You should see the presentation in the webcast. If you'd like to receive a copy, simply email me: glenngillian@bristolir.com. We'll break for questions at the end of the formal presentation. As a reminder, this is not an earnings call, but rather a general introduction and overview presentation. We're only going to take questions through the web portal and encourage those questions to help you better understand the business. If you're listening over the telephone, please access the web link that we sent earlier today to ask that question. Remember, you can submit a question using the text box within the portal at any time. I'll ask the questions on the air for everyone to hear, and then Amit will answer. I'm not going to reference any names, but simply read the questions asked. As we have a fairly large audience today, if I can't get to your question online in time and it has not yet been addressed during the call and can be, I'll come back to you by email. I'm not going to read the forward-looking statements, but if you state that they apply, I'll reference them on page two of this PowerPoint. With that said, once again, thank you for joining us. Remember, this is fairly informal, and we do encourage questions to help you better understand the business and its growth path. Now I'll turn the call over to Amit to start his part of the discussion and presentation. Thanks, Glenn. Thanks for the introduction. And thank you, everyone, for attending this call, both existing shareholders for whom I hope to give you the latest update, and for new shareholders for whom I hope to introduce you to the company and explain why we are so excited about what we are doing as a company. As Glenn noted, excuse me one second. We're in trouble with, okay, there we go. Forward-looking statements apply. Before I get into discussions in detail about the programs that we're developing, I want to take a few minutes, a couple of minutes, to really talk about the history of the company, the strategy of the company, how we think about the company, and some of the financial aspects of the company, how we built this company. Because a key attribute of what we are trying to do is create a lot of value, not only through the programs, but also how we've structured our company and the strategy that we're executing. As many of you know, this company was reinvented in 2017 when I took over as CEO of the company, and current management and the board got involved. In 2017, late 2017, we turned this company into a biotechnology company. Since that time, we've built a very robust pipeline of products. Two of those products are in clinical trials right now, which I'll talk about in a little bit more detail in a moment. Both products are demonstrating very, very positive results in our clinical trials. It is also important to understand the strategy behind how we built the company. We have always tried to establish strong partnerships with highly credible organizations that have scientists and infrastructure that are world-class. We have key partnerships with some of our research partners, such as the Cleveland Clinic, which is one of the top hospitals, perhaps the top hospital system in the world. The Moffitt Cancer Center, which is one of the top 10 cancer centers in the United States out of the 3,500 that provide cancer care. In addition, a number of our programs are funded by top organizations like the U.S. Department of Defense and the National Cancer Institute, providing us non-dilutive capital to move our programs forward, enabling us to conserve our burn. All of our programs are addressing very large markets. We are not like many biotech organizations that are focused on rare diseases. We are addressing the markets of breast cancer, ovarian cancer, and eventually lung, colon, and prostate cancer. Now, on the corporate and financial front, we have maintained a very strong balance sheet. Unlike many companies in the biotech sector, we have over two years of cash on the balance sheet that will enable us to get to many clinical milestones, catalytic milestones as we go forward. In addition, we've maintained a very clean capital table. What that means is that we have been able to maintain a capital structure where all we have is common stock. We have 32 million shares of common stock. We do not have any warrants, any preferred stock, nothing out there with ratchets and resets that many other companies have had to accept from investors because of the challenging market environment for biotechnology. We have, as I said, a clean capital table, $32 million and change of common stock only. We anticipate continuing that clean capital structure going forward. I think that's very important for everyone to understand because as we create value and as that value is recognized by the investor community, the value will accrue to common shareholders as opposed to warrant holders and others that hold derivatives of our stock. Another characteristic of our company is the strong and consistent insider buying since 2017. I myself have bought over $2.5 million worth of stock on the open market because I'm incredibly bullish about the company. Many of our, all of our insiders, I should say, including our board, have all been buyers of stock in our company. I anticipate that that will continue as we go forward. We have limited windows in which we can buy. In fact, just a couple of weeks ago, I bought some stock, but when those windows open up, we typically see buying. The most important thing about our corporate structure and strategy is that we have a very capital-efficient business model. What that means is that that enables us to run this company with very low cash burn that allows us to not have to go to the markets very frequently to raise money. In fact, our last financing deal transaction that we did was in 2021, over four years ago. As I noted earlier, we have two years of cash on the balance sheet, $16 million, which is not a lot in most contexts. Considering that we're only burning $5-$6 million a year, and last year, last fiscal year, we burned a total of $7 million. We anticipate that that burn level will remain consistent going forward, at least for the next fiscal year and moving forward. It may increase slightly, but only very slightly. The reason is because we have developed a business plan where we leverage the existing infrastructure of our partners, our partner organizations, which have world-class infrastructure and world-class scientists who work with us on our R&D programs. That allows us to maintain a very low overhead and low cash burn. It also enables us to strategically work on different types of projects, enabling more portfolio diversification and having multiple shots on goal, so to speak. The other characteristic of our business plan, which we are beginning to execute now, is to monetize our programs early. As many of you know, biotechnology products take a fair amount of time to develop and get to market. They require a significant amount of R&D, as well as clinical trial work that takes time. Ultimately, we would like to get our programs to a point where they're providing enough clinical data and they're de-risked enough that large pharmaceutical companies would be willing to partner with us to eventually commercialize these programs. It is not our intent to build expensive manufacturing infrastructure as well as sales marketing distribution infrastructure, which takes a lot of time and a lot of money to build when organizations like big pharma companies already have that infrastructure in place, and they're looking for additional products to pump through that infrastructure, which is a sunk cost for them. By outlicensing or partnering with pharma companies, we will be able to not only create a win-win situation where we can commercialize products sooner and more efficiently, but also enables us to monetize the assets that we are developing for our shareholders so our shareholders will get a benefit much earlier than when the products appear on the market or become commercialized. That's a little bit of background. I also want to highlight a couple of key sort of intangible factors about our company. We have built this company very carefully to make sure that we are