Anixa Biosciences, Inc. H.C. Wainwright 28th Annual Global Investment Conference

Thank you, Catherine, and I want to thank H.C. Wainwright for having us for this conference. I also want to note that this presentation is being recorded on August 21st, even though listeners will be able to see this in the middle of September. All of my statements are accurate as of August 21st, within the context of our forward-looking statement. Let me begin by talking a little bit about Anixa at a very high level. The company was initially founded in the 1980s as an electronics company and went through the decades in a number of failed businesses. In 2017, I took over the company as CEO and converted it into a biotech company. In reality, the company is about 8 years old. Since that time, we've built a very robust pipeline with two products in the clinic, which I'll focus on during this presentation.

Both products are demonstrating very good, very positive clinical data. We execute a business plan that involves very strong partnerships. We keep our burn low that way, and that enables us to work with multiple experts in different scientific areas. We're addressing large markets, ovarian cancer and breast cancer. We have a strong balance sheet, no debt, a very clean capital table with no warrants or overhangs of any sort. Over the last 7, 8 years since I've been CEO, there's been a tremendous amount of consistent insider buying by myself and other insiders, including our board of directors. I myself have bought over $2.5 million worth of stock on the open market. This is what our balance sheet looks like as of the last reported date, which was April 30th, which was the last fiscal quarter.

We have $14 million of cash on the balance sheet, which doesn't sound like a lot for a biotech company, especially one that's in clinical trials with two products. Because of the way we run our business, we've been able to move both of these clinical trials forward with very low burn. We've been burning about $5 million-$7 million per year. Last year, we only burned $7 million. We have 34 million shares outstanding, and as I noted, no debt and no warrants to produce an overhang for the stock. The strategy, as I noted, is to develop our programs with our partners. We're able to leverage existing infrastructure that exists at our partner sites.

For example, our two biggest partners are the Cleveland Clinic, which is one of the best hospitals in the world, and the Moffitt Cancer Center, which is one of the top cancer centers in the world as well. This partnership approach allows us to maintain a very low overhead and not have to raise tremendous amount of cash frequently like most biotechs, and also enables us to maintain a very clean capital structure. Our plan long term is after we have innovated the products that we're developing, which I'll tell you about in a moment, we want to out-license these programs to pharma companies for potential commercialization. As I noted, we have a number of programs that are ongoing, but I'm only going to talk about the two that are in the clinic today. One is a CAR T therapeutic targeting a solid tumor, ovarian cancer.

These are recurrent and resistant ovarian cancer patients who have failed multiple approved therapies and their disease is still progressing. That's in phase I at the Moffitt Cancer Center. The other program I'll talk about is a prophylactic vaccine for breast cancer. I should say prophylactic and therapeutic vaccine for breast cancer. We recently completed the phase I study, and we are now in preparation to do the phase II study. That program was partnered with the Cleveland Clinic, and it was funded by the U.S. Department of Defense. Let me begin with the ovarian cancer CAR T therapy. Many of you may know what CAR T therapy is, but essentially it's the ultimate personalized medicine. We take T cells, specifically T cells from a patient who has cancer. This is autologous. We take the T cells from the patient, we take them to a laboratory and genetically engineer them, quality control them, expand them, and then go back to the patient and reinfuse them back into the patient.

The intent is that those T cells that have been engineered are potentially better able to find the cancer and destroy the cancer. This type of therapy created a tremendous amount of excitement a few years ago when the first CAR T approaches were approved for certain leukemias and lymphomas, specifically B-cell leukemias and lymphomas. B-cell is a type of white blood cell. Unfortunately, since that time, the approaches to utilizing CAR T in other types of cancers, especially solid tumors, has been unsuccessful.

