Alright, I'm very happy to introduce you to David Mazzo, the CEO of Lisata Therapeutics. Thank you, and good morning, everyone. I appreciate you taking the time out of your schedule to allow me to introduce Lisata Therapeutics and provide an update on our development activities. As with all the other public companies that are presenting here, I'll just remind you that I'll be making forward-looking statements throughout the presentation and ask that you please keep those in mind as you make development and investment decisions. Let me describe Lisata initially at a glance. We are a clinical-stage pharmaceutical company working in the field of solid tumor cancer principally. We do have some other areas of interest, which if we have some time, I'll get into, but mostly we're a cancer company and we're working specifically in the area of solid tumors because that's the area of the highest unmet medical need that still exists today. We have a very seasoned management team. This presentation, including the appendix, which I will not have time to go through, which gives details on all of the clinical trials, is available on our website, as are the bios for all of the people that I'll be mentioning here. Our management team has about two centuries of combined development experience in both big pharma R&D and small emerging pharma successful drug development internationally. We have a very strong intellectual property portfolio protecting our products out through 2040, a development plan across the board of the portfolio that provides for a number of milestones that should be value creating over the course of the next 12 to 18 months, and a platform technology that we believe has been validated by the fact that we now have existing licenses and collaborations with a number of other companies which have assessed and determined that the product and the platform have value. Importantly, we also have cash runway through early 2027, so unlike many companies, more than a year of cash on the balance sheet. As I mentioned, a strong management team with international drug development experience working across all therapeutic areas, including, of course, oncology. We're working in the area of solid tumors because more than 90% of all newly diagnosed cancers are actual solid tumor cancers, and they still represent an area where treatment effects are not optimal. Additionally, many of these solid tumor cancers are growing in prevalence at an unprecedented rate. For example, pancreatic cancer, which not too long ago was not very well known, will become the second leading cause of cancer death in the United States by the end of this decade, which is now only about four years away. The reason for this is that these cancers present with a very challenging morphology. They create a tumor stroma, a mixture of cells that encapsulates the tumor and acts as a physical barrier preventing anti-cancer drugs from accessing the tumors optimally. In addition, that stroma and the tumor cells that are adjacent to it are immunosuppressive. There's an immunosuppressive microenvironment, and that helps to hide the tumor from your immune system and actually prevents many immunotherapies from being effective as well. Really, until very recently, the most prevalent way of getting around this problem was by trying to create a larger concentration gradient, pumping more drug, in most cases chemotherapeutics, which are poisons, into the body to try to force more into the tumor. Because they were non-specific, you ended up with many off-target side effects, and eventually patients quit the therapy because the treatment was worse than the disease, and then they succumbed to the disease. We found a solution that we believe overcomes this problem, and that's SERTEPATIDE. It is a proprietary internalizing RGD cyclic peptide. The RGD is just the sequence of amino acids or the motif that is in this particular compound. It's an adjuvant, which means we use it in combination with other anti-cancer agents, and its function is to target the tumors, open up that stroma so that you can penetrate the tumors with the appropriate drugs, and also to reduce the immunosuppressive nature of the tumor microenvironment. It converts the tumor stroma from a barrier to a conduit. It reduces the immunosuppressive T cells and actually recruits cytotoxic T cells to the tumor, and it inhibits the metastatic cascade, so it prevents these tumors from spreading. It is also interesting because it can be used in combination with any modality of anti-cancer drug, you know, chemotherapy, immunotherapy, radiotherapy, etc., ADCs, etc. I won't spend a lot of time on this just to say that we have fundamental composition of matter protection on SERTEPATIDE now into the 2040s. A nice strong intellectual property portfolio. As I mentioned earlier, a number of important strategic alliances. We just recently announced last week a strategic license, a global license with Catalent for their ADCs in combination with SERTEPATIDE as a payload on their SmartTag ADC technology. We have a strategic alliance with JTC Health Corporation, which is an AI discovery company based here in Irvine. They are generating new compounds and we're their exclusive translational and development agent for JTC Health. We have a diagnostics application license to Cuva Laboratories, looking at their nanomark technology being enhanced and being able to use MRIs as opposed to CT scans to be able to better diagnose and measure solid tumors. We have an agent in China that has the license for the product in Greater China, and that's called Qilu Pharmaceutical. The way that SERTEPATIDE works, it's this nine amino acid peptide that has a very high affinity for alpha-3, beta-3, and beta-5 integrins, which are upregulated on solid tumor cells as well as the cells that make up the stroma. This is the targeting portion of the technology. Once SERTEPATIDE is activated on these integrins, it becomes susceptible to proteolytic cleavage, and the result of that cleavage is a five amino acid CN rule peptide fragment. That