seen as one of the premier companies in the biotech sector. Even though we are a small development-stage biotechnology company, unlike many companies in that category, we are doing all of our clinical trials at the top hospitals in the United States. We're not doing clinical trials in places like third-world countries or China or places like that. Our data is coming out of the top places in the United States. We also have associated with us advisors, business advisors, board members, as well as clinical advisors that are some of the most credible and highly experienced people in the world, scientists that have been involved in some of the biggest drug development programs in the world in cancer, as well as vaccines, as well as some people that are some of the top-notch business advisors in the world. I encourage you, if you are so inclined, to go to our website. I do not have the time to go over the backgrounds of these people here, but go to our website and please take a look at the list of advisors, and you'll be quite impressed. Let's now talk about the programs that we're developing, incredibly exciting programs that are potentially game-changing for a number of different types of cancers and cancer in general as a broad category. The two programs that I'm going to speak about today in a little bit of detail are the CART-T therapeutic for ovarian cancer, which is targeting terminally ill ovarian cancer patients. These are patients that have exhausted all other possibilities on the market today, and they have been effectively told by their physicians to go home and get their affairs in order. That's when we get them—excuse me—that's when we get them, and then we treat them with our therapy. I'll explain how that therapy works and the results that we're getting in our clinical trial. This therapy has been licensed from the Wistar Institute and is in clinical trials at the Moffitt Cancer Center in Tampa, Florida. The second program I'll talk about is a breast cancer vaccine that is designed to not only treat women with breast cancer, but also prevent breast cancer in women who are breast cancer survivors to sort of prevent recurrence, as well as to prevent breast cancer in women who've never had breast cancer. The market opportunity for this is massive. Potentially, this is a game-changing type of vaccine that could enable a new type of, a new paradigm in thinking about cancer, not only breast cancer, but other types of cancer as well. This program is in clinical trials with our partner, the Cleveland Clinic, and this program is being funded by the U.S. Department of Defense. The other programs on this slide are also in our pipeline, and they include an ovarian cancer vaccine that is being funded by the National Cancer Institute, as well as recently initiated programs addressing lung, prostate, and colon cancer. I won't be talking about those programs in much detail at all today, but if anyone is interested, please feel free to reach out to me, and I'll be happy to talk about them. Let me begin with the ovarian cancer therapy. This technology is called CART-T technology. CAR stands for Chimeric Antigen Receptor T Cell Technology. This is a new type of immunotherapy that has been developed over the last decade, 15 years or so. It created a huge amount of excitement amongst the medical community as well as the investment community a few years ago when it was shown to be incredibly successful for certain types of leukemias and lymphomas. The way the process works is one takes the blood of individual cancer patients, isolates white blood cells, specifically T cells from that patient, and takes those T cells into a laboratory, genetically engineers them, and then puts them back into the patient with the intent that those T cells that have been genetically engineered outside the body in a laboratory, those T cells become much better cancer fighters than the native T cells that exist in the patient's body. As I noted, this type of technology created a huge amount of excitement for certain leukemia and lymphoma patients. These were terminally ill leukemia and lymphoma patients, patients who, again, as I noted earlier, had been told to go home and get their affairs in order. Yet CART-T technology was able to not only treat a large number of them, but in a significant number of them, the treatment was curative, meaning after the treatment, the patients exhibited no indication of disease. That type of treatment does not happen for metastatic late-stage terminally ill cancer patients. It created a huge amount of excitement. The unfortunate thing, however, is since those early successes in the leukemia and lymphoma situations, there have been no successes in solid tumors, which is obviously a much bigger market and would have a greater impact in cancer. There are a number of reasons why or a number of theories why CART-T technology has not worked in solid tumors. Our CART-T approach identified some of those. Based on the learnings that we have gained from many of the clinical trials that have failed, we have designed a CART-T platform, which we think will be potentially the very first successful CART-T platform against solid tumors. Incredibly exciting opportunity here. We are already starting to show incredibly promising data, even though it is a very early stage in our T cell clinical trial. I am going to go through the three unique attributes of our CART-T technology that we think are going to enable it to be very successful for ovarian cancer. Stay with me if you can. I am going to get a little bit scientific, but I will stay at a relatively high level. I want to really teach our shareholders why we think this is incredibly exciting and why we think we're already starting to see positive results. This is a complex slide here, but I want to highlight a couple of key points. The right-hand side is a cartoon that describes what the CART-Ts that were successful in the leukemia and lymphoma patients look like. In that case, in the B cell leukemia and lymphoma patients, these are a certain type of blood cancer where the B cells, one component of the immune system, become cancerous. In this case, one wants to be able to kill all of those B cells, ideally just the B cells that are cancerous. If you kill all of the B cells, that's still okay because you've eliminated the cancer and the patient will live. In this case, the scientists had identified a protein that exists on the B cell. It's called CD19, depicted by that black arrow on the right-hand side. This is a very unique protein because it only exists on B cells, and it's not found on any other cell in the human body, no other organ system, no other blood cell. The thought here was that if we could take a white blood cell, which potentially can kill B cells, the T cell, and engineer the T cell to have a homing missile on the surface that would enable it to go and find that B cell, then that T cell would go find the B cell, attach to it, and kill it. That's exactly what happened. The genetically engineered T cells were engineered with an antibody fragment, which is depicted by that orange crown on the right-hand side, that would then become a homing missile that would direct that T cell to the cancer cell, bind to the cancer cell, and then kill the cancer cell. That worked incredibly well for that particular situation. Unfortunately, for solid tumors, until now, there has never been a target like that CD19 protein that's been found on a solid tumor that would allow the homing missile to target just that cancer cell and not other cells that are healthy cells in the patient's body. In our case, we have identified such a target. We've identified a compound or a protein called follicle stimulating hormone receptor, FSHR, that is found on the ovaries in women and on the testes in men, nowhere else in a human body. Because it's an endocrine receptor, part of the endocrine system, it has a cognate ligand, which is called follicle stimulating hormone, that over millions of years of evolution has become a really good binding protein for the follicle stimulating hormone factor. As a result, if we engineer our T cells with the follicle stimulating hormone, it becomes a really good homing missile to find the follicle