For this session, we'll have a presentation by Anixa Biosciences. Anixa is a clinical-stage immuno-oncology company with a pipeline of candidates targeting breast cancer and ovarian cancer. Presenting for the company is Mr. Mike Catelani, President, Chief Operating Officer, and Chief Financial Officer of Anixa. Mike.
Thanks, Yi. Thanks, everybody, for being here. And for those of you listening webcast now or in the future, just want to make sure we point out that this presentation is given on May 20th. As you'll see our forward statement, if I can advance the slides. There we go. We got the slides working. So our forward-looking statement disclaimer: this presentation is given as of May 20th. Things can and will change in the future. Quick overview of Anixa Biosciences. We're a clinical stage company based in the Bay Area of Northern California. We have a robust pipeline of immunotherapy products. We've got a CAR-T therapeutic platform, and we've got a number of cancer vaccines. Our two lead clinical programs: one is a breast cancer vaccine, and one is an ovarian cancer CAR-T therapy.
Both of those are in phase I clinical trials currently, and we're seeing very good and promising clinical data. It's very exciting for the stage we're at. They're seeing very strong data. One of the really important parts about our business model is that we have important key partnerships with top-tier academic research institutions. Our partners include the Moffitt Cancer Center. They include the Cleveland Clinic, so both top-tier research organizations. Moffitt Cancer Center, based in Tampa, one of the leaders in cell therapy development. Cleveland Clinic, very well-known worldwide, is one of the best hospital systems. The diseases we're going after, all oncology, the top ones we're looking at are ovarian cancer and breast cancer, both very large markets with a lot of opportunity. Breast cancer, obviously, is a huge market. Everybody has been affected by breast cancer in one way or another. It's, unfortunately, a very common disease.
Ovarian cancer, smaller market, not quite as common, but a much greater unmet medical need with very poor outcomes in that disease space. We have a very strong balance sheet. We've got ample cash, unheard of in this industry at this time right now, but we've got a two-and-a-half-year runway, which puts us in a very comfortable position. That strong position has led for us to have a very clean cap table. There's no warrants outstanding, no preferred stock. We're very clean, which puts us in a good position for any future transactions or any other things we're doing going forward. Another aspect of our business is that we've had strong, consistent insider buying over the years. Over the last seven or eight years, millions of dollars of Anixa stock have been purchased by directors and management in the open market.
We all very much believe in what we're doing, and we've all been consistent buyers of our stock. We have a very capital-efficient business model. It's very important to understand that while we have this long runway I will go to the next slide you'll note that we only have $17 million in cash, and that seems like not very much. We have been burning, historically, on average between $5 million and $7 million a year. We do not go through a lot of cash. We can last a long time on very low cash. We are very efficient about how we spend. It puts us in a great position. As I mentioned earlier, we've got about a two-and-a-half-year runway. It puts us in a great position. We do not have to burn a lot of money to make a lot of progress. Now, how we do that, it's really not that complicated.
We're very disciplined about how we spend money. We leverage the infrastructure of our partners. I mentioned earlier, an important aspect of our business model is the key partnerships that we have. We leverage the infrastructure of these partners. Instead of having to go out and build a massive cell therapy manufacturing facility, which would require millions of dollars of investment, instead, we're working with the Moffitt Cancer Center, who's already made that investment, and we can leverage that infrastructure. We have access to the level of scientists that we could never afford to hire internally by having these great partners that we have. By keeping our burn low, by keeping our team small, keeping our investment low, we're able to use that infrastructure of our other partners and keep our overhead low so that we're not constantly just burning through cash.
We're burning less per year than most companies in this space are burning per month. It is just a really key aspect of how we run this business. It has positioned us well for, frankly, the last four years. In the microcap biotech space, it has been tough for a few years now. We have been able to come through that very well financially because, again, we do not burn a lot of capital while moving two clinical programs forward. Important to point out that we do not have any warrants. There is no preferred stock. There is no debt. Any financings we have done in the past few years have been very clean, and we have tried to keep it clean, keep it simple going forward. It is just a better situation all the way around if we can avoid those more toxic financings that other people have had to do.
One other important aspect of our model is that because we are working with partners and we use their resources, their expertise, we do not have a lot of investment in any one specific area, meaning we can work on orthogonal projects. We can work on CAR-T therapeutics, and we can work on vaccines. That is very efficient for us because we do not have—we have not committed a bunch of capital in people and in facilities to one therapeutic area or one modality. We can do a lot of different things. Of course, our goal, like most biotech's, is to eventually outsource our programs to pharma. It is important also from a business model perspective. We are not gearing up to build out commercial manufacturing facilities or sales and marketing to commercialize.