peptide fragment then dissociates from the integrins and immediately binds to an adjacent receptor also upregulated in the tumor microenvironment called Neuropilin 1. Neuropilin 1, once activated, initiates the CN rule active transport mechanism, which is a naturally occurring biochemical transport mechanism manifested by the formation of microvesicles on the surface of the cell, which then encapsulates the co-administered drugs and percolates it through the stroma, depositing them deep into the tumor. That's the penetration portion of it. The presence of SERTEPATIDE in the microenvironment disrupts the immunosuppressive nature of these tumors and actually recruits cytotoxic T cells and allows your immune system to contribute to the combat of the tumor. Additionally, it actually activates immunotherapies, which traditionally have been ineffective in solid tumor treatment. The next several slides, which I mentioned, are all on the website, just demonstrate how well this works using a variety of models, whole animal models, as well as in vitro cell models, looking at a variety of modalities of different drugs, checkpoint inhibitors, non-drug entities, as well as a whole host of different modalities of drugs going from chemotherapeutics all the way up to adaptive cell therapies. You can mix and match with almost anything. Additionally, we have data that now shows that SERTEPATIDE actually improves immunotherapy efficacy in these solid tumor models preclinically, which are the data that are here. I apologize for going fast, but we have a lot to cover. I have clinical data that I will show you as well that shows that durvalumab can be activated with SERTEPATIDE. Our development platform consists of a two-pillar approach. On the one hand, we're most advanced in metastatic pancreatic ductal adenocarcinoma, and we have now completed phase 2b and are phase 3-ready in metastatic pancreatic ductal adenocarcinoma. We also have a multiple number of phase 2a proof of concept studies across a variety of standard-of-care regimens in a variety of different solid tumors, and those data will be coming out over time as well. Some were recently reported from the Sendifox study, which reported data in appendiceal, colorectal cancer, as well as pancreatic cancer. I'll show you some of the metastatic pancreatic ductal adenocarcinoma data. This is the phase 1 data. We have data from our phase 1 trial, which was conducted in Australia and New Zealand, as well as our partner's independently run phase 1 trial, which was done in China, in comparison to the standard-of-care data for gemcitabine and nab-paclitaxel in this. You can see here in these studies we both showed significant improvement, major improvement in overall survival. This is the thing that most patients and physicians are concerned about. It's not, you know, whether or not my biomarkers go up or down. It's how much longer will I live and what will be my quality of life during that period of time. We can increase survival by five to six months in these patients, which is a major, major improvement since the average lifespan of a metastatic pancreatic cancer patient is about nine months from diagnosis to the date of succumbing to the disease. You know, 150% improvement. Additionally, we can show across all those other efficacy endpoints consistency of improvement. That's important because in a clinical trial, you don't want some of your markers going in the positive direction and others going in the negative direction. You need to see internal consistency, and we see that across the board in all these studies. That led us into our phase 2 trial, which we actually acquired when the phase 2b had started. It was being done as an academic trial, and in that regard, it had been powered for an unusual endpoint, six-month PFS as opposed to median PFS, which is not a standard regulatory endpoint. It was using a single cohort of dosing and a number of other things that were purely academic. We redesigned that study to add a second cohort for dosing, to add overall survival as a major endpoint, as well as median PFS, as well as a number of other critical regulatory endpoints. Because we added that, the two cohorts are coming out sequentially rather than being reported at the same time. Cohort A data were actually reported at ASCO GI back in January, positive data. We just reported cohort B preliminary data at ESMO GI in July, also positive data. The combined data set will be presented at ESMO very shortly in Berlin, followed by final data and the CSR late this year, early next year. Just to give you a sense of what the data is looking like and why we're so excited, by the way, this is a double-blind, randomized, placebo-controlled trial, two-to-one randomization against the standard of care, which is the placebo group. Here you can see initially, and this is why we're so happy we redesigned the trial, when looking at six-month PFS, you saw no difference between active and placebo. What is significant here is that the median PFS from these groups was almost identical to the median PFS seen in every pancreatic cancer study. That gives us a good indication that the population in this trial is highly representative. That was the one good thing that came out of that analysis. What was really important from cohort A is the improvement in overall survival. You see we have almost 13-month versus 9-month in the standard of care overall survival. Again, a corroborating significant improvement in overall survival. I'll ask you to take note of the overall response rate as well. We have four complete responses in the SERTEPATIDE group and zero in the standard of care group. That's fairly typical. It's very unusual to find a complete response in people who are receiving standard-of-care chemotherapy in metastatic pancreatic cancer. We consistently show complete responses in combination with SERTEPATIDE. Cohort B, which is the same as Cohort A except a second dose of SERTEPATIDE alone is given four hours later, is just to simply keep the active transport mechanism open