stimulating hormone receptor and destroy those cells. That's one characteristic that's unique about our CART-T therapy that has not been found on any other CART-T therapy that's been tried in solid tumors. In addition, as I noted, the Follicle Stimulating Hormone Receptor is only found on the ovaries and testes in women and men, respectively, as you can see on this left-hand side. However, a few years ago, a publication came out in the New England Journal of Medicine. That first page of that publication is depicted on the right-hand side. You do not need to read it, although this deck is on our website if you are interested in reading at least this first page as well as the article. You can pull it down. The key here is that this research team found that even though the receptor, that protein, FSHR, is not found on any other organ system, when a tumor is found on any of these other organ systems, the vasculature, the blood vessels of the tumor express follicle stimulating hormone receptor. What does that mean for our situation? In our situation, we are targeting ovarian cancer, ovarian lesions. Think of this cartoon on the left-hand side, this blob of tissue as the lesion, as the cancer. As solid tumors start to grow, they induce a process called angiogenesis, which is the process of forming blood vessels within the tissue, within the cancer tissue. The reason is because in order for the tumor to grow, it needs to have nutrient and oxygen brought in and waste and CO2 removed. It forces the body to create these blood vessels. What that research study found was that the blood vessels within this tumor express follicle stimulating hormone receptor. The reasons for that are not completely known yet, but the point is those proteins are there. In our case, we believe our CART-T therapy will not only attack the ovary cells directly, but also the blood vessels that are providing the nutrient for the lesion to survive. We're going to have a dual mechanism of action targeting this tumor that is going to occur even though we're only treating it with a single agent. That's important because typically when you have two agents, multiple agents to enable combinations of mechanisms of action, you often have multiple and synergistic side effects. In our case, we're not going to have those synergistic side effects. We're going to get a dual mechanism of action with only one agent being added. The third characteristic, which also is important and it's unique to ovarian cancer, is that the ovaries exist in an abdominal sac that exists in all our abdomens, lower abdomens. The sac is called the peritoneal sac, which is depicted by this yellow membrane. Within this sac, there exists a lot of different organs. For women, ovaries exist within the sac. When ovarian cancer starts spreading, most of the lesions, if not all of those lesions, remain within the sac, within other organs within that sac as well as the membrane of the sac itself. In our case, we are delivering the CART-T cells directly into the peritoneum. We do it through a port as opposed to delivering the CART-T cells through the vein. When CART-T cells are delivered through the vein, they go immediately throughout the body. They cause side effects everywhere, including in the brain, cardiotoxicity, and a number of other things. In our case, because we're delivering directly into the peritoneum, not only are we sending the T cells in direct proximity to where the lesions exist, but also we are keeping them away from the system, away from the bloodstream. Because they're staying away from the bloodstream, they're not causing all of the side effects that in many other CART-T trials for solid tumors have caused death of the patient. In addition, we feel that we can go to much higher dosages of our CART-T cells because we are keeping those T cells away from the bloodstream. We're starting to see the effects of that already. As I noted, the patients that we are getting are terminally ill. They have a median life expectancy of about 12 weeks, about three months, maybe four months at the highest. We are treating them with CART-T cells, their own engineered CART-T cells, as I've described a moment ago. We're beginning with very low dosages and increasing the dose. So far, this is what the dosage scheme looks like. We started out with 10 to the 5 cells per kilogram, and now we are at 3 times 10 to the 6 cells per kilogram, and we will continue going higher. This is the data. At this point, we have only treated 10 patients. I cannot make statistically relevant conclusions from this small number of patients, but the data is incredibly promising. First of all, we have verified that the safety profile of this CART-T therapy is incredibly good, much better than many other CART-T therapies that are delivered through the vein. We have treated 10 patients so far, and we already have—and while we were not expecting many of these patients to have responses because some of these dosages are subtherapeutic—we are already starting to see some incredible outcomes. We have one patient that is alive over 25 months when she was expected to pass within three. We have another patient that's alive over 13. We have several patients that are alive much longer than their mean life expectancy. As we go further in dosage, we anticipate that we're going to have even more positive results going forward. It is incredibly exciting, incredibly positive. We're keeping women alive that were not expected to be alive at this stage. We are looking forward to additional data, and that data will be provided over the next few months before the end of the year going forward. In addition, because of the results that we have seen so far, CART-T therapy is typically utilized as a one-and-done type of therapy. In our case, because of the results we have seen so far, and many of these early women that are responding have had very low dosages, we went back to the FDA and asked if we could give some of these women a second dose. The FDA gave us the approval to do that. That is significant because the FDA does not provide these types of approvals willy-nilly, and we have that approval now. As we go forward, should a woman start responding and not have enough response to curatively treat her, we anticipate being able to give her a second dose to perhaps get her either closer to a curative treatment or a complete curative treatment. We are looking forward to more data from this trial, which we will be providing on a rolling basis, on a patient-by-patient basis as we go forward. Each of those results, assuming they're positive, which we think they will be, we expect those to be catalytic for us. Let me switch subjects now. Let me talk about our breast cancer vaccine. This is a vaccine, as I indicated, that is designed to treat breast cancer as well as to prevent breast cancer. Breast cancer—I should say cancer vaccines in general—have failed because we believe the mechanism of action, that molecular mechanism of action and targets that have been tried before have been the wrong targets or flawed approaches. This approach was invented at the Cleveland Clinic about two decades ago, and it's a brand new approach that has never been tried and is the subject of this clinical trial that we're doing right now, or the phase one, which is pretty much complete. We are targeting triple-negative breast cancer, which is the most lethal form of breast cancer, but this approach we expect will work on all types of breast cancer. The way this product works is that we've identified a protein called alpha-lactalbumin, which is a lactation protein that is only produced in the breasts of women during lactation. When a woman is nearing childbirth, this protein is produced, enabling her to produce milk to feed her child. After she stops breastfeeding, the protein disappears, reappears again when she has another child and another child. Eventually, after she's no longer going to have children, the protein completely disappears and is never seen again in most women. In the one out of eight women that will get breast cancer, it turns out that the majority of those cancer cells, breast cancer cells, are producing this protein. The concept here developed at the Cleveland Clinic years ago