Hello, welcome to the CohBar and Morphogenesis conference call and webcast. As a reminder, all participants are currently in a listen only mode. At this time, I'd like to remind our listeners that except for statements of historical fact, the remarks on today's conference call may include forward-looking statements within the meaning of the securities laws. Forward-looking statements are based on current expectations, projections, and interpretations that involve a number of risks and uncertainties that could cause actual results to differ materially from those anticipated by CohBar. These risks and uncertainties are described in our registration statements, reports, and other filings with the Securities and Exchange Commission and applicable Canadian securities regulators, which are available on our website at cohbar.com, sec.gov, and SEDAR.com, as well as in the safe harbor statement included with today's press release. You are cautioned that such statements are not guarantees of future performance and that our actual results may differ materially from those set forth in the forward-looking statements. CohBar does not undertake any obligation to update publicly or revise any forward-looking statements or information, whether as a result of new information, future events, or otherwise. Joining me on today's call are Dr. Joe Sarret, Chief Executive Officer of CohBar, and Dr. James Bianco, Chief Executive Officer of Morphogenesis. I'd now like to turn the call over to Joe Sarret, CohBar's Chief Executive Officer. Please proceed. Thank you, operator, and thank you everyone for joining us today. We are very pleased to have announced earlier today the proposed merger of CohBar and Morphogenesis and are looking forward to walking you through the exciting value proposition that we believe it represents for our current and future stockholders. As we communicated in November, CohBar's board of directors determined it was in the best interest of the company and its stockholders to conduct a comprehensive review of available strategic alternatives with a focus on maximizing stockholder value. We believe that the merger with Morphogenesis represents the highest potential value creation opportunity for CohBar stockholders and provides the opportunity to build a great oncology-focused company by bringing the best of both companies together. We are excited about the tremendous promise of Morphogenesis's technologies, which are designed to overcome two major obstacles that limit the effectiveness of cancer immunotherapies. We believe this approach will have a significant impact on the treatment of patients with a wide variety of cancers that are resistant to current immune therapies like checkpoint inhibitors. The combined company is expected to have a strong balance sheet and a network of world-renowned collaborators with a commitment to leverage its innovative science to bring powerful novel therapies to patients in need. This merger would provide CohBar stockholders with a risk-diversified development pipeline with a late-stage clinical program. Morphogenesis's ImmuneFx or IFx personalized cancer vaccines are designed to overcome tumor-intrinsic factors which allow tumors to escape recognition and attack by the patient's immune system. IFx is designed to prime the activation of an innate immune response which can target and destroy cancer cells. The company's lead product candidate, IFx-Hu2.0, is being developed under the FDA's accelerated approval pathway for the treatment of an aggressive form of skin cancer called Merkel cell carcinoma. Morphogenesis expects to initiate a phase 2/3 registration study early next year. Impressively, in an ongoing phase I-B study, IFx-Hu2.0 demonstrated the ability to produce durable systemic antitumor responses in 80% of patients who initially failed therapy with checkpoint inhibitors. In addition to its cancer vaccine technology, Morphogenesis is also developing modulators of the tumor microenvironment designed to overcome factors outside the biology of the tumor that lead to acquired resistance, causing cancer immunotherapy to stop working. Cells called myeloid-derived suppressor cells play a central role in acquired resistance by creating a highly immune suppressing microenvironment in which the tumor can live and escape immune attack. Along with researchers at Moffitt Cancer Center, Morphogenesis has identified a novel delta receptor on tumor-associated myeloid-derived suppressor cells and is developing a new class of bifunctional antibody drug conjugates targeting this receptor, which can both block their immune suppressing capabilities while also localizing checkpoint inhibitors in the tumor microenvironment where the tumor lives. As you can see, a combination of Morphogenesis would transform CohBar into a phase III-ready company with two innovative technology platforms that have the ability to fuel a growing pipeline for years to come. With the proposed transaction that we announced today, I believe the combined company would