I'm pleased to announce our next speaker is Dr. Amit Kumar, who I've known now for a couple of, well, five or six years now, who is the CEO of Anixa Biosciences. Anixa is a clinical stage biotech that is taking a very unique and capital-efficient approach to, capital-efficient and partnership approach to oncology and drug development. Rather than building out, rather than building out a costly infrastructure, they collaborate with top-tier institutions, including the Moffitt Cancer Center and the Cleveland Clinic, to move their programs forward while keeping cash flow burn low and optionality high. The company has two lead programs. First, a novel CAR-T therapy for ovarian cancer designed to overcome historical challenges using CAR-T in solid tumors. The program is in phase one right now, and they're progressing into higher dosing, higher doses of, higher dosing for their cohorts.
The second is a first-of-its-kind breast cancer vaccine developed with the Cleveland Clinic, targeting triple-negative breast cancer, the most aggressive subtype. Phase one data has shown strong immune response, and the company is gearing up for a phase two trial later this year. Looking ahead, Anixa expects multiple catalysts in 2025, including new clinical data, trial initiations, and progress on additional cancer vaccine programs targeting ovarian, lung, colon, and prostate cancers. With $20 million in cash, no debt, and a clean capital structure, they're in a strong position to deliver. With that, I welcome Dr. Amit Kumar.
Thank you, Eric, for that introduction. I think you pretty much told the whole story right there, and I want to thank you all for attending here. Let me begin by talking a little bit about some of the corporate aspects of our company before I talk about what we all are really here to hear about, and which I like to talk about, which is the magic of our technologies. From a corporate standpoint, here are some highlights. We've built a very robust pipeline of products. Many are, two are in the clinic and others in the preclinical stages. The clinical products are producing a lot of very good data, which I'll talk about in a little bit more detail. We've established a lot of very strong partnerships with organizations that help us do our R&D in a very capital-efficient manner.
We have been very good about, you know, taking care of our capital as well as maintaining a very clean capital structure. Why is that important? The reason that that's important for investors is that if you have a very clean capital structure, then the true value of your products and technologies can be realized by shareholders. We do not have any overhangs like lots of warrants and preferred stock. We have a very clean 32 million shares outstanding. In addition, all of us, including myself and board members, have bought millions of dollars of stock in our company on the open market because we all are very bullish and excited about our technologies, especially since we are seeing some fantastic, fantastic data. A little bit more corporate information. As Eric mentioned, we have been very, very frugal and careful with our cash burn.
Unlike most companies in the biotech sector, which spend a tremendous amount of capital in developing their technologies as well as running their clinical trials, we've been able to do all of our research and development as a publicly traded company, as well as run two clinical trials and burn very little cash. In the last 12 months, we've burned $7 million, which is a very, very modest amount. As a result, we have over two years of capital on our balance sheet, enough to get to many catalytic clinical milestones. We have, as I noted, no debt and a very clean capital structure. Let's get to the things that we're here to really hear about. I'm going to talk primarily about the two programs that are in the clinic.
We have other programs in our portfolio, but these are the two programs that people want to hear about because we're getting data on human beings. The data is really, really good. Early stage, these are early stage studies, but so far we are very, very proud of the type of data that we're getting. I'm going to talk a little bit about the science here, and I hope you can stay with me as we get into some of the details behind these technologies because that'll really help you understand why they're differentiated from many other technologies that have been tried in these arenas but have failed. The first program I'm going to talk about is our CAR-T program addressing ovarian cancer. These are for patients who are terminally ill. They have been given practically weeks to live.
Most of the patients that we get into this trial have a median survival expectancy of about three months. We are already showing that several of these patients are living much further, much longer than that, even though we are at the earliest stages of this trial. That trial is going on at the Moffitt Cancer Center, which is one of our strategic partners. The second program I am going to talk about is our breast cancer vaccine. We have close to 30 patients that we have treated with this vaccine. That trial is nearing the end of phase one, and we are beginning a phase two trial. That trial is being funded currently by the United States Department of Defense. Let's begin with the CAR-T program. CAR-T technology, it is a big, big, big word or a big phrase, chimeric antigen receptor T cell technology.