was that if we could 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 target cells making this protein, the immune system will be ready and trained to attack cancer cells as they arise at their earliest stage, at the two-cell stage, the four-cell stage, and so forth, long before they have a chance to reproduce and become a multi-billion cell mass that can be seen in a mammogram, for example. An early experiment was done, which was quite interesting because of the molecular mechanism of action that this approach takes. It was done to demonstrate how powerful vaccination could be. Those of you who may be following the world of cancer vaccines and the research that is coming out will note that many vaccines are showing results indicating indicators of efficacy, meaning they're showing immune response, which our vaccine is as well. When those studies are taking into phase three clinical trials, the clinical data does not show clinical benefit, even though immune response was seen in an early phase one study. This experiment demonstrates that not only do we see an immune response, but we see very clinical outcomes, in this case in an animal, but we anticipate that that's translatable into a human as well. Here's the experiment. The experiment here is we took a female mouse, normal female mouse, gave her the vaccine, and then allowed her to mate and have children. The pups were normal, the litter size was normal, but the mouse, the mother that had been vaccinated, could not produce milk because what's happening is the vaccine has induced her immune system to destroy any cell making that protein. The cells making the protein are the lactation-enabling cells. As a result, the mouse could not lactate. What this tells us is, at least in the mouse model, that the immune system of the mouse through vaccination became so powerful and cytotoxic at destroying the target cell that it was able to destroy billions and billions of cells that are enabling lactation. The assertion here is that if we can teach the immune system of the mouse to destroy billions of cells, we can certainly teach the immune system of the mouse to destroy a handful of cells of cancer as they arise. Those studies were done as well. On the right-hand side is a study where we took genetically engineered mice that are designed to spontaneously develop breast cancer. Half the mice were vaccinated, the other half were given a placebo, and the vaccinated mice remained, 100% of the vaccinated mice remained cancer-free, which is amazing because in biology, you never get a 100% response for anything. Obviously, these are mouse experiments. Now we're in the middle of doing human, or I should say we're completed with the phase I human studies targeting three groups of women. The first group of women, cohort 1A, are women who've had triple-negative breast cancer, have gone through their journey, have had their surgeries, and they're now worried about a potential recurrence. We're giving them the vaccine. Obviously, we're looking for safety and indicators of efficacy, which I will show you about in a moment. In a second cohort of women, we are targeting women that have mutations that predispose them to cancer. These are women who do not have cancer at the time, but they've decided to have a prophylactic breast mastectomy. They're having their breasts surgically removed so that they reduce the risk of cancer in the future. These women, we're vaccinating before they have their mastectomy, and then successive to the mastectomy, we can look at their breast tissue to see if the vaccine has induced their immune system to surveil their breast tissue, which is what we saw in the animal studies. This is an experiment. We have not provided data to the public about this study yet, and we plan to provide this data sometime later this year. The third group of women are an interesting group of women. These are women that have gone through triple-negative breast cancer surgery and adjuvant therapy, but they happen to have residual disease, meaning they still have some cells of cancer in their bodies. Most of these women, in fact, all of these women will have a recurrence. These women are being treated by a number of different therapies, the latest of which is immunotherapy, particularly a therapy called Keytruda. Keytruda does not work on everyone. Keytruda has a lot of really bad side effects. We are seeing if we can add our vaccine to the Keytruda therapy to enable a better response in these women than just Keytruda alone. Our goal for this study, which we have achieved, was to verify that by adding our vaccine to Keytruda, we do not create intolerable side effects. As I noted earlier, when combinations are used for cancer treatment, often you get synergistic side effects. We wanted to verify that we are not seeing synergistic side effects in this group of patients. That has enabled us to help us design our phase two study, which I'll get into in a moment after showing you the data that we've presented on the phase one so far. This is our first 26 patients. We've done a total of 35 patients. We'll provide all of that data, hopefully in December at a scientific conference. This is a busy slide, but there are some key attributes that I'll highlight. One is that a large percentage of these women are seeing a very strong immune response, which I indicated was an indicator of efficacy. As you may recall, previously on a previous slide, I indicated that at least in the mouse model, we're seeing good cytotoxic response. In phase two, we will evaluate the strength of that cytotoxic response, but at the current time, we're seeing good indicators of efficacy, meaning we have taught the immune system to target that alpha-lactalbumin protein. In addition, we've achieved the goal of verifying that this is safe to give to these women because ultimately, a vaccine like this could potentially be given to a very large number of women, and so we want to verify that it's safe. The only side effect women saw was irritation at the site of the injection. The data so far, as well as the additional data that we'll be presenting later in the year, has indicated to us that we can go into a phase two breast cancer vaccine trial, which will be addressing women in the neoadjuvant setting, meaning newly diagnosed women that have not gone through their surgery, but they're headed towards surgery. What we will be doing is having two arms, one arm that will be, let me take a step back for a second. Women who are newly diagnosed typically get some therapy before they go to their surgery. The purpose of that therapy is to reduce the tumor burden as well as to reduce the possible recurrence after their surgeries. Typically, a lot of these women are getting immunotherapy like Keytruda. What we're going to do is have half of these women get standard of care. The other half will get vaccine plus standard of care. As I noted earlier, we showed that the vaccine plus Keytruda did not increase side effects. We think this is going to be a tolerable combination. We will see what the response is between the two different groups of women, and that will tell us how effective this vaccine is. In phase I, we got the indicators of efficacy, indicators of effectiveness, but since we did not have a placebo group, we really could not compare one versus the vaccine versus non-vaccine. In this case, we are going to be able to compare vaccine versus non-vaccine. This is going to be a very, very telling trial. We are looking forward to this data. All indicators, the animal studies and the early human studies, all indicate that this is going to be effective. The market opportunities, obviously, are very big. I do not need to go over the numbers here. The idea here is that initially, this vaccine would be available as a neoadjuvant therapeutic treatment, meaning it would be treating women who have been newly diagnosed with breast cancer. We want it to be available as an adjuvant treatment. Women who have already gone through their surgeries and are now considered cancer survivors, but they are worried about a recurrence. They wake up every morning worried about whether, say, they have a headache, whether the cancer has come back and moved to their brain, or whether