longer. This was not powered for PFS, yet you can see here a 7.5-month versus 5-month overall median PFS, so an improvement in PFS. Standard of care at 5.29, meaning the population looks like it's behaving as others have. There is also an improvement here in overall survival with a complete response in this group, as well as none in the standard of care. I apologize for going quickly, but we have a lot to cover here. We also showed that the time to treatment failure and the treatment duration favor the SERTEPATIDE groups. People stay on treatment longer, and the chemotherapy works longer than it would without SERTEPATIDE being present. We see that there's no increase or exacerbation of the safety profile of the chemotherapy. Whenever we administer SERTEPATIDE, either in preclinical models or in clinical studies, we almost always see an improvement in efficacy of the associated co-administered products, and we've never seen an exacerbation of safety. We haven't found a dose-limiting toxicity for SERTEPATIDE, and the safety profile in these studies is always the safety profile of the co-administered drugs as if they were given alone. That's a very important factor. We're giving more drug to the tumor with less off-target side effects. Here's a summary to date. Basically says what I just told you. Everything is pointing toward an improvement in efficacy in a safe manner with the addition of SERTEPATIDE, with magnitudes of improvement that are consistent or better than those that were achieved by the most recently approved drugs in pancreatic cancer. We're very positive about the prospects. We also have a study called iLSTA, which looks at using gemcitabine, nab-paclitaxel, and durvalumab, so that's AstraZeneca's checkpoint inhibitor, in locally advanced non-resectable pancreatic cancer. Here, the goal is to be able to shrink the tumor sufficiently so that they can be surgically removed. This study is being used with durvalumab because previously checkpoint inhibitors alone or in combination with chemotherapy showed no improvement whatsoever. This is partial data. The study is now completely enrolled, and full data will be available in January. Partial data already shows that we have a disease control rate with SERTEPATIDE of 100% in combination with durvalumab and the chemotherapy, an ORR of almost 70%, and we have two complete responses in this area as well. For the first time now clinically, we show that we could potentiate immunotherapies as well as just chemotherapies alone. I also have here just another example to show the broad applicability of SERTEPATIDE. This is in metastatic gastroesophageal adenocarcinoma. This was a very unfortunate 53-year-old man who had significant nodal metastases. They had tried standard-of-care, which was FOLFIRINOX, which is a pretty nasty chemotherapeutic regimen. They combined radiotherapy. They added pembrolizumab to try immunotherapy on top of that, and none of that resulted in anything more than a partial response. Based upon a compassionate use request that we honored, he got SERTEPATIDE added at about cycle seven, and after about 10 cycles later, after exploratory laparoscopy, he was disease-free. A complete response in gastroesophageal cancer. He is now more than three years out and still disease-free. That is a really wonderful outcome for that. As we mentioned, SERTEPATIDE can be mixed and matched with almost anything, and it's not important to know what stage of growth the tumor is at. It can be when the tumor is just forming or when it's already trying to metastasize, because as soon as the tumor cells are present, the requisite receptors are present to allow SERTEPATIDE to work. You can use it across the treatment paradigm quite broadly in combination with that. We've actually found non-oncology applications where we can look at it in black lung disease, as well as a number of other places where the receptors exist that can allow for targeting and penetration, including a disease like endometriosis, which is non-cancer, but actually behaves like a cancer and also shows the requisite receptors. On the regulatory side, we've done very well. We have Fast Track designation in the U.S. in pancreatic cancer. We have Orphan Drug status in the U.S. and in Europe for pancreatic cancer, and in the U.S. for malignant glioma or brain cancer, osteosarcoma bone cancer, or cholangiocarcinoma, which is bile duct cancer. We have a rare pediatric disease designation in osteosarcoma, which comes with the possibility of a pediatric voucher as well. We're poised for phase 3 initiation in pancreatic cancer, and we're currently looking to do a combination of raising some capital to contribute to that, but mostly to complete the development in combination with partners who are either interested in using their checkpoint inhibitor and/or chemotherapeutic biosimilars to have a specific proprietary product in combination with SERTEPATIDE that would have an efficacy advantage and obviously at that point a premium pricing. We're looking at licensing the product and the development to complete that mostly in pancreatic cancer, as well as to complete all of the scale-up for phase 3. The process is finalized, the specs are finalized, and we've actually scaled up for phase 3. We just have to take one more scale-up to be ready for commercial on the CMC side. We have a phase 3 design that has already been approved by FDA. The protocol is well known, and we're in discussions with the EMA to now get that protocol applicable for a global registration trial. The challenge here is that the EMA still, in their guidances, require placebo-controlled trials, blinded trials, and the FDA has switched over to open-label trials in pancreatic cancer. We'll have to thread that needle. As I mentioned, we have studies ongoing in a number of other cancers. As you can see, first and second-line cholangiocarcinoma, we'll be reporting data on that probably early next year. Sendifox, which was in pancreatic, colon, and appendiceal cancers, data was just presented, preliminary data that was positