Good morning, ladies and gentlemen. Welcome to the 42nd annual J.P. Morgan Healthcare Conference. I'm Louisa from JPM China Healthcare Investment Banking team, and today, it will be my honor to introduce Dr. Jasmine Cui, founder and president of InnoCare, to give a company presentation on the latest development and highlights. InnoCare is a commercial stage biopharma dedicated to developing innovative drugs for cancer and autoimmune diseases. So without further ado, let's please welcome Dr. Cui.
Thank you, Louisa. Good morning, good evening, ladies and gentlemen. Our thanks first go to J.P. Morgan for the presentation opportunity here, especially on online presentation. Also, thank you all for your support, attention to InnoCare. InnoCare is a drug innovation company. Our vision is to become a global pharmaceutical leader that develops, delivers innovative therapies for patients worldwide. Our therapeutic focus are oncology, autoimmune diseases, the two therapeutic fields with a lot of huge unmet medical needs. This slide summarizes our exciting eight years journey of innovation and development. At the bottom, the corporate milestone. The company was founded in the second half of 2015 by myself and Professor Yigong Shi. By 2018, we established R&D center in Beijing and in 2019. In 2018, we started to build manufacturing facilities.
By 2020, in March, the company got listed, IPO'd in Hong Kong. That's during COVID pandemic. We were the first healthcare company IPO'd by virtual roadshow, virtual ceremony, and we raised $311 million. In 2021, we raised another $393 million. We in 2022, we successfully listed in STAR Board, in Mainland China, raised another $400 million. So from the inception of the company to now, including the pre-IPO rounds, we total raised $1.34 billion. The good thing is we still have $2 billion in cash, demonstrating our effective and efficient operation.
At the top is a progression of orelabrutinib, a BTK inhibitor, our first drug, and the project started at 2015, and by 2017 and 2018, IND cleared in China, Australia, and the U.S. The first patient was enrolled in April of 2018, and we got two indications approved in China by end of 2020. So it means from first patient in to the NDA approval, launch, commercial launch, took us two and half years. It's quite of a record for the clinical development of a drug. Orelabrutinib also approved in Singapore for MCL in 2022, and also MCL in Mainland China in 2023. All the indications approved in China being covered by NRDL. In the middle is our progression of other assets, including autoimmune disease and the solid tumor.
Other projects started 2015. By 2020, all those products, more than 10 products, got onto the clinic and are being developed for different indications. 2021, our first biological IND approved in China, this collaboration with Keymed, and we licensed in tafasitamab from Incyte, is anti-CD19 antibody for DLBCL treatment. And the tafasitamab launched in China, in Hong Kong, in Bay Area by 2020 and 2022 and 2023. Here are the highlights of InnoCare's strengths and advantages. First of all, we have established fully integrated and efficient drug innovation platform from basic research, discovery, clinical development, manufacturing, and commercialization. Majority of assets are coming from our internal discovery. By far, we have 13 assets in the clinical trials, 12 from our internal effort, and we have two marketed products and have over 30 clinical trials ongoing.
By far, we have filed more than 350 patents and established two GMP-compliant manufacturing facilities. The second advantage, we are positioned to build leading hematology oncology franchise. In there, we have a comprehensive coverage of indications and MOAs. Just imagine, we have two marketed product in the liquid cancer and six differentiated asset in the pipeline, and we have best-in-class BTK inhibitor being marketed and the first-in-class asset, like tafasitamab and the anti-CCR8 antibody and et cetera. Our pipeline can be effectively used alone and also in combo with ourselves and with others. The third one is we're well positioned. We have a well-positioned portfolio in autoimmune diseases. In there, our assets cover both B and T cell pathogenic pathways.
Currently, we have six large indications ongoing in phase II and phase III, and we have three clinical assets together with a few preclinical assets in autoimmune space that will cover more than 15 indications in the next couple of years. And we have two innovative TYK2 inhibitors that offer us a good opportunity to win, and we have a global leading BTK inhibitor in autoimmune disease, developing indications in SLE, ITP, NMOSD, MS, and others. Finally, but not least, we have a fully-fledged commercial and a healthy financial position. As mentioned, we still have $1.2 billion, amount of $1.3 billion we raised; it mostly is still here. And we have a commercial team of over 320 team members covering over 1,000 hospitals.