it is just a headache. It is an anxiety-ridden situation for all cancer survivors, not just breast cancer survivors. We want to be able to prevent that recurrence. Eventually, the holy grail here is to prevent cancer in women who've never had cancer, primary prevention. We want to be able to—every woman potentially in the world who's worried about cancer becomes a potential customer for this because hopefully, we can give the shots to these women and never have to worry about cancer arising in the first place. Those are the two programs. Incredibly exciting data, incredibly positive, and looking forward to additional data in the phase two as well as additional data in the phase one on the ovarian cancer situation. I'll just mention the other programs in the pipeline without getting into detail. As I indicated, we have an ovarian cancer program that is in collaboration between the Cleveland Clinic and the National Cancer Institute, funded by the National Cancer Institute that is in preclinical studies, animal studies stage at the current time. We have initiated lung, prostate, and colon programs. We feel that if the breast cancer vaccine is successful, it'll change the paradigm of how we think about cancer. Research teams all over the world will start looking for new vaccine targets for different types of cancer. We and our partner, the Cleveland Clinic, have decided based on the data that we're seeing in the clinical studies for breast cancer that we want to take the lead, continue having the lead in other types of cancers, including the big three, which are lung, prostate, and colon. We've initiated those programs, and I look forward to updating all of you on many of the advances that we're making in those programs in the coming months. With that, that's the presentation, and I will go ahead and turn it over to you, Glenn, to manage the Q&A session. Perfect. Thank you so much. Again, to our audience, if you have a question, please use the question text box within the Zoom portal. We do have quite a few questions in the queue, and we'll try to get through most of them in the remaining time, and we may go a little bit over if you're available, Ameet. First question. With over two years of cash runway, what are the key inflection points over the next 12 to 18 months, I guess, milestones that could drive financing decisions or partnership opportunities? For a typical biotech company, the clinical or the catalytic outcomes tend to be clinical data. For the breast cancer vaccine, we'll be presenting all the comprehensive clinical data, we hope, in December at the San Antonio Breast Cancer Conference. We are in the process of creating the abstract to apply and present there. We'll also be presenting at that time the report to the U.S. Department of Defense for the final results of this vaccine trial, which they have funded. We'll also be putting together a report for the U.S. FDA and discussing with the FDA the trial design and the metrics for the phase two study. A lot of that is going to happen near the end of this year, in a few months. For the CAR-T therapy, we are going to be providing updates on a rolling basis. When we treat new patients and as previous patients continue living for periods of time on a monthly basis, we'll be providing updates. Catalytically, each of those updates will be telling us how long these patients are living. We have biomarker data on these patients, but we think overall survival is the key metric. The longer these patients live, the better it is, obviously, with good quality of life. That's what we hope to be able to provide over the coming months. Super. Thank you. I guess I'll paraphrase this question because it's related. Given some of these timelines and these milestones, where are you in discussions with potential pharmaceutical partners and your current programs? Have these types of discussions begun, or are you waiting for that data to begin those discussions? All of those discussions for both of these programs have begun. We are talking with potential pharmaceutical partners on the breast cancer vaccine. We are talking to partners on the CAR-T ovarian cancer therapy as well. It's very hard to identify when a deal can get done. I am not going to predict, but I am hoping that 2026 is a really good year for us. Thank you. How did the Department of Defense get involved in the Cleveland Clinic study for breast cancer vaccine? The Cleveland Clinic, the data that I showed you, which is just a subset of the data that has been published and disclosed by the Cleveland Clinic research team. The U.S. Department of Defense, obviously, most people realize the U.S. DOD funds things related to defense, but they do fund certain types of medical research that could be game-changing. The Cleveland Clinic went to the U.S. Department of Defense and submitted a request for funding for this vaccine, which could be game-changing. The U.S. Department of Defense obviously saw the merit in that program and how it could completely change the landscape of cancer. Imagine a world where you could just give women a shot and not have to worry about breast cancer. That's the thinking there. The U.S. Department of Defense allocated some multimillions of dollars to the Cleveland Clinic to fund not only the final preclinical development, but eventually the clinical study that is nearing completion now. The U.S. DOD is providing all of that capital. Does the current administration health policy affect your funding and support? That's a really interesting question, Glenn, and I get that all the time. It's really hard to answer that question because there are a lot of things that are up in the air. I will say a couple of things about the current situation. First of all, with the caveat that things are still up in the air and things have not completely settled, we do believe that there will continue to be some funding for various types of revolutionary research, and we've requested some of that funding. We'll see how that works out in the next probably few months. We'll know. One thing I also want to say about the vaccine, and I get this question often, is that there's a lot of controversy about vaccines today. In fact, there was recent news today about the RSV vaccine and the new committee that Robert RFK has installed regarding vaccines. The one thing I want to say about a breast cancer vaccine is it's not an infectious disease vaccine. All of the vaccines that are sort of controversial are related to government-mandated vaccines. The idea that the federal government or even a local government or a school system can mandate certain types of vaccinations for you to be able to attend school or get a job or whatever. There's been a lot of controversy about that, a lot of discussion about that. I don't want to get into the politics of that. I do have my own scientific opinions about that. What I want to say about our breast cancer vaccine is that because it's not an infectious disease, you don't get breast cancer by hugging someone who has breast cancer. This is not the type of vaccine that will be mandated by the government to enable you to get a job or anything like that. This is the type of vaccine that you, as an individual, if you're worried about breast cancer, if you have a history of breast cancer in your family, if you don't want breast cancer, once the product has been approved, it'll be your own personal decision. It'll be a decision that you and your physician make regarding whether you take that vaccine. This will not be a vaccine that the government will say, "You've got to take or else you can't have a job." I hope that answers that question. I can talk about that issue for a long time. It's probably beyond the scope of this presentation to have an in-depth discussion about that. Thank you. How do you avoid T-cell exhaustion? Are you using an armoring approach to deal with tumor-suppressive microenvironment? That's a really good question, and it gets into a little bit more—it's a sophisticated question from someone who obviously knows a little bit about CAR-T therapy and T-cells and how the immune system works. We are not using any sort of armoring approach. We think while those approaches have had some interesting results in animal