Okay, good afternoon, everyone. We're going to start our next presentation. I'd like to introduce Lewis Bender with Intensity Therapeutics. Welcome.
Well, thank you very much, and I appreciate everybody's round of applause now. So thank you, happy to be here. Good afternoon. I'm going to talk about cancer, and I'm going to talk about something that I think is very exciting: a new weapon in the war on cancer. My background is I'm a chemical engineer. I have helped to develop products with sales of over $1 billion, and the drug that we use is an oral form of Ozempic, if you know it, which uses this very unique delivery technology. What we're going to talk about is intratumoral delivery using this delivery technology, and I think I'm going to show you some pictures that you would not have seen before. I may be making forward-looking statements. Please refer to our regulatory filings.
So we have a new approach to treating cancer, using this delivery technology that causes cancer to die in a new way, in an immunological way that leads to an immune response. We've treated over 200 patients in our studies. We have a phase III study beginning, in the beginning of this, the middle of this year, in metastatic sarcoma, a deadly cancer. But we also can work not only in metastatic disease but in presurgical cancers, like breast cancer, and I'm going to show you some exciting data in that in a few seconds. Everybody in the company uses a picture that is 15 years younger. If I get to time, I'll show you what I looked like 15 years ago. But right now we have a veteran team. We are phase III, focused, and we are experienced in developing drugs through phase III.
We have patents in 37 countries, multiple industry partnerships, government and university hospital partnerships as well that helped us in our phase II studies, and a de-risked, cost-efficient business model. We turn on research when we need it, and we turn it off. These are some of our partners on the research side: the National Cancer Institute, with whom we've published jointly, Merck, Bristol, some of the best clinical hospitals in the country, Fox Chase, Johns Hopkins, Columbia here in New York, Keck School in USC. Our drug is a water-based drug, 100% water, and yet if you inject it into the fat-dense environment of a tumor, it is highly absorbed. And what you're seeing is this molecule shell. This is a molecule that has a component of it that is lipid and a component of it that is water-loving.
So lipid-loving and water-loving, and it makes 2 of the world's most potent cytotoxic agents that are gram-for-gram some of the best killing agents there are, given intravenously, and we can now get them to diffuse through the tumor and treat orally, intratumorally when we inject directly into the tumor. Cisplatin, well-known drug. Vinblastine, a well-known drug. These three components are all mixed together in water with excipients, and they form a supramolecular complexation that makes these two drugs temporarily soluble in fat and water at the same time. They are not covalently bound. The drugs are unchanged. They just now have a very unique physical property when they're combined together, and soluble in fat and water. We are, as I said, starting a Phase III study in sarcoma in the middle of this year. We have all of the necessary regulatory approval from the United States.
We're filing with Europe. This is a metastatic disease. This, we are going head-to-head against the standard, best standard of care in second line and third line, with a local therapy, and I believe it's the first time the FDA has ever approved a local therapy or authorized a local therapy to go head-to-head against metastatic disease in a randomized controlled study, compared to the best standard of care. We also are operating in a breast cancer program where we will treat women who have the highest risk of disease recurrence, triple-negative breast cancer. We will inject two doses of our drug in advance of the standard of care, and then we will compare it to the standard of care, the idea being to kill all the cancer when it comes out, which has been shown to delay the progression of the disease, delay the recurrence of the disease.
Then if we had the money, we would do a breast cancer study in metastatic disease. But we have received from FDA orphan drug status, which gives us a lot of advantages in terms of working with the FDA and getting proprietary time for our drug beyond expiry of patents, if that should be the case, and fast-track in metastatic cancer. So the FDA has reviewed this, and these are not small markets. Metastatic sarcoma is 157,000 patients in the U.S. There are 6,000 deaths. It is a deadly disease. You die, you're in about 13 months, 14 months. It is a straight line to death. The median survival is very, very low. Presurgical breast cancer is high unmet medical need. We think we have a new weapon in the war on that. This is what we do.