From 2021 to the third quarter last year, we have got a cumulative revenue of $310 million. Despite we have a cash, and we have ability to generate revenue, the company still keep strict cost-effective operation and culture. The few slides talking about the hemato-oncology franchise. So, we have a comprehensive coverage in the liquid tumor space, both indications and mechanism of actions from multiple myeloma to non-Hodgkin lymphoma to leukemia. So, so far we have approved the BTK inhibitor and tafasitamab as our cornerstone product. On top of that, we have a small molecule, BCL-2 inhibitor, and also ubiquitin ligase, the molecular glue, and also large molecule, and CD3/CD20 antibody, and the CCR8 antibody, covering NHL and as well as T-cell lymphoma from B to T cell.
Our ubiquitin ligase is also covering multiple myeloma and the BCL-2 inhibitor covering leukemia, such as AML. Orelabrutinib is a marketed BTK inhibitor, has potential best-in-class clinical advantage, including the significant BTK target coverage close to 100% at 50 milligram and above. And due to the target selectivity, we have much improved the safety profiles. For example, we don't have the cardiovascular liability, AFib fibrillation, and for all the clinical trials we observed so far, it's once-a-day dosing. And we have three marketed indication in China under coverage of NRDL. And we have a first and only BTK inhibitor for marginal zone lymphoma, and we also approved in Singapore for MCL.
In 2024, we have three NDA submissions for orelabrutinib, the MCL in U.S., and the first-line CLL/SLL in China, and the MZL in Singapore. Also, we have a number of ongoing clinical trials focused on the first line and the indications outside of China. As mentioned, for orelabrutinib, we already have a commercial team effectively covering the hospitals and the clinical centers in China. Orelabrutinib has a unique structure design, provides much improved target selectivity. On the right-hand side is a design of orelabrutinib. Comparing to other irreversible BTK inhibitors, the key feature is in the middle, there is a single ring on core.
Because of a single ring core, comparing with the double ring in the middle, the compound has less hydrogen bonding sites, it's more stable, and a smaller angle in the molecule, and that offers target selectivity for just BTK, not other kinases. And also because elimination of the double ring, we eliminated the chiro center. So the compound itself is target-specific and is stable and easy to synthesis. So indeed, the orelabrutinib is very target selective. Among a panel scan of 456 kinase at a micromolar, it only hits BTK, not like other BTK inhibitors, hits other target besides BTK. So that's why orelabrutinib can be used for not only cancer indication, but also for autoimmune diseases. So orelabrutinib is a potential best-in-class BTK inhibitor for B-cell lymphoma. And so we—those are the indications, CLL, SLL, MCL, MZL.
Orelabrutinib all have leading, class-leading efficacy in ORR, overall response, and also in CR, like CLL, other BTK inhibitors barely has a CR above 10%. We have a 30-some% of CR, and the PFS for MCL, as well as OS for MZL. Another big advantage is the safety profile. I just mentioned, the AFib fibrillation is a significant cardiovascular adverse effect associated with other BTK inhibitors, but we don't see it in... By now, we have over 1,000 patients in the clinical trials, and we have much reduced diarrhea and infections. So let's switch the gear to the second key molecule that we internally discovered. That is, BCL-2 inhibitor, ICP-248. This molecule- design again and provide very unique matrix.
For BCL-2 inhibitor, by far the only approved drug is venetoclax. But in venetoclax, and there is metabolic soft spot in the middle, as pointed by the arrow. And so venetoclax has active metabolites, M27, count 12% in human plasma. Both venetoclax parent compound and the active metabolites have CYP inhibition, therefore has a drug-drug interaction potential, and also inhibit the PGP, BCRP, inhibition by venetoclax and active metabolites. So our design 248, and we eliminated the active metabolites by blocking the metabolic hot spot, and of course, reduced drug-drug interaction potential, significantly improved the PK and efficacy, and so far, we observed very good safety profile. So this is early clinical results, showing 248, have outstanding efficacy.