That being said, we have developed a new approach, or I should say a more nuanced approach, which we feel will identify ovarian cancer much better and target the cancer for destruction. This is a little bit of a busy slide, but stay with me for a second. I'll explain the key differentiators between our CAR T therapy and other CAR T therapies that have failed in the solid tumor clinical trials. On the right-hand side is a cartoon of the CAR T therapies that have been utilized for the B-cell leukemias and lymphomas, many of which are approved now. In that case, the T-cell, which is the cell on top, is genetically engineered, so it will present an antibody fragment on the surface. That's the CAR. That antibody fragment acts as a homing missile to find the B-cell, which is the cancerous cell, healthy and cancerous B-cells, to bind to the protein CD19, which is what that antibody fragment has been designed to target.

Once it binds to that protein, and hence the cell, it destroys those cells. In our case, or I should say in all other solid tumor CAR T therapies that I am aware of, there has never been identified a protein that could be targeted by the engineered T-cell that only exists on the cells one wants to destroy. The proteins that have been targeted in the past also exist on healthy cells and healthy organs, so that limits the dosage that can be used in those therapies. In our case, we use a T-cell that has been engineered with a follicle-stimulating hormone, which is an endocrine hormone.

It is a small protein, and it targets something called the follicle-stimulating hormone receptor, which is expressed exclusively on the ovaries in women and the testes in men. So when we engineer our T-cells and reinfuse them back into the body, those T-cells will only attack the ovaries and no other organ system. That is one key attribute of our technology. A second attribute is the fact that, as I noted a moment ago, the only expression of the follicle-stimulating hormone receptor is found on the ovaries and testes. Since we are dealing with ovarian cancer, we are only dealing with ovaries. Recently, however, a publication showed that the follicle-stimulating hormone receptor is also expressed on the vasculature, the endothelial cells, the inner lining of the blood vessels that exist in tumors, not in the healthy organs, but in tumors, in multiple types of organs.

What does that mean for our T-cell therapy? In our case, the left-hand cartoon shows a tumor, ovarian cancer tumor lesion, for example. Solid tumors, when they grow, they induce a process called angiogenesis to enable the formation of blood vessels within the tumor that allows waste and CO2 to be removed and oxygen and nutrients to come into the tumor. As I noted in the previous slide, the studies had shown that the inner surface of these blood vessels within the tumor, not outside the tumor, but within the tumor, express follicle-stimulating hormone receptors. So in our case, our T-cells, we expect, will not only attack the cells, the ovary cells themselves, but also disrupt the vasculature that is enabling nutrients to come into those tumor lesions. So it will be a dual mechanism of action that we believe is acting in our situation.

The third key advantage of our CAR T therapy is that we are delivering the T-cells directly into the peritoneal sac, which is the abdominal sac in which many organs exist, and in women, ovaries exist in that sac. The ovarian cancer as it metastasizes, largely all of the lesions stay within the sac. They form on the sac surface itself, as well as other organs within the peritoneal sac. So by delivering our T-cells directly into the sac, it never gets into the bloodstream and causes the side effects that people see with bloodstream with IV delivery. It also traffics better to the lesions because we are delivering it into a somewhat enclosed sac that contains all of those lesions. So this has a couple of different advantages.

One is the trafficking aspect. Because the cells never get into the system, into the bloodstream, we believe we are able to get to much higher dosages without dose-limiting toxicities. This is our dosing scheme. We have to date dosed the first four cohorts, and we are in the fifth cohort dosing right now. Just dosed an initial patient recently. We have dosed 14 patients so far. This is the key slide here. This is a swimmer plot representing the length of time that patients have lived on our therapy. We have one patient that went 28 months, several that have gone over a year. I should note that most of these patients are expected to pass within 12 weeks. So we have demonstrated significant improvement in their overall survival.

However, we have not yet completely curatively treated a patient, and we anticipate that that will happen as we increase our dosages at the current cohort and two additional cohorts above that. So very exciting data and more to come as we move forward. The vaccine program is also a very exciting program. This is a vaccine that is designed to not only treat breast cancer, but also prevent breast cancer, primary prevention. Those of you who are familiar with the world of cancer vaccines know that we have never really developed a cancer vaccine. Recent news from Merck and Moderna shows a personalized cancer vaccine that has demonstrated some efficacy in melanoma. Besides that, most clinical trials have failed. In our case, we are utilizing a different molecular mechanism that has ever been tried before.