Thank you for joining us for Healthy China 2030 Oncology Innovation Summit, R&D Day, Innovent Biologics. Today, we feel very pleased to share the great stage together with the experts, the scholars, as well as the partner organizations, so that we can do some thought taking for, like, oncology innovative drugs, so R&D, from the right, the one right in the way to the one leading the change. I am the moderator on behalf of the organizer for this conference. I would like to say my heartfelt welcome to everyone. Thank you very much for joining us for the summit. Thank you. Healthy China 2030 is not only the honorable mission entrusted to us by the time, but also it is going to require some collaboration so that we can chart a course forward.
Let's use scientific-based evidence as the driver to make sure that we engage on this maiden voyage above life. Okay, without further ado, let's bring to the stage our VIP guests so that we can jointly have this exciting moment to everyone. Without further ado, let's welcome Professor Huo Jianqing, Professor Shen Ling, Professor Zhu Zhenggang, Professor Zhou Caicun, Gao Shougang, Xing Ligang, Cao Guochun, Zhou Qi, Liu Zihong, Xiong Jianping, Xu Nong, Matthew Yong, Zhou Jianya, Dr. Hong Zhang, Dr. Shi Yao, Dr. Michael Yu, Xi Hao, Zhang Qian, Dr. Zhou Hui, Youfei, Rachel Yu, and Dr. Kaijie He Dr. Kaijie He , please come to the stage so that we can launch this exploration voyage. Thank you.
You'll see the guests for honoring our launch ceremony with your presence. Let's together have the inauguration ceremony and launch this voyage for scientifically based R&D research and innovation. Everyone is super modest, so please come to the stage so that we can have a countdown to launch the voyage together. [Foreign language] Today we are pleased to be joined by the heavyweight group players so that we can become the eyewitness to this joint voyage of life. Let's come to the anchor point of innovative drugs for treating oncology, to make sure that for the hugely unmet clinical needs, that's human innovation, that's the engine to make sure that we believe the truth for therapeutic areas. Let's use the collaboration to set the sail for our R&D global voyage.
Ladies and gentlemen, please put your hand on the push bar so that together we can push the bar to launch our voyage. The audience on site, let's have a countdown of five numbers: 5, 4, 3, 2, 1, launch. Push the bar. Thank you [Foreign language]. Congratulations. Congratulations on the successful setting of the sail of the life voyage. Super duper for men. Please take a photo to record in our current memory this exciting moment. Thank you very much for making sure that we inaugurated the life journey so that you use the innovative spirit to lead on the voyage into the blue ocean. The VIP guests, please stay on the stage for a while so that we are going to capture you in the same family group photo.
So please come here so that we are going to take another photo of you because there is a rare chance that we can put together so many best minds in your industry. Ladies and gentlemen, please stay on the stage for a while and come to the front so that we can capture you in the big family photo. Okay, audience on site, would you like to give a round of applause to congratulate on the successful inauguration of the voyage and journey for life?
Thank you very much for joining us [Foreign language]. Camera ready? So please smile. We are going to have innovation beyond borders. Thank you so much for joining us for Healthy China 2030 Oncology Innovation Summit and R&D Day for Innovent Biologics. Let's give a thumb up for the inauguration ceremony for today's conference. Thank you so much, everyone. Please take your seats.
As you make your way back to your seats, we are going to say thank you to everyone. As always, cancer and oncology is a major threat for health and life for people, no matter if you're poor or wealthy, no matter of your background. Everyone should enjoy, actually, the results of technology improvement and innovation. For this life-threatening threat, we are going to put together all your wisdom as well. Professor Fan, due to other engagement, cannot make it here. That's why Professor Fan did a video to share with us about the cutting-edge forefront of the innovative drugs R&D for oncology. Let's look at the screen.
[Foreign language]
Thank you very much, Administrative Fan, for your kind words and sharing. Let's try to collaborate together with our dream so that together for the oncology treatment diagnosis, I can give you that wisdom. Okay, without further ado, let me introduce you to someone who is at the forefront for innovative biological drugs for the fighting against the cancer. We have with us the Founder and the Chairman of the Board and Chief Executive Officer of Innovent Biologics, Dr. Michael Yu. For information, he is not only at the forefront of domestic R&D for oncology drugs to, like, blaze the trail for China for the rest of the world, but also is also the practitioner for developing world-class Innovative Biologics company. Dr. Michael is going to decipher the topic for building a global premier biopharma company. Welcome, Dr. Michael Yu.
Morning, everyone. First of all, a big welcome to you all. Thank you to the chair. Thank you to experts and investor friends. My thanks also go to the shareholder and the shareholder to be of Innovent Biologics. Thank you very much for joining us for Healthy China 2030 Oncology Innovation Summit. As is known to all, everyone is on a super busy schedule, especially we really appreciate you sparing some time out of your quality time with your family members to join us for the summit. I'm very pleased to host you. Thank you so much for joining us. This is a rare chance. I can do the stock taking of what happened over the past decade. Think about the biomedicine industry. What about for China's landscape? What we have been through? I am going to take some time to have some outlook for the next decade.
What about the anticipated new development on the horizon as well? Of which for the landscape, Innovent Biologics is a very simple, we do not claim to be the best casing point, but we are a casing point. About one decade ago, 10 years ago, since our establishment in 2011.
Way back then, I believe that was the era for generics in China. A case in point. Back then in China, there was almost no biologics. Taking monoclonal antibody as an example. We had seven products in total, out of which six were imported. We had the CD3, kind of a murine antibody, which was domestically produced. I believe a lot of experts know about this. For mAb, in mAb drugs in China, as I mentioned, the drug accessibility was very poor. Not only were patients not able to access the drugs, but they were not able to afford the drugs as well, because the drugs were like 30%-40% more expensive than those available in the United States. After a decade of growth, there has been an ocean of changes that have taken place. These days, we have almost 90 monoclonal antibodies.
More importantly, price-wise, the prices are only a fraction of those of the United States. Right now, basically speaking, it's fair to say those accessibility and affordability problems have been gone. What changes have taken place in the past decade? I think there are four reasons. For example, the change of regulatory science. When I returned to China, the first product we filed R&D, then upon approval, it took us like two years and six months for approval. Now, for R&D filing, it only takes one month for you to gain approval. Second, the biggest change is access, especially with regards to innovative drugs that are not covered in national reimbursement. Although there were higher pricing possibilities for access and a reimbursement payment, now has managed to change some of the difficulties in payment, as well as hospital listings.
Because of these changes, capital markets, especially Hong Kong, 18A opening. Now the capital markets, we have closed the loop on capital. A lot of talents come back to China as a result. The best decade is the golden decade for biologics industry in China. When it comes to Innovent, we are fortunate because we were founded during a golden window, and we have been growing throughout that period. We were founded back in 2011. As of now, we've launched 16 products. We have over 20 products which are in the middle of R&D. Over the past decade or so, we invested over RMB 8 billion, and we established production capacity that goes in tandem with these products. We've got 140,000 liters production capacity, or 20% of China's total capacity.
In recent years, and we are open-minded, we have been interacting with those good players from across the globe based on the principles of a win-win. Companies such as Roche, Eli Lilly, and Sanofi. We have a lot of partnerships with this multinational pharma. At present, our headcount, or we have over 2,000 employees who are dedicated to R&D. You look at this investment and output we are driving. All these are based off of the wonderful, you know, business environment in China, a very favorable environment for biologics in particular. We launched 16 drugs within 14 years. As you may have watched the information in the video, in the past five or six years of our sales activities ongoing, there has been over 5 million Chinese people. Because of our new drugs, these people have been treated effectively.
We are an example as a result. In monoclonal antibody drug and a world company with most mAbs, as we move along with our efforts, and we stay true to our mission, namely to develop high-quality and affordable biologics for the general public. In oncology, if you look at IQVIA numbers last year, China's oncology drugs in terms of sales growth, the top 10 products, out of which three come from Innovent, on many segments, including PD-1, VEGF, and CD20, these segments where we are a leader. In terms of PD-1 oncology, active mission Fan Jia also delivered the message in a video, and we have actually done a lot of creative efforts, our pioneering actions because of your contributions. First, in 2019, we were the first to enter in our NRDL list, of which the selling price is only 1/30th that of the United States.
For all patients who have the needs, almost all of them have the opportunity to access Sintilimab, right? As a result, these days, Sintilimab is the PD-1 with the biggest market share in terms of patient count. Because of the gradual approval for our products, we have made substantial headways in our business. In 2024, our total revenue exceeded RMB 9.4 billion. The taxes we paid exceeded RMB 1.3 billion, almost RMB 1.4 billion taxes, although we had yet to turn a profit. In many areas, as we know, there are good targets available. Innovent has been fortunate because over the past decade or so, we actually, you know, for example, got two phenomenal targets, namely PD-1 and a GLP-1. As for PD-1, we've got Tyvyt or Sinti limab, and GLP-1, and we got approval not long ago. We got Mazdutide.
These targets and our solutions around these targets benefit a lot of the general public and the patients. More importantly, we've managed to advance the R&D level in China. At Lancet, JAMA, as well as NEJM, the main journals where we've published a whole host of publications. This is due to your contributions, dear experts. Because of these products, we're confident that back in 2022, we put forward our operational objectives, saying that by 2027, and we're hopeful that our product revenue is projected to achieve RMB 20 billion. Upon gradual approval of these products, we are more confident now about these targets. Innovent is only one example in this country. Over the past decade or so, golden window in China, we have quite a few innovative companies taking Suzhou as an example.
In Suzhou City, in the downtown area, there have been over 2,000 biologic firms. A lot of capital flocked to this place and is making investment. We also have private sector capital which is coming in as a result. There is a boom and a prosperity in innovative drug undertakings in this country. At the beginning of this year, Wall Street Journal wrote that there has been a deep sea moment for Chinese biotech. CNBC also tallied some numbers, talking about, for example, the BD size. For those large-sized deals, around 42% of those large BD deals are involved with China. At the beginning of this year, our partnership with Roche, for example. In a recent ASCO meeting, I'm sure you've got your perception, be it oral presentation or the number of presentations from Chinese experts. Yes, indeed, we have a very important stature.
We have over 20% of those oral presentations are about China. The total number of clinical trials and MRCT quantity overtake the United States already. This is like the golden era for innovative drugs in China. If you look at multinational pharma, all multinational pharma as their CEO must pay a visit to China, because of the new drugs and the medicines you're developing. Now China has become an innovation engine, as a matter of fact. Therefore, when it comes to our planning for the next decade, I think we're on very solid ground. We have put forward our new R&D objectives by 2030, based on oncology and non-oncology product lines. By 2030, we're hopeful that we're going to have like five assets in MRCT phase three. Maybe, you know, 10 or 20, right?
As of yesterday, we got two products for which we started the regulatory registration trial. We are more and more confident to deliver on these objectives. These products are based off of new generation technologies, for example, the new generation IO and the next generation ADC. During ASCO this time, one company, namely Innovent, delivered eight oral presentations, or 2% of the ASCO total, among which three are about IBI 363. For 363, it is a PD-1 IL-2 fusion protein. The engineering of this very molecule is based on our lab and our basic research. In our basic research, we found, for example, in the microenvironment of the T cell of the tumor, the highly expressed PD-1 and also CD25 available. In the peripheral bystander T cell, there was no expression of T cells or CD25, while CD25 is one of the targets for IL-2 receptors.
IL-2 has three receptors, alpha, beta, gamma, and CD25 is the target of alpha receptor. Based on the findings of this basic research, the paper was published at Nature Cancer. We designed IBI 363, the interleukin-2 R-alpha bias agonist, which enhances anti-tumor immunity by invigorating tumor-infiltrating CD25, CD8 T cells. IL-2 promotes T cell proliferation. This is quite established, right? Everybody's using it because in 1994, upon approval of IL-2, then, however, not a lot of people are using IL-2, though. Why? Because people couldn't control its toxicity. Now, thanks to our novel design, we have disrupted people's stereotypical thinking about IL-2. We're able to bring to full play its strengths. We're going to have three talks later on to focus on oncology.
Actually, for many diseases for which we have no therapies, or for those patients who are failing IO therapy, yes, indeed, we have very good potential to treat these patients really well. We believe IL IBI 363, this may be the next-gen PD-1 in IO therapy for cancer. We also focus on honing and improving our ADC tech. Right now, we've got three platforms. Based on our internal Topo1 inhibitor platform, as we control the toxicity, at the same time, we're able to deliver therapeutic effects on treating cancer. For example, IBI 354, for which we have ushered into the registration trial. Due to the good characteristics of this asset, we have built the dual payload. For dual payloads, the first molecule is IBI 3020, and we entered clinical trial phase. Our partnership with Roche is based on this payload.
These are new tech and new molecules. We believe together, yeah, especially with many of our experts, it is possible that we stand a chance to reshape and redefine cancer treatment. Because of this progress, and we work hand in hand with a lot of innovation pharma, we have drawn up our blueprint for the next steps. From 2011- 2021, that was the first decade. At the strategic conference of Innovent in 2021, we proposed the second 10-year goal. By 2025, we were hopeful that we would achieve break even. Last year, we achieved this goal already. Although we were not profitable last year, we stopped loss-making. We were break even last year. By 2027, we hope our product sales revenue can go up to RMB 20 billion. What about it?
Because in China's industry, excluding unknown players, maybe one of the top five in terms of sales revenue by 2027. By 2030, we aim to become the world-class biopharma. All Chinese biopharma claim they are world-class. There are criteria we've got to meet. One of the criteria is five pipeline assets in global MRCT phase three, and two products shall be marketed in the United States. Size-wise, these products must be blockbusters.
How do we define a blockbuster? The peak value should be no smaller than the revenue of sales of about $2 billion. That's the first indicator for being a blockbuster and a world-class. The second one is about internal KPI for overseas sales should be no less than a certain threshold of proportion.
Third indicator, because of the different promotion and progress, the market value and market capitalization for a company as a result of that should increase and move upward as well. We talked about actually on like 37 or 38 by the year 2030. We really hope that we are going to increase into the ranking of our market valuation, et cetera. If we can achieve all three different indicators, which means that we can claim ourselves to the world-class biopharma company for Innovent Biologics, I have the full confidence by working together with everyone here, especially given all the expertise level by all the best brains in our expert teams in the audiences. I guess together we can co-cultivate a lot of world-leading, like China-originated biopharma innovator companies originated from China, but also carrying world weight.
I would like to quote one punchline from a poet. We have to keep swimming until we can see the blue water coming from the other end of the ocean. There is an author who is a world-famous scholar in China called Yu Hua, who was a native in Hangzhou. After Yu Hua was brought up, he relocated to Haiyan. Dr. Zhou Hui is originated from Haiyan. Haiyan is a seaside town and city from Zhejiang Province. Think about keep swimming until you see the blue like ocean water coming from the other end of the ocean. At the same time, whenever I see the bluish water, it means that I also see the light coming from the other end of the tunnel. When Yu Hua, the author, in the late 1980s, wrote like essay.
There is this one night, and Yu Hua spent about 13 hours trying to keep swimming, swimming all the way to the Hangzhou Bay. After swimming for a dozen hours, and Yu Hua actually is finally getting to see the blue ocean water coming from the other end, which means that this is a metaphorical way. This famous author, a lot of very excellently authored essay, because I'm quoting Yu Hua, is because this is exactly renewable for us. Think about the anti-oncology and biologics drug innovation universe for China can be better and better because we have the honorable past of which we jointly work together to achieve a lot of breakthroughs, but it's still a lot of oncology, it's a many clinical areas as well. You'll find that now the position for biologics here in China.
We wouldn't claim ourselves to be world-class or number one from China, right? China is not world number one yet. Let's swim together. Let's keep swimming and never give up until we see the best purified like blue ocean water coming from that. This is a metaphorical way to describe that better innovative drugs and better innovative companies are going to come on the world stage.
Thank you so much, Dr. Michael Yu, for your very excellent sharing, especially given that Dr. Michael Yu shared with us like a punchline, which means that you're a passionate person with a lot of aspirations. You not only think of yourself and Innovent Biologics, but also you have a mission.
You really want to develop biologics affordable to everyone to develop the world-class biological innovative companies to make sure the effective anti-cancer treatment approach is made available to all the patients in the world. This is a dream come true, and we are into the golden stage for China's innovative drugs. Okay, let's give a round of applause to say thank you to all the scientists, for all the researchers, and all the entrepreneurs like Dr. Michael Yu. Thank you for bringing China's innovative drugs into the golden age. Thank you so much. Now let's go to the keynote presentation session. Hereby, I'm very pleased to bring to the stage our moderator for the keynote session. Let's give a round of applause. The Beijing Cancer Hospital, so Professor Guo Jufang is going to chair the keynote session. Welcome. I've got to note that Professor Guo is a very passionate and a very knowledgeable person, so we'll be in good hands. Thank you.
Thank you so much, everyone. Now it's my turn to have an academic session. Without further ado, let's bring to the stage a heavyweight player in our oncology world. We have Professor Zhou Caicun with us. Professor Zhou Caicun, for your information, actually, we have a lot of very good relationships with each other. First of all, we are long-term friends with each other, and I personally admire you and respect you as an academician as well. Professor Zhou actually has a lot of productive results throughout the career of yours. You are a good person. You are a very good practitioner at the forefront of the medical world. Needless to introduce.
If you work in the oncology world in China, if you do not understand who Professor Zhou Caicun is, then you are not the real person or insider. Let's welcome Professor Zhou Caicun.
Thank you, actually, Chairman Guo and the Secretary General and Professor Guo. I give you multiple hats because you are wearing multiple hats. You have a lot of capacities. Thank you very much, Moderator Guo. We have learned like IO therapy from you. You are the pioneer. You are the forefront. Think our perspective. I believe that. We are thinking about we are at the inflection point right now. It is totally reliant on our efforts. Thank you so much, Dr. Michael Yu, for passionately and confidently presenting what has been through by the development history of Innovent Biologics.
I really have the full conviction that it wouldn't take you long before Innovent Biologics really becomes world-class. To make it a top rank amongst the global innovative biologics industry. Why do I have such a confidence? Because you have a great pipeline. You have solid science. More importantly, you have a great vision that I see from Dr. Michael Yu. Without vision, we cannot travel further. You have a very decent team building around your vision. Hereby, I'm going to let you understand the topic, which is like IO and the lung cancer treatment in the post-PD-1 treatment era. Do we see any hope for the lung cancer treatment? Of course, we see the like, for example, you find that the melanoma also see the light coming from the other end of the tunnel.
But think about the lung cancer. It is going to be more tricky than melanoma, right? Even melanoma can do it. Like lung cancer has some hope. We have made a lot of improvements for treatment of lung cancer. It is great to be someone treating lung cancer because you have chemotherapy, you have RT, you have surgical operation, you have it all. Now you have IO as well. At the same time, it is going to be very soon that you are going to have ADC. Professor Shen is here. We have bispecific antibody. We have a triple antibody. Let you understand that the progress of the treatment for lung cancer is making a lot of inroads as well. Think about the IO immunotherapy by far across all the optional ways. I think this is still the key.