be well-positioned to make a true difference in the lives of patients suffering from cancer while also delivering near and long-term value to our stockholders. Before turning things over to Jim, I'd like to summarize the key details of the transaction. The proposed acquisition is structured as an all-stock transaction and includes a $15 million private placement from an accredited investor. Combined with the balance sheets of CohBar and Morphogenesis, we expect the combined company to have a cash runway through 2024. Assuming stockholders approve the merger, each holder of CohBar common stock at the closing of the transaction will be issued a dividend equal to 3.3 shares of CohBar common stock. On a pro forma basis and based on the number of shares of CohBar common stock expected to be issued in the merger and the concurrent financing, and taking into account the issuance of the stock dividend, the CohBar stockholders immediately prior to the transactions will own approximately 15% of the combined company immediately after these transactions are completed. Additionally, CohBar stockholders of record and certain warrant holders will receive a contingent value right or CVR. Holders of the CVR will be entitled to receive certain payments from net proceeds received by CohBar, if any, related to the disposition of our legacy mitochondrial assets for a period of three years following the closing of the merger. The combined company will be led by Dr. James Bianco as CEO and existing members of the Morphogenesis management team. The board of the combined company will consist of seven directors, with five to be designated by Morphogenesis and two to be designated by CohBar. The transaction is subject to stockholder approval and customary closing conditions. We expect the closing to occur in Q3 of this year. With that, I will now turn the call over to Dr. Jim Bianco to provide additional background and details on Morphogenesis's technology, pipeline, and strategy. Jim? Thanks, Joe. Before I begin, I'd like to state that I couldn't be more excited about this potential merger. I've done a number of successful business combinations, I believe the merging of Morphogenesis and CohBar has all the components to build a successful company and create significant stockholder value, as well as providing CohBar stockholders the upside opportunity of substantial dividend at a contingent value rate. As Joe mentioned, Morphogenesis has developed two unique technology platforms. Our ImmuneFx personalized cancer vaccines are designed to overcome tumor-intrinsic factors which allow tumors to escape recognition and attack by the patient's immune system. In addition to our cancer vaccine technology, we're also developing modulators of the tumor microenvironment, which are designed to overcome factors outside of the biology of the tumor that leads to acquired resistance, which cause cancer immunotherapies to stop working. We're leveraging these technology platforms to advance several product candidates, spanning preclinical development for our bifunctional antibody drug conjugates to IND-enabling studies for our novel intravenous tumor-targeted mRNA vaccine to a late-stage phase II, phase III registration trial for our pDNA vaccine in Merkel cell carcinoma, providing the company with a well-balanced, risk-diversified pipeline. IFx 2.0 is our first personalized cancer vaccine product that is entering late-stage clinical trials, let me outline how it differs from other cancer vaccines, present some of our early clinical trial results, as well as follow on plans for advancing IFx 2.0 towards FDA approval. Checkpoint inhibitors have clearly revolutionized the treatment of cancer, making them the fastest-growing class of oncology drugs, which are forecasted to account for $70 billion in annual sales by the year 2028. However, despite their success, up to 75% of patients who receive checkpoint inhibitors may not respond to them. We've demonstrated that IFx-Hu2.0 administration allows patients who failed checkpoint inhibitor therapy to achieve an anti-tumor response. In our phase I-B trial, 80% of patients with Merkel cell carcinoma achieved a long-lasting anti-tumor response when they were rechallenged with the checkpoint inhibitor. Those data guided us to have discussions with the FDA on developing a protocol design for a single phase 2/3 registration trial utilizing the FDA's accelerated approval pathway. Accelerated approval not only potentially shortens the time to approval, but significantly decreases the cost. We expect to start enrolling patients in early 2024, with the potential for a BLA filing in the second half of 2026. IFx 2.0 also has orphan designation, which extends the regulatory exclusivity for up to seven years post-patent expiration. The mechanism of action for IFx 2.0 exploits the fact we're all born with an immune system that's pre-wired to recognize foreign pathogens like bacteria or viruses. Our immune cells have what are called pattern recognition receptors, with