On the left is, we have six patients at 100 milligram dose, and six out of six showing the ORR 100%. And then the CR is three out of six, 50% of complete response, as well as 33%, the MRD undetectable. So comparing to marketed drugs in the West on the clinical trials, and 248 has outstanding performance in terms of efficacy. We're excited about the drug. And on the right-hand side, showing the BCL-2 inhibitor 248, has great synergy with orelabrutinib in the animal models. So for 248, we are going to develop it alone for leukemia and develop it in combo with orelabrutinib for a number of indications.
For NHL, particularly in the large indications such as, first-line CLL, SLL, and we have a plan to develop it in China and the global market. So in addition to the two molecules, our-- we are continuously enriching our, liquid cancer portfolio and the modality, and we have four other molecules listed here. Tafasitamab, CD19 antibody we just mentioned, and, CD3/CD20 antibody, and, we, potential first best-in-class, and we have a, a subQ formulation, developed with, Kmed together. And, so far, in follicular and DLBCL patient, we see 100% OR as well. CCR8, first-in-class target, and we are evaluating in both liquid cancer, solid tumor. We have observed, the, the PR, single drug response. And the molecular drug 490 and in clinical development for both multiple myeloma and NHL.
So now let's move to the autoimmune disease portfolio. Autoimmune disease, we have asset covering B-cell, the orelabrutinib, and the T-cell pathways, the TYK2 inhibitors. B-cell, we mentioned, we have SLE, phase IIa positive. That's first BTK inhibitor for SLE being showing efficacy. And MS finished phase II, and also positive, as well as ITP. We are in phase III registrational trial. We are going to finish the patient enrollment and have clinical results next year. NMOSD, we are in phase II trials. So for the T-cell pathway, we have two TYK2 inhibitors will cover a number of indications. 332, which is finished phase II for atopic dermatitis, and we've got positive result we'll show you later. Psoriasis and 488, we're doing phase II for psoriasis.
So, autoimmune disease has enormous unmet medical needs, and there are over 150 indications. Globally, 500 million patients, and in China, also over 40 million patients. Autoimmune diseases have six categories, as listed here, and we have covered four out of the six: dermatology, hematology, neurology, rheumatology. And the orange covered are the indications currently in phase II and phase III ongoing by our asset. Orelabrutinib, we just mentioned for MS, is best-in-class efficacy and excellent brain penetration. ITP in phase III registrational trial, and we are striving to finish the clinical trials next year and have it launched. And also SLE, we have a phase IIb, we'll get interim result for this year, and NMOSD in the phase IIb trial.
As we mentioned before, orelabrutinib evaluated in a six-month MS study at three doses, 50 mg QD, 50 mg BID, and 80 mg QD, and all met primary endpoint. 80 mg gave us 92.3% efficacy. This is class leading, and because it really has good brain penetration, and we are still figure out a way for the MS. We think the compound, by acting as B-cell and microglia, will give really benefit for a variety of MS patient. Let's switch the gear to TYK2 inhibitors. We have two inhibitors, ICP-332 and ICP-488. Left-hand side is the structure of a JAK family, and you can see, the TYK2 has JH1, a kinase domain, JH2 allosteric domain. And our ICP-332 inhibits TYK2 very potently, 0.5 nanomolar.
JAK1, 90 nanomolar is 40-fold higher, and JAK2 is over 190 nanomolar, over 400-fold selectivity. For 488 , only hit JAK2, 5 nanomolar, TYK2, not hitting any of the JAK2s.... So 332 will perform the phase II for atopic dermatitis, AD. Because AD is a serious disease. Globally, over two million patients, especially the young patients, is quite a severe disease, reduce of quality of life because of itching at night. You lose sleep and cause depression and even the suicide. Globally by 2028, there's a huge market, over $20 billion. On the right-hand side, showing why we chose to do AD. Since AD pathway need the heterodimer of TYK2 and JAK1. So 332 has major TYK2 inhibition plus minor JAK1 indication.