We have been talking about IO for so many years. It's about like the doctor is going to prescribe the drugs for the patients and trying to have the injection for you. You find that to have a very good mental balance. If good mental balance can treat everything, then cancer is not called cancer. Cancer is very sneaky. It is very smart. Think about PD-L1 expression is the key. Think about actually the T cell killing the cancer cell actually is going to express the PD-1. Once the PD-1 and PD-L1 is being combined, as a result of that, there is a loss of the function for the T cell. Think about PD-1 and PD-L1.
It turns out that in the modern IO therapeutic approach, this is the key for the combination of PD-1 and PD-L1. Think about the PD-1, PD-L1 expression. There are two different ones, the structural expression. Think about like a driver gene induced expression. The other is about like an immunogenicity. Think about like for interferon gamma, actually, is going to actually result in or have a high relationship for the immuno escape. This pathway is very important. That is why we designed the antibody to make sure PD-1 and PD-L1, so the pathway could be blocked, the blockade for the pathway as a result of that, so that T cell can be actually the anti-tumor activity of the T cell can be coming back.
Think about the monotherapy for the PD-1, PD-L1, or like for example, the dual drug has already become the SOC for lung cancer. PD-L1, if you do not know about that, you are not expert in that. We have so many different products as well. We have IO products. At the same time, the big beauty about IO approach is to make sure that we can let some patients survive longer. In the chemotherapy, we would not talk about long OS. You will find that if the OS could be two months or three months, that would eat up. That is already a great deal, but that is about the chemotherapy. The target actually, you will find the PFS improvement and the OS is not being arrived at yet. Think about for the IO, I believe that if you have a five-year OS, that is good.
Think about for a lot of clinical trials, you'll find a five-year OS is about 18%. You'll find that the highest could be 32% or even higher. What does that mean? Which means that one-fifth of the patients or one-third of the patients could survive longer than five years. Think about lung cancer, which is unimaginably now doable right now. Think about the IO. When it's applied for lung cancer, it's very effective. Also think about the melanoma. You'll find that actually, there are so many different types of tumors. Melanoma is one where we can see the IO work wonders. A lot of tumors still doesn't work for like the IO. You think about lung cancer, its efficacy rate is 20% using IO.
Which means 80% of the lung cancer patients did not achieve the PR, only SD or PD, et cetera. Think about the PD-1. Still, it suggests that there is a lot of upside room for improvement for efficacy. As a result of that, you will find that there is a glass ceiling for its efficacy as well. You will find that actually the ceiling effect. In the chemotherapy era, we talk about ceiling effect. Now for IO, there is another ceiling effect, et cetera. The thing is that how can we break the glass ceiling for the efficacy of IO? What are we hoping for? We are hoping to make sure that the immune escape mechanism could be better understood by us. It is because think about it, it is different from the targeted points.
Because think about the escape starting from the antigen and all the way to the T cell. You find any problem in the process of this. You'll find that we can only establish the pathway for anti-tumor activity. When T cell is going to give up and then the tumor cell is going to proliferate. That's what we already know. Think about that to say that for IO therapy, there are different therapeutic approaches. Think about the PD-1. We hope that we are looking for the new products. We're looking for some of the new combo approach, et cetera. Like ADC, when worked together with the IO, et cetera, we hope that we can have a synergistic efficacy. Think about the ADC, it actually can induce the immunogenic cell death and also the exposed antigen cell of the tumor.
It can induce anti-tumor immune memory, et cetera. ADC at the same time can induce the maturization of the T cell. Also, you'll find that when those cells are becoming mature, then they can have the anti-tumor activity. Think about when we let IO combine together with ADC. That's the next most important actually R&D direction for us. You may probably say that, okay, I didn't see any hope for ADC. Why is that the case? It's because we have done so many clinical trials. The second line treatment, no matter, is actually you'll find that actually for the, for example, compared with docetaxel, you'll find that actually still there is no statistically significant difference. You'll find that is it going to be better than chemo or something?
I can assure you that for the ADC monotherapy in the second line, where there is no difference before and after, I think it's because the first line, you are using the chemo plus IO. Think about the IO plus chemo. You'll find that carry-on is efficacy in the second line. You'll find that actually it dropped to ADC. You'll find dose CPExo, actually, for example, efficacy is already having the carry-over efficacy factor from the first line. Dose CPExo, actually, PFS no longer than three months in the past, but now you can have four months of PFS, dose CPExo. In the past, OS never go beyond 10 months, but now we can go beyond the threshold over the 10 months.
Which means that the ADC, actually why it is actually on is being applied in the late lines, but if you apply it in the early lines and first line, you have a chance. That is to say that when we talk about actually, the ADC, one month or two months or three months or et cetera. The antibody and also its mAb and also have the payload, the toxin, et cetera, linker as well. The three all in place to kill the tumor cells. Think about the ADC, the conjugate compared with the mAb, monoclonal antibody, is more complex because any misstep in a single process and the ADC expected efficacy will not be arrived at. You'll find that like a toxic AE is going to increase.
You'll find that actually the toxic linker and also, for example, actually all three being put together has already composed the very important three attributes of ADC. What about the ADC applied for first line treatment? We find that a TROP2 ADC plus PD-1. Think about the clinical trial combining all those. TROP2 ADC plus the PD-1. You'll find that actually TROP2 ADC plus plasma-based, no matter the cisplatin or carboplatin. There is like a triple therapy being combined as such. You'll find that the bi-act PFS is longer. At the same time, PFS is about 11 months. About the three drugs, it's about 6.8 months for PFS. It's not head-to-head comparison, but you'll find that it's not head-to-head.
But as a result of that, at least the data suggests that ADC plus the IO and also the bi-act therapy is better than the three therapy. Of course, you'll think about it because of one less because the safety profile is better. Think about lung cancer as a major change for that. In the past, we are so platinum-based chemotherapy, but in the future, we are going to talk about ADC plus the IO. That's going to be the new treatment. Platinum-based actually is going to be staying further away from us, et cetera. We have seen clinical trials like this one. It's called Long 07. You find that TROP2 plus ADC plus PD-1, et cetera, NSCLC first line treatment for the phase three pivotal research ongoing.
In China, there is ADC plus K versus K plus chemotherapy. We believe this data are going to come out momentarily. You can look at these criteria, the ADC plus PD-1, and what about it? I'd like to say the data are going to be even better because PCR could go up to 35.2%, NPR can go up to 63%. Therefore, the chemo era, during chemo era, we did a lot of clinical trials. The PCR was about 20%, NPR of about 50%. However, now ADC plus IO, look at it. We've obtained better PCR, and we've obtained better NPR as well, meaning the curing of cancer is possible. This is huge progress. Post-PD-1 chemo era, we look forward to ADC plus IO, yes, some of those newer therapeutic strategies. What else? We look forward to more bispecific antibodies. Chinese, we are very experienced.
If I cannot beat you alone, then we can fight you as a team. If we add some targets, I believe we stand a bigger chance to pull it off because one single target is very difficult to cure cancer because there is huge heterogeneity of cancer. There is temporal spatial heterogeneity of cancer. With one single target, it is impossible to eradicate and annihilate tumor. The most simple form of therapeutic strategy is to add targets. Hence, we have bispecific antibodies, PD-1, TIGIT, PD-1, VEGF, PD-1, CTLA-4, and also T-cell engager, et cetera, et cetera. PD-1 interleukin 2, which is Innovent product. Dr. De-Chao Yu is very confident when he talked about this product. This one is AstraZeneca's product, PD-1 TIGIT. The efficacy is good, especially for those patients who express high level of PD-1. For these patients, there is even better efficacy.
They are making an advancement and started phase three trial for this product. You need to be careful because the message we got from Roche is TIGIT is quite a hard nut to crack. The second pathway, which is performing very well as well, namely PD-1 VEGF, domestic products are licensed out and are earning tons of money. In terms of clinical trial is concerned, the Harmony 2 has made great contributions. For example, $9 billion or $5 billion, those revenues come from Harmony 2. Based on this trial, what messages have we seen? Yeah, we've seen very good data because for clinical efficacy, we need to look at endpoints like PFS, not only median PFS, but also the shaping or form of a PFS because in many clinical trials, the PFS looks like a banana shape.
Which target and which drug has yet to play a positive role? Different targets may play very different roles without synergistic effect. You look at this trial, the two curves started separating from the get-go. Over time, they become larger and larger. They indicate there is synergistic effect achieved of these different targets. As a result, more patients will benefit from treatment. We also have a lot of products for PD-1 CTLA-4 in China, for example. Professor Shen is an example of the first PD-1 CTLA-4. The trial around lung cancer is spearheaded by Dr. Shen with very positive outcome. We see good objective response rate. The safety of bispecific antibody is way better than that of two monoclonal antibodies combined. More and more phase III trials are still ongoing. T-cell engager, for example, CLDN CD3.
Globally, this has been launched. For products like this, DLL3 T-cell engager, it's difficult to pull off the research, but once you succeed, it's going to give great help. There is a second line treatment of small cell lung cancer with this agent. The remission is very good, as high as 30%. PFS is as long as seven months or eight months. What matters more is it helps extend survival of patients. The two curves are completely separated. DLL3, you look at tarlatamab. Innovent also has the DLL3 ADC compound. For patients, we definitely look forward to the compound from Innovent, which may yield even better efficacy. IL-2, I'm sure many of you have experience in IL-2. Twenty years ago, people started to use LAK cell, which was IL-2 to treat lung cancer. Very expensive. RMB 10,000 for 10,000 units.
With that money, you could purchase several square meters of home in Shanghai, but the patients had to pay big money, RMB 10,000 for treatment. The efficacy was not very good. IL-2 is indeed a target that is worthy of our attention. In terms of dose, there is big cardiac toxicity, so people could not tolerate it. From Innovent, there is PD-1 IL-2B, the alpha bias of the bispecific antibody. There is unique molecular structure. You can look at the molecular structure. We're going to skip the details, but it yields better efficacy. There is a distinct improvement to the PFS rate. Professor Zhou delivered a presentation during ASCO this year. The wild-type adenocarcinoma patients, there is even wider separation OSIs. For a product like this, we have seen better opportunities as far as response rate is concerned.
For the standard dose of 3 mg , for a squamous cell, 37%. The EGFR wild-type, it is 24% LOR. PFS are 9.3 months and 5.6 months, respectively. For 9.3, this is about the same level as chemo IO. We need to advance this product quickly. It will become like a new standard of care in the future. PD-1 IOT, for a squamous cell, it works very well. PD-1 negative and a PD-1 positive patient, no matter what, yet this works on both cohorts. For PD-1 negative patients, the results are even better. Unluckily, right now, there is no good product yet to treat those patients with PD-1 negative patients. In the previous trials for such patients, there was no product that indicated marked improvement to the OS. With this product, we're hopeful and we are paying attention to it.
Summary, we have like chemo IO or IO monotherapy to treat lung cancer. We have seen very good kind of efficacy. These kinds of treatment regimen is the cornerstone of a treatment now. The efficacy is preceding. Five-year OS ranges between 18-20%. How can we go above and beyond? We call for newer drugs. We call for newer combo strategy. For example, ADC plus IO. This may be a new direction to go. We are more hopeful about products like bispecific antibody. This is where Innovent's PD-1 IL-2 come in. This may be a very good candidate. Please make sure that you launch this product to market and to benefit patients not only from China but from the rest of the world. Thank you very much. Yes, thank you, Professor Zhou, for a fantastic presentation.
Although I'm no expert on lung cancer, but upon hearing his presentation, I agreed to his arguments because Professor Zhou put forward several concepts which I deem as very important. First, the ADC plus IO, not only in the treatment of lung cancer, for urothelial endothelium carcinoma. This is already achieved. For example, 061 and also 342. These are for urothelial endothelium carcinoma. ADC plus CD1, PD-1, not only extend, for example, PFS by a factor of one, but also double the OS. What does that mean? This is unprecedented, as a matter of fact. That means those previous standard first-line treatment is actually beaten. The ADC plus PD-1, this is the recommended first-line treatment based on the strong evidence. I agree to Professor Zhou. This is like the future trend. Second, the combo with IO or novel IO therapy.
Melanoma is one of the leading tumor types that we look at. For Professor Zhou, the earliest IO approval, a lot of those earlier approvals were about melanoma. No matter the first approval of PD-1 or CD3 or LAG-3, all these were around melanoma. As of now, as we can see, I can agree with Dr. Hugh's point more. 363, there is the possibility that it might develop into the future standard PD-1 because we try to combine it with CTLA-4 and combine it with LAG-3 and a lot more, like we mentioned. In the old days, we were imagining those IO combo with regards to melanoma, basically. We have got a picture about how to combine different agents, including LAG-3 or LAG-3, CTLA-4, PD-1. This triplet, right? We are shaping our understanding. Some of those combo regimens may not work.
I believe when it comes to 363, as a matter of fact, was it meticulously designed or does that come by out of chance? I think it's like a godsend. It's a wonderful gift. From my perspective, IBI 363, I firmly believe it stands a big chance to make a difference and become the future standard PD-1. Now, on top of that, we can have more combo regimens we can figure out. Hence, there are going to be new hopes for the future oncology treatment. With that, we're going to invite the next heavy-hitter speaker. Like a very mysterious and magical lady, we call the Professor Lady Shen or Aunt Shen. We respect Dr. Shane a lot. I think this is like a magic Shane. Actually, Magic Shane is my years-long friend and a comrade for the past two or three decades.
I cracked a lot of jokes with Dr. Shen, but I really respect her tremendously, not only because of her academic achievement, but also because of her great spirit. GI tract cancer, this is quite challenging. In terms of IO, if you look at melanoma, and they told me that you made a lot of successful achievements in melanoma, but she suffered a lot of failures in GI tract carcinoma. She never gave up, and she hung on in there. As of this year, the biggest highlight with regards to China voice is Magic Shen's voice. In China, the first to report the solid tumor kind of treatment with great accomplishment. This is due to her perseverance throughout the years. Now, let's invite Professor Shen Lin to deliver her presentation.
Thank you for your kind words. I feel very encouraged, and my heart is moved with a lot of emotion and passion. We are old colleagues. We used to work with the same organization. You never let me know that you appreciate me really for my great contribution. You never say such high words for me. I really appreciate the nickname. You call me Grandma Shen, which means that I'm a veteran in this one. It is not easy to crack the nut for the GI tract tumor, but I'm still keeping up. Melanoma is developing very fast now, especially when we develop some small molecular drugs. As long as there actually is a treatment area like lung cancer, if it works to some extent, with certain advocacy, we're going to stop the efforts for the GI tract tumor and then put all the bets on the lung cancer.
Once there are some hopes, we are going to shift back the efforts on the GI. I really respect Professor Guo Jun and Professor Zhou Caicun, but I respect you with all. Sometimes I'm fearful for both of you. Whenever I see you, that means that resource is going to be there for yours as well. Let me share the status quo for the drug development innovation for GI tumor. Luckily, because of the consistent and persistent efforts, we are trying to already keep it up. In the past, we admire others, but now all the admiration is for China innovation. The China researchers and China clinicians have more available drugs, more intervention methods to treat our patients. In the past, we were begging others to join the global multi-center ongoing clinical trials.
Now, so actually, people are begging us to join us for our ongoing clinical research. This sea change is a result of the fast innovation efforts of development of innovative drug makers here in China. I'm going to talk about cancer treatment in China and ADC development in GI tumor. I'm going to talk about this issue from the following different ways . I still remember that at this year's beginning, JP Morgan Summit, it has been mentioned that. Think about for the innovative drugs in different China in terms of the total deals, China accounted for more than 30%. Now half a year has already passed, and China is already accounting for 40%, 40%. Next year, JPM organ Summit is going to be 50%, I guess.
Clinical trials in China for the first time in history is on a par with that of the U.S. I think I'm not using the word overtake that of the U.S., but at least that I understand that China companies initiate clinical trials is increasing a lot on the same par with the U.S. We're going to overtake the U.S. in the future. We have a bigger patient population, we have a different pathogenesis profile for the Chinese patients. I remember that in 2022, when I was giving a lecture about R&D here in China, first-in-class was less than 1% back then. If you take up all the numbers, it's five, first-in-class. Now, first-in-class in China is a growing balance in China. That's a sea change.
The sea change is indicative of the fact that, so think about Healthy China 2030, indeed, that we are really innovative. We are putting some serious efforts to the innovation. It's not like a follower as well. Instead, we are going to meet the medical needs, whatever clinical needs we have. We're going to target our research on meeting those needs. In 2024, 48, for example, first-in-class new drugs have been first-in-class launched here in China. Which means that you can claim safely that China is the most proactive place here in China. For the forty-eight class one novel drugs, you'll find that actually, you'll find that a lot of European companies are trying to go for a shopping spree here in China. U.S. going for a shopping spree here in China.
It only happens in a recent two to three years, etc. You find that you understand this a lot. Think about the fastest growing one is anti-tumor, anti-oncology drugs. Not only growing fast, the quality is high, and the volume is growing. For innovative drugs, you find that oncology is hugely a med area. That is a lot of patient need for that compared with other different disease and therapeutic areas. They are admiring us right now instead of us admiring them. Think about immunotherapy. It has been very fast. I am happy to see the great efforts and the expanding presence and efforts of innovation for innovative biologics. From a clinician perspective, we are happy to see that happen. This is something we are aspiring to.
All the MNCs over the past two years, generally speaking, if you look at the number one guy and the number two guy, so CMO and CSO, they all come to China not only to talk with the biotech company here in China. With Dr. Michael Yu, not only to communicate with them only, and they are traveling to the frontline clinical trial. To look at a medical need for China, they never bothered checking that out 10 years ago. Let me give you one example. Ten years ago, Roche brought a team. You are early champions. You brought the delegation of 20 different people. Dr. Zhou Hui worked for Roche back then. Whatever you say, they did not care. There is no way for you to communicate ideas with them because they think the China market and the R&D level for China is too low.
It's way out of their league. So Professor Zhou Jianya and me, together with the other two professors, were really angry, honestly. We were so pissed off. There's no way to communicate with those foreign companies. It's not because we were so bad or so lagging behind because of the R&D level for China, status quo for China back then, and level of research is a look-down pound by foreign companies. Things have already experienced a sea change just after 10- 15 years. That makes a huge difference. You'll find that now in the international arena, we can stand up upright. We can feel very proud right now. In the area of anti-tumor and anti-oncology, I guess there are a few areas of why China is ahead of the curve globally. ADC, second one is bispecific antibody and trispecific antibody, but most importantly, the bispecific antibody.