studies and maybe some early clinical trials, the complexity of CAR-T therapy is high enough already based on our understanding of how we can manipulate T-cells that we think a simpler approach is better. You're right. We are susceptible to T-cell exhaustion. We are susceptible to the tumor microenvironment. What we've seen in some of the early patients, especially our patient who has gone 25 months, is that our T-cells are infiltrating her tumor. They're knocking out. They're creating tumor necrosis, meaning they're killing the tumor cells. We've seen that through a biopsy result. We do think that there will be different levels of exhaustion for different patients. That is one of the reasons why we went back to the FDA and said, "If patients are showing a response, but the response is not strong enough to curatively treat them, will you give us the permission to give them another shot, another treatment, essentially?" The FDA, looking at the data that we presented them and the results we presented them, said, "Yes, we're going to give you the ability to do that." Other CAR-T treatments, I'm not aware of any other. Maybe there may be one or two other CAR-T treatments that have received that approval, but we're one of the first that has received that approval from the FDA to address some of these things. We will learn more about T-cell exhaustion and persistence as we go forward. We do not have all of those answers right now. Thank you. What evidence do you have that T-cells can effectively expand in the peritoneum? Is there sufficient antigen presentation, other growth factors? Yeah. We believe there is sufficient antigen presentation because that's where all the lesions are. We think there's enough growth factors. We don't know exactly how these T-cells will proliferate, but in the end, and we'll be studying all of those things, but in the end, the bottom line is overall survival. Whether it's one of the questions people ask me also is, "Are your T-cells working based on the anti-angiogenic mechanism because of the FSHR on the blood vessels, or are they working because they're targeting the cancer cells directly?" We don't know the full answer to that. We believe it's a combination, but we don't know the answer yet. The bottom line is it really doesn't matter what the answer is. If you're keeping the patient alive and she's got a good quality of life, we'll eventually figure out what the mechanism is, or we'll eventually figure out if there's enough expansion. In the end, if you're keeping the patient alive, that's really what matters. That's what we're focused on. Thank you. Were there any radiological biomarker responses? Yes, there are radiological. I'm assuming the question is radiographic responses, and we did see responses of necrosis in, and this is obviously for the CAR-T therapy. We did see radiographic responses indicating that there was necrosis in some of these patients. That's also a little bit confusing because what we also see often in some of these patients, when I say often, it's a small number because we've only treated a small number, but we often see the tumor after treatment expand. We call that pseudo-progression because it looks like on the radiograph, on a CT or an X-ray, the tumor has gotten bigger, which is not good, but it turns out that the tumor in many of these cases was getting bigger because our T-cells were getting in there and expanding them. The T-cells are getting in there to kill the cancer cells, and that on a radiograph actually looks like pseudo-progression. That's the technical term. Thank you. Is it possible to attract the attention of big pharma with your current phase I and low patient count, or do you need a more substantial phase II? It depends on which of the programs you're talking about. I do believe that the breast cancer vaccine will require some initial phase two data because, as I indicated, all of the results in phase one were incredibly promising. In phase II, we will start getting an indication of effectiveness. Initial data there will get, I think, the whole world excited if the data continues to be positive. In the case of the CAR-T, I think we only need a few more patients that are demonstrating good overall survival because CAR-T therapies are being, this therapy is being tried on terminally ill patients. These patients have zero other options, and they're going to die. If we can save a handful of their lives for a significant amount of time with good quality of life, then that becomes very, very interesting and attractive to pharma companies. Thank you. I think you just answered part of this question, but I'll ask it and maybe have you expand on it. In a phase two trial, what sort of patient enrollment count would you be looking for given how terminally ill patients would be? We're looking for phase two for the CAR-T therapy is going to be a very different animal than the phase two for the breast cancer vaccine. In the CAR-T therapy, again, we're going to be targeting terminally ill patients. Typically, for this type of trial, you do a phase two/three study at the same time. We will be looking at terminally ill patients who have basically no other options. A phase two trial will pretty much be an expansion of the phase one trial. Not too many things that will be different there. In the phase two trial for the breast cancer vaccine, that's a different situation. We anticipate on the order of about 80 patients, half of whom will get the standard of care. The other half will get standard of care plus vaccine. The intent there is that that phase two is not going to be a registrational trial, meaning it's not the trial that's going to determine whether you get FDA approval or not. It's the trial that demonstrates that you are going to be successful with the vaccine. By doing an 80-person plus or minus trial, we'll be able to get results much faster. We'll be able to tell whether this vaccine is doing what we need it to do. We'll be able to tell if it's 60% of the patients that are responding or 100% of the patients that are responding. That data will have two effects. One is that it will scientifically tell us what the chances are of a successful phase three trial. Number two, it will create a huge amount of excitement with potential pharma partners who will want to jump on board and continue the final development and eventual commercialization of this program. The data from the phase II trial is going to be incredibly catalytic, assuming it's positive, which I truly believe it will be. Super. Thank you. I'm just doing a time check. I noticed we're just before 3:00 P.M. East Coast time. We do have a number of questions still in the queue, but I think a lot of them overlap, so we probably will only need to ask about a quarter of them. For anybody that needs to drop off exactly on the hour, this is being recorded. We'll make the recording available sometime tomorrow if you want to pick up from where you left off. I'll continue now with you, Amit. Can you just go over the process of registering participants for such trials? Has it been easy to sign up patients, or is this a slow process? Trial enrollment is always a slow process. In the breast cancer vaccine, we have a waiting list, or we had a waiting list. Now that enrollment has been completed for phase I, we're no longer enrolling patients. I would be getting phone calls from patients all over the world and their families asking how they could get involved in that trial. That was a unique situation. The CAR-T trial is a little bit different because these are patients that are terminally ill that have failed everything else, that have gone through a lot of treatment, and they've been beaten up a lot. Sometimes these patients would rather just spend the latter three or four months of their lives without having to rush to hospitals and do all kinds of other treatments. Sometimes these patients are just not able to logistically and physically come to Tampa, Florida, which is where the trial is going on. They are just not able to get into those trials. There are lots of logistics. Each of these trials and all trials in general have inclusion criteria and exclusion criteria that are designed to take patients in a way that allows us as the