If you look at a cancer, most common cancers are not immunogenic. That means they don't have the ability to get T cells in or immune recognition. They're also very, very avascular, meaning they don't have a lot of blood vessels. So if you give systemic drugs systemically like you do, IV or orally, the tumors just don't get the drugs just don't get to where they need to be. So what we have is a new approach. We now can saturate all the tumors that you see on X-rays and scans, on CT scans or MRIs. We can inject them. It's just like taking a biopsy, except we're putting drug in. The cytotoxics will then go in. We will inject, and the tumor will start to die. And we can saturate the entire tumor. We dose based on the size of the tumor.
Large quantities of the tumor are starting to be released. The immune cells can come in. The immune system can now start to recognize the cancer, and we convert your own tumor, the tumor with your DNA, how it was mutated, into your own personal anti-cancer vaccine. Polyvalent. We get all the clones. We are, honing the immune system onto your cancer. We do not have to inject all the tumors. So current therapies are really a one-size-fits-all. If two people are the same height and weight and one person has two tumors, another person has six large tumors, but you're the same height and weight, you get the same dose. That's inefficient because weight and height have nothing to do with your outcome, but the amount of cancer you have has to do with your outcome. So what we are doing is we are treating the tumors.
We take our drug. We inject into as many tumors as you can, and you got it. You can hit the tumors just once. You don't have to hit all the tumors. In fact, we don't even try to hit the tumors one centimeter or smaller. But now you can kill these tumors, and you can get the patients debulked and immune-activated. And we treat based on the size of your tumors. The dosing is set by the tumors. And what's the result? The result is what we believe is the people will live longer, and they will live longer, we believe, with good quality. This is what you would see. The red curve is what, you know, when we were underloading and underdosing and the patients really weren't getting much drug, and that means the median survival and typical for people who failed all approved therapies.
These were people who failed everything, including many experimental. Normally, their median survival is about 3-6 months, and that's what you see with the red curve when we were underdosing. And what happened is as we got to dose more and more and treat more and more tumors, we were able to see a dramatic increase from 3 months median survival to 18 months in the population that got the better dose. All right? This is not a randomized study, but this study shows the proof of concept of the ability to kill tumors and give people longer life with good quality. This is some data in mice. This is what you see. We put a dye. This is what you would see on the left here with water being injected into a tumor. This drug, this is containing cytotoxics. We put a dye in.
You can see the drug doesn't stay. Tumors are fat. They're dense. They don't have blood vessels. They don't absorb water, and they're going to have the drug excreted out, and you don't see any absorption in the little circle. So a mouse here, injected into its tumor, excised open, you can see the drug doesn't stay. Now you see what happens when we add that shell molecule, that chemical that I showed you. It's black and white different. As fast as you're pumping the drug into the tumor, the drug is diffusing through the tumor and getting into the cancer cells and killing the cancer. And it's killing the cancer in a new way with an immunological mechanism of action. Cisplatin and vinblastine both have direct killing and immune-activating properties. We dose based on the tumor, as I said. I just showed you mice.
Now I'm going to show you data from women in a breast cancer study. We did a 91-patient breast cancer study, and what you're seeing is a resected tumor. It's a large tumor. It's almost the size of a tennis ball, 3.9 cc. We gave this woman one dose, 7.4 cc, then we gave her 14.8 cc, and then she had her surgery. We killed 85%, but that's not good enough because we saw that what it looked like was we were in the, in the center here on the first dose right here, and then we were given the second dose. We killed the same part of the tumor twice. So we stopped, and we said, "What happens if we were to do one dose of that same amount in a tumor 40% larger, and now we could kill 95%?" So think of it as diffusion.
You spill a gallon of milk. It goes a certain distance on the floor. You spill a quart of milk. It goes less. By dosing more, by dosing proportionately to the size of the tumor, and now we understand how that mechanism works for tumor sizes up from 1.5-15 centimeters, we can now kill very large tumors very quickly and with immunological activity. The drug stays in the tumor. 95% of the drug will be in the tumor even at the highest doses, and we are dosing three times what the IV dose is of some of these drugs. So we are giving all of the, drug that would go throughout your whole body, very little reaching the tumor. We are now treating with all of that into the tumors as much as we can hit. Obviously, the safety is very good.