Innovent has it all. At the same time, cell therapy, etc. All three are the fastest growing areas in the world. China is already among the top ranks in the world. This is something we should feel super proud of. Transaction volume, the deal size is very big. You can refer to the numbers. I think it's not just about deal size or the volume. For the multinational companies, MNC, they have been deep diving in the industry for so many more years than China. They can see the future trend, and they are mindful of the great need and medical clinical need globally for the China innovative drugs, etc. That is why it's being reflected that way once. More importantly, we have China data made available to them in the past. Global trial without China data.
But now, if they are going to claim themselves to be global, but they don't include the China data, they are not truly global because China patients account for half of the global patient pool. If you don't cover the Chinese patients, you cannot claim yourself a global one. In the past, we called the China research local or domestic. We are not calling a China research a regional clinical trial. Now, in China, at least it represents the Asian. Especially for esophageal cancer and gastric cancer, etc. These are the biggest change before and after. Such a sea change is happening over a very short span of time. Of course, in my area, like GI tract cancer, safe to say that the mAb and the bispecific antibody ADC.
MAB represents the monoclonal antibody, not only just ADC, but also you have a specific targeted payload, etc., dual payload. At the same time, there are other different drugs being added to the combo. Fast-growing small molecular and the small peptide, for example, etc. A lot of fast development here in China in the market. That is to say, for the R&D efforts for China's anti-tumor drugs, we can claim that China is no longer lagging behind. We are amongst the top. We are making a lot of amazing progress as well. Another thing is that anti-tumor drug in China finally is going to attract the world's attention so that all the eyes of the world are on the clinical development for China. This is something we should feel happy about.
Next, I'm going to talk about the progress for ADC in GI cancer. Think about the ADC progress. There are so many happy news to share with you, a lot of progress. Think about the development. You find non-small cell lung cancer. Dr. Zhou is not around here, right? That's why I feel safe to talk about it. It seems he's not around here. Lung cancer, you'll find that actually for the GI tract, actually on, for example, being put together, it's like this volume of this one. Uneven distribution of the research efforts because of global disease. GI tract cancer, hepatic cancer, esophageal cancer is a high incidence disease here in Asia.
So hereby, I guess, because of the efforts of innovative drug makers in China, as a result of that, the world attention is on the unmet patient need for the GI tract cancer patients. This is a very important sea change before and after. In this area, we find that for the ADC actually is originated from the gastric cancer. Safe to say this is a sea change for us. Because think about actually, for example, for the breast cancer after being successful. You find that, but it failed for the GI tract after more than 10 years before we are thinking about using the HER2 ADC for gastric cancer. T-DXd globally. For example, RC48, etc. It is like taking off, starting from the GI tract gastric cancer. When I talk with Dr.
Zhou, so we find that all the small molecular drug is within Dr. Zhou's hands. I used to respect him so much and admire him so much, but now we are sitting on the same level. Think about for all the different ADC, different areas, just like PD-1, PD-L1, etc. Once it's happening, and then it's already at the peak. You find that HER2 ADC, whenever it happens, it arrives as the prime state. Ever since then onward, all the ADC drugs actually never surpassed the peaking level of the efficacy and the safety level of the HER2, etc. Think about it. I think it's already almost another 10 years. Think about PD-1, up and running for about 10 years. I really hope that. As Innovent shared with everyone.
I guess that the IO, interleukin 2, etc., it can make a positive change for the world. I really hope that the ADC drugs can go above the previous ceiling. If we think about the ADC drug, you have to understand this is a cytotoxic drug, etc. Especially under the popular landscape for that, how can we make it precise and targeted to make sure that we find the balance point between its efficacy and safety? This is something we really should bear in mind. Also, the ADC type of drug needs to have a targeted, precise treatment. Because if it's not precise, it doesn't make any sense. If you actually, for example, cover all actually, and then the ADC, what about the effect of the ADC? You find that antibody drug conjugated. You'll find that.
Compared actually for the albumin-bound paclitaxel , what's the difference between that if it's not targeted and precise? This is something we have to think about. We have to precisely use that for exactly the same target patient population. This is something we have to work on. Because for the ADC, people are mindful of the fact of HER2, so EGFR and Claudin 18.2, etc. Of course, the CK5, etc., and also TROP2, etc., nectin- 4, etc. For example, the 5T4, etc. The ADC drugs, there are so many possible target points we can try. The first one is about the cell because think about a bench and a bed actually unlimitedly can be closer. The second one is that the ADC, whether target point works. The third one is that you do the monoclonal antibody, the bispecific antibody, etc.
You have to balance that against the long-term benefits. Think about the ADC. The near-sight ORR can be a telltale sign for efficacy. ORR is everything you want to aspire for, but you have to look at the long-term survival, whether the patients on this drug can tolerate this drug over the longer run. We have to make sure the OS can be extended a lot so the long-term use can become the biggest barrier. We have to crack nuts for that. We have to focus our efforts on that. That's super important. Luckily, think about those as the different target points. Aside from the solid tumor, for the GI tract cancer, it is the largest research area for ADC drugs.
Think about the distribution for that GI tract cancer. It is already forefront for being some hope for breakthrough and trying to find the right target points and find the right target patients, etc. We understand that HER2 is already widely applicable, areas for HER2. We learned that from breast cancer and later on together with the Gajewski's team. You will find that urothelial cancer, so that is his team's efforts. We are trying to refer to their development at the same time. We tried to learn from them because urothelial cancer, think about the distribution compared with gastric cancer. Suppression efficacy is very strong. Because of strong suppression, for ADC drug for GI tract gastric cancer, the great upside as well as the anti-suppression, etc., I see the benefit of ADC drugs. That is to say that actually they are already mindful of this fact.
In the recent ASCO, you find that T-DXd, so trastuzumab deruxtecan for the second line, the gastric cancer has been successful. Think about throughout the research history of the GI tract cancer, usually line two will fail. You find the levocirumab actually on monobody is going to be fine, but it's difficult. You find that we do about 400 different cases for bridge trials. It is very difficult. Now only two available choices for them. This is like any small step will be a major breakthrough. In the past, the CRC, HER2 expression is very low. We take it for granted. Now we understand that. You find that membrane protein, high expression, medium expression, low expression, better for the patient. There are some certain proportion. High expression is about 5%.
For CRC clients, the patients, it's very interesting that for the ADC, so think about actually, so it's related to payload. Payload accounts a lot for the success for its efficacy. You'll find that actually, for example, about TACO, he summarized one inhibitor is going to be very important. Think about for the CRC patients, for the tubulin, the drugs actually are not working effectively. Very interesting that as long as the protein expression is declining a little bit, the efficacy is going to degrade a lot. Every different type of tumor has a different molecular biological structure. It's related to the different drugs you have chosen for this one. Now CRC, but also for the solid tumor, for other different things, actually there are different expression, etc. You'll find the urogenital and reproductive system cancer, etc.
Like for ladies, female and other rare cancers, they have different kind of level of expression as well. For HER2, not only gastric cancer and the non-small cell lung cancer and the breast cancer, but also the lung cancer, lung cancer and the CRC and other so many tumors. Like HER2 has a lot of expression. If you do it right now, actually you're going to do a lot of experiments and research for that.
Moreover, for Innovent product, yes indeed, there is very good efficacy and a safety. Therefore, because we're talking about HER2, we need to be worried about the pulmonary damage. FDA actually proposed a black box warning for some of those other drugs. How can we have early detection of those side effects and early warning in order to prevent the potential risks for patients?
We try to minimize these side effects, but we need to pay attention to toxicity of those other drugs. As for Innovent, the side effect rate is only 1 point something. In T-DXd, instead, it was 13%. Innovent is a lot safer as far as the data are concerned. Another hot topic is Claudin 18.2 because they're solely expressed in GI tract, for example, the gastric, the bile duct, and the pancreas. For pancreas, around 4%. And seldom other solid tumors. I was really concerned about the possibility of its expression in lung cancer. I'm afraid Dr. Goh's team may get this opportunity, but now I'm rest assured because it's not expressed in his tumor type area. I told Dr. Yu, "Yeah, you've got to give us some chance, right?
We want to take the lead for some trials for GI tract tumor. Some earlier trials were ground to a halt for 10 years. The market is very attractive for GI tract tumor, and we're under pressure, and we're nervous when we carry out trials, which is understandable. Innovent has ushered into a new era. They are both capable to do this. Claudin 18.2, with regards to their plans, yes indeed, they have paid substantial attention to the GI cancers. Yes indeed, this is very interesting. On our part, we also did some cellular therapy because there is mucosa of the stomach. Then there is payload, the cytotoxic drug for other organs. Overall speaking, it's very safe. Of course, 343 design, yes, there is uniqueness of the design. This is site-specific conjugation as a result.
In terms of the target, as well as the stability, are very good. There are very few free-form cytotoxic drugs or substances. Hence, it has minimal side effects or toxic effects on GI tract. The main adverse reaction is like GI tract reaction and also the low proteinuria in a third nucleotide marking. We found there is exudates from the damaged mucosa of the stomach. Once we emulate the efficacy, then safety is the main battle. This is where IBI343 comes in because it has distinct advantage on safety. Three days ago, Nature Medicine, as we know that, it proved, for example, the therapeutic effect in the second-line setting in the treatment of gastric cancer. Efficacy is very good, but in interest of time, I'm going to skip some details. In pancreatic cancer, which is refractory condition, there are some promising results as well.
343, there is early preparations targeting these tumor types. There is positive efficacy discovered. The patient group is different from the patient group for gastric cancer. Neither 75% nor 40%, but 40%-60%, rather. You need to identify the corresponding target patient for whom your drug is most likely to work. There are other ADCs as well. It is quite a rat race, quite a contestant. We're going to check out who is going to be the winner. For Innovent, in terms of the efficacy and its plans, yet Innovent does things a chance to make a difference in the world. There is also EGFR, MET, and HER3, etc., etc. A lot of developments in this area, but people are most concerned about toxicity. It's fair to say for ADC drugs, toxicity is the biggest constraint.
Going forward, the role of ADC drug, they're intended to replace chemo agents. If you combine it with other target agents, if you combine it with a carrier per se, it's definitely worthy of our attention. Also, combo with IO drug. Professor Goh is one of the pioneers on that regard. We are making parallel efforts on our part, but we're enjoying less support from pharma than we do IIT for five years. I showed them our evidence. Finally, at ASCO, we start to cover first-line setting. It's quite a tedious journey, but now finally, we have targeted the first-line setting. We need to find those target patients with continuous improvement of ADC so that globally we can demonstrate the China charisma. In the interest of time, I'm going to skip some of the details.
Innovation-wise, not only are we talking about ADC, but all those other innovative drugs to fight cancer, we aim to become world number one as well. Thank you very much, Professor Shen, for your fantastic presentation. I heard your remarks, and your remarks struck a chord with me. Yes, it's no easy job, as a matter of fact. Professor Shen, for decades in the past, I still remember a little anecdote or a story back then. HER2 ADC, it was initially designed for gastric cancer. Then Grandma Shen was invited to participate in clinical phase one, but she lost her confidence as she went along. She invited me to recruit some urothelial endothelial carcinoma patients. We recruited three cases. Those were u rothelial endothelial carcinoma. On that front, the drug demonstrated very potent efficacy. With monotherapy, the response rate was over 50%.
However, it was way less efficacious on gastric cancer. Different tumor types, the same agent may have different efficacy levels. This is a message to pharma. Traditionally speaking, your compound may target a certain group of patients, but on many occasions, our hypothesis turns out to be incorrect. Sometimes I'm confused if you look at HER2 mutation. If the agent works on those mutating disease, but why? It also works on non-mutation. If you look at EV or HER2 ADC, we do not even test for HER2. Because even if HER2 is negative, yeah, some of the agents work very well, right? We have got to ask why. At the end of the day, we have to validate those arguments through clinical results. All right, with that, let's thank Grandma Shen with our one round of applause again for her fantastic talk.
Next, we have the next heavy hitter, the next speaker, Professor Lawrence Fong. For Professor Fong, for urinary carcinoma, there was MCRPC, which was approved back in 2010 by FDA. That was the first true cellular product known as CPT. For CPT product, actually, it was a dendritic cell or DC cell-based cellular therapy. Back then, for CPT, as of now, this is like the first cellular therapy product ever approved by FDA. Now we have a lot more like TIL and CAR-T, which came out later on. It is fair to say Lawrence Fong was the leading PI of CPT. In IO oncology, Professor Fong is definitely one of the pioneers from the United States. Now, let's invite Lawrence Fong to start his presentation.
Hello, everyone. Thank you for having me join your meeting, and I'm sorry that I couldn't be there in person. It really gives me great pleasure to provide a perspective on cancer immunotherapy and innovation in China from a U.S. academician. It is really exciting to see all the progress that has been made in the field. These are my disclosures. I should point out that I have been serving on the SAB for Innovent for a few years and it really has been a great experience in seeing some of these ideas come to fruition in the clinic. Now, when we think about cancer immunotherapy and the global trend, you can see with regards to the different therapies that we think about, cellular and gene therapy, multi-specific antibodies, PD-1, PD-L1, these actually are given to a significant proportion of patients, both on the solid tumor side and on the malignant heme side.
Going forward, we would anticipate that these modalities will continue to be a significant therapeutic modality across multiple diseases. This is where particular molecules with regards to immunotherapies, like checkpoint inhibitors, have an advantage where a singular drug may actually be active across multiple disease indications. I think we'll see that with some of the molecules that I'll highlight later on in my talk. Now, when we think about the development of immunotherapies, this is just a timeline. As you all know, we use anti-PD-1 and anti-PD-L1 antibodies across multiple diseases. We can actually see that with regards to the different modalities that were highlighted in the prior slide, including bispecific cell therapies, they actually have been approved across multiple diseases with multiple modalities.
Probably the best example of that are obviously lymphoma and multiple myeloma, where we have multiple cell therapies and multiple T-cell engagers. Importantly, in the context of, for instance, lung cancer, we now not only use immune checkpoint inhibitors, but over the last year, we actually had FDA approval in the United States of tarlatamab for small cell lung cancer. That has really been a watershed moment in terms of T-cell engagers transitioning over into solid tumors. Now, for my talk, I was going to divide the discussions into the two approaches that we take with regards to immunotherapy and really separating these by mechanisms of action. On the one hand, I'll start out first talking about immunotherapies where we're actually redirecting immune effectors within a patient.
With this type of modality, what we would be thinking about is reprogramming cells, like with CAR-T cells or with TCR-T or T-cell receptor transduced T-cell therapies, where we're engineering T-cells from a patient with receptors to confer antigen specificity. Also within this group are the T-cell engagers, where they're binding tumor antigens, but recruiting T-cells, whatever their specificity, into the tumor microenvironment to mediate tumor killing. This is a modality that does not rely on a patient actually being able to generate T-cells that have specificity to tumor antigens. In contrast to that, we could think about the alternative approach with regards to immunotherapy. This is enhancing endogenous immunity in our patients. The key element here is this treatment approach relies on the patient to actually have T-cells that can ultimately recognize the cancer.
You could envision that in some malignancies, patients may not be able to induce those T-cells, in which case we may not, this treatment modality may not actually be able to get tumor responses in these patients. These are therapies where we can think about vaccines, checkpoint inhibitors, TIL therapy being another example of this, where even though it is a cellular therapy, we are actually harvesting T-cells from the patients. The patients had to generate those T-cells. We expand them in the lab, and then we give them back to the patients. Obviously, cytokine therapies, where again, we are driving endogenous T-cells to recognize cancer. A critical component is I do not view these different modalities as being mutually exclusive. You could really think about ways in which you could combine these different approaches together.
Indeed, there have been examples now where CAR-T cell therapies have enlisted vaccines or checkpoint inhibitors or cytokine therapies to enhance their efficacy. I think going forward in the field, we will see more of these combinations where we utilize treatment modalities from each of these different types of mechanisms of action going forward. I am going to start out focused on redirecting immune effectors, and then I will close with treatment approaches enhancing endogenous immunity. Starting out with redirecting immune effectors, the greatest example of this is actually CAR-T cell therapies. Where this has made the most impact so far is in the context of multiple myeloma, where we now have in the United States multiple CAR-T cells targeting BCMA for multiple myeloma. The FDA-approved molecules are IDACEL and SiltaCel. This is an example where innovations from China have really propelled the field.
Now, importantly, with these BCMA-targeted CAR-T cell therapies, there are high rates of response, and it's really been transformative for patients. The first cell therapy that was FDA-approved was ide-cel or BB2121. Just highlighted here are the really high rates of clinical response that we can see with the patients. If you look with regards to overall responses, on the order of 80% in this context. When we look at that in terms of longer-term efficacy, you can see that with these patients and high rates of response, we can see overall survival now actually extending out to about a year with these CAR-T cells. One of the things that we're seeing with CAR-T cells is that these patients actually go on to progress. Now, with regards to the second CAR-T cell that was FDA-approved in the United States, this is cilta-cel.
This is the product that was developed by Legend and acquired by Johnson & Johnson. With this product, we can actually see also high rates of response, but we can actually see much more durable responses that are highlighted here, now going out beyond two years and out to almost three years with regards to median overall survival. As a result, this product that was developed by Legend is actually now the treatment of choice for multiple myeloma in the United States, making a huge impact in our patients. Just to follow on with this and highlighting the innovations that are taking place in China, the field is actually now moving to multi-targeted CAR-T cells. This is an example of one of the studies moving forward, which is with a BCMA-CD19 CAR-T cell in multiple myeloma that actually has entered clinical trials.
This product was also developed in China by Gracell Bio and was actually acquired by AstraZeneca. This product is now in two phase three clinical trials. Even in the early clinical trials, you can see, again, really high rates of response, now on the order of greater than 90% response rates. The median duration of response also is quite durable. We think that perhaps this CAR-T cell may actually eclipse some of our existing FDA-approved CAR-T cells, especially with these randomized trials that have launched. These are really transformative therapies from a perspective of CAR-T cell therapies. Again, the leading products in this field are originating from Chinese biotech. To switch gears on enhancing endogenous immunity, this is the context where we're relying on a patient to have tumor-reactive T-cells that we can then activate and drive with our therapies.
The prototype for this is obviously PD-1 targeted agents. These immune checkpoint inhibitors really tip the balance towards T-cell activation. By targeting this one immune checkpoint pathway, we can actually have disease activity across multiple diseases, as highlighted by the slide. In the U.S., our indications are a bit more limited than they are in China. Just to highlight, those diseases in red are where PD-1 blockade is actually frontline therapy for patients with metastatic disease. However, when we think about checkpoint inhibitors, PD-1 is actually one of many immune checkpoint inhibitors that's highlighted here. The idea is that we have both co-inhibitory molecules, of which PD-1 and CTLA-4 are the prototype for, but we also have co-stimulatory molecules that we could envision targeting and activating. These would presumably activate T-cells that recognize antigen, the signal one that basically delivers antigen specificity.