researchers to get good information on those patients. It breaks my heart, as I am sure it does for many of the physicians working on these trials, to have to say no to a patient that wants to get into a trial because they do not meet the inclusion criteria. We end up saying no to a lot of patients. I think it's important for us to understand, and I want to say this carefully, that we've been very careful about the patients that we have taken in our CAR-T trial. People have told me that it's going too slow. Absolutely, we all want things to go fast, but we don't want to rush it to the point where we potentially cause harm to patients, including perhaps cause death to some patients. I will tell you that certain CAR-T trials that I have seen clinical data for in other situations, they have perhaps pushed it too aggressively before they understood the science well enough, and they've hit the wall. They've had patients die that perhaps may not have had to pass. As a result, they've had clinical trials shut down, suspended by the hospitals or suspended by the FDA. That's disastrous. We are being very careful. We want to make sure that that doesn't happen to us, and we want to make sure that we're treating the patients as ethically as possible. If that means it takes a little bit longer, we would rather do that than hit the wall, so to speak. The benefit of our business model, which allows us to operate with very low burn, gives us a little bit more flexibility in terms of time and enrollment. Whereas other companies that are burning $50 million-$100 million a year, they need to push their patients quickly through these trials to get data to enable financing. We're not in a rush. We have intentionally built our company that way so that we can properly drive these trials and obviously benefit patients as well as our shareholders with positive results. Super. Thank you. You led into this next question, so I'm going to go with that and then followed by others. Can you talk about the total spend of the programs, including CAR-T and the breast cancer vaccine? What is the allocation between you and your partners in terms of cash used? Maybe get into the economics between the partnerships. Okay. I guess there are three components. Regarding specific spend on each program, we don't disclose that information. Based on my comments and public statements, you can probably figure it out. As you know, if you assume we spent $7 million last year in total costs, assume that the CAR-T program, I'm sorry, the breast cancer program is fully funded by the Department of Defense. The bulk of the spending outside of our public company costs and overhead is on the CAR-T program, which is still very tiny. As you know, as many people who are familiar with CAR-T therapies and other companies, those programs cost tens to hundreds of millions of dollars. Yet we spent $7 million and cut out half of that for overhead being a public company, accountants, lawyers, all those things. You can sort of back into how much was spent there. The second question, actually, I sort of lost my train of thought. What was the second component of the question? I guess the split in economics between yourself and your partners. Oh, yeah. In all cases, we owe a very small, modest royalty to our partners. In the case of Cleveland Clinic, a small royalty there. In the case for the breast cancer vaccine, and by small, I mean low single digits. In the case of the CAR-T therapy, because we licensed it from Wistar, we owe them a small single-digit royalty. In the case of Moffitt, we're supporting the effort there financially. Basically, all of the economics remain with us, whereas going forward, we will share that bulk of the economics with a potential pharmaceutical partner. Thank you. And then touching, I guess, continuing from that form of discussion, can you talk about the technology IP and the ownership and the splits between your partners? Yeah. The ownership of all of these technologies through an exclusive 100% owned license, worldwide license, the ownership basically belongs to us as the commercial partner of these academic centers. As far as IP is concerned, I typically don't talk about detailed IP strategy in public forums, but I will say this: we have lots of patents that have been issued on all of our technologies, not only in the United States, but in international jurisdictions. We are very aggressive in prosecuting and continuing to file patents on things that we've already done, as well as anything new that we learn that could be the subject of an inventive disclosure. We're very, very, and by the way, these patents belong to the academic institutions, but we have 100% license to those patents. Thank you. Can you provide a little more technical insight into how the breast cancer vaccine can not only prevent breast cancer, but also cure it in patients and put them into remission? Yeah. The idea here is that this is a type of immunotherapy. Chemotherapy is basically a chemical that goes in and tries to destroy the cancer cell. It tries to destroy the cancer cell at a rate faster than it harms healthy cells. That's often a challenge. Immunotherapy, the broader umbrella of immunotherapy, is that you're not trying to target the cancer cell itself. You're trying to impact the patient's immune system to go after the cancer, with the idea being that the immune system, which is native to the patient, is much better at distinguishing between a cancer cell and a healthy cell. In our case, we are trying to teach the immune system to target any cell that makes that target protein. Because that target protein we have discovered is only found on cancer cells, we hope that the immune system will attack cancer cells without creating autoimmune disorder, meaning without attacking healthy human cells or organs. This is getting into a little bit more technical detail than probably is in the scope of this presentation, but I will say this for the person who asked that question: the reason that previous approaches have been flawed is because previous approaches tried to target proteins that were overexpressed on cancer cells versus healthy cells, meaning cancer cells exhibited large numbers of this protein, and that was a characteristic of the cancer cell, whereas healthy cells exhibited low numbers. When you target that protein that's overexpressed, you may be able to kill the cancer cell, but you're also creating autoimmune disorder against a whole bunch of other organs that exist in your body. In that situation, it really doesn't work very well. That's been the approach that's been tried before. That approach has been tried and successfully done with therapeutic approaches like Herceptin, which is one of the biggest and first monoclonal antibodies for breast cancer. The idea was that certain breast cancer cells express a higher level of protein called HER2/neu. If you target that protein, you can kill the cancer cell before killing a lot of healthy cells. Healthy cells have that protein too. The thing about a therapeutic is if you start seeing these really bad side effects because the therapy is attacking healthy organs, you can stop the therapy. With a vaccine, you cannot do that. Once you have vaccinated and taught the immune system to target a particular protein, it is on. You cannot shut it down. With a vaccine, you really need to find a good target. That is the target that we have identified for this breast cancer vaccine called alpha-lactalbumin. We have also identified a similar target for ovarian cancer that is being, as I indicated, worked on with the National Cancer Institute. We are in the process of discovering those targets for lung, prostate, and ovarian. I will say this from a shareholder standpoint. As the breast cancer vaccine continues down through the trials and continues to show positive data, we already have these other programs and other types of cancers. Once the breast cancer vaccine is shown to be successful or heading in a very positive direction, for shareholders, the value of these other assets, which right now are science experiments, the value of those other assets just increases dramatically because the first asset is now showing good positive clinical results. That is one