Normally, you'll have somebody with 80% grade III adverse events. We saw less than 10% people with minor grade III adverse events, mild pain at the injection site, some fatigue, and some nausea on the day of dosing. Very safe, so far, very favorable safety. What happens to the tumors? They don't go away. They get crushed. They die, and they become fibrous scars. So we are looking at, tumors. You're going to look to see what's the RECIST. That's Response Evaluation Criteria in Solid Tumors. That is only looking at the longest diameter, and what we're doing is we're changing, we're stretching the tumors when we put the drug in, and the immune system is coming in. The tumors get bigger, and then they get smaller on diameter, but their volume is crushed on the shorter dimensions. We are lowering the volume.
We are killing the cancer, but the tumors are still there as fibrous, dead, benign necrotic tissue like a scar. But what do we see immunologically? What you're seeing on the left is a biopsy sample. The blue is cancer. The yellow, green, and orange are immune cells. On the left side, in ovarian cancer and liposarcoma, which are not considered to be immunologically active cancer types, what you're seeing on the left is very little immune response in the tumors prior to dosing. We take a biopsy. We dose. Then we take another dose at day 14. We take another biopsy at day 28, and what you see is tumor block full of immune cells. 13 out of 14 matched-pair biopsies had a significant increase in immune cells, and that's what you want. You want the tumors to get immune-activated, and then we see it go systemically.
In sarcoma, what we see is exactly what we saw when I showed you the entire population. We see, when you underdose, we see people dying in 3 months in 4 months. We would have estimated these patients to have about 6.7 months of survival based on their health status, large tumors, over the parts of the body with poor nutritional quality, and we would have expected these people to be dead in 6.7 months, half of them. Well, we kept them alive 15 months longer than you would have expected, and that's when we knew that's the red line and the green line, which is when we gave a reasonable dose. The blue line, what we're talking about, that blue line is a 21-month median survival versus a 6 or 7.
Remember, in people who failed 1 or 2 lines, which I'll talk about in a second, it's about 14 months. We are modeling like the blue line, and what you see in sarcoma is, are these curves. The people in the group, the colored lines, underneath the blue line are what the best drugs do, and you can see from 100% people alive at day 0 to about half the people dead by day 14 by month 14, what we're seeing on our worst case when we were underloading and underdosing, a 21-month survival. We are not modeling like the green curve or even better. We are modeling like the blue curve. We have overpowered and oversized this study.
The study we will be running in phase 3, hopefully by the middle of this year, is going to be in 333 patients with metastatic sarcoma, first line or second they fail one or two lines. We will randomize 2 to 1. 2 patients out of 3 will get our drug, monotherapy, intratumoral delivery, compared to the best standard of care. And let me tell you, the best standard of care, such as eribulin, is dosed on day 1. It's dosed on day 8. By day 9, you're vomiting for a week. You start to feel better. You get it again and again until either you die, until you progress, or you can't take it, and you go on something else. That's the best we do in this disease right now, and we're going to inject. We're going to kill your tumors.
We're going to set up an immune response. We've seen multiple sarcoma patients have an immune response, and we hope we'll keep people alive a lot longer. Overall survival, you live or you die, that is our endpoint, not a RECIST endpoint, and we think we'll also see a good quality of life improvement as well. That is our phase three study. We hope to start it. It'll be a historic study if it works. All the pieces of the phase three and let me just say this. There is so much complexity to phase three that there isn't in phase two. It's like playing in the NHL versus pond hockey. You have to get the study, the protocol, the final protocol, has to be reviewed by the FDA.
You have, like, two days to respond to them to get your answers from all of their groups. You have to meet with the chemical manufacturing group to show that you've got control over the processes that make this drug. You have to have supplies that can be logistic throughout the world. We are going to have nine countries in this trial. You have to have contracts and budgeting and sites, training videos, release drug through manufacturing depots. All of these things with a worldwide study are critical, and it is really not an easy thing to start, and that's why you don't see a lot of companies making it to phase three because the FDA and the regulatory bodies are absolutely meticulous in what they expect.
This has to be a final product ready to go to market, and we are excited that we will start that study soon. We have authorization from the FDA. We did a study in breast cancer. I showed you the results. What we saw in that breast cancer study in 91 women, where we had 60 patients in our group, we saw no surgery was delayed. The doses that we got could cause 95% of necrosis. We did not affect the cosmetic look of the breast after the surgery was done. We understood the safety was excellent, and the patients love this drug.