As it turns out, I use the slide that's now over a decade old because we now have had drugs that have moved into the clinic that have targeted each one of these different checkpoints. You can see that while we have broad efficacy with anti-PD-1 antibodies, and we have some efficacy if we use some other checkpoints like anti-CTLA-4 or anti-LAG-3 antibodies, particularly in combination with anti-PD-1 antibody, we basically have failed to see significant clinical activity with all these other checkpoints. I think this has created a challenge for the field, is while everybody had such excitement around PD-1, we really have had challenges replicating antibodies targeting other checkpoints resulting in clinical efficacy.
I think one of the big challenges that we face is that when we give antibodies that target these other immune checkpoints, they really have not been targeted in any way to a tumor-specific response or to the tumor microenvironment. In fact, when we give these antibodies, including anti-PD-1 antibodies, they'll bind to T-cells and immune cells everywhere in the body. It actually is really amazing that with PD-1, this is actually sufficient to drive anti-tumor immune responses, but really has not been the case with most of the other immune checkpoints that have been studied to date. This is where I think innovations that are being born by China biotech have really pushed the field forward.
I wanted to highlight two particular molecules that really demonstrate the importance of having tumor-targeted checkpoint inhibition to really focus the immune response within the tumor microenvironment have really been demonstrated. The first of these is actually with regards to the molecules that target PD-1 and VEGF. As you all know, this is now a clinically validated approach where, in this case, a molecule that binds both VEGF as well as PD-1, the presumed mechanism is that this molecule would actually bind VEGF within the tumor microenvironment and actually cause multimerization of these molecules to better stimulate or deliver anti-PD-1 within the tumor microenvironment. Although I would say that the mechanism of action is still not fully elucidated. I think this has been a critical component with regards to skepticism about this particular molecule, is that we do not fully understand that MOA.
I will circle back to that, as I think is an important future direction at the end of my talk. Nevertheless, with this particular molecule, there has actually been a high rate of response in a few different malignancies. The one that has really caught everyone's eye abroad is in the context of non-small cell lung cancer. The example that I wanted to convey is with PD-L1 positive non-small cell lung cancer, the activity of immunotherapies as a monotherapy. In this particular clinical trial that now has been published in The Lancet, there are actually very high rates of response with ivonescimab and actually is superior to pembrolizumab, which is our benchmark in the U.S. You can see that the rates of response are actually superior with this new molecule. In fact, with this randomized clinical trial, there is now progression-free survival data.
If you actually look at all patients, there was an advantage with regards to progression-free survival. Actually drilling down on specific subtypes, if we look at those patients with the highest level of PD-L1 expression, you can see an advantage. Even with patients with less than 50% TPS, we can actually see an advantage. What is also critically important is we can see an advantage in PFS for both squamous and non-squamous non-small cell lung cancer. These results are actually really striking. We are awaiting eagerly the results with regards to overall survival. From a progression-free survival standpoint, this drug looks to be highly active and could represent a new standard of care. Obviously, this drug now is moving forward in multiple randomized trials in the U.S. This is being developed by Summit.
Again, we're all eagerly awaiting the results of these follow-on randomized trials with a particular eye towards looking at improvements in overall survival. The other example that I'd like to give is actually with regards to a phase I IL-2 drug, IBI 363, that Innovent has developed. This is an approach that I recall discussing at scientific advisory board meetings in the past. It's really exciting to see this molecule actually move forward into the clinic and show really impressive clinical responses that has also caught everyone's eye. I should point out that in this case, again, we're not relying on an anti-PD-1 antibody and an IL-2 molecule. Both of those have been tested. In this case, this is a unique drug where it basically is bringing these two together in a singular molecule.
I really want to emphasize that point because we're now thinking about this as a synthetic biology approach to actually improve the efficacy of these immunotherapies. The other component, just to highlight in terms of novelty with this type of approach, is this IL-2 molecule is actually an alpha-biased IL-2. What you'll find in the field is that there really have been two camps in terms of people thinking about how best to use IL-2. We know that native IL-2 hits the alpha receptors, which are the high affinity receptors, but it also hits the beta-gamma receptors, which are lower affinity. There has been some thinking that by biasing IL-2 in one direction or another, you can actually enhance the efficacy of IL-2 and/or reduce the toxicity of IL-2. Most of the field has been focused on the beta-gamma-biased IL-2s.
In this case, the Innovent molecule actually is biased towards the alpha receptors, which are higher affinity. There is always concern with regards to toxicity and/or impacts on regulatory T-cells. Because this molecule is actually targeted to PD-1, that actually enables this molecule to preferentially target effector T-cells better. At least that is the idea around this molecule, which, again, is contrary to many of the molecules that are being developed out there. What has been shown is indeed this actually does do what we think it would do in terms of driving T-cell activation. In this case, looking at patients who actually are clinical responders having more T-cell activation that is shown here. In fact, this molecule has been looked at in multiple diseases, including patients with MSS colorectal cancer having significant clinical activity in this context and having progression-free survival, particularly in patients without liver metastasis.
I think this has been also a pretty impressive response for a therapy that actually has no clinical activity in the context of a PD-1 antibody by itself. In fact, this has been borne out in larger clinical trials, in this case, looking at progression-free survival as well as overall survival in this context, non-small cell lung cancer. Again, quite promising results that should enable follow-on trials, randomized trials to basically demonstrate efficacy in this context. I think it was really quite dramatic at this year's ASCO presentation where this molecule IBI was actually highlighted in multiple oral presentations. This actually was one of multiple molecules that were developed by China biotechs. If you look at the number of oral presentations and late-breaking presentations, really making a huge impact at this year's meeting.
Just comparing that to 10 years prior, it's really unprecedented. With that, I just wanted to close, just really to highlight and congratulate you all on the successes of novel immunotherapies based upon innovation from China. Already, the dominant CAR-T cell in multiple myeloma is a product that was developed in China. I think there are now multiple first-in-class, in this case, bispecific molecules that are really leading the way. In my mind, this is really just the beginning with more innovation on the way. I just also really wanted to highlight the importance of a fast generation of clinical signal that you all are able to accomplish. That really is unprecedented and I think is really a significant competitive advantage.
I also want to highlight the critical importance of validation of these findings abroad, including within the U.S., that really will hopefully take these forward to registration strategies worldwide. I think the other point that I wanted to highlight was the critical importance of really understanding the mechanism of action. Oftentimes, companies will want to just focus on clinical activity and get that over the finish line. I think the thing is, if there is clinical activity but not a firm understanding of how the drug works, that actually results in a lot of skepticism and challenges in terms of adoption abroad. I think that's another opportunity that could be leveraged earlier and I think would be possible in IITs in China, but also through studies abroad, including the U.S.
Thank you very much. Thanks to the four top experts for fantastic presentations. Also, my remarks or thanks go to Professor Guo for his chairmanship. Through the four talks, the post-PD-1 era IO explorations and a GI tract ADC R&D breakthroughs and a global oncology treatment landscape and a renaissance in this area. We have heard a great blueprint going forward. We are deeply touched by the scientists and the researchers because they have great perseverance in insisting on their efforts. From this perspective, they can actually make great efforts and forge ahead much toward the blue ocean for life science and healthcare. Today, it is a very invaluable gathering and academic feast. Let's take a photo op and memorize this moment. Let's invite the photographer on stage and then take a group photo. Please just remain in your seat. You look at the camera.
You can wear your confident smile as the photographer is doing their job. All right. All right, photographers and a drone will be deployed to take a group photo. Please look at the camera and wear a smile on your face because we're ready to take this photo. Let's remember this beautiful moment. On my count, three, one, two. [Foreign language] And let's actually give our like to this event and wish this conference a complete success. You're smiling very happily. This is a very invaluable moment that we memorized through photographs. Thank you very much. We're going to take a 10-minute tea break. You can talk to each other, enjoy some snacks and tea during the break. Please come back in 10 minutes. Thank you. [Forging language]
Honorable guests, ladies and gentlemen, welcome back for the next session. Thank you for joining us back for the Healthy China 2030 Oncology Innovation Summit and R&D Day for Innovent Biologics. My name is Li, and I'm the moderator for the whole session. Next, I'm going to have the privilege to moderate the next session for you as well. Next, a highlight for today, it's about Innovent R&D Spotlight. During this session, we're going to have a global vision where we deep dive into talking about the most cutting-edge innovative therapeutic approaches for the treatment of oncology and strategic layout to make sure that we can create enough for R&D. Let's welcome to the stage the moderator. We have actually Professor Huo Jianqing, who is with the number one affiliated hospital to Guangzhou. Let's welcome Huo Jianqing. Hi, Professor Huo. Dr. Michael Yu, experts, ladies and gentlemen, hello everyone, my industry peers.
It's my pleasure to join one for the stage. This is a part of the session for Healthy China 2030 Oncology Innovation Forum Summit. Think about the thank you very much for the organizer Innovent Biologics for innovating new technologies. Thank you for the excellent innovation efforts you have to make sure that you benefit not only for China, but also the whole world as well, so that you can keep us updated on our vision and the new mindset and philosophy. I personally am a big fan of Dr. Yu. Think about like IBI 363. This is a very important entry point. Think about a lot of innovative drugs in the world. Most of the cases, China used to be a follower following the footsteps of others.
There are cases of which like PD-1, and also you find that actually on Soh, actually for the for other different combined approaches, there are a lot of breakthroughs being made. Think about the PD-1 and also the IL-2 being combined together. This is a very innovative philosophy by any global yardstick. This is quite unprecedented. This is a really disruptive innovation as well. Think about the IL-2, interleukin-2. We have been hearing of that for a long time. We have been using that for a long time. When I was in university days, there is an immune research institute in my university. They really like the IL-2 and also the interleukin, et cetera, and interferon. At the same time, TNF. You find that my university professor told us that like the IL-2 is very effective.
When I become a clinician doing clinical research, we understand because of the high toxicity profile of that. As a result of that, we only apply it locally. Also after the lympho depletion, you find that it works its wonders. That is why a big surprising note and happy news for everyone. Innovent team, with the leadership of Dr. Yu, you find the PD-1 together with IL-2. Thank you very much for putting them together. This is a very epoch-making innovative, like a great, greatly challenging existing approach. Think about actually behind every research, there are a lot of different courage, hard efforts, as well as difficulties you have overcome as well. Me together with Dr. Yu, back in the COVID years, we research on antibody.
Not a lot of you will know about me. My name is Huo Jianqing. I come from the nationwide Guangzhou Center for Respiratory Diseases. I'm in charge of respiratory diseases as well as the surgical department. For the transplant department, I'm also overseeing that. Ever since COVID, Academician Zhong Nanshan told me that you really have to focus on the research so that you can save a lot of lives. For a lot of different localities, whenever it's a rescue therapy, Henan, Anhui, and also all the way as far as Xinjiang, when they find that, wow, you come from the National Respiratory Disease Center, that's why those guys actually are trying to give us the patients who are suffering from late-stage respiratory diseases as well. Like 80 years old, like senior citizens. If I really want to save them, there are a few interventions you have.
The first one is you have the respirators and actually also ECMO that could be used as well. These are only like life support. How can you treat them? Together with Dr. Yu, we are trying to use antibody. The antibody is very effective. The antibody is so effective that for all the ICU patients, especially in the senior citizens. In our center, respiratory disease, we use this antibody and also trying to treat the severe critical symptom patients suffering from COVID. There is no single fatality or death in our team. I mean, for the other patients we have treated, we got a lot of esteem and respect. At the same time, actually we are applying that for, for example, compassionate as a compassionate drug and save a lot of lives.
Let's go back to the topic for oncology. It turns out that as always, Innovent Biologics team, as you always do, stay committed towards innovation and you are making this epoch-making disruptive innovation step in the world without further ado. In other two, like for example, topic we're going to have with us actually on, so someone who is engaged in the transformation for the oncology treatment. Treatment of oncology is different from others because on the early line, like therapeutic approach is more effective and even later line is also very effective. Think about usually in the past, when we treat someone suffering from lung cancer, maybe half a year, that's the OS, but now they can survive for two, two, three years. In the past, if the like patients can survive five years or ten years, it's a miracle.
But now so many miracles right now. Thank you for the contribution from the innovative drug makers. Next, we're going to have some joint discussion as for actually about the strategic layout as well as the systematic exposure and efforts for the global innovative anti-tumor drugs. This is about the forward-looking scientific insights, but this is about the industry transformation as well, especially since COVID. We are very happy to be joined by the next speaker coming from the leading example of the representative of innovative biologic innovator company. The Vice President, Innovent Academy, Innovent Biologics, Dr. He Kaijiee, to moderate this next session. For information, Dr.
He has been deep diving into oncology biologic mechanism for so many years and also the ADC antibody like drug conjugate, who is at the forefront of research for that, who is going to have the early strategic research like strategy for the anti-oncology drug and to let you understand that from a multidisciplinary perspective, what about the early stage and early line R&D strategy? Let's welcome Dr. He Kaijie.
Thank you, Professor He, for your kind words. Honorable experts, distinguished leaders, guests, and investor friends, ladies and gentlemen, good morning. Thank you very much for representing the Innovent Academy from Innovent Biologics to give you an update on what we have done from our academy, especially for our thinking about innovative new approaches for the anti-oncology treatment and our strategic layout, et cetera. Our Innovent Academy was established in the year 2020.
Think about within Innovent Biologics, we are the innovation engine for our company. We aim for a world-class R&D platform. First-in-class and best-in-class drug are our key research priority. Think about we have more than 500 different scientists on our team for the academy, Suzhou, Shanghai, and also California. These are the three different R&D centers we have. The 500 scientists are working in those three different centers. We want to leverage the synergistic resources in China and the U.S. and develop the global market, like intelligence collection, as well as the innovative drug R&D innovations platform, et cetera. Think about the Innovent Academy based on our antibody and the protein drug research prowess of Innovent Biologics companies. We developed a new generation bispecific antibody platform and a multi-antibody platform, as well as a cytokine platform and ADC platform.
Yeah, I'm going to talk about the dual payload ADC platform as well. We're making efforts on planning for newer modalities, for example, siRNA, polypeptide, and broad-sense SDC drug, et cetera. Disease-wise, we focus on four areas: oncology, cardiovascular metabolism, immuno, and ophthalmology. The promise we deliver to our companies, we aim to deliver at least six or eight innovative molecules, which will be ready for R&D stage. In terms of our plan and strategy for early stage R&D of oncology, we focus on two pillars, namely next-generation IO, next-generation ADC. For next-generation IO, we hope following PD-1, we can create IO 2.0 or next-generation IO. Strategy-wise, there is PD-1 and a cytokine. We can have fusion of these two, then PD-102, and also a PD-1 IO-12. Moreover, we have a T-cell engager platform targeting solid tumors in various hematological carcinoma.
In an all-around fashion, we aim to cover those hard-to-treat tumor types. Another pillar of ours is ADC drugs. Right now, in the pipeline, we have, for example, monotarget ADC. We are making plans for next-gen bispecific antibody ADC and a dual payloads ADC. Here is the simple introduction of our next-gen IO plan. IBI 363 is very important. This is a fusion protein featuring PD-1 IL-2. Experts before me already talked about it. It is in the middle of clinical phase three, and we are thrilled to see some of the early-stage data. There is a brother of this compound, namely IBI 3036. A new cytokine, IL-12, is deployed. We got very good clinical data. We are enabling R&D for IBI 3026 plus for colorectal cancer. There is IBI 3019. We are on preclinical stage for IBI 3019.
These are multiple domains, multi-mechanism of action. We want to modulate, for example, the immune environment and the microenvironment. The next, the interleukin-2 receptor, some of the design thoughts we put in. IL-2, as a cytokine, has a long history. It goes way back, for example, to the 1970s by NIH. Actually, for supernatant expression, it has a very strong role to provoke lymphatic proliferation. With cloning and recombination, there has been clinical progress in human beings, for example, with regards to melanoma and kidney carcinoma. The responders have long survival benefits. For the experts mentioned, it is toxic and poor drug ability and a poor PK over the past two or three decades.
In industry and academia, one of our biggest goals is to increase the therapeutic window of IL-2 and how to reduce its toxicity as we maintain the efficacy by optimizing the drug administration. There is a lot of efforts ongoing in the past two decades along these lines, both in terms of industry and academia. Those re-engineering is based on a gradual and a deepening understanding about the mechanism of action of IL-2 early on, prelooking by Rosenberg. This is recombinant interleukin-2 protein, yet there are limitations. By the beginning of 2000s, Wu lab put forward a very interesting theory believing through bias, the IL-2 signal can achieve, say, decoupling of efficacy from safety. One of the theories they put forward is non-alpha bias IL-2.
Based off of the theory, the whole industry spent over 10 years of time, companies such as Roche, Nektar, Sanofi, and other biotechs, which are working hard on this direction. PK improved, dosage enhanced, but systemic toxicity remains as a problem. On our part, as we started out with this initiative, and we stood on the shoulders of a giant, then we kicked off our research. We found Boyman theory was, for example, not that comprehensive. We put forward newer theories, namely the alpha bias theory based on our research evidence. According to our previous findings, something important that we've discovered, tumor-specific T cells, or TST in short, not only are they expressing PD-1, but they can upregulate CD25, as Dr. Yu mentioned. IL-2 receptor alpha upregulated. It distinguishes TST in a way. It has the very functionality to kill tumors.
This is a very critical factor. There are those non-related T cells that do not express PD-1, neither CD25. We have a clear design target. PD-1, IL-2 alpha bias is bispecific antibody, so it can selectively stimulate the T cells. In our clinical data, on the leftmost column, 363 for naive or bystander T, as double negative cells, there is no activity whatsoever. On the right side, for TST, there is dual expression of PD-1 and CD25. On that front, the compound is very active. The selectivity and activity increase by a factor of thousands or even tens of thousands. We have a huge selective window. We have an interesting animation here.
to this innovative design, IBI 363 has shown significant benefit advantages in the treatment of multiple solid tumors. Its unique dual immune activation mechanism is expected to break through the limitations of immunotherapy and open a new future for immunotherapy. A brilliant animation, because the message we can hear from the animation is a lot more clear than my message. The hypothesis, the mechanism of action of 363 is to explain the tumor-specific T cells. We did a lot of preclinical models for validation. This model, for example, this is a PD-1 resistant lung cancer model. The blue chart, the area C1 over, the blue antibody, because it is drug resistant, so it does not help. Murine 363 produced a very good inhibitory effect on the tumor. We remove the tumor sample and look at the analysis. In the upper right corner, the IgG control group, no change.
On the rightmost chart, the IBI 363 treated group, the TST cell population expanded by a factor of two or three. This data directly speaks to the mechanism of action of our molecule. To sum it up briefly, IBI 363 has a dual immune activation mechanism, including PD-1 checkpoint blocking and also selective activation of TST. It is a dual immune activation mechanism. Because of the design of interleukin-2 alpha bias, it has very good tolerability. Not only can you use it in monotherapy, you can combine it with chemotherapy, ADC, or other IO compounds. There is a huge scope of applications going forward. Plus, on the preliminary clinical trials, by the way, we're going to have another speaker who is going to go into detail. For PD-1 resistant tumor, cold tumor, and PD-1, PD-1 low expression tumors, we have actually demonstrated preliminary efficacy.