It's a relatively new type of chemotherapy or immunotherapy that involves taking blood from individual patients, isolating their white blood cells, specifically T cells, which is a type of white blood cell, and taking them out of the patient, taking them to a laboratory, genetically engineering them to make them better cancer fighters, and then reinfusing them back into the patient. It's a very complicated process, and it's expensive as well. If it can save patients' lives, then obviously it's worth it. This technology created a tremendous amount of excitement a few years ago for certain types of leukemia and lymphoma patients, blood cancers, liquid cancers. These were patients who were terminally ill, again, who had weeks, weeks to maybe a couple of months to live. As many of you who are, you know, all of you here are very familiar with cancer.
When you have really late stage metastatic, terminally ill cancer patients, it's almost impossible to keep them alive. It's a battle to keep them alive, and especially trying to keep them alive with good quality of life. CAR-T technology was able to address many of these patients, and a large percentage of them had responded to this therapy. Many responded well enough that they were effectively cured. By cure, I mean no indication of disease after the treatment. Many of these patients have lived years and years and are continuing, continuing strong. It created a lot of excitement. The problem was that this technology, when it was tried in other types of cancers, especially solid tumors, failed miserably. There is no solid tumor CAR-T technology, CAR-T therapy that has been approved to date.
We hope that our therapy will be the first addressing terminally ill ovarian cancer patients. There are a number of reasons or theories about why CAR-T has not been successful in solid tumors. Our T cell technology is designed to address many of these. I'm going to talk about three of the unique attributes and get into a little bit of detail about these three attributes, which are very different from any other CAR-T therapy that's been tried in solid tumors. Those three are that we have identified a very unique target, a unique protein that our T cells are trying to attack. In addition, our T cells have, we're going to have, are going to have an anti-angiogenesis effect. I'll explain that in a moment.
That'll, and because it has that anti-angiogenesis effect, it's almost like our T cells are acting in combination. We're adding one agent, we're dosing the patient with one agent, but that agent is acting like we are, it's a combination of drugs. The third characteristic, which is unique for ovarian cancer, is that we're delivering the T cells not through the vein, but through the peritoneum. Again, I'll explain why that's important. First characteristic, and Eric, keep me honest on the time as well, okay? The first characteristic, this is a little bit of a busy slide, but this describes a couple of key points about our CAR-T technology. The right-hand side is a cartoon that depicts the CAR-T technologies that have been approved for the leukemia and lymphoma indications that I noted a moment ago.
In that case, the T cells are genetically engineered with an antibody fragment, which is depicted by that orange crown. That antibody fragment acts like a homing missile that drives the T cells to the B cells, which are the cancer that it's trying to attack. B cells have become cancerous, and these T cells that are circulating in the blood supply will find those B cells, bind to those B cells through that combination of the antibody fragment, targeting a protein on the B cells called CD19. The name is not important, but the characteristic that is important is that the CD19 protein is uniquely found on B cells and no other cell in the body. These T cells only home in on those B cells and destroy them.
They destroy the healthy B cells as well as the diseased B cells, but that's okay because a patient, an individual can live with no B cells, but they can't live with cancerous B cells. Now, on the left-hand side is a cartoon that depicts our technology. In this case, we've identified a protein on the ovaries that is called follicle- stimulating hormone receptor, FSHR. It's very unique in that it's only found in the ovaries in women and in the testes in men. Obviously, we're treating ovarian cancer, so the fact that it's found on testes is irrelevant, but it's only found on the ovaries and nowhere else, no other tissue in the body.