specific molecular patterns or motifs conserved through evolution are present on all bacteria and viruses and are recognized by these pattern recognition receptors on our immune cells. This is our first line of defense against foreign pathogens, which leads to the activation of what's called an innate immune response. When IFx 2.0 is injected into a tumor, it will deliver a gene which makes the tumor cell produce a bacterial protein, which is then transported to the surface of the tumor cell. Irrespective of what your tumor does or doesn't look like to your immune system, IFx 2.0 will make that tumor look like a bacterium and will activate an immune response against the tumor. Importantly, IFx 2.0 is not an intratumoral therapy like oncolytic viral therapy, which is injected into a tumor to cause it to shrink and die. Because oncolytic viral therapy only works in injected lesions, their applications are limited to localized stages of cancer. Instead, IFx 2.0 is injected into a tumor as a cancer vaccine to activate an immune response throughout the body against the tumor's foreign antigens anywhere they're present in the body, not just in the injected tumor, thus making our therapy applicable across a wide range of cancers. By making a tumor look like a bacterium, the molecular pattern of the bacterial protein will activate dendritic or antigen-presenting immune cells, which then digest the tumor cells just like they're a bacteria. In doing so, all of the tumor's foreign antigen neoepitopes, a neoepitope is the portion of the tumor's foreign antigen that's not recognized as being part of us, and those are presented to newly produced T cells and B cells, which then educate your immune system to the patient's tumor and primes an innate immune response, and this process is called primary epitope spreading. Now that the immune system is activated and educated to foreign tumor antigens, tumor-specific killing T cells can seek out and destroy tumor cells. Similarly, activated B-cells will produce tumor-specific antibodies which also seek out, bind to, and destroy tumor cells. Destroying tumor cells then releases new foreign tumor antigens, which further educates the immune system to different-looking tumor cells than those first attacked. This process is called secondary epitope spreading, and that's the hallmark of an adaptive immune response. It's the adaptive immune response that confers memory to the immune system, potentially preventing the recurrence of tumors. Our skin has a high density of dendritic cells, which are very efficient in presenting foreign antigens to immune cells. We chose skin cancers for our proof of concept trials. IFx-Hu2.0 was investigated in the treatment of advanced Merkel cell carcinoma, which is a rare aggressive form of skin cancer with approximately 2,500 new cases diagnosed each year in the U.S. Now, Merck's KEYTRUDA, which is a checkpoint inhibitor, which by the way recorded $5.8 billion in sales last quarter, is the current standard of care in first-line treatment of advanced Merkel cell. Approximately 50% of patients will see their tumor shrink, and up to 20% will have complete disappearance of their tumor, what we call a complete response, which can be very long-lasting. Unfortunately, 50% of these patients exhibit primary resistance to checkpoint inhibitors, and they won't respond to KEYTRUDA. Unfortunately, there is no approved or effective therapies for these patients, with 60% of them dying before entering a clinical trial. The potential for IFx-Hu2.0 to overcome primary resistance could increase the number of patients who can respond and benefit from a checkpoint inhibitor like KEYTRUDA, and we believe that would address an unmet medical need. We have an ongoing two-stage phase I-B trial among patients with advanced Merkel cell carcinoma or squamous cell carcinoma. There are three cohorts of three patients in each cohort where IFx is administered weekly for one, two, or three weeks. The primary objective for this trial is to determine the optimal dose and schedule for our planned phase 2/3 registration trial. The second stage expands enrollment for an additional 11 patients at the weekly for three weeks dose schedule. Data on the first three cohorts of nine patients will be presented at the American Society of Clinical Oncology meetings this June. This slide graphically shows initial anti-tumor responses in our phase I and I-B trial. Of the nine patients enrolled in the first stage of the phase I-B trial, seven patients had primary resistance to checkpoint inhibitors therapy. Five of those patients had Merkel cell and two had squamous cell. You can see on this slide, all seven patients exhibited primary resistance to a checkpoint inhibitors therapy. PD is progressive disease, that shows that their disease progressed between 2.5 and five months, at which point the checkpoint inhibitor is discontinued. Patient received IFx 2.0, when these patients were rechallenged with a checkpoint inhibitor, you see four of the five patients, over 