Ten years ago, PD-1 antibody worked. The inventor got a Nobel Laureate award. In the past ten years, there was a vacuum. Although people were bullish on IO as a whole, people are in constant search for the next PD-1. I'm very proud. I take pride in saying there is indeed potential to this molecule to become IO 2.0 product. Furthermore, we have a T-cell engager plan. A case in point is GPRC5D, BCMA, CD3, trispecific antibody for refractory and relapsed multiple myeloma. Leveraging our trispecific antibody platform, we have designed complex energy molecules in low energy expression xenograft model and also a J&J control. The red curve refers to our 3003, which is superior to the J&J control molecule in terms of efficacy. Plus, we made comparison with their phase one trispecific antibody.
Our potency is distinctly higher than that of the J&J molecule because we have balanced design of the three Fabs. Right now, we're on ramp-up stage for clinical phase I. We look forward to the future results. Moreover, on ADC, this is a very important direction of goal for our efforts. We've created three ADC platforms earlier on. We had Synaffix E by partnership with another company. Then there is also, for example, the Claudin 18.2 and the ADC. From within, we have our own Topo1 inhibitor with brand new structure. This is actually a Solo TX platform. We have 10 ADCs, which are in the middle of clinical development. Plus, we have a Dual TX. This is kind of a dual payload platform. This is our first of its kind, which is ushered into clinical trial phase. From this perspective, we have differentiated advantages.
We have hydrophilic group for linker. So we enjoy advantages on PK and efficacy. More importantly, if you look at our payload, the clearance is fast, especially in vivo human beings. With the same level of dosage compared with DXd ADC in human PK trial, the free toxin volume is only 10%-15% of a DXd. So it provides a very important safety window. Same, our off-target toxicity is way lower than DXd and other Topo platforms. Very low kind of a hematological toxicity and low rates of ILD. What about next-gen ADC? We're going to focus on bispecific and a dual payload ADC development. For the former, there are two different tumor antigens because of tumor inhibition, no matter intratumor heterogeneity or interpatient heterogeneity. If you try to have like a mono kind of targeting ADC, there is likely to be antigen escape.
If we target two different antigens that not only are able to cover a broader cohort, but also we would induce deeper response. More importantly, if we have good enough design of bispecific antibody through unique kind of an epitope, so the, you know, let's say kind of an endophage or autophagy effect is stronger, then this is EGFR ADC. We're on clinical phase I stage, targeting two solid tumor antigens, EGFR and another one. There is a big overlap. As we design, the kind of effect is stronger than those monotarget EGFR or B7H3.
That's why we want to conjugate the payment for the bispecific antibody. No matter which one you look at, you find that the 301 molecular has a strong efficacy. In monkey, we have already finished the GLP independent trial.
You find that it could have a high tolerance of 30 mg per kg. Now you find that the phase I clinical trial is being conducted in Australia and in China, and for U.S. multi-center, like randomized trials are ongoing. Think about dual payload and ADCs makes easy sense. Dual play and also triple play and like chemo, etc. Think about for the single payload, there is going to be an easily drug tolerance. We are thinking about complementary ones are going to be loaded on the ADC together. It has been backed up by clinical trial data, for example. Recently, there are some important data. Think about two ADC, Trodelvy. It is the Topo1 inhibitor ADC and also the other ones based on different mechanisms like ADC.
After using ADC of a different MOA, you find the response rate is increasing a lot. This is an important reminder for us. Given different mechanisms of action, like toxicity and payload, we can work in combo with them. The thing is that how can we make sure we mix and match them to the right proportion? On the same, like the antibody, they can become the same converged ADC. Over the past three years, at first, we have successfully developed the first dual payload ADC platform. Also, you find that CCAM FEM, and IBI 3020, is already at a clinical phase one, and then they are trying to be used for some patients as well.
On the right-hand side, you find that like the efficacy data prior to clinical trial, which proves that the dual payload is effective in the sense that we use two different mechanisms. The first one is a DXd tolerance. The other one is a different model for tolerance. Think about for actually the ADC user as like the monotherapy, that's not very good, but dual on the same ADC is going to have a strong tumor killing capability. You find that tolerance and the safety window is great. That is why actually we are already promoting it to the phase one clinical trial. Let me summarize a little bit. I think think about Innovent Academy. We have ambitious targets, vision, goal, and mission.
We aim that we really want to become China's first global leading advanced science and technology research application research institution to work out the epoch-making, revolutionizing new drugs. How are we going to achieve this target no matter what happens? Actually, we're going to aim for that. It's going to be like a make-or-break moment for us to the Red Ocean or the Blue Ocean, or if we have a big enough addressable market. Of course, from our perspective, we have full confidence. We are optimistic that we are going to achieve our mission, vision, and target. Thank you. Thank you very much, Dr. He Kaijie, for your presentation about the global early research systematic interpretation of the R&D for oncology. Very professional presentation. Thank you very much. If we can use the animation to illustrate the points, maybe this is going to interest the clinicians more.
Thank you for explaining to us a lot of different complex things in our pipeline so that you are developing a lot of navigation new pathways to meet unmet clinical needs. This is much anticipated. Antibody, bispecific antibody, and then tri-antibody, etc. There are a lot of research upside for our improvement. There are a lot of technology challenges still ahead of our way. Thank you very much for broadening our horizon.
Thank you very much, Dr. He. Next, we have with us Senior Vice President of Oncology R&D, Innovent Biologics, Dr. Zhou Hui, who is going to talk about redefining the cancer treatment for the next-gen therapies. Dr. Zhou is going to share with us like a deep dive insights. Welcome, Dr. Zhou. Thank you, Professor He. Honorable experts, investor friends, ladies and gentlemen, good morning.
I feel very pleased and privileged to be able to present to you from a clinical perspective. What about our oncology pipeline? What about the strategy for the outlook for our future? Here today, I feel very pleased. Super fantastic because think about what we have been through from the past era to a new era as well. I remembered correctly from the last R&D day was held in 2019. It was a PD-1 era. Now it is 2025, the new R&D day, etc. We are already on a new platform to face the future. I would like to echo the great points raised by you. Difficulties, courage, and taking on the challenges head-on, these are the three important things. Ahead of the new opportunities and challenges, we have to be brave enough to take on the challenges and undertake our responsibilities.
This will not be possible with Professor Guo and Ansheng without your great guidance and expertise, without the trust of investor friends. So we cannot become who we are. Let's jointly have the take for the future of development of anti-oncology treatment. I'm going to assume the perspective of a clinical perspective. Let's try to look at the PD-1. From the design perspective for the trial, this is an add-on role, which means that on the basis of a chemotherapy and other different therapies, how can we have an add-on like a PD-1? Think about a PD-1 as addressing the hot tumor issue. If you add on the PD-1 on top of the chemotherapy, this is going to make a difference for the treatment of oncology. There is a watershed in the sense that you'll find that a cold tumor.
These are the examples of cold tumors. For example, the CRC and also the prostate cancers, pancreatic cancers, we need a lot of new different approaches for intervention and treatment. That's to say, given the sea change for the paradigm shift, how are we going to make some breakthrough? This is the issue for us. Ever since the year 2020, we have already done some attempts as well. For example, we are trying to use ADC to iterate like a chemotherapy, use a bispecific antibody to iterate a PD-1 or PD-1, so the anti-clonal monobody, monoclonal antibody, etc. We already have seen that happening. More importantly, we really want to see the iteration for the double ones, which means that for the IO, we can use a bispecific antibody and the next gen, so the next gen ADC.
For the chemotherapy trajectory, we are going to use a bispecific antibody or dual payload ADC to iterate to make sure we have a double. The one plus one bigger than two stronger synergistic effect is going to be generated, which means that we need to make some breakthroughs on either end of the two sets of feasibility needs to make some breakthrough as well. For Innovent Biologics, Kaijie had already introduced to everyone as to how we have been through and what other work we have done. Think about for the IO end, in the past, we have done a lot of bispecific antibody job. The past acceleration efforts come to the realization that, think about the cytokine in terms of like the very unique and very strong role it plays for, like for example, the treatment.
The IBI 363, the new gen like PD-1 products, and at the same time, the IL-12, etc. You find that actually this is going to work together with the different cytokines. We hope that we arrive at the optimal combo to make sure and leash more possibilities in the future as well. Another thing is that ADC as well, because we always hold it to be sure that the chemotherapy and also if you use ADC to replace the chemotherapy, that's going to be the trend for sure. For ADC, there are a lot of yet to be addressed problems. You find that DXd, for example, DXd has already made a lot of breakthroughs and likewise as well, give us more hope, but we need a differentiated like linker payload platforms as well. That's why for Innovent has done a lot of work.
Kaijie has already, Dr. He Kaijie has already introduced to you about the internal differentiator advantages for us. Dr. Shen Lin, her two ADC, which with your help is the first one out of the Innovent platform, we are happy to see it making a difference. It is a differentiation. On the basis of what we have already done, we have the next gen like a PD-1, like with the example IBI 363 and also some ADC platform. The bispecific antibody ADC, dual payload ADC, we have it all. The combination we have can give us more opportunities as well. For IBI 363, I'll call it 363 for short. Three RO presentations at ASCO 2025 and ever since the year 2016. Dr. Yu mentioned that we started the efforts. Think about the PD-1 and the IL-2, etc.
You'll find that nine years has already been put in place and three years clinical trial. It doesn't happen overnight. It's not possible with the incremental efforts we have made throughout the way. Think about the 363. I think the mechanism of action for that is something that we still need to explore with. Now we have come to the clear realization that from the clinical perspective, these are things straightforward. First one is that it can turn the unfavorable design into the favorable design because our concern is about a Treg issue. That's why the gen one, generation one. Think about a knockout, actually. For example, it is, for example, the original design.
We are trying to do some bias design, which means the epoch-making innovative to turn the negative things into favorable things in our design to make sure that for the peripheral toxicity, we can control it to make sure that actually in low dosage, Treg can be activated. Once activated, they can better control the peripheral toxicity. The second one is about a dosage for a therapeutic window. Think about the IL-2. Think about the treatment dose for IL-2. Usually, you'll find that it is about 6 mg per kg, etc., like Sanofi. They take it for granted that they can already do multiple times better, but I think 24 micrograms per kg is the best they can do. The dosage is constraining their actually phrase efficacy.
Like CAR-T, why they can use IL-2 to do it is because think about it, it is for individual. You can apply it at a high dosage. You'll find that actually we already go above the glass ceiling for the interleukin-2. At the same time, we can design it into the dual functional so that we can use a PD-1's affinity capability. The molecular make sure intra-tumor can play a better role as a result of interleukin-2. Actually, for example, can be amplified or extended as well. By stimulating that, the special bifunctional molecular design can help to make the full utilization of interleukin-2. How do we position this IBI 363? I think this is going to become a difference-making. The new generation of IO can go beyond the constraints of IO. We target two ones.
IO tolerant and the cold tumor, these are the two target population we have. Also, the IO naive people could be added as well. That is why for the 363, the three different patient populations are the main different population we want to cover. 363, August 2022, going for the clinical trial. In the U.S., Australia, and China, we have already enrolled about 1,000 patient population. MRCT, multi-center randomized trial, has been ongoing as well. That is to say that based on all the data we have right now, this is about across different regions and across different geography, it spans people of different ethnicity or people from different countries. This is giving us a more diversified data, more representative than a single data point.
Melanoma, the CRC, and the lung cancer, we have already arrived at a POC and a regulatory breakthrough as well. You'll find that the BTD and FTD, each in China and the U.S. We have already got the approval and the vote of confidence from the regulator as well. We are going to fast track the global development of that. Hereby, I wouldn't have enough time to go through the lengthy data. The ASCO and RO presentation, and you can refer to the information. Think about how we target important patients. Lung cancer, like immunotolerant, you find a gastric cancer and also the tolerant, like IO, for example, melanoma, etc., PFS and OS has been extended as well. Compared with the SOC, it has shown clear significant improvement for the IBI 363.
Think about what about for the differentiated mechanism of action. This is most important addressing three issues. The first one is about the breakthrough for efficacy as well. Think about the breakthrough in efficacy. You'll find that the VEGF, PD-1, so on the basis of bispecific antibodies called the dual immune activation. It's not about just the breaking mechanism is activated and the interleukin-2. We are going to activate it, like for example, the PD-L1, etc. As a result of that, it's just like a very strong engine. We're going to turbocharge the engine from the gen 1 to 3.0 version to make sure that it has a turbocharged engine to make sure that when you hit loose, the breaking, which means that the strong functionality of the auto can be given a full play.
Because otherwise, if you do not address the breaking issue, you cannot release it and it cannot make a breakthrough. It is going to break the glass ceiling for the efficacy. The second one is the safety. Because without the safety as a guarantee, you cannot make sure that the efficacy can be maximized as well. We have to make a breakthrough for the design. Beta-gamma reduced alpha is going to be a bias design to make sure the peripheral toxicity can further decline. Even though we have already seen that, the IL-2 related toxicity, these are managed by the clinical level. For example, we have already come up with very comprehensive management experiences as well. The third one is drug ability. Drug ability is about, for example, PK profile.
Because the prior IL-2 has very poor PK, the next ADA. The breakthrough of the three topics as a result, we have huge room and a potential for 363 and to find a breakthrough on the limitations of IO. We have come up with a very clear strategy. First wave, how can we obtain the blank market of IO, namely those who IO failed and who are IO resistant, these lung cancer patients, and led by Professor Guo, there is IO naive, mucosal acro subtypes or groups, then also intestinal carcinoma where there is almost no presence of IO therapy as of now. On top of these two patient groups, we are getting rapid entrance into first line setting in terms of lung cancer and intestinal carcinoma. The POC trials are ongoing rapidly. For a broad spectrum IO product, the POC explorations are well ongoing, be it in terms of gastric cancer or liver cancer.
We're going to increase our presence or explorations in GI tract cancer and esophageal carcinoma, then also in gynecological carcinoma and urinary carcinoma where we're making plans. We're making plans for new adjuvant setting as well. Another product of ours, as Dr. Kaijie introduced, we have a specific trispecific antibody platform. This is 303. This is actually, for example, GPRC5D, BCMA, and CD3 trispecific. Johnson & Johnson already entered ASCO and delivered a presentation. We benchmark against the Johnson & Johnson. Our affinity and the potency are way stronger than that of the Johnson & Johnson compound. Now, for those who are treated with BCMA or GPRC5D patients, our product still works on these patients, meaning we have delivered on the original design purpose because we aim to overcome drug resistance. Another important thing for this molecule, we want to achieve higher CR.
In the future, the patients do not have to be CAR-T treated anymore. Speaking of ADC, the three platforms, as we alluded to, from a clinical standpoint, we checked the current progress. The Claudin 18.2, for example, in gastric cancer, phase three trial is ongoing. Pancreatic cancer, phase three trial is about to be kicked off momentarily. We have registered with a CDE website already. 343, gastric cancer and pancreatic cancer. We are making headways on both fronts in parallel. We are trying to advance from a late line to front line setting. Also, the 35C HER2, this is a platform we developed specifically. For example, whether we can achieve high potency and low toxicity to meet the clinical expectations because the current status quo for many ADCs is high toxicity despite high potency. We want to address this problem. Dr.
Kaijie, who spoke before me, talked about the differentiated advantages. The peripheral free payload concentration is very low compared to the market benchmark where like 15% or 10%, meaning the off-target or systemic circulatory toxicity level is very low. There are great possibilities for ADC. You may combine our ADC with other assets or we may develop a dual payload platform on top of this. Bispecific ADC, you can look at the EGFR B7H3. This is a first in our company. We are conducting phase one trial very quickly. The expression of these two targets is broad spectrum. We have discovered positive signals in some early research. The efforts are ongoing in the United States as well. The first dual payload molecule, which is being developed on our proprietary platform, the American IND is approved.
The first patient in the U.S. is being recruited as we speak. In China, we are on rapid ramp-up. For the early doses, they demonstrated very good safety and efficacy profile. We need to ramp the dose up to a certain level so that we can bring to full play the advantages of a dual payload platform. For these two payloads in combo, this is the first of its kind that has ushered into the clinical phase. When it comes to Innovent, our overall objective is to face the whole world. We're innovation-driven and we're going global. The molecules we listed out here, they have the potential to be developed globally. For several colleagues, we're making headways development-wise on both fronts in China and the U.S. in parallel. For clinical development, by innovating in China, we have established process.
We have about 800- 1,000 people in China who are dedicated to clinical development. While in the States, 363, 343, and other potential and promising ADC molecules that we're taking advantage of, our American team has reached a certain size. We have built a full-functional team out there in the States so that we're able to advance the global development of these IO molecules quickly. Going forward, what will be the future milestones for us? What matters the most is to advance IBI 363 and IBI 343 global development. New POC, what matters more is how can we migrate from late line people to front line people and to drive more POC readouts. Overall speaking, for Innovent, oncology, we have all-around configuration. We target the future direction to go of oncology treatment.
IO serves as a cornerstone on top of which we can redefine the next-gen PD-1. We can also have more powerful combo regimens. We can have like double upgrades and double iterations. At the end of the day, we aim to bring about brand new therapies for patients and to go above and beyond where we're now and make a breakthrough on the upper limits or ceiling. Yeah, thank you again, dear experts and investors, for your support. Thank you very much, Dr. Zhou Hui, for your presentation. Yes, indeed. Comprehensive talk with a lot of information. The IO works on oncology. It took us 30 years for us to see the first drug in IO therapy, the PD-1. IL-2, actually, I looked at IL-2 for a long time. For IV use of IL2.
In the past, for decades, I had been observing and looking for IL-2 without toxicity. Yeah, we know IL-2 works, but whether we could create a dosage form based on IL-2, which was administered IV route. Now, Innovent is making great headways on this. You combine it with PD-1, that helps address the instability problem. Third, for other trials, there are precedents we can refer to, but PD-1 plus IL-2, there is no precedence for you to refer to whatsoever. This is true innovation that we respect substantially. Next, we have three brilliant presentations. For example, advances in melanoma and non-small cell lung cancer and CRC treatment. Three angles from which we're going to have discussions about a mAb and a bispecific antibody or even trispecific antibody. Next, it is our great honor to invite Professor Guo Jun.
Professor Guo shared in the previous session a very impressive style. In melanoma treatment, Professor Guo has had wonderful accomplishments. We look forward to Professor Guo's talk. The title is "Advances in Melanoma Treatment: Clinical Progress of a PD-1, IL-2, Alpha Bios." Let's welcome Professor Guo on stage.