When a woman gets diagnosed, and I'm sure a lot of you have had friends or family or, or yourselves being diagnosed with breast cancer, that is a terrible diagnosis, but if the doctor says you can come in in the next couple of days, and we will inject your tumor, and we will possibly knock that tumor out and, and set up an immune response, the women are empowered. They would love this drug. They love this study. We could have enrolled the entire country of Canada if we had the money to do it, but we, we saw a good improvement in quality of life. People were able to go back to work much faster. We will do our drug two doses upfront.
If we can debulk and kill 95% of the tumor in the larger tumors in triple-negative breast cancer and then give the standard of care, we hope we can increase the pathological complete response rate. That is when the surgery happens, the tumor, and the nodes are dead, no live cancer. Unfortunately, in the current standard of care, women go through this brutal chemotherapy, immunotherapy regimen. Maybe half of them will have a pCR, and some 0.6%-1% will die from the chemo, and that shouldn't be. So if we can knock out these tumors, we can give a lot more of the women to go through these processes, a higher pCR rate, pathological complete response rate. We will not only help these women get, the disease from coming back, but we will give them a lot more confidence that it was worth it to try.
We have a lot of milestones. We're going to start our studies. We hope to complete enrollment by the third quarter of 2025. We're taking a very conservative. This is not a blinded study. It's randomized controlled, but doctors will know what their patients are getting in the metastatic study, and that's what the FDA agreed to because it would be really logistically and very risky to give the people these standard-of-care chemo and an intratumoral injection. Our drug is safe. The chemo is dangerous. The FDA was more concerned about making sure we monitor the chemo rather than our drug. So we're starting the breast cancer study. We're starting the metastatic study. The breast cancer is local, as I said.
We have papers coming out, and we anticipate that we will be able to complete the enrollment in both studies by, you know, the third quarter of next year. We have $14.8 million in cash at the end of last year. We have no debt. We have only 1.2 million options, mostly to staff, 13.7 million shares outstanding, very few warrants, and we have a runway through the first quarter of next year. So, obviously, we will need to raise some capital, but right now, we are focused on getting these studies started and seeing how quickly we can enroll. This is a new way to kill cancer. It is unlike any other cancer therapy out there. I am an entrepreneur. I did the first chemistry work in my basement. I was written up in Forbes. I own. I am the second-largest shareholder.
I'm trying to buy more so I can pass the first-largest shareholder, but we have the majority of this is management, and I'm the second-largest shareholder. I bought in on the IPO, and I am intent on doing what we need to do to get investors and patients what they need for this drug to be approved. We have shown things that have never been shown before, the induction of almost 100% necrosis in a tumor, activated immune response on tumors that are normally considered cold, and favorable safety, significantly favorable that more favorable than what we've seen so far with chemotherapy for the sarcoma patients. So we have a good management team. There you get to see me, like, from 15 years ago. I should update this picture, by the way. And then our CFO is here.
We've got a great new team that we've added over the since we did our IPO. We did our IPO last year in June. It was, as everybody knows, not an easy market. It took us two years to do it, but at the end, it resonated with investors. We were upsized, priced top of the range. We held our own. We had some events where we announced some great data. The stock tripled in one day, and we're looking forward to, you know, a day someday where we'll announce the success of our phase three study of a local therapy and against metastatic disease. It will usher in a new era of safe, effective treatment, when we get there. Great board, great management, and that's it. And do I have time for a couple of questions? I do. Five minutes. I have five minutes. All right. Good.
Maybe you can go back over some of the milestones that we can look forward to in the next, say, 3-6 months. So clearly, we want to start by the middle of this year, either second or third quarter, where we're going to have these two studies started, the phase 2, where we're going to size a phase 3, and then, do I have the laser pointer there? I can see it on the wall. I guess I can't see it. Could you see it there? No. All right. Maybe do this. So this you can see that arrow a little bit? Yeah. So this one is the big one. This is the, the, you know, a study that we think will be very exciting, our drug head-to-head against the standard-of-care toxic chemotherapy.