of the reasons why for shareholders and for us as scientists and physicians, we wanted to start these programs in these other cancers as well. Thank you. I guess this is a competition-type question. Are there other companies that are also creating cancer vaccines, breast cancer vaccines? Are there any that are near-term approval? Yeah. There are lots of other companies that are working on cancer vaccines, and that's been the case for decades. The most recent types of cancer vaccines that are in clinical trials are primarily mRNA personalized cancer vaccines, not only for breast cancer, but for many other types of cancers. Those vaccines have shown some initial positive data in clinical studies, and many of them have also failed miserably, epic failures that have resulted in companies that have raised hundreds of millions of dollars or even billions going bankrupt. The challenge with mRNA vaccines is that they have to be personalized. You have to take a tumor sample from each patient. You have to sequence the DNA of those tumor cells. You have to identify specific mutations that could be targets of the mRNA vaccine. You have got to create, you have got to choose which of those mutations are going to be immunogenic, and you have got to create a group of mRNA or, in some cases, DNA fragments that you inject back into the patient. That process is expensive, and it has got to be personalized for every patient. It is incredibly expensive. Our approach is to have an off-the-shelf vaccine that is inexpensive because eventually, who knows? If this thing is approved for primary prevention, we may be giving it to hundreds of millions to billions of women in the world. You cannot personalize a vaccine for that many people. You have got to be able to have something on the shelf that you can distribute to everyone. Thank you. Can you address how the quality of life has been for those patients that have responded favorably to the CAR-T treatment well beyond their estimated life expectancy? Again, it's a small number of patients, so it's hard to broadly generalize. For example, the patient who is at 25 months, her quality of life has been fantastic, although I will admit she's starting to have some issues now. Some of the other patients, while they have lived, their quality of life has improved, but it could still improve more. We want these patients to be able to live independently, and some are doing that, and some are still having some challenges, even though we're having potentially an impact on their lesions. They're not completely independent. As we go forward, we will hope that higher doses will give these patients a much better response and a much better quality of life going forward. I will also say that some of these patients to whom we have given the vaccine have passed. Some have passed within a month. I'm sorry, not the vaccine, the CAR-T. Some of these patients have passed within a month after we've treated them. Part of the reason is because they are so far along that the treatment came a little bit late. I believe that if we had gotten them three or four months earlier, we would have had a bigger impact. As we go forward, we'll have a better statistical representation of the results. Thanks, Amit. There's a number of questions related to your market. I'm just going to sort of qualify them all and characterize them all in one general statement, and then I'll let you just answer it. The general comment is that your technology appears to be extremely exciting, but the sentiment is that the market doesn't understand or appreciate what you're actually building as a business. Can you just address how you think about, I guess, the current valuation, your market, access to investors, and just generally anything IR-related that you think should be said to current shareholders on the call? A couple of things. This is creeping into a discussion about stock price, which is something that I tend not to discuss in general. I'll say a few things here. The valuation of the company is driven by a number of factors, which includes an understanding and excitement about our programs, the clinical data, etc., but also driven by macroscopic effects that a lot of our shareholders perhaps are not aware of. That is that the development stage biotech sector has been under tremendous pressure for the last four or five years. In fact, if you were to go look at the XBI, X-ray Bravo India is the index that tracks smaller cap biotechnology companies. If you look at that chart over the last five years and compare it to us, look at it over the last six months, one year, three years, whatever period you want, you will see that our company has performed better than the rest of the sector. However, if you compare our sector with the technology sector, for example, you'll see that the technology sector has performed a lot better. That has to do with macroscopic things that we, as an individual company, really can't control. If you look at a lot of other companies in our sector and their performance, specifically the smaller cap companies, you'll see that many of them have had to do financing transactions that are very, very painful and that have taken all of the value away from their shareholders. There are companies that may have the greatest program, and they're providing very positive data in their clinical studies, but their valuations are not going up because they've created capital structures where they have huge amounts of warrants and overhangs, preferred stock, ratchets, all these things. Sophisticated institutional shareholders are not going to buy those stocks unless they get the same warrants and other derivative securities. In our case, we've tried to stay away from all of that because we want the value to accrue to common shareholders, which is including myself and other members of the insider group. That being said, our company is often classified in the same bucket, painted by the same brush as many of these other companies that are under a tremendous amount of stress. I believe that as everything is cyclical, as interest comes back into the biotech sector, which it has to eventually because we're the companies that are keeping people alive, as interest comes back, our company will be recognized for the value that we are creating and the shareholder-friendly approach and strategy that we are executing versus many of the other companies that have really, to be blatant, have screwed their shareholders. I don't know when that's going to happen. The key is that we have enough capital to get us to a point where I believe that that will happen. I think I don't know what else I can say about that, but when you compare our performance versus Nvidia or Apple, you'll see a big discrepancy. When you compare our performance versus anyone else in the biotech industry, including large cap biotech companies, you will see that we've performed better. On a relative basis, in our industry, we're sort of one of the cream of the crop, but on a relative basis, comparing to other sectors like technology or AI and things like that, we have not performed well. I eventually want us to perform better than those other sectors, and I'm working very hard to do that. I'm also buying a lot of stock because I think that will happen at some point. Super. Amit, you've done a fantastic job. We've still got a vast majority of our attendants that are participating live. Again, this is being recorded, so we'll circulate it to anybody that had to drop off. We'll maybe let you give some parting words and statements, and then we'll end the presentation. First of all, thank you, everyone, for listening to this presentation. Thank you, Glenn, for holding this. I look forward to engaging with any and all of you going forward, shareholder or not shareholder, big shareholder, small shareholder, patient. I make it a point to call everyone back who calls me, especially patients who are interested in how we could benefit you. If anything, please stay tuned with our keep watching our company because we have a lot of really exciting things in the works, and I hope to be able to update you as we go forward. Thank you, everyone. Super. Thanks, Amit. Thank you to our audience, and this concludes this presentation.