Thank you, Dr. Hui, for your introduction. Honorable Dr. Yu and Professor Shen. All right. In the interest of time, I will not name all the names here. Dear colleagues, for melanoma treatment 363, for the first slide, I'd like to elaborate because Hui approached me talking about the plan to develop, for example, the IL-2 PD-1. I asked him why I was not very confident. Why not confident? You look at history. It goes back to 20 years ago, around 2003.
I was young, and Grandma was like Sister Ma back then, or Grandma Shen was Sister Shen back then. The founder of our team, Professor Shen, and also several other experts were put together in a team that there was a Pudu Jin clinical trial or Proleukin trial that was started. That was the first generation wild-type interleukin-2 in the United States. I was responsible for melanoma and kidney carcinoma. We recruited 50 patients, respectively. On melanoma, the efficacy was just so-so. While for kidney cancer, the response rate was 15% versus 10% for melanoma. Proleukin was not marketed in China anyway. Those efforts sort of stopped because I perceived toxicity of IL-2. Of course, once it works, it would be very potent, and the efficacy would last for a long time.
The route of administration was IV, so a million units versus like 18 million units of interleukin-2. That was the maximum dose whatsoever for interleukin-2. People thought maybe the imported products were less toxic given a high dose. Then NKTR- 214 came about. Many of you may not have had experience with it, but I've had a lot of experience with it for NKTN- 214 trial, I was the PI for melanoma and kidney cancer in APAC. Why? It was not very famous because it failed. I lost my confidence. We took up on this project, and we started recruiting patients. I was amazed. I started the proven of this very drug. This year, on the ASCO stage, I felt particularly confident. After I was done with the presentation, all the questions came to me from the audience.
I spent around 20 minutes of time answering questions on the ASCO stage. That speaks to people's passion for this product. People are very interested in this product, indeed. Second, my background is on immunology. Otherwise, I wouldn't have been able to answer those immuno-related questions. The expert asked, "Alpha bias, why don't you activate CD25? Would you activate TREC T cells?" If the answer is yes, you would have immuno-inhibitive effect, right? That drives the point home. Given my immunology background, I was able to answer that very question very well because I was focused on this topic. Actually, like Hui mentioned, to turn the QQ car into a BMW car, but there is more to that kind of transition. Melanoma, this is like a template cancer. Why do we call it like a template cancer?
Because on this very template, you can do all types of validations as you wish. In the concept of IO, melanoma serves as a template, kind of a testing ground. So we do a lot of tests. We are inspired. For cutaneous type melanoma, the indications were approved first on cutaneous because for cutaneous type, with monotherapy PD-1, the response rate was around 50% already, and the duration of the response was long. People were thrilled. That was brought to China, and we tried it on various types of melanoma. Our colleagues said, "It seems PD-1 was not that magic after all. It seems it was not very efficacious because there was disease progression one trial after another." There was a huge difference between the typing. 75% of the melanoma in China are acral and mucosa. These are cold tumors, while the cutaneous type in the U.S. is hot. With a hot tumor, PD-1 works very well. In a cold tumor, it does not work
Why is that the case? Because our car engine has never been ignited yet. For others, they are fully turbocharged. It is just that they are going to let loose the braking, etc. You use the PD-1 to release the braking, and then it will take off. Actually, for your car, it has never been taken off. Think about it, actually the car is not going to set off because the engine has never been ignited, even though you hit loose the braking mechanism, right? Think about the interleukin-2 alpha bias, which is the design of PD-1. I am not going to talk about the T cell story.
My personal view is knowledge is more than just a T cell. It's more about making sure, changing the tumor microenvironment to make sure that the cold tumor has been turned into the hot tumor. Why is that the case? Because think about the interleukin-2 is not only about trying to activate the T cell. And more importantly, it's about the NK and the macrophage, etc. Think about the NK and the macrophage actually are the ones igniting the natural innate immune system because you never ignite the immune system, which is innate for you. How are you going to have to acquire the immune system? Think about interleukin-2. You find that the macrophage, as well as the activated NK, is going to, for example, TNF alpha chemokine. Those things are being released, etc. Think about actually for all those different things as a result of that.
Because of the ignition capabilities, there is going to be the cold tumor turned into the hot tumor, not about the amplification, extension of the T cell, but also for other different kinds of cells being involved in the process. I've talked too much about the background. I'm going to speed up a little bit. Melanoma. Think about I'm going to skip a couple of slides for this one. I already talked about this one already. Think about China's melanoma versus overseas. It's the difference because we have some difficulties. We have some challenges, but at the same time, some opportunities as well. All the different challenges are the opportunities in front of your eyes. When you are coming across challenges, don't feel down.
You'll find that actually for the mucous and as well as the acral melanoma, those two different types, we can make a positive difference. Even though that, at a global level, from our perspective, we are going to compete with overseas drugs for, about, for example, the subcutaneous melanoma. We cannot compete with them, but for competing with the overseas approaches for the sacral as well as mucous . For example, we have the hope. For example, think about the 70% of the Chinese patients suffering from melanoma is because of the sacral and the mucous , those two different types. I enrolled 100, but for the U.S., they enrolled just 10. Because of the huge size of patient population, we have natural advantage on those two different types of melanoma so that you can turn your disadvantages into advantages as well.
Think about the mucosal as well as the acral. Think about this cold tumor to start with. Why is that the case? Because originally, you'll find that the survival for those ones compared with non-mucosal, which is subcutaneous, like the OS, is so much weaker. The existing PD-1, no matter if it's imported or for the pembrolizumab, nivolumab, and also toripalimab, etc., they're actually 0-8%, etc. No matter what you are talking about, for subcutaneous, it's the same as foreign countries, but for the acral and also for the mucosal, it's even worse. Think about the subcutaneous ones. Also, acral and mucosal, it's about 0-15%. You'll find that it's very small. Like I said, the car engine has never been ignited yet. No matter how you hit hard on the braking, it's not going to work.
PFS, even worse. Pembrolizumab approved for actually the first-line indication for melanoma. It is about December. CDE gave it approval for that, for the first-line treatment, pembrolizumab. The data is very low. PFS is 2.3 months only. Also, please bear that in that pembrolizumab is 2.3 months, still get approval already, even going to low ones. Think about it at a global level. No matter if we are in China globally, it is very hard because melanoma. Think about what you take for granted is chemo free, right? It should be using IO. IO is the first choice, but what about IO felt? There is no way to save the patients. Of course, for foreign countries, they approved the TIL. Think about the TIL study. It turns out that they are mentioning.
Think about the lifileucel is approved because of the IO failed. They can use a lifileucel , etc. Think about, do you think you're subjected to enough of the IO? Do you need to go for the last result of lifileucel ? Think about after TIL and also the lifileucel . What about for the patients? Is there no way out? We ran out of choices in our ammunition box. We have to, like IO, work effectively, especially for this IO failed. For melanoma, we could develop some case in point. For example, PD-1 failed and also CTLA-4, actually on plus, for example, left 4, actually all failed. By the way, we ran out of options, but if you're rich enough, you can use the most expensive drugs, but you ran out of expectations or options. What are we going to do?
Thank you for Professor Kong. They have done a lot of basic research on the left-hand side. Think about actually refer to this one. This is about single-cell sequencing. Single-cell sequencing proves that the one in red is about mucosal melanoma highlighted in red. Within the tumor, think about a lot of reddish cell is a macrophage as well as a myeloid cell. These are the typical immune suppressive type of cells. Think about mucous and also the acral, the subtype. Think about they are strong, the immune suppression capability. That's why you find it's cold tumor by definition. The CD4, CD8 has a very low proportion. Think about the subcutaneous melanoma. It's mostly CD4 and CD8. There are not a lot of immune suppression cells, etc.
This indeed tells us that, of course, the acral as well as mucous is a cold tumor. How are we going to address that issue? Here comes the one. The IBI 363. I have undertaken a lot of interleukin-2 trials, just like Dr. Shen. I failed and failed and failed through a lot of downs and downs until we have absent successful. I have been a PI for so many multiple different researchers and clinical trials. It's a rare chance that I'm going to be a successful PI, etc., for successful clinical trial. I told Dr. Yu is that phase three clinical trial. Think about the small molecule melanoma. Pembrol is being benchmarked against IBI 363. Think about pembrolizumab is a global first-line standard. We can undoubtedly compare against that.
In case that for head-to-head, we can be outperforming the pembrolizumab. That will be the ultimate victory for us. Think about the phase three. About two months ago, we already initiated that initial round here in China. The speed of the enrollment is just taking everyone by surprise. Think about what more patients you can cover with your melanoma. Two months, how many enrollment? Less than two months, more than 70, 70 patients melanoma within just two months. That's us. We're amazing. The total enrollment target should be 200 before the end of the year. We're going to achieve the target. Just now, Dr. Michael, you asked me, when are we going to enroll 200 before the end of this year? I think it's going to be before the end of this year.
If we can outperform pembrolizumab, that's a major thing. I'm going to point by Dr. He. They have already said a lot about it. I'm not going to repeat what has been said. For the mucous ones, we have already proved it. Think about the mucous like melanoma. If you use the IBI 363, one microgram per kg prior and after the therapy, you'll find that actually for the tumor infiltrating T cell and CD8 and also the FOXP3 and PD-L1, etc., you'll find that actually things have been changed before and after using this without using it. What does that mean? It means that if you use IL-2, like the basis PD-1 bispecific antibody, it can turn the cold into hot tumor. It's not about amplification of the T cell.
More importantly, you'll find actually the infiltration of the CD8 positive T cell is increasing. It's on FOXP3 and also the PD-L1 expression has been increasing. That's why for the IO naive patients, the efficacy data is taking us by surprise. Of course, if you look at the data, we don't cover actually a big sample size. Sample size is still very humble. Think about 20 for mucous . R is 60. Pembrolizumab is only 14%. 0%- 14%, etc. Think about our performance. Also toripalimab . Think about is zero, actually two, 14%, etc. I think it's almost the same, etc. Think about the IBI363 on efficacy is about 60%. Think about acral is 66%, it's even better. Of course, subcutaneous is going to be better. Of course, think about subcutaneous, etc.
I believe that is going to add oil to the fire. I'm not quite sure about adding oil to fire is going to make any positive difference. The biggest difference is that the baseline is very low, but now it's very high. You find that this is very helpful because for subcutaneous melanoma, the baseline is usually very high, elevated level. For the naive melanoma patients, IO naive. This is for China. The red one is acro. The blue one is a mucous one. You'll find that actually the red and the blue ones actually show clear efficacy improvement in significant breakthrough ways. Technology has already proved that the cold tumor has been turned into the hot tumor, etc. As I said before, think about the clinical trial, phase three clinical trial. Now, only up and running for two months.
We are fast tracking enrollment efforts before this end of the year. Think about when I research on the melanoma, there is only one center of ours, but now we are running multiple centers for melanoma. Guangzhou Center and other different centers as well. In Shanghai, we have a center as well. Domestic here in China, we find that the sites, actually to the number of more than 30, more than 30 different sites could join the clinical trial. Very good. You find that ASCO, our representation. Think about the global melanoma experts really care about this issue. In terms of IO felt patients, what about actually lifileucel TIL? Aside from that, what else do we have? We tried 363, etc. A lot of different experts tried a lot of different ways, like globally.
Like three and two more three, like in combo, etc. They tried putting those together, so many different attempts, etc. Like cytokine at the same time, Nektar like 214, but they all failed. From our perspective, we're thinking that, say, for already the treatment-failed patients. What about the 29 different patient population we have? I guess that there is a clear improvement of efficacy. The ORR, it's 23.3%. You fid that acral is 25%. You may wonder that just a 20-something. Why are you so confident? Think about the first line is only less than 15%. Think about these are the IO-failed patients. Think about the secondary time. Think about the 23%. Compared with the first line, it's even better than first line. For melanoma, it's already creating a lot of repercussion positively.
At the same time, we understand that the disease control rate for the mucous is 85%. Also, generally speaking, it's about 77%. This is amazing because the multiple IO failed patients and chemo target IO also has been tried on all the patients where they failed. Still, even you try this one on them, still have a high decent efficacy and DOR is very long, 14 months, duration of response. Aside from the DOR and the PFS, 5.7 months. As I said before, think about Keytruda. First line is only 2.3 months only. Think about actually for the multiple relapse patients failed all the previous lines of therapy, it's about 5.7 PFS in terms of months. This is a wow effect for everyone.
That's why in this year's ASCO, I guess that this is like the shining star. This is taking everyone by positive surprise at ASCO for this year. At the same time, I'm the year oral presenter for the education session for that, talking about mucous subtype melanoma patients. For mucous subtype melanoma, I did an oral presentation talking about the future hope for the 363. Not only the vs lifileucel , but also think about the new IO, new gen. The new gen like PD-1 is going to stand a chance to replace and substitute for the legacy one. For the new PD-1, if we can do it very well, think about if it's being applied, maybe the efficacy is not going to be inferior to the subcutaneous.
Sometimes you'll find that this is going to mean big things for the mucous and the acral. This should be the pride of, for example, the breakthrough designation and a fast track designation achieved by Dr. Rees team. Think about the IBI 363. Think abut melanoma in this leading poster child. The treatment is going to be rolled out to the cold tumor and other cold tumors as well, including the ones we said before. In the past, we take it for granted that maybe the IO failed. Like Dr. Shen's team, the cold tumor as well, gastric cancer and the CRC, like intestinal cancer. Why did IO in the past few years fail? From this perspective, if you look at lung cancer, PD-1 initially had to work, but when it comes to GI tract, it seems it no longer works.
Maybe it's still a cold tumor, like a car is yet to be started. You're busy with putting your foot on the brake pedal. It doesn't work. You need to start the engine first. You lower down the parking assist, then the car will start to move. Melanoma is like a role model for other solid tumors to follow. Thank you very much.
Thank you very much, Mr. Guo, for a wonderful presentation because the response rate of a new drug is 80%. That's like the peak or pinnacle you can reach. There's like the 20/80 law, right? No matter where we're talking about, the law of 80/20 basically applies everywhere. After hearing Professor Guo's talk, since we're like a technological and a science innovation summit, this seems like a competition between martial art masters. Hundreds of years ago, we had Dr.
Yu initially who talked about those new drugs, right? We heard the presentation from Professor Guo, who was like the Kung Fu Master, Mr. Guo, in Chinese martial art mythology. There is Grandm a Shin, Professor Shin. We also heard the talk from the Kung Fu Master of Grandma , who was more like the founder of the Emei martial art camp. That may be like a better kind of analogy. Indeed, this is like a martial art contest. Professor Shin, last year, when there was like a medical committee of selection and there were objective rankings, there were experts in that committee as contestants. From a clinical perspective, it's an easy job for surgeons to publish papers. Professor Shin actually ranked ahead of me in terms of that committee member selection rankings. I was deeply impressed with Professor Shin.
No matter how hard I try to stay on the top rankings, it seems Professor Shen was always ranked before me. I think Professor Shen is like a top master. All right. This is a brilliant track. Dr. Yu, the next speaker, Professor Zhou Jianya from Zhejiang University School of Medicine, No. 1 Hospital. Lung cancer is one of the most important tumor types. At ASCO this time around, one of the most eye-catching trials. Professor Zhou is going to walk us through some of the experience in terms of the lung cancer multi-site clinical phase one, focusing on 363 for IO-treated advanced stage non-small cell lung cancer patients with respect to safety and efficacy. These results are catching worldwide attention.
Without further ado, let's invite the next speaker, Professor Zhou Jianya from First Affiliated Hospital to School of Medicine, Zhejiang University. Floor is yours now. Thank you, Dr. He, for your introduction. Honorable Dr. Yu Dechao and Professor Guo, Professor Shen, Professor He, and the dear experts, many of you are my mentors. Today, I'm very honored to have this opportunity to report to you the progress of IBI 363 in lung cancer. I'm very excited because I had dinner with Professor Guo. Professor Guo took deep pride after he delivered his presentation during ASCO. I still remember in IBI 363, I showed perseverance in lung cancer. Why? Because I was inspired by Professor Guo with regards to his experience in melanoma. Now, from this standpoint, the patient group is way bigger than those patients in melanoma.
Since this asset works on melanoma, we're hopeful it could work in lung cancer as well because in the solid tumor arena, regarding efficacy, lung cancer always follows in the footsteps of melanoma. Now, from that perspective, after I talked to Professor Guo time and again, yeah, in bio or IO, this is going to be a potential asset which you can add on. Yes, indeed, this may be like a new kind of a molecule. All right. The outline of my presentation today, several parts. First, I'm going to talk about the research status of IO resistant advanced stage non-small cell lung cancer. On lung cancer in China and the rest of the world, the incidence and mortality rank number one. It is a huge economic and a societal burden.
Across the world, there are more than 2.5 million new cases every year, while we have 800,000 new cases of lung cancer in China. It is a grand picture. We are receiving a lot of attention from industry and capital markets. At present, for driver gene negative non-small cell lung cancer, there are a lot of unmet clinical needs. In a first-line setting, as for PD-1 negative patients, there is about one-third of the patients falling in a bucket when it comes to non-small cell lung cancer. If we combine chemo with IO, the median survival is between one year to less than 1.5 years. Basically speaking, 18 months or 15 months, that is what we are talking about. In terms of IO treatment, back then, we perceived the influence of IO on lung cancer, very good efficacy. Despite that, most patients face the challenge of a drug resistance.
For IO, the charm of IO is we're able to cure some stage four lung cancer patients, but there are a few patients belonging to that category that are able to be cured. For the vast majority of patients who may suffer resistance to IO, right? In that context, how are we able to overcome IO resistance? How can we diversify our regimens? How can we modulate the immune microenvironment? How can we prevent the depletion of T cells, right, and apoptosis? How can we have more precise treatment based on driver gene testing? Multiple targets, multiple mechanisms, we can shape new strategies. We have made a lot of endeavors along these lines. Now, following IO resistance, there are multiple trials, right? Indeed, we have gone through ups and downs. In terms of multi-target TKI, there is LEAP-008 and a CONTACT01 and also 301.
These target, multiple targets, these are kind of drugs. However, there is no long-term OS benefit. What about ADC, represented by TROP2 ADC? There is TROP2-Lung01 and EVOKE-01. On resistant patients, we have not seen the benefit compared to the control group of docetaxel. There is two-target combo or combo with CTLA-4 and with TIGIT and a PD-1 plus LAG-3. For all these combo regimens, we have yet to see crystal clear clinical benefits. There is no active response. Plus, there is poor safety and tolerability. When it comes to the squamous cell carcinoma subgroup, it is very difficult to see the trend of showing efficacy. Cytokine, there are cytokine inhibitors, right? And explorations thereof and therein. For example, the growth differentiation factor 15 monoclonal antibody. For resistant patients, the ORR of 19% based on 83 patients. PD-1 plus cytokine agonist.
are two drugs combined. What we are seeing here is interleukin 15 receptor, the WOC data readout last year, indicating the median OS of 14.1 months. Then IBI 363, which I am going to place my emphasis in in the latter part of my presentation. There is also the angio kind of a genesis inhibition drug. There is some ongoing trial which are on the phase three stage. There is T-cellular therapy, there is ADC, there is oncolytic virus as well, and some of those explorations which are underway. Next, let us zoom in on the research progress of 363 in lung cancer. As I mentioned, there are a lot of cold tumors that are existing out there. There is also IO resistance. Design-wise, through the dual immunoactivation, and we hope it will work, like Professor Guo mentioned.
