Okay. Good afternoon. I am Sara Nik from H.C. Wainwright's healthcare research team, and it is my pleasure to introduce Kairos Pharma, ticker KAPA, a clinical-stage oncology company whose lead antibody, ENV105, targets CD105 to reverse acquired drug resistance and restore the effectiveness of standard therapies currently in clinical development in prostate cancer and lung cancer. Presenting today on behalf of the company is CEO John Yu. Please join me in welcoming them. The floor is yours. Good afternoon. My name is John Yu. I am the CEO and chairman of Kairos Pharma. It is a pleasure for me to be here today. I would like to first thank the team at H.C. Wainwright for the invitation to present to you today. Our mission is to advance therapies that address real challenges in cancer drug resistance and immune suppression. As a neurosurgical oncologist, I believe that my main role is to provide hope to patients that really have lost a lot of hope, particularly when their cancer comes back. This hope is based not on a Pollyanna theory or some false hope, but one based on real science and the identification of mechanisms of cancer drug resistance that we can actually reverse. The problem is that resistance develops to even blockbuster drugs like anti-prostate therapies, TAGRISSO in non-small cell lung cancer. We have identified a protein on the cell surface called CD105 that becomes elevated with the treatment of these drugs and as the cancer becomes resistant to these drugs. The solution to this is a neutralizing antibody that we call ENV105 that targets this protein. This is a large opportunity in prostate cancer, non-small cell lung cancer, and other tumor types. Our lead drug, ENV105, is in a phase II trial in prostate cancer, randomized with apalutamide or with apalutamide. ENV105 is also in a phase I trial with TAGRISSO in non-small cell lung cancer. We also have an IND for KROS-201, which is an activated T cell therapy for glioblastoma. We have an experienced team that drives enrollment, and non-dilutive funding that has brought us to this point. These are the portfolio of drugs. Our phase II trial in prostate cancer is at three centers at Cedars-Sinai Medical Center, where all the technologies are derived from, City of Hope, and the University of Utah. In addition, we have a phase I trial in non-small cell lung cancer, with TAGRISSO at Cedars-Sinai Medical Center, and an activated T cell trial within the IND, as well as an IND-ready small molecule called KROS-101 that we hope to bring to trial within a year. We have several other preclinical assets that are under development as well. There are many mechanisms of resistance to cancer therapies. In TKI resistance, there are secondary mutations to EGFR drugs like TAGRISSO. There are bypass signaling through other pathways like the c-Met pathway or other EGFR pathways. Tumor dormancy is also a mechanism by which tumors slowly divide so that they are no longer activated or targeted by these TKI drugs. Radiation therapy is also something that a resistance develops to when tumors can evade apoptosis or a mechanism of cell death, and they can develop improved DNA repair mechanisms so as to repair all of the breaks in the DNAs that is caused by radiation. This is caused by cancer stem cell-like phenomenon. Immune therapy resistance occurs through T cell exhaustion, PD-L1 expression. Hormone therapy resistance are caused by androgen receptor splice variants and receptor mutations, and as prostate cancer cells become dedifferentiated into small cell cancers. All of these mechanisms have one common theme, and that is that these cancer cells become more cancer stem cell-like. This is very parallel to normal stem cells in that normal stem cells have to be very hardy and resistant to the environmental stressors like radiation and toxins so that it can replenish the cells of a particular organ. For instance, brain stem cells provide all the cells of the brain. Liver stem cells provide all the cells of a liver. In a parallel fashion, cancer stem cells provide all the cells of a particular cancer and make all the heterogeneous cell types that make it so difficult to treat. In addition, the cancer stem cells, which account for approximately 2%-5% of the cancer, are the only cells that can divide ad nauseam. All of the other cells have a limited growth potential, and these cancer stem cells also have the ability to withstand radiation and other types of stressors like the therapeutics that we throw at it. As cells become more cancer stem cell-like, they become more resistant to the drugs we use to treat them. CD105 gets expressed during the treatment of cancer cells, and as CD105 gets expressed, it signals a common cancer stem cell pathway called BMP4 signaling. As this molecule is signaled, the cancer cell becomes more dedifferentiated into a stem cell or a cancer stem cell phenotype, thereby allowing it to survive all of the onslaught of the therapeutics that are thrown at it. You can see in this survival graph that patients treated with TAGRISSO, those that have high CD105, live a lot longer than those patients with a low CD105 expression, suggesting that this molecule has an impact on survival of these patients. So in non-small cell lung cancer, EGFR-dependent non-small cell lung cancer accounts for approximately 45,000 patients per year. These patients are treated with TAGRISSO, and TAGRISSO is a fantastic drug and works great for one to two years until it doesn't. We showed that CD105 gets overexpressed on lung cancer cells as they are being treated with TAGRISSO. As these resistant cells are treated with TAGRISSO or osimertinib, they are able to grow despite the use of this drug until we add ENV105, otherwise known as carotuximab, which decreases the growth of these tumors. So based on this preclinical study, we went on to a phase I clinical trial wherein patients are treated in a Bayesian design in a dose escalation. Patients are then placed in one of two categories, either those that become resistant to TAGRISSO or those that are incompletely treated with TAGRISSO that have circulating ctDNA from these tumor cells. We recently reported the interim safety results of these patients, showing