We think that it provides a better efficacy and a new possibility for effective treatment of AD. Indeed, this is a phase II result we just released, and the primary endpoint, the percentage change from baseline in EASI, so the Y-axis is EASI score. Comparing to placebo, the two doses, 80 mg QOD and 120 mg QOD, give us a significant decrease of the EASI scores. 78.2%, 72.5%, comparing to the placebo, 16.7%. And the middle graph shows how quick the response is. First week, we already see significant decrease of EASI score, so as second week and week four, even more. Right-hand side is showing the EASI 50 and 75 is the phase III clinical endpoint.
We see both doses and both EASI 50 and 75 showing a significant decrease comparing to the placebo. Here showing the best efficacy of ICP-332 offers. The left-hand side is a comparison with the upadacitinib. Upadacitinib is a JAK1, purely JAK1 inhibitor. Efficacy is pretty good for AD. ICP-332, in any cases, the four-week treatment compared to upadacitinib four-week treatment of 50 milligram, we see this better in EASI 75, EASI 90, and IGA zero and one, and also the itching score, NRS, NRS 4. So we see the better efficacy for every parameter. On the right hand, we comparing with all the AD drugs approved, JAK1s, IL-4, IL-13.
At the four weeks, 332 has the whole leading better efficacy comparing to the 16-week 12-week treatment. So we are really happy that our hypothesis turned out to be right. And this left-hand is the itching score. And because DUPI, the IL-4, which works okay, is actually being marketed. But the first two weeks, it has a delayed response. It doesn't do much for reducing the itch, the disease. And we look at it from day two to day 14, and we see from day two, we already see a significant decrease of ARS score and the last to the 14 days of course, by four weeks, and it, it show even more improvement. Right-hand side is improvement of patient quality of life.
Based on those data, of course, we see very significant improvement of the quality of life, both at 80 and 120, 120 milligram QOD. And here is the safety tolerability profile. Just to mention, Upa has good efficacy, but does have a black label for the safety. So here on the top line is the total adverse effect. We call it the TRAE. And comparing to placebo, 80 and 100 milligram, just no different from placebo. Very similar. At the bottom, it's a severe infection. The infection cases, which is outstanding problem for Upa, and we don't see any severe infections in 80 and 120 milligram, no different from placebo. If we see anything at 80 milligram is better than placebo.
Of course, we did not see any of the black box labeled for venetoclax, like thrombosis, like severe infection, and et cetera. So 333 gives excellent safety, tolerability profile and also, the efficacy profile. So our solid tumor, very quickly, and we have precision medicine. We have also immuno-oncology first-class asset. And I'm going to go quickly. SHP2, we are in phase I, seeing excellent efficacy, the safety profile. We are doing with EGFR third generation for lung cancer right now, and CCR8, we are doing both liquid cancer, solid tumor. We already see single-drug efficacy. So next is our robust growth outcome.
So in short term, before 2023, we have two drugs launched, and in short to mid-term, listed middle, we'll have a number of five or six drugs that will be launched in the next three years, three to four years. Orelabrutinib, we are continuously developing oncology outside of China. In China, for the indication, tafasitamab will be launched in about a year in mainland China. ICP-248 will be a high priority project developed in China and global, and also the antibodies, we will put effort to development. For autoimmune disease, we just mentioned orelabrutinib, ICP-332 and ICP-488. That will cover a lot of big indications. By these three compounds, we have others in the preclinical stage. And on the right-hand side, we continue to push our clinical pipeline.
In discovery, that's our strength point, strong point, where establish new platforms, like, a larger molecule, bispecific antibody, conjugations, protein degradations. We are also expanded to CNS, the CNS autoimmune disease franchise. Finally, 2024 milestones catalyst. Just to mention, during the talk, 2024, this year, we have a lot of milestones. NDA submission for auto- for orelabrutinib. There are three. tafasitamab, we have NDA submission this first half year. 332, we are moved to phase III, and also, other progress is all moving pretty well. Thank you for your attention.