Actually, once you put your foot away from the brake pedal and onto the oil throttle, so the car will accelerate, the T cells activated, and kill more tumor cells. How can we overcome T cell drug resistance and overcome the problem of a cold tumor? Yes, indeed. The MOA design here is completely different from those conventional designs. Non-small cell lung cancer, 2025 ASCO, we delivered all our presentations. I'm very pleased to have this opportunity and enjoy myself in the grand feast of ASCO. I received the passion and interest from the expert panel and the participants. We had over 20 minutes of discussions around IBI 363, but out of a pity, I didn't purchase Innovent shares ahead of time. I missed that train.
Anyhow, based on this data, so quickly, we got like the fast track approval from the FDA, and we got the designation of a breakthrough therapy from CDE. A couple of years ago, we kicked off the trial to evaluate the advanced stage solid tumor. There is another speaker to talk after me, right, with more details. In solid tumor at my hospital, we explored for different tumor types with IBI 363. So we centered our efforts around not only efficacy, but safety. Earlier on, with my early experience with the drug, yeah, I was always asking the questions about safety because I was mostly concerned. But for this drug, not any single IL-2 was able to be tolerated by patients at the same time with inhibiting tumor.
Until April 7, 2025, we included 136 non-small cell lung cancer patients, including 67 squamous cell and 58 EGFR or driver gene negative adenocarcinoma and eight cases of EGFR mutant adenocarcinoma, plus the other three non-small cell lung cancer types. Baseline characteristics, yeah, they're in line with the previous trials. I would like to emphasize the PD TPS expression. We have more than 30% of the patients with a TPS of below 1%. For squamous cell carcinoma, one case not treated by IO. All those other patients are IO treated. Furthermore, more than 60% of the patients have gone through two lines or more treatment and failed. When they're on IBI 363, more than 60% of the patients are in third line or even seventh and eighth line of treatment. ORR and DCR indicate very strong activation of immunity.
3 mg, which is defined as high dose group. 1.5 micro per kilo is defined as low dose group. For high dose group, the confirmed ORR is 36.7% for squamous and 24% for adeno. DCR is 90% for squamous versus 76% for adeno. Low dose group is 10.2% for squamous and not to yet DOR for adeno and not reach the DOR at the 3 mg yet. This indicates the response may be long lasting.
What about a high dosage like a cohort PFS? Squamous cell is about 3.3 months and 4. Adenocarcinoma is about 5.6 months, etc. Squamous cell is 9.3 months. We can compare with historical data. You can see very clearly that a lot of experts are following attention for the special feature for the 363. It has a longer duration.
You'll see that actually the 17.5 months OS is achieved at four for the low dosage. The high dosage, about 12 months OS has not been achieved yet. You'll find that squamous cell is about 70.9% and adenocarcinoma is 71.6%. The 3 mg per kg, you'll find this is over 70%. If you try to use that and compare that with historical data, from my perspective, I always really want to check to compare with like the CheckMate, like the study, etc. Of course, this is not going to be the controlled group and cohort for this trial. The CheckMate study actually is not about IO treated as the first line, but our patients actually have gone through the first line IO. Think about 2024, the DCO publication, etc.
You'll find that actually, so you'll find that like the data from this one perspective. You can see that the control group, actually, they have been through the IO and they become tolerant. For this study, you find dosetaxel, the ORR is about 12% no matter if that is adenocarcinoma or squamous cell carcinoma. For our one, high dosage is about 36.7 months and the low dosage is about 25.9, etc. This is very exciting, giving us a lot of hope and confidence. You'll find that actually the ORR doubled for the adenocarcinoma and also the PFS is extended by about 1.5-2.5 times, etc. Now let's try to look at this IO tailing effect, dosetaxel, 12 months OS. If you refer to the dosetaxel, median OS is about 9.4 months.
Adenocarcinoma is about, for example, the 12.3 months, no matter the high dosage or the low dosage, you'll find that as a result of that, based on the data, we are so much better than docetaxel. Of course, there are a lot of questions being asked about, say, for example, what about the smokers and the non-smokers? What's the difference between this one? Model therapy in the second line, driver gene negative, you'll find that the PFS and OS and ORR, so the non-smokers data is being shown hereby. People might be wondering, why adenocarcinoma actually isn't worse than those suffering from, for example, squamous cell carcinoma? It's quite counterintuitive as well. Hereby, let me give you some explanation. Think about the lung adenocarcinoma patients in our enrolled patients group.
It turns out that in our cohort, so think about actually, so we do not enroll a lot of patients suffering from the carcinoma. It only accounts for 56%-71%. The CheckMate study 017 is about 79%. Keynote 189 is 88% of the patients that way. The smokers. Think about which means that for the U.S. clinical trial, there is a different patient profile being enrolled in the study. We enroll a smaller proportion of the smokers. If you are trying to put that on the international stage, maybe I guess that maybe the efficacy can be better. We are trying to think about actually for nivolumab is being compared as well. Firstly, docetaxel, you will find that no matter if it is adenocarcinoma or the squamous cell carcinoma compared with nivolumab, you will find that the benefit profile is similar to that.
We can clearly see that for nivolumab, the monotherapy, the OS and PFS, the clear benefits, etc. In general speaking, I believe that IBI 363 is similar to that. What about the non-squamous cell carcinoma? PFS for nivolumab is limited and OS significantly improvement. Back then in a study, you'll find that the CheckMate 017 and also the nivolumab for the non-squamous cell, the IBI 363, if we reconcile against the nivolumab in CheckMate study, is similar. Adenocarcinoma is not as obvious as the squamous cell for the late line patients therapy. The OS improvement is bigger. Compared with nivolumab in the CheckMate study, it is similar. Now, let's try to look at the PD-L1 expression. Once it is bigger or equal to one or smaller than one.
Think about the ORR based on the data. Maybe that's a smaller than one expression might be better. I think there are a lot of questions about this one as well. A lot of attention has been directed to that issue, but in our data. We can think about, say, for example, from our perspective, we give you the data, we give you the phenomena, but from a scientific perspective, compared with the PD-L1 negative patients, are we showing better? Probably not. I really hope that we can have a bigger sample size so that we can do some statistical analysis to the point that we can get a bigger sample size. Also, your PD-L1 negative patients, we have the confidence for those ones.
Multiple lines of, like for example, the treatment using our drug can benefit more, especially for the IO, like failed or IO tolerant patients, they can benefit a lot. Safety profile in our study, you'll find that the TRAE is about arthralgia as well as a rash, etc., or some of the fever, etc., actually eosinophil, etc. Think about actually I can come to the realization that this is the drug, actually there are two side effects. You find the PD-1 as well as the interleukin 2, like the bad effect is already being there. Arthralgia and a rash, generally speaking, I think it's related to the interleukin 2, etc. That is to say, my view is that it already works, it's effectiveness, because otherwise there wouldn't be treatment-related AE like those ones.
The thing is that how can we better manage those ones and overcome the negative effect? Also, once like the 363 is being launched into the market, we are going to subject that to more discussion. The AE issue, TRAE, safety is controllable. It is manageable because for the TRAE, grade 3 above drug discontinuation is a rare occurrence. Hereby, we have the data hereby. People are asking me, so they take it for granted that you are a conservative person. Maybe when you go back to like the first line treatment, we have to wait for the data from the first line treatment. I guess that, from our perspective, we have to emphasize that. Think about the grade 3 above TRAE data. It is about 43.9% in our data.
PD-1, as well as VEGF, so the bispecific antibody, EGFR, and also the MET, etc. Think about the grade 3 TRAE is bigger than 60%, 60%. Why am I so modest? Why am I so modest by claiming that we have to treat it very precautiously when it applies to the first line approach? We can promote it to early lines and like a first line to explore its effectiveness. Okay, that is like from my perspective, because prior to that, we are always wielded with over precaution. We have to strengthen the management, etc. By far, if you look at the data, data supports us to use that as a first line treatment. Let me summarize a little bit for the content I have covered.
Think about the 3 mg per kg, you'll find that 36.7% ORR, which is exciting to everyone, squamous cell like carcinoma. The PFS is 9.3 months in mean level. Compared with other IO, I guess that this is going to be a major breakthrough, which means sure is that actually the IO treated like lung squamous cell like carcinoma and PD-L1 low expression patients. You find that monotherapy, the 363 is safety controlled. Let's have the outlook for that for the first line, the non-small cell lung cancer and in the juvenile therapy. We can think about like IBI 363 plus chemo plus ADC. We can open up more possibilities and also in the first line as like the monotherapy has a lot of advantages or possibilities. Thank you. Thank you, Dr. Zhou. Thank you for an excellent presentation.
Think about for the lung cancer is different from other different cancers in the sense that, so think about the target therapy seems to be working effectively. So target effective and target failed like patients. So what are we going to do? Maybe IO is going to be the most applied approach if they failed like a targeted therapy. What about the PD-1 is negative, which means that it does not work for them. We are so concerned about it. That is why we are happy to hear that IBI 363, especially for the one suffering from the squamous cell carcinoma. This is more effective. Think about in the past the pain points for the treatment of lung cancer. IBI 363 is a very good viable data showing to everyone.
Actually, you'll find that the OS is not being arrived in two years already, which means that it's longer than that, it is very effective. Thank you very much, Professor Zhou, for your excellent presentation. Thank you so much. I guess that just like it can too long like a martial arts. At the end of the day, we have more hopes. The TCM, you'll find that for lung is great, and then the CRC may have hope, etc. Let's welcome Professor Xu, who is coming from the Zhejiang University School of Medicine First Affiliated Hospital, talking about the IBI 363's advantages in the CRC treatment. Welcome.
It's the first time I am going to make a presentation like this one. Thank you, Dr. Yu and Dr. He and Dr. Shen, etc., my peers. Good noon, everyone. From my perspective, I'm going to talk about IBI 363. What about the CRC treatment of the initial results? First of all, let's try to look at the CRC. Think about actually this is a major oncology tech that at the same time is increasing a lot, especially for China. Think about for the outpatient clinical level, there are a lot of different endoscopic treatment. Sometimes you think it's, for example, the minor issue, but it's going to be a very big incidence as well for the GI tract cancer. China, like adverse countries, you'll find that this is very often seen, especially when you identify endoscopic polyps. For example, molecular subtyping has always been there.
From this one, I think it's like the, for example, immune inflammatory and immune activated is very high and also the immune exclusion and the desert one is also a lot as well. At the same time, what about like the IO effective like CRC patients? Very rare occasion. That is to say that most of the time it's a cold tumor and also the latest stage, the vessel stage. MSS has a high DMMR patients. 5% will have a very good prognosis as well. On the right-hand side, you'll find that most of the first line treatment for CRC patients as a code like. You find that the MSI, MSS, and pMMR. You'll find that actually, the EGFR targeted VEGF and also the chemo and the second line, third line.
That is to say IO across all the, like, the treatment for, like, CRC maybe is not working that effectively. What about the early attempts for, so think about the immuno checkpoint inhibitors. For example, the pMMR, MSS, latest stage CRC patients, you'll find that the cold tumor, tumor regression is usually, for example, the dMMR, like the, for example, so the dMMR actually for the CRC patients, which means that most of the time the tumor still is not regressive. It's still growing as well. Let's try to look at this one. Think about the immuno, like, checkpoint inhibitors plus, like, the targeted therapy, the ORR smaller than 10% is 8.7%, 3%, and 7%. PFS and OS respectively very low as well. It's about 1-3 months, etc. PFS and OS is no smaller than 10 months, etc.
Let's try to look at like the ICI plus the ICI, so the IO. You'll find that, for example, PD-1, PD-L1, so and LAG-3 and PD-1, etc. By using those things in combination, they're not very effective. We're not very happy. The PFS and ORR, you'll find is 0.8% or sometimes 0.8%. PFS is less than 2 months. OS is about 6-7 months, etc. Of course, what about the chemo plus like the IO, the first line approach, etc.? Think about those ones. As a result of this, it's a rejected to non-hepatic metastasis patients being enrolled for this one. We can see that Nivolumab for FOLFOX6 and Bevacizumab.
The SOC and plus like the IO, so targeting like the latest stage, like first line pMMR, MSS, metastasis CRC, no matter the second, like phase two, phase three trial compared with the SOC, we did not see the PFS and OS increasement or improvement. We did not see that. For the full morning session, we are talking about the IBI 363. Actually, it is about a different MOA, mechanism of action. We are trying to find this difference to turn that cold into the hot tumor. What about the mechanism of action that is obtaining for the conversion of cold to hot? It is about overcoming the issue of a cold tumor. For the latest stage CRC patients, for the cold tumor, it is effective.
CD8 cells in a CD25 in a PD-1, PD-L1, etc., etc. Yes, indeed, there is marked increase in these cells. As a result, these cold tumors in theory and in practical research, as a result, there is like the ground for cold tumors to show response. There are solid grounds for that to happen. Now, from 2000 up to now, some of those colorectal cancer patients we recruited. This is the baseline characteristics of our data. As we can see, 363 monotherapy treated 68 subjects, then 363+, 305 for bevacizumab in 76 or 73 cases treated with that regimen. For those patients, you look at MSS pMMR patients. Not a single patient of these are dMMR, and around 20% of the patients who are on previous IO therapy. As we can see, the overall response rate is around 16.1%. And 17% without liver metastasis and 14.4% with liver metastasis. These are late-line treatment, for example, line three and above and beyond line three.
Yes, indeed, the efficacy is pretty eye-catching. The next, the increase in response rate, 73 cases, among which 15.1%, and at bevacizumab combined with 363, this is 3 mg per kilo. Thirty-three patients is 19.4%. And without liver metastasis, it is 31.3%, which is pretty shining. The waterfall plot shows you those messages very clearly. Now, what about PFS? As we can see, out of 73 cases, the total is 7.4 months. For the group without liver metastasis, it is 7.4 months. In the combo group with bevacizumab, the PFS is 5.6 months. The two survival curves are pretty clear. This slide, this is a typical case. There is liver metastasis in a patient treated with 363+ bevacizumab in the first line setting with treatment. The hepatic lesion regressed distinctly.
As shown on the left panel, 107 cycles of medications from April 2023 to May 2025. That long period of time. On the right panel of the slide, it's also one of the case studies where there is liver metastasis. The treatment works on this liver metastatic lesion. Compared to previous three line or third line above crux, the blue bars refer to 363 or 363 plus BEV. In terms of ORR and PFS numbers, they are markedly superior to the gray bars, which are SOC and common therapies. These are current standard of treatment. In comparison, you can look at a better ORR and PFS of the blue bars. The OS has doubled, 363, just like lung cancer. There is a strong tailing effect. As we can see here, TACE 102, the longest is like 10 months for frequent TINIP.
For this drug, the total survival is like 16.1 months longer than the control. The MSS advanced stage colorectal cancer, there are some of the ongoing trials, 363 plus bevacizumab and CapeOX in the first line setting. For this trial, this is a randomized phase two trial. One group is with an add-on of 363, while another group is SOC, namely BEV plus CapeOX. Recruitment is happening very fast. We're hopeful that the data readouts will be available by 2026. Overall speaking, most tumor types are code tumor and phenotypes, on which we have seen some optimistic results and hopes with 363. The critical phase two trials are ongoing. Thank you very much for your kind attention. Professor He, do you want to sum up? All right. In the interest of time, we are about to transition to the next session. Thank you very much, Dr.
He, for your fantastic chairmanship. The next part is a round table discussion, globalizing China's biopharma innovations. So China's innovative biopharma going global and China is gradually taking the lead. We're going to talk about the globalization opportunities. We have four panelists who will be invited on stage: Fengdian Imagine Partner, Lilly Asia Ventures, and Dr. Hong Zhang, Asia Partner Head, Roche, and Professor Shen Ling from Beijing Cancer Hospital. And Mr. Richard Yu, CFO, Innovent Biologics. Please come on stage. Let's have a dialogue. Welcome. Welcome on stage. Yeah, we talked about the R&D results from a professional perspective. Next, let's look at the industrial perspective with regards to how China pharma can go global in a better fashion. All right. Welcome to the four panelists. First, we'd like to extend our welcome to the four panelists. First, for Dr. Hong Zhang.
Thank you for joining us. First, in recent years, the multinational pharma is very active in PD transactions in China. What's your take? What are the reasons behind? What are the drivers behind these active PD deals between China and multinational pharma? To be here today.
Thanks for the invitation. Great to see all the science explained here by the scientist. Yeah, the question is about the Chinese innovation. What have we seen here? I go back to 2020, the time that I was interviewed for my role at Roche. I'm currently working for Roche, the Head of Asia Partnering. The question was often asked for me, "Armian, do you think there is innovation in China? Innovation such that is first in class or best in disease?" I said, "I don't know." In 2020, it was unknown.
Maybe there is something in phase one, maybe earlier. I said, "I believe in the future, there will be innovation." I also think it has now been proven that there is innovation. We have seen a whole wave of ADCs now coming. We have also seen one of the parts here that is a trust in data. In the past four years, we have signed about five deals, all the five deals in the field of oncology. Now, the question that I got in the beginning is sometimes, "Can we trust the data?" "Can we trust the data?" was a question that with the first deals were asked. The answer was the data was reviewed by us. We looked at the data, and we felt comfortable because we did our due diligence.
Now, this has now been repetitively the case that we have seen more and more that we can repeat the data that we see. At Roche, we often, when we do an assessment of a molecule, we do a due diligence. This due diligence is also including an MTA, a material transfer agreement. In this material transfer agreement, we get a molecule of the partner. We do the assessment. Now, in the four and a half years that I'm here, in all the cases, with all the biotechs, we could repeat the data of the Chinese biotech to the letter. We could just confirm this. This is not a case with the Western biotechs. There were cases of European biotechs or U.S. biotechs that we could not exactly replicate what they are doing. Now, what is part of the success?
Part of the success is part because of my neighbors, right? The neighbors that put the financing in place and the neighbors that lead the clinical trials that make it really successful. I would say without the help of people like E, who is really supporting innovation and is not only supporting it financially, but also with advice and staying close to the companies, I think this is a big differentiator because it is not only important to give the money, the cash, but also follow up with the companies and stay close with them. Another part is the close collaboration with the CROs. We see at Roche, where we do a lot of internal work, that sometimes you need to work closely with very efficient CROs that are lean in setup and can work almost seven days a week, 24 hours.