that there were no grade three or four toxicities and that the patients tolerated the drug very well. We hope to report the interim efficacy studies in the next few months. In prostate cancer, those patients that are treated with anti-androgen agents like enzalutamide become resistant to it. You can see one aspect of this here, where in this PDX tumor of a patient treated with enzalutamide has these positive cancer cells in pink that regrow despite the drug. When we add ENV105 to it, those tumor cells disappear and only the blood vessels survive. Here you can see when you add ENV105 that the growth of these tumor cells are significantly decreased when added to enzalutamide, again, another anti-androgen agent. One of the mechanisms of this is that these decoy receptors called androgen receptor variant 7, that gets expressed to take away the anti-androgen therapeutics, when we add ENV105, gets downregulated so that these decoy receptors no longer work. Other receptors that are mutated are no longer expressed so that the tumor cells are susceptible to anti-androgen agents once again. This led to a phase II trial that we're enrolling on at three centers at City of Hope, the Huntsman Cancer Institute at University of Utah, and Cedars-Sinai Medical Center, and reported the results of the safety lead in these patients some time ago. A companion biomarker study is done with the help of a $3.2 million grant from the NIH to confirm a biomarker that we used previously. These patients were treated with one to three different types of anti-androgen agents prior to being placed on ENV105 and apalutamide, which is the drug that will be used in the randomization process. We chose four months as the baseline of progression-free survival in these patients because in these two large trials in the New England Journal of Medicine and The Lancet where a chemotherapy agent was added to the anti-androgen agent or PLUVICTO to the anti-androgen agent. When the anti-androgen agent was changed to another one, the progression-free survival in both these trials was either four months or 5.6 months. That was the baseline that we chose as the comparator. In this case, these patients had a progression-free survival of 15.8 months, much higher than the four months that we anticipated. In addition, there was a significant decrease in PSA or 35% mean decrease in PSA in these patients. So we went on to study radiation therapy resistance because patients with prostate cancer are treated with radiation very commonly. Radiation therapy resistance occurs through many pathways, through enhanced DNA damage repair, through tumor hypoxia. They become more cancer stem cell-like as I discussed and several other mechanisms. As we add ENV105 and block BMP4 signaling, we showed that these radiation-resistant cells can become more radiation sensitive. So we recently reported a strategic collaboration with Bayer Pharmaceuticals to test XOFIGO, which is their radium agent with ENV105 in an animal model with the rationale supporting a phase II trial of XOFIGO plus ENV105 as a combination in bone metastatic prostate cancer patients. This was based on previous preclinical data showing that when you add ENV105 to radiation, there's a significant impact on radiation to decrease the growth of the tumor. Moving on to immune suppression agents. We are developing a small molecule that targets the GITR ligand or glucocorticoid-induced tumor necrosis factor receptor-related protein ligand. What it does is it trimerizes this ligand and enables signaling of both the receptor and the ligand, showing increases in effector T cells, CD8 T cells, which are the killer T cells. It decreases Tregs and increases T8 to Treg ratios. In addition, it prevents exhaustion of T cells and allows the T cells to be more killer or cytotoxic to the tumor. We've also developed an antagonist called KROS-102, which we're developing for autoimmune diseases, which does the opposite and increases Tregs and decreases T effector cells for self-targeting T cells in autoimmune diseases that we're developing for an IND as well. One of the important aspects of starting at Cedars-Sinai and having all of our investigators at Cedars-Sinai is that we've developed an academic CRO consortium between major medical centers, including the Mayo Clinic, Stanford, Vanderbilt, and Rutgers. This allows us to do is start clinical trial activation concurrently in each of these centers and enroll onto the trial at each of these centers in a cost-efficient manner because of the investigator status of the trial. We see this as a platform to take our therapeutics forward and test therapeutics in a very efficient and cost-effective manner. We've come through with significant non-diluted funding from the NIH through donor support, which supports our phase I trial in lung cancer, Department of Defense trials funding, which supports our clinical trials as well. Our IP extends to 2040 and supports the molecule as well as the methods of use. We have a small team that are all investigators at Cedars, and people ask how we can compete with these pharma companies with hundreds of scientists each. The true fact is that we are collaborating with these pharma companies and co-developing these drugs rather than competing with them. Our directors are well-heeled in pharma collaborations, and that's how we've begun to create these collaborations and co-lead these trials. We're a clinical stage company with an antibody that impacts a resistance mechanism for cancer drug resistance in a host of cancers. We're targeting immune suppression as a means of targeting cancer drug resistance as well. We're enrolling on phase I and II trials with interim data in 2026, as well as top-line data in 2027. We have strategic collaborations that are in place and more to come in the field of radioligand therapies. We have a strategic relationship with Cedars-Sinai Medical Center and an academic consortium co-led between Cedars and the Mayo Clinic to actively develop these therapeutics, as well as other therapeutics that we bring into the company. This year will be a year of strategic collaborations to develop technologies enabling us to transform cancer therapy. Thank you for your time