80% of those with Merkel cell cancer, experienced a major anti-tumor response. Two of those patients had complete disappearance. One of the two patients with squamous cell also experienced a major anti-tumor response. Importantly, these responses are durable. They're ongoing anywhere from 10-24 months in duration. We showed similar results in another phase I study, which we conducted in advanced refractory melanoma, where four patients progressed on first treatment with a checkpoint inhibitor. Again, following IFx-Hu2.0 rechallenge with a checkpoint inhibitor, three of those four patients also experienced major anti-tumor responses. Biomarker analysis demonstrated that these patients produced antibodies that recognized hundreds of new melanoma neoepitopes that were not present before IFx-Hu2.0. The melanoma neoepitopes recognized by antibodies differed from patient to patient, showing each patient's tumor is unique and that IFx activates an immune response specifically targeted to each patient's unique tumor antigens. The simplicity of IFx technology and this broad personalized anti-tumor response is really what separates it from other personalized cancer vaccines. For example, some vaccine technologies require biopsying a patient's tumor, taking the tissue to the lab, sequencing the entire tumor genome that produces thousands of tumor neoepitopes. They have to use proprietary computer algorithms to try to predict which 34 of these neoepitopes amongst the 1,000 sequenced are actually relevant to the patient's tumor. They make an mRNA for each of the 34 neoepitopes, combine it into a single mRNA, then they go and inject it back into the patient. This process obviously is cumbersome, time-consuming, costly, and clearly fraught with a variety of regulatory hurdles. Okay, here's a pretty dramatic example demonstrating that IFx 2.0 works by priming and activating a systemic immune response, not just limited to the injected tumor. This patient progressed within 3 months of starting therapy with a checkpoint inhibitor called Avelumab. IFx was administered in two skin lesions not shown here on the slide. Following IFx-Hu2.0, this patient was rechallenged with a checkpoint inhibitor, and you can see near complete disappearance of that extensive skin involvement with these Merkel cell carcinoma. In addition to our data in melanoma, we also have biomarker data from our phase I-B trials amongst patients with Merkel cell carcinoma that also demonstrate the production of tumor-specific antibodies, again, confirming IFx-Hu2.0 is priming a systemic immune response. Here's a patient with metastatic Merkel cell carcinoma with a lymph node involvement who progressed within three months of KEYTRUDA. Following IFx-Hu2.0 injection into a skin lesion, not the lymph node shown on the slide, the patient was retreated with KEYTRUDA and responded with over 80% reduction in the size of the tumor, which on surgical removal was shown to be cancer-free. We demonstrated that IFx-Hu2.0's ability to overcome resistance to KEYTRUDA in patients who failed KEYTRUDA. It makes sense to test IFx-Hu2.0 in patients who are receiving KEYTRUDA for the first time and see if we can make KEYTRUDA work better in more patients than KEYTRUDA alone. We've been in discussions with the FDA, including the Deputy Director of CDER's Oncology Center of Excellence, in finalizing a phase 2/3 registration trial design. The study design we've agreed to in principle will be a randomized placebo-controlled trial in the first-line therapy of patients with advanced Merkel cell carcinoma. Patients will receive KEYTRUDA per its label indication versus weekly IFx-Hu2.0 for three weeks alongside a standard treatment with KEYTRUDA. The primary endpoint will be overall response rate, and we'll utilize a blinded independent radiographic review committee to evaluate tumor responses. The FDA considers response rate as a surrogate endpoint that would likely predict clinical benefit, and also that this patient population has an unmet medical need, thus meeting the requirements for the FDA's accelerated approval pathway. The trial will look to enroll 116 patients at approximately 30-35 centers in the U.S., and enrollment is projected to take approximately 18 months, then an additional six months before we analyze the primary endpoint, and we expect to start enrollment in that study early next year. We're also developing IFx-Hu3.0, which is our mRNA cancer vaccine for intravenous or autologous whole cell administration. This will allow us to expand the utility of our cancer vaccine technology to blood-related cancers, which are not amenable to intratumoral administration. We're working on a proprietary antibody fragment, termed an scFv, which is coupled to a lipid nanoparticle carrying the mRNA vaccine. There are a number of benefits for using an antibody fragment over an intact antibody, most notably biodistribution, allowing more of the payload to reach its target. For IFx-Hu3.0, that target is the CD22 receptor, which is