In addition, because it is a receptor, it's an endocrine receptor, a hormone receptor, there is an existing natural hormone that we can put on our T cells, genetically engineer our T cells to express on their surface that will act as the homing missile. Why is this important? The reason is because over millions and, or I should say hundreds of millions of years of evolution, the follicle stimulating hormone in mammals has become a very good binding molecule to the follicle- stimulating hormone receptor. We have a really, really powerful mechanism to drive these engineered T cells to the cells we want to destroy. That is unique and that has never been developed for any other solid tumor, CAR-T therapy. Now, I fibbed a little bit.
I said that the receptor FSHR is not found anywhere on any other organ system, and that's true, as you can see on the left-hand side, only on the ovaries and on the testes. However, recently a publication, a research paper was published in the New England Journal of Medicine, the first page of which is on the right-hand side here, that indicated that the follicle- stimulating hormone receptor, while it's not found on any other organ system, it tends to be found on the vasculature of tumors, the blood vessels within a tumor. What does that mean? That's the case for ovarian cancer, which is what we're trying to treat, but all many, many other types of cancers, and we believe probably all solid tumors. What does that mean?
If you look at the cartoon on the left-hand side, the visual on the left-hand side, what we're doing here is, what we're depicting here is blood vessels that come to the tumor and blood vessels within the tumor body itself. When it's, you know, I think some of the previous speakers talked about blood vessels and vasculature within the tumor. When a tumor, a solid tumor starts getting bigger, it induces a process called angiogenesis, which is the process of building blood vessels. It does this because the tumor needs oxygen and nutrients to come in and waste and CO2 to be removed. It creates these blood vessels in a very rapid manner because the tumor is growing rapidly, much more rapidly than normal tissue.
It turns out, based on the study that I noted a moment ago, these blood vessels express follicle stimulating hormone receptor on the inside of the vessels, the endothelial cells. What that means is that our CAR-T cells are going to attack the tumor directly, but they are also going to disrupt the vasculature, the blood vessels. This T cell therapy, we believe, is going to act as a dual combination approach and synergistic, in fact. Previous speakers today have talked about the fact that there are anti-angiogenic drugs on the market. Avastin, which is the most leading drug, is often used for ovarian cancer and other types of cancers to try and disrupt blood vessels. That is what we are doing here with our CAR-T cells. We are disrupting the blood vessels in ovarian cancer as well as attacking the cancer.
Those of you who follow the latest approaches to treating very difficult to treat cancers know that one of the biggest rages today is to try and use combinations of drugs to treat cancer. The challenge is when you use two drugs or combinations of drugs, you often increase the, you know, increase the side effects and make the combination intolerable to patients. In our case, we're using one drug, but it's acting like a combination of two drugs. We have the best of both worlds, fewer side effects and a synergistic dual mechanism of action. The third characteristic that's important for us, especially for ovarian cancer, uniquely for ovarian cancer, I should say, is the intraperitoneal delivery. Most CAR-Ts have been delivered through the vein.
When you deliver these engineered T cells into the vein, they go all over the body immediately, and they create side effects everywhere, many of which are intolerable or have caused deaths in the patient. In our case, we're delivering directly into the peritoneum. The peritoneal sac is a sac in our abdomens in which a bunch of organs exist, depicted by that yellow membrane. Within that sac are the ovaries. When a woman gets ovarian cancer and it starts to spread, metastasize, most of the lesions remain within the peritoneal sac. The lesions are found on other organs in the peritoneal sac as well as the peritoneal membrane itself. Eventually, at really, really late stages, they can escape the peritoneum and go into the pleural cavity, which is where the lungs reside, and then move on from there.
Most women have most of their lesions within the peritoneal cavity. By delivering into the peritoneum, we're sending the CAR T cells directly where the lesions are. They're trafficking well to the lesions. Because they're not getting into the veins, they're not getting into the system, they're not creating these systemic side effects that often become intolerable for the patient. The third thing is, because again, they're not getting into the system and they're gonna, you know, they're not getting into the bloodstream, we believe that we can go to much higher doses than has been used in other IV-delivered CAR T therapies. All of those characteristics are important.
I should say that we are doing these studies in terminally ill cancer patients, as I said before, and I want to emphasize that these are patients that have been given weeks to live. These are patients that have failed at least two, sometimes up to five or six previously approved therapies, and nothing is working and their diseases are progressing. In this case, we start out with very low doses, what we call subtherapeutic doses, doses where we do not expect to see any efficacy. In this case, we are starting to see some efficacy, which I will tell you about in a moment. The point is we are starting out with very low doses and we are increasing the doses every time we verify safety for one particular dose. We are at the fourth dosage level right now. We will continue going higher.
In the first three doses, we've treated nine patients with very, very good safety results. I need to update this slide. It's a little bit old, but basically all of the patients experience very, very good and tolerable safety. Some of the patients are living a lot longer than their expectations. In fact, one patient is alive close to two years. We have another patient that's alive 12 months and another patient that's looking like this patient that's going to be, that has lived over two years. Now, all of these patients, by definition, have what's known as progressive disease or stable disease. What that means is they still have the tumors.
We have not completely cured them, but we have increased their overall survival from a few weeks, a couple of, two or three months to up to two years, which is incredibly exciting, especially since these patients are all terminal. This data is incredibly positive data for any CAR-T trial that is going on. We are very, very excited about this study. It is still early stage. As I mentioned, it is going on at the Moffitt Cancer Center in Florida, nine patients so far, and we are about to begin our 10th, 11th, and 12th patient. As we go to higher dosages, we expect to be able to get better responses, you know, fingers crossed.
The one thing I also want to say is that the FDA is incredibly supportive about this because with this first patient that I mentioned who's alive almost two years, we took her data to the FDA and asked them permission. We filed an emergency IND, or I should say a single patient IND, to ask permission to dose her again with the belief that had we dosed her at a higher dose in the initial dosing, we might have been able to have a bigger impact. We gave her a second dose recently, and we'll see what those results are soon. She is still alive, doing really well, good quality of life. Now, the second program that we're talking, you know, that I want to talk about is our breast cancer vaccine. This is really exciting.
We're nearing the end of phase one, but this is a vaccine that's designed to not only treat breast cancer, but also prevent breast cancer. This is something that has never been done before. Many vaccines in cancer have, or I should say all vaccines in cancer have failed. We're starting to see in clinic certain vaccine studies that are showing some interesting and positive results, including ours. Now, I'll talk a little bit about how this vaccine works because it's important to understand that it's very different from the approaches that other people have used for vaccine development in any type of cancer. I don't have the time to talk about some of those other approaches, but please feel free to come and, you know, talk to me if you want to talk about that, the molecular mechanism.
In this case, there's a protein called alpha-lactalbumin that's expressed in the breast or the mammary glands of mammals when they give birth. This is a protein that is only expressed at that time. When a woman gets pregnant, as she gives birth, this protein is produced in the mammary glands because it enables lactation, enables the production of milk to feed her infant. After she stops breastfeeding, whenever that is, the protein disappears and it does come back again when she has another child and another child and so forth, but eventually it's gone. In most women who are not going to have any more children, the protein never comes back. In the one out of eight women that do get breast cancer, this protein is produced by the breast cancer cells.
We're focused initially on triple-negative breast cancer, which is the most lethal form, but we believe that this approach will work on other types of breast cancer as well. The idea here is we vaccinate a woman after she's no longer going to have children, say at the age of 40 or 45, and teach her immune system to destroy cancer cells as they arise. These cancer cells are going to arise initially as one bad cell, then two, then four, eight, sixteen, and they continue reproducing until they become a multibillion cell mass. What we do is train the immune system so it's ready when those cancer cells emerge. The immune system will destroy them at the earliest stages of tumor formation, neogenesis. As a result, the cancer never has a chance to become a tumor.
We did a bunch of interesting studies, or I should say our partner, the Cleveland Clinic, did these studies. One, you know, a little bit of context about this particular experiment. As many of you who may follow cancer vaccine research know, vaccines now are showing immune responses, meaning when you give them to animals or to, in some cases, patients, human patients, you see immune responses, you know, specific immune responses, meaning certain white blood cells are being trained to attack the cancer. That does not always translate into clinical response, meaning the cancer is being destroyed or at least caused to shrink. The reason is because sometimes those immune responses are not, perhaps not strong enough.
This experiment, because of the circumstances of this particular molecular mechanism targeting a lactation protein, enabled us to show that this vaccine creates a very powerful immune response that's cytotoxic, meaning it kills the cells you want it to kill. This is an experiment where we took a normal, healthy female mouse, vaccinated her, and enabled her to mate and have litters. She had perfectly normal litters. The pups were babies, the pups' babies were perfectly normal, but she could not produce milk after she had given birth. The reason was because the vaccine had trained her immune system to destroy any cell making that protein. As a result, the billions of cells that were making that protein in her mammary glands were all being destroyed by her immune system because of the vaccine.
This is a very powerful proof of concept experiment that showed that there's a very good cytotoxic response. I'm getting the time warning here, so I'm going to go fast. That was a mouse, you know, that was not a cancer study. We did a cancer study again in mice. The right-hand side is the experiment I want you to focus on, which is we took these mice that are genetically engineered to spontaneously develop cancer. We gave half of them the vaccine, the other half got a placebo, and the vaccinated mice remained 100% cancer-free, whereas all the placebo mice developed cancer. Now we're studying this vaccine in humans. We're doing it in three groups of women.
One group of women are women who've already had breast cancer, triple-negative breast cancer, have gone through all of their treatments and are worried about a recurrence. We're giving them the vaccine to verify it's safe and also to determine if we're seeing an immune response. A second group of women are women that are, you know, positive for certain mutations that predispose them for getting breast cancer. These are women who, many of them are choosing to have prophylactic mastectomies. They're having their breasts surgically removed before they get cancer because they don't want to deal with cancer in the future. We're going to vaccinate these women before their surgeries, and after their surgery, we're going to look at the resected tissue, and I'll have more data to report at some point in the near future on that.
The third group are women who've gone through their breast cancer journey and are, you know, they still have residual disease. As a result, almost all of these women are going to have a recurrence, and we're vaccinating, we're providing these women with the vaccine along with immunotherapy to again see how it goes with them. Initially, our goal is to determine if the side effect profile of the vaccine with immunotherapy is too toxic or intolerable. We found in the few women that we've treated here that it is not intolerable. This is data. By the way, all of these slides are available on our website as I'm going through them fast, and I'm going to go through this one fast. What we see is that the majority of women are having a good immune response. The vaccine is tolerable, very safe.
The only side effect that we see are irritations at the sites of injection. As a result, we have decided to begin a phase two study, which we're preparing for right now as the phase one is ending. In that case, we're going to have two, you know, we're going to do it in a neoadjuvant setting. These are newly diagnosed breast cancer patients. We're going to give them the vaccine as well as standard of care and compare that with standard of care and see how the vaccine group versus the placebo group responds. This is the only way you can determine efficacy because in phase one, we studied indicators of efficacy, immune response, and safety.
In phase two, we're going to have a control group, and we're going to be able to tell is it, are the people who got the vaccine 60% responsive, 80%, or 100% responsive like we saw in the animal studies. I'm not going to talk about how big the markets are. I think everyone here knows someone who's had breast cancer. The goal here is to bring this product out initially as a therapeutic and then eventually for adjuvant treatment and recurrence prevention. Eventually, the big holy grail here is to be able to prevent cancer in women who've never had cancer. In principle, we could give this vaccine to every woman in the world who's worried about breast cancer to prevent breast cancer.
My vision, our vision is potentially, it's a big, bold vision, especially with just a few patients treated so far, but our vision is that we may be able to eliminate the majority of breast cancer, sort of like we've eliminated with vaccines, major infectious diseases like smallpox, polio, and others. I'm going to just finish up. There are other products that we're developing. These are all in the preclinical stage. I'm not going to have time to talk about them, but that's all I have. I'm happy to take questions. I did such a good job.