With Chinese biotech, when they tell to you, including Innovent, "We have certain data at a certain date," they will deliver, A, ahead of the data, ahead of the date, or at the date. It is very reliable. Whereas other companies, sometimes they might deliver on the date, but it might also be a few days later. I think that is very important to see. Also, I think it is very important to see how is the corporate culture? How is the leadership? That is what you also see here in Innovent. I come later back to that on number two. You see here an inspiring leader who is leading the company with vision. You need to have a vision. You need to understand and go after novel targets because this is the big difference, right?
If you see in 2018 and 2019, the companies would go after MeToo, biosimilar, but now they go after novel targets. Not only very novel, if you now look who publishes novel targets, many publications are of Chinese origin. So not only are they there to work on the novel targets, but also the novel target selection is now happening in China. So overall, I think it's really impressive what China has done so far.
Okay, thank you for your profound and professional points of view.
[Foreign language]
Which means that the excellent innovation capabilities have already been enriching the cross-border PD deals and making the landscape better and better. Question to Professor Shen Lin: Just now, Guo Jun used a very humorous way to describe you, call you Grandma Shen. Grandma means not you are old, which means you are senior.
As the bridge between China and the rest of the world, you are the proactive participant in international conferences. What about your observation? In the ASCO meeting, what about for global, like the multinational practitioners, and how do they view the innovative drugs in China? Did you see any difference in their comments for China, for Chinese companies and global, leading the global R&D for innovative drugs? What are the different attempts we have to make?
This is an excellent question. As a matter of fact, I can feel very strongly about the question you are asking me. The first one is that, think about elective for China-specific high-incidence tumor for China. Relatively speaking, in Western countries, it is low incidence. Think about actually the R&D capabilities for Chinese companies. It is based upon the great experiences.
We are part of the global ongoing clinical trials. We scale the learning curve by being part of the global. A lot of the researchers for different companies. Think about the marketing guys, decision makers, the high exposures who are working for MNCs as well. As a result of that, all the different researchers have already been there for the global clinical trial. We have been through there. We have seen what's the best advantages of our inventory. What about shortcomings for China? Everyone is working super hard ever since the year 2015 until the policy has been given an upgrade for China domestically for the innovation of the development of the new drugs. We are in a fast track of development as well.
Just now, thank you so much for our speaker who mentioned that we have to look at the corporate culture for the company. The most important thing is about think about the data from your innovative drugs as well. Traditional medicine told us that it's based on the experience, but we don't have the data. We only have the experience. Now it's quite the opposite. Now it's the time when we have the clinical trial experience, and we are using like the cutting-edge new innovative drugs to make sure that we get the data and present it to the rest of the world so you can find this reliability and high quality as well.
That's to say that actually for the international stage, as we showcase a lot of innovative drugs and the reliable data, nobody had any concerns about the data reliability for China. They wouldn't say, "Oh, this is a China data." So it's dubious. Nobody is going to say that. As long as it's based on the clinical problems and based on unmet clinical needs, as long as it's based on that and you do the innovative research on basis of that, it's fully reliable and trustworthy. That's the first point of observation. Secondly, you'll find that the researchers in China have the difference of the role. In the past, we are looking up against the best innovators globally. We are following their footsteps. Now in some areas, we are ahead of the curve.
We are ahead of the pack, not just on the same level with them. You'll find an ADC type of drugs at the same time, bispecific antibody and also the gene cell therapy, et cetera. Think about all three areas. For example, means that the fastest growing area of the anti-tumor. Think about all over the world, China is already ahead of the curve. That's undoubtedly. That's why you can see that very clearly that here in China, in terms of R&D as well as our innovation, we have done a lot. In the past, we are not having enough courage to do so much highly risky innovation because for emerging new guys in the market, nobody is so strong to fight against other risks or to resilient against other risks. Now it's different.
It's okay that we learn some trials and errors because if one failure, we have so much more successes. I can feel strongly about this one across multiple disciplines. It's a great cross-fertilization, et cetera, especially for think about the IBI 363. Think about actually for the cancer area and based on the field, the past experiences is offering the telltale sign for everyone. The new drug has been developed filling the shortcomings and then go to clinical trial. Also, I'm doing the GI tract cancer, right? I have learned a lot from everyone's intervention. Professor Guo Jun, think about we are working for the same hospital. We don't have a lot of communication with each other. We often like a spat with each other from like, but think about the mucous -related melanoma.
It turns out that, so you find that the B cell, so MBNC, MACVISH, so related to that compared with a GI immune system, is quite similar to each other, which means that we can cross-fertilize each other by learning from other disciplines so that we will benefit the patients. Because you cannot afford to say that all the patients will go from day one, from the first attempts, which has a chance of good or not or something. If we do cross-fertilization by learning each other, we can reduce the gap. Clinical resources, the doctors, and also the innovative drug makers, the R&D capability has already positioned us at the top of the world arena. That is to say that maybe in the future, people are going to have eyes on China and try to find the problems for us. Then again, on the trajectory of innovation, now we are going to take more firmer steps and more confident, etc
Thank you very much, Dr. Shen Lin. Wow, that's super passionate. It's about the solid research capabilities of Chinese companies that has won the respect of all the global peers. Our data has indicated our research capabilities as well. LAP, as one of the successful long-term investors in China's biopharma, just like Wall Street mentioned, the deep-sea period for China's industry is already there. Innovent Biologics, the innovators here in China, had a performance which is still a performance in HCL. What about Dr. Yao? How do you view, for example, the reevaluation of the Chinese companies creating the re-rating of the Chinese biopharma? How might the investment strategies evolve going forward? What will be the role of the capital market in this process?
Okay, let's try to look at the past, the current, and the future for industry development. If you're asking me about the history, a lot of things are like purely like over there. If you do like specific analysis because industry is composed of different companies. Of course, aside from companies, we also have our principal investigators, PI, et cetera. Think about the industry. You have to look at what is the PI up to, what is the leading guys, what are they up to, what are they working on? From my perspective, I guess that not only the barometer for China's biopharma innovator is the leading company here. Let's try to look at where Innovent is traveling towards.
This is going to become a very good indicator as to the future innovative pathway for China's innovative drugs. We are very pleased to invest in Innovent. Actually, in the year two since the inception of Innovent, the reason we invested in Innovent is because back then of all the companies who are doing the, like, for example, biogenetics. Innovent is one of the earliest campaigns. We really appreciate that, like, of the biogenetics. I remember that actually at the meeting year 2012, Dr. Michael Yu told me one thing, there is actually a very viable target point, which is a PD-1. He told me that Michael said that I, that's something we must do. Innovent must be there for PD-1.
The board meeting actually is going to produce a lot of people who are surprised because they really want to do the generics of biologics. They understand, they don't understand a PD-1 or what is a PD-1 exactly. Michael Yu said that it's worth it. Actually, if you are not a decision made, I think I will spend my own money trying to do it. We need to do it. Actually, it sounds very arrogant if you are claiming something where others don't understand. The reason we put money in Innovent is because we don't understand what is PD-1. I was wowed by the sincerity and the passion of Dr. Yu.
Then in 2015, you understand that Innovent Biologics, so across all the players here in the world, has become the first one in China to go out for globalization. 2015. Second one, it is 2017. The Nanjing company called Chuanxi Legend. Think about actually, since it is launched in the market and covered by the National Health Insurance Leader. Prior to Innovent IPO, I can feel strongly about the execution capability of Innovent Biologics company. After the IPO, I retired from the role of the Director of the Board, but I came up with a new appreciation for Innovent because for me, Innovent represents a company who is very strong to constantly challenge the existing self. From the antibody, small molecular, anti-oncology, metabolism, and immune therapy IO, and also under trajectory of a PD-1.
Think about also who used to do PD-1. A dozen companies did PD-1. It is a rare chance that actually Innovent and Roche could be the rare players who can always do the better version of yourself on your platform. Others are just happy selling for revenue, but you are already figuring out the next generation PD-1, PD-L1, and interleukin-2. You have strong capability to have execution power, and you always try to make breakthrough by challenging the old self to do better self. These are the two attributes I really appreciate from Chinese innovators like Innovent Biologics and China PI. That is to say innovation 1.0 to 2.0. That is why you are there for me, for Innovent and for China innovation. I am of the full confidence.
You mentioned confidence, right? As a matter of fact, in the future, how do you see the trend for the capital market? Do you have any expectations or aspirations, etc ? I think biopharma by its very nature is a high-risky industry. It's a risky trade. In the invest, the alpha and the beta investor jargon. We really appreciate the alpha better. You find that there are successful biopharma companies, but on the basis of successful wave, there will be like a bankrupt companies as well. What kind of company investors really appreciate it? Really, if you need to invest into. I guess the science is quite unpredictable. It has its own pace and tempo. Think about the ADC is making a lot of waves positively. When I first joined the industry, ADC about 15 years ago.
You find that because one failure after another, nobody would like to touch upon it. Same is true. GLP 20 years ago, but there are the founding fathers actually that, for example, GLP five years ago who started to do it, become like the most successful pioneers in our industry. We invest in a company who has the capability not in predicting the scientific trend, but the company has the capability to write down the opportunities brought about by scientific like innovation or progress. We find a case in point in Innovent. As an investor, I would not say that actually, I like all the companies who are doing innovation. I do not like most of the companies in the industry. As for the few companies I really like, the company must be someone.
As the investors, I guess that actually they will assist on the opportunities. They will trust in the opportunities coming at the same time. They constantly do the better themselves and create a next round of opportunities for those companies. I really appreciate as an investor. I really trust on that ground, I really trust Innovent Biologics. Think about ever since the year 2012, we first invested in Innovent. We have established six funds ever since then. All six funds have exposure to Innovent. When we exit like the previous funds, we really want to follow up with money coming from the next round of the fund. We really appreciate it. Thank you so much, Dr. Shi. Let's give a round of applause to say thank you to Dr. Shi. We were encouraged and moved by you.
Like, excellent companies can always understand what's the next opportunity for us. Exactly these opportunities brought down, and Innovent exactly has the capability. The first round, we are talking about the Chinese companies going global for China innovation. The next one, we're about, let's focus on Innovent Biologics as a role model for China innovation going global. How can we formulate the strategy and seize on the opportunities?
My first question is Richard Yu coming from Innovent Biologics. You find that, like Dr. Shi mentioned, that Sintilimab, Tyvyt has become the, like, for example, the highlights of the PD-1 brand in China going global. Yesterday, much anticipated, dual-target waste management therapy sign now, which is a must-do type injection, is already being approved by the market approval. It's a new threshold for a new era of global expansion.
As the representative for innovative Chinese pharma companies, how do you see the opportunities and challenges for your company going global and from the financial strategy and the investment and pipeline planning perspective? How do you plan for your globalization strategy?
Thank you very much, the moderator, for your excellent questions. As a matter of fact, in the keynote presentation of Dr. Yu, he mentioned one thing I would like to quote. This is a golden era for the innovative drugs for China. In this golden era, we have a lot of opportunities as well. First of all, in terms of the policy, we can see that policies for innovative drugs in China over the past 10 years, there are a lot of changes as well, say from the speed of the approval of the drugs.
It used to take about three to four years before you can give a go ahead for the new drugs, but now it's shortened to about 12-18 months. You'll find that MAH has been made possible as a result of that. A lot of innovative concept companies have the capability, innovative molecular can be turned into clinical drugs, and then they can market that in the market and sell them. In terms of innovative drugs, the pricing for China, we have a lot of supportive policies as well, introduced commercial insurance to make sure that the innovative drugs are, to give it more pricing flexibility as well. I guess all those things can give us confidence that for innovative drugs in China, we can see a lot of policy support.
Second, innovative environment in the past 10 years or so, Dr. Shi Yao, a professional investor, as well as those secondary market investors, a lot of capital has flocked into the very industry of innovative pharma. Many talents returned from overseas to China. These talents brought with them avant-garde innovation and R&D concepts. No longer are we lingered around, say, generics for the true innovations. Plus, we have experts like Professor Shen with very high-level clinical data and a clinical execution power. From discovery of innovation to the landing of innovation ideas on the ground, we have fertile soil and environment. We believe we're going to have more innovation-oriented molecules. Third, regarding internationalization or international partnership, I believe there's going to be more opportunities. The speakers already mentioned in the past two or three years are the innovation pharma.
There was quite a few, for example, global BDs and deals. The year beginning with Roche, we have our product partnership with Roche, right? Indeed, for a global pharma, this speaks to their approval of China's innovations. With China innovation results, we're able to enable a global pharma and enrich their clinical pipeline. We have high efficiency and a relatively low cost. The partners are able to bring the drugs and have them commercialized globally. Going forward, cooperation-wise, the Chinese pharma are going to have a whole host of more opportunities. What will be the challenges for Chinese innovation pharma going global? The first big challenge is we are very familiar with the domestic regulatory environment, for example, clinical production and sales.
As we reach global markets such as Europe and America with higher regulatory scrutiny and a higher bar of requirements for quality, are we able to fulfill those higher-level regulatory requirements in every step of the process from the early stage production all the way to commercialization? These are very demanding of the soft power of a company. How can we attract talents and how can we promote the cooperation and synergy between domestic team and overseas team? We are subject to higher standards and more requirements than capital. I believe for global clinical costs, yeah, the costs are way higher than those in China. For innovation pharma like Innovent, yes, indeed, we aim to become a globalized biopharma. How can we allocate our resources and maximize our pipeline value?
As a CFO, this is like the sweet puzzle that I face because we have a very strong pipeline with a lot of innovation. How can we maximize the value of our products? I think for a comprehensive investment model, there are high risks associated with it. We want to partner with our partners, right? Based on partnerships, we would be able to reduce the investment risks and maximize our pipeline value. There are different ways, shapes, and forms of cooperation: joint development and license out and a new co-model as well. I believe different models have their pros and cons for Innovent.
We hope leveraging our product characteristics, if we can maximize the value with our products and select the most suitable kind of molecule and a partnership model that suits the best of those each and every molecule, we can learn from our partners as well. Finally, we believe we can make a difference.
All right. Thank you, Ms. Yu, for your response. Because we have institutional investors, I believe we're now more confident. If we mention made in China, we think about those labor-intensive industries. Now, the new era of globalization, when we talk about made in China, we think about innovative pharma like Innovent, the new product forces from China going global. From Roche, Dr. Hong Zhang, what are your thoughts? In your eyes, what unique advantages of Innovent made you decide to partner with this company? What is your future plan for long-term cooperation? Thank you.
Yes, there was the impression already in the beginning that the platform was really validated because this is an ADC platform. We, as Roche, have brought 12 ADCs to the clinic, two to the market. We knew about ADCs. What we liked especially about the platform here is the therapeutic window, also shown with the HER2 ADC, because we believe HER2 ADCs as monotherapy or ADCs as monotherapy is possible, but probably you need to combine. The broad therapeutic window triggered our interest. Also, it is how Innovent thought about a development plan. We, as Roche, can handle programs, phase one, phase two, phase three. These days, it is competitive. If you work with a partner, you need to make sure that you do not have a delay in a program.
When we start talking with Innovent, early on, we figured out that they could do the phase one. Currently, Innovent is overseeing the phase one. The patients are now recruited in Australia as well as in China and hopefully soon in the U.S. as well. Also, this is one of the challenges in working with us. If we do a due diligence, we ask questions. We ask many, many questions. Adrian this morning reminded me, we ask over 200 questions. These are detailed questions to understand the whole system. It is the capabilities and the competencies and, of course, also the data. We look to the preclinical data. We're really convinced this is the right thing. The future is difficult to say. I only can say that if you look to the people in the past, many people of Roche moved to Innovent.
Now, two people here in the audience, Adrian He and Tracy Shu, ex-members of Innovent. Michael, you maybe still know them. They're now working in my team. It is also people business. We feel that we have a very good link with Innovent, not only the collaboration, but also the collaboration that we already have in 2020. It is people, it is science, and probably it is also a bit of luck that we find out what the next time is, how we collaborate. Okay, thank you. [Foreign language] Yes, thank you very much. All-around cooperation between the two sides. Last but not the least, from LAV, Dr. Shu Yi, because today our experts showed brilliant viewpoints. LAV is a long-term partner investor of Innovent. You have borne a witness of Innovent, the transition from a biotech to bio pharma and to go global from China.
In your eyes, could you describe what Innovent is like in your eyes? What expectations may you have for Innovent in the past 17 years? This is the most successful project we've ever invested in. We invested in over 100 projects. Innovent was the most successful one we ever did. We had more failures than success, but this one is a success because for other failures, we learn a lot, right? We learn more than the successful cases. As we invested a lot, and we felt throughout the development of a company for two or three decades, what about the status, the form, way, and shape of a company? Is the company like a baby or like an adolescent or a young talent or elderly, right?
I think the way, shape, and form of a company is a lot to do with the way, shape, and form of the founder and the pipeline status as well as the industry position. I would like to share with you some of my thoughts now about Innovent. I would like to say Innovent is a very young company now, the youth stage. We are very confident about this company. Going forward, I expect the company to stay hungry and stay young. This is the very reason why I invested in Innovent and also why we are very confident about this company. Yeah, Dr. Yu, right? Dr. Yu heard these expectations, I believe. Dr. Yu is very thrilled because this is a young company and going forward, let's march forward. Lastly, we invite every panelist to say one sentence as expectation of the future innovative bio pharma.
Let's start with whom. Now, there are too many positive things. For example, China right now is in the middle of a deep-sea movement for biopharma. I'd like to say we need to be cool-headed because we transitioned from a low trough to the current level. Everybody is claiming going global and the partnerships are brilliant. We need to be mindful about risks of innovation pharma. When you select a partner or a company from an investor perspective, beta is very important. To pick a good company is more important than picking a good industry. All right, thank you. It's a perfect place where we have capital, clinical competence, novel ideas, AI in a perfect combination can really make things change in a thing that the world will remember in 100 years. Thank you. [Foreign language] Yeah, for innovative medicine in China, I'm very confident.
Going forward, I believe people would be more rational and able to grasp those opportunities at a good timing and to promote the development of this area and fulfill the clinical needs. Yeah, for Innovent, we would like to say this is a new beginning. This is never the end. We adhere to this vision and mission. Working with our experts, investors, and partners, including those from the secondary market, we are determined and confident we would bring more China innovative medicines to the world stage and benefit global patients. Yes, your points are well taken. This speaks to a more mature kind of innovation environment. We have an ocean of data. We have AI, right? The artificial intelligence and talent and different factors and how they're combined. Indeed, this is a deep-sea movement. China is going global with China solution.
We'd like to say going global is not the end. It is a new beginning of our journey. We need to meet those unmet clinical needs globally. We're able to make a difference on a worldwide stage and create benefits for patients across the globe. Let's actually put our hands together for things go forward. Finally, again, for the remarks. Thank you. Really appreciate you for your remarks. We have our photographer who's going to take a photo opportunity for panel.