We'll start that, hopefully, sometime between the second and third quarter, and, I should have moved this over a little bit, maybe, but sometime in the second quarter, the third quarter, we'll be doing this one too. And then, we believe that we'll enroll. We're saying 15 months, but remember, the doctors are going to know what their patients are getting, and if they see what we saw, why did we enroll so many sarcoma patients in our phase 2 study? 30 patients were sarcoma out of 110. It's a rare disease because the doctors saw that the drug killed the tumors, and the people didn't die. They would die they had failed three lines of therapy. They should have been dead in six months, half of them, but they weren't. They weren't dying, so more and more were coming in. I didn't find sarcoma.
Sarcoma found us. Same thing with breast cancer. I said, "Well, sarcoma is like breast cancer. They're fatty tumor types. Why don't we, why don't we dose? Why don't we see what we can do with chemotherapy to get pCR when we're getting almost all the cancer killed upfront? Let's kill the cancer upfront, then give the patients the chemo, and hopefully, we'll get a better outcome for these patients. We'll get an immune response activation in breast cancer as well as sarcoma. We also have great data in sarcoma in metastatic breast cancer. We have ideas, like, for prostate cancer and pancreatic, where we showed great results, but right now, we're focused our efforts on getting these studies started, enrolling as fast as we can, starting the phase 3 for breast cancer, and finishing the phase 3 for sarcoma and getting the first readouts.
We will be taking readouts at 20%, 30%, and 40%, with the endpoint being at 80% of deaths. So if this drug is really working, if people are keep being kept alive, we'll see it, and we'll see it soon after enrollment, and that's, how fast can we enroll and how fast can we get the data, that's going to show the survival benefit that this drug hopefully will offer. Then there's other things that could happen which I don't mention, but we are doing BD, and we do a lot of business development and talk to pharma companies, all the time, and we'll be announcing some more data from our phase 2 studies. So it's a one-time injection. How much would that cost?
Well, it's 1 or 2 times in the breast cancer, but, you know, what we like to do is when people have metastatic disease, we like to give it to them over 5 doses every 2 weeks. So you dose as many tumors as you can. You hit them as many key times as you can over 5 weeks, kill them as thoroughly as you can, and then you just monitor them every 3 months, and if there's new tumors or if the tumors are not going away or growing a little slowly, you whack them again. So it's, you know, treatment over 2 years. Remember, their median survival, half the people are dead, usually in 14 months, so if we are treating a lot of these people for 2 years, that will be a good thing, and that's what we're going to do.
The cost, you know, the cost is to be determined a little bit. I did not create this drug so that people can't get it. I will make sure that people can get it, and we'll work with if we have a partner or if we're marketing it, we'll make sure that this is priced fairly and effectively to get people to, be able to have this drug if it works. Have a insurance partner? We, you know, we have insurance consultants. We look, again, we're going to work with patient groups. It's a deadly cancer. It's a rare cancer. Usually, the payers know that if you have something that doesn't have the morbidities, like the current standard of care, your costs to treat these people, and if they're dying, they're in hospice. They're in a lot of expensive care.
We think we're going to justify any price we have, because of the potential of life-saving, feel-good effects that this drug has. Thank you. About one minute left. Okay, so for your anticipated phase 3, is that going to be a global trial? Yes. In the U.S., Europe, and Asia. And Japanese descent? It'll be; it may not be Japan, but it'll be of, you know, Japanese descent. But typically in California, right? You get a lot of those patients there, so you can file them. Yes, we actually will have a lot of patients in the U.S. of Asian descent. We did about 10%. How close are you to your process validation campaigns for your drug substance or your drug products? Validations for drug product is done at the scale that we did.
I mean, this is the part of the CMC that we need. A couple of things we still have to do that we had to do. I mean, this is not an easy thing to do. It took months and months and months of testing, but remember, these are simple molecules we know. So validation is that the API validation, we're just working finalizing that, because we make one of them. We buy the other two. We buy the drugs, and we make the delivery enhancers. So validation is that is done. We've made 4 GMP batches, 2 at very large scale. We need to make 1 more. That's our registration batches. We will make that probably at the end of this year or early next year, and then we'll make our commercial batches. It is readily scalable.
It's simply taking the drugs, mixing them in a pot, but our validations on the assays had to be done. You couldn't release under a phase three program without validated analytical methods. Okay. I'm out of time. Sorry. Thank you.