Again, we can keep our burn low by not focusing on those things and instead focusing on advancing programs through early clinical stages and then partnering with pharma for the later stage and commercialization. Also, one last thing to note is that we advance these programs very carefully, and we try to conserve cash as much as possible as we move these things forward. Last year, for example, we only burned $7 million in cash, so very, very efficient. Let me talk about really quickly our pipeline. Sorry. We've got a CAR-T therapeutic against ovarian cancer that's currently in phase one trial. We've got a breast cancer vaccine in phase one that's partnered with Cleveland Clinic. The one thing I want to point out is with two of our vaccine programs, the breast cancer vaccine has a U.S.
government grant that is fully funding that phase I trial, another aspect of keeping the burn low. One of our preclinical programs is being fully supported by the NCI. Again, we keep our burn low through a lot of different things, including trying to find non-dilutive capital opportunities. Let me talk about our ovarian cancer CAR-T. I think most people are probably familiar with CAR-T. Briefly, it's a custom product for each patient. You take blood from the patient, you separate the T cells, you engineer those T cells so that they will bind to a target on a cancer cell. You reinfuse those T cells into the patient. Now they've got a new population of T cells that effectively act as a therapeutic to destroy the cancer cells.
I'm sure many of you who have heard of CAR-T know that there was a lot of exciting news in the CAR-T space a few years back with some multi-billion dollar acquisitions. CAR-T really came around big a few years back with amazing responses in a lot of different patients. The biggest challenge in CAR-T—one of the biggest challenges in CAR-T has been there hasn't been a lot of success in solid tumor CAR-T. CAR-T has been successful more in lymphomas, leukemias, these B-cell cancers. We've got some unique attributes to our approach where we believe this will work in solid tumor and in ovarian cancer specifically. We've identified a unique target. We believe that our approach also has an anti-angiogenic effect, and we're taking a slightly different delivery approach because we can—with ovarian cancer, we're delivering intraperitoneal.
I'm going to talk about each one of these things briefly without getting too much into detail here. CAR-T works because you've got a cancer cell that has some type of antigen, some protein on it, and then you take the T cell, you design something that will bind to that, typically a synthetic antibody fragment that will bind to that antigen, and then that will cause the T cell to destroy the cancer cell. The challenge, of course, is it won't just kill cancer cells. It'll destroy any cell that's presenting that protein. The challenge, especially in solid tumors, is finding those proteins that are only expressed on the cell of interest and not on some other organ system, causing some potentially devastating side effects. A discovery was made that follicle-stimulating hormone receptor—it's a hormone receptor—is only expressed on the ovaries in women.
The idea here is we take the natural cognate ligand, the follicle-stimulating hormone, we engineer that onto the T cells. Now we're taking advantage of that hormone-hormone receptor binding affinity. Now these T cells have FSH on them. They'll naturally want to bind to FSHR, and they'll destroy those ovary cells. Made it sound simple, but it's pretty straightforward. The key here now is the next stage. I really want to point out, again, only ovaries and testes in men is where it shows up. Some research published in the New England Journal of Medicine a few years back showed that FSHR, for reasons not entirely understood, is also expressed on the endothelial cells in blood vessels within a tumor.
When a tumor—if we go to the next slide here—when a tumor starts to develop through a process of angiogenesis, it starts to create its own vasculature and starts growing its own blood vessels within the tumor. Those blood vessels in the tumor, the endothelial cells that line the blood vessel walls, are expressing FSHR. As soon as you get outside the tumor, there is no longer any FSHR expression on those endothelial cells. It only happens in the tumor. We believe what is happening with our CAR-T cells is they are having a dual mechanism of action. They are having the direct kill effect by attacking those ovary cells, but they are also having an anti-angiogenic effect in destroying the vasculature within the tumors. Finally, the third key attribute is intraperitoneal delivery. Ovarian cancer, ovaries in general, are contained within the peritoneal cavity, the peritoneal sac.
The peritoneum houses essentially all the abdominal organs. Even in later-stage ovarian cancer, those metastatic lesions tend to stay within the peritoneal sac. By delivering intraperitoneally, we believe we have two advantages. One, it is a more localized delivery. We are getting the CAR-T cells delivered into the peritoneal cavity where they are then more easily trafficking to the tumor lesions. Second of all, the peritoneal sac is somewhat conserved from the rest of the body. When we infuse the T cells into the peritoneum, not a lot is getting out into the bloodstream. We believe we can dose higher. We can have a better safety profile than you would typically see in CAR-T. I am sure many of you have heard of cytokine release syndrome. It is a common side effect in CAR-T.
We don't believe we'll see that as soon as we would in an IV delivery. Now, we do plan in our phase I trial to try this IV as well, but so far, all the patients have been treated IP. We want to understand the differences. Where we are in this clinical trial is we've completed the first three doses, and every three patients, we tripled the dose. The first three doses were what we assumed would be subtherapeutic doses, but we're now getting to a dose level where we think we should start seeing something pretty meaningful. We should be starting treating patients at this fourth dose cohort very soon. Results so far—now again, it's only nine patients treated so far, so we have to understand that this is a very small number of patients so far, but it's very exciting what we're seeing. It's very encouraging.