overexpressed on a number of B-cell cancers like aggressive lymphomas. We plan on identifying a lead candidate later this year and begin IND-enabling studies early next year. Our second technology platform addresses the underlying cause as to why immunotherapies stop working, and that's a condition called acquired resistance. An emerging area of intense industry research focuses on the cause of T-cell exhaustion, which is the primary reason immunotherapy stops working. Over the past three to four years, research has turned its attention to the relevance of the tissue in which the tumor lives, which is called the tumor microenvironment. Tumor microenvironment exerts a really potent immune-suppressing effect on immunotherapies, causing them to stop working. Central to that immune, immunosuppression is a cell type called tumor-associated myeloid-derived suppressor cells, which are a major component of the cells that make up the microenvironment. Myeloid-derived suppressor cells are normally produced during pregnancies, where they migrate to and populate the placenta. They create an immunologic sanctuary for the fetus. Since half of the genetic makeup of the fetus comes from the father, this is necessary to prevent the mother's immune system from attacking the fetus. Well, in cancer, these cells are hijacked by tumors to create an immunosuppressive environment in the tissues in which the tumor lives. Tumor-associated myeloid-derived suppressor cells secrete multiple immune-suppressing factors like iNOS or Arginase-1, and these molecules prevent T-cell growth and proliferation by depriving T-cells of amino acids that they need to grow and survive. They can inactivate immune-activating cytokines or even produce immune-inhibiting growth factors. Inhibiting the ability of myeloid-derived suppressor cells to create an immune-suppressing environment for tumors to live and escape immune attack represents a novel approach to overcoming acquired resistance to cancer immunotherapies. Our researchers, along with those at Moffitt Cancer Center, are the first to demonstrate the presence of a novel delta receptor, which is highly expressed on tumor-associated myeloid-derived suppressor cells. This receptor plays a central role in controlling their immune-suppressing capabilities. Inhibiting the delta receptor blocks the ability of myeloid-derived suppressor cells to produce multiple immune-suppressing factors, thus making the tumor microenvironment now susceptible to immune attack, allowing checkpoint inhibitors and cellular therapies to keep working. We're developing novel bifunctional antibody drug conjugates that target the delta receptor on myeloid-derived suppressor cells, and this represents a paradigm shift for this class of therapeutics. Traditional antibody drug conjugates have one function. They utilize an antibody to carry a cellular toxin to a tumor cell. In contrast, our antibody drug conjugates have two functions. We use a small molecule to block the delta receptor, shutting off myeloid-derived suppressor cells' ability to shield the tumor in an immune-suppressing environment, while at the same time carrying with it a checkpoint inhibitor. T-cell exhaustion is prevented, and checkpoint inhibitors can do their work amplifying immune attack against the tumor where the tumor resides. Before I close, I just wanna highlight some of the upcoming potential value-driving milestones that I touched on earlier. First, we plan to initiate a single phase 2/3 registration study for IFx-Hu2.0 for the first-line treatment of Merkel cell carcinoma early next year. We anticipate that trial to be conducted under an SPA with the FDA. The top-line data is expected in the first half of 2026, with our BLA application following shortly thereafter. We also expect to start a phase II basket study for IFx-Hu2.0 with the potential to expand its utility to a variety of cancers beyond Merkel cell, which also exhibit primary resistance to checkpoint inhibitors. In parallel with these clinical activities, we plan to complete lead optimization for our IFx-Hu3.0 program, targeting B-cell malignancies by the end of the year, with the goal of initiating IND-enabling studies early next year. We plan to start our phase I study for this program in 2025. Finally, we are advancing our discovery research activities for our tumor microenvironment modulator program, targeting the initiation of IND-enabling studies in 2025. I believe this business combination with CohBar positions us with a strong balance sheet to advance the development of our novel immunotherapies, which can make a meaningful difference in the lives of patients suffering from cancer while also delivering near and long-term value to our stockholders. Thank you for your attention this morning. This concludes the CohBar and Morphogenesis conference call and webcast. We would like to thank you for attending today's presentation. As a reminder, a webcast replay of today's event will be accessible on CohBar's website. You may now disconnect.