Excellent safety profile. There have been no safety issues at all. We're very encouraged about that. We've got patients that have had very good overall survival. We've got one patient who is now 24 months since treatment, and she's still alive. Another patient that's still alive 12 months after treatment. We have several others that have all outlived their expected survival. We're really excited about what we're seeing here in these patients that looks like we're getting extension of life. All of these patients had a median survival of about four months, and most of them are outliving that, and some by very significant amounts. Some are still alive today. Every day, we get longer overall survival with these patients. We're very excited where this is going and the kind of data that we've been seeing.
I'm going to jump over to our breast cancer vaccine. Completely different technology. We're going to switch gears here. This technology was discovered at Cleveland Clinic, and we've exclusively licensed this from them. What was being researched was there are proteins that are, as they refer to them, retired proteins. These are proteins that are expressed at certain times in life or for certain functions in life, and then expression goes away. The interesting discovery is that some of these retired proteins, even though they should no longer be expressed, start getting expressed again in cancer cells. When a cell becomes cancerous, it starts expressing it. What was discovered in the case of breast cancer is there's a protein called alpha-lactalbumin. It's a lactation protein. It's only expressed in breast tissue and only expressed during lactation.
If a woman is not lactating, no cells in her body should be expressing alpha-lactalbumin. What was discovered, though, is that when cells become cancerous, they start expressing alpha-lactalbumin. The idea here was, what if we were to vaccinate women after they're done having children, vaccinate them against this protein? Could we prevent the onset of breast cancer? Now, what we're looking at initially—actually, one of the first proof of concepts we did was in mice, and we vaccinated a bunch of mice, bred them. They had totally normal and healthy offspring. The interesting finding was that the mothers couldn't produce milk. They weren't able to feed their pups.
What it showed was that by properly vaccinating a mouse when its body went to—when its cells started to produce alpha-lactalbumin so that it could lactate, the immune system was destroying all those cells and not allowing those cells to grow and continue. They were killing off all the cells, and these mice could not lactate. It was a really great early proof of concept. In another study that was done—and obviously, many, many studies—but this is another study on, if you look on the right side, most compelling. This study was a line of mice that are designed to spontaneously develop breast cancer. We took a bunch of these mice at a control group and then a vaccinated group. The control group, as we would expect, virtually all of them developed breast cancer. None of the vaccinated mice did.
It showed that in a model where these mice should be developing breast cancer, by vaccinating them against this protein, they were not. This data, plus a lot of other data, is what was all put into the grant with—it was the U.S. Department of Defense. That grant has paid for, at that time, all of the remaining preclinical studies as well as the entirety of the phase one study. Where we are on the phase one, we've been looking at three groups of patients. I want to point out it's a phase one trial. The key here is safety and looking for immune responses. These three groups are essentially a recurrence group. These are women who have had triple-negative breast cancer. It's the most lethal form of breast cancer. These women had TNBC, currently cancer-free, but at risk of recurrence.
We have the prevention group. These are women who have never had cancer but have certain genetic mutations that indicate they have a higher likelihood of developing it in the future, and they have elected to have a prophylactic mastectomy. We have the third group, which is the treatment group. These are women who have been treated for triple-negative breast cancer. They have had surgery, but they still have residual disease, and they are currently on Keytruda. In looking at all three of these patient profiles, this is the data. We have actually treated or vaccinated about 30 patients so far. The data here on the right is on the first 26 patients. This was presented at SITC back in November. The key findings here are, first of all, that this is very safe. Any adverse events at all were all injection site related, so no systemic issues whatsoever.
We saw that there's greater than 70% of the patients had a protocol-defined immune response. We saw that at every dose level and in every patient group, we were seeing robust immune responses. The other thing is in the treatment group or the Keytruda group, we know that Keytruda already has some pretty rough side effects since we want to ensure that a combination with our vaccine did not create more problems. What we've seen so far is there have been no additional safety issues with any of those patients. Overall, this data has been very exciting. It's very compelling. Now we're seeing very robust immune responses across the board. We are very excited about where we can go with this next. This phase I trial, at this point, enrollment's complete.
We've still got a few vaccinations to do and some patient follow-up over the next few months. Our plan is to present the final data for the trial at the San Antonio Breast Cancer Symposium in December. Really quickly, the phase II trial is now—we're starting to plan for that once we finalize the phase I. We're looking at the neoadjuvant setting. Our plan is to vaccinate women shortly after diagnosis. The reason we're going after this therapeutic setting first is because it's the fastest path to showing efficacy. We believe this can work as a primary prevention to prevent cancer from ever arising. The pathway to that is much longer than going to therapeutic setting first. You can see there's a number of different markets we can go after from neoadjuvant all the way to primary prevention.
We believe we can get to each one of those stages, again, starting in the neoadjuvant setting. Obviously, the market is huge. Just really quickly, we've got a few other vaccine programs in the pipeline. These are all targeting different retired proteins. Ovarian cancer, that program is being worked on at the NCI right now. The other cancers are all still in the discovery stage as we're seeking to find the best targets to go after and to create a vaccine around. I believe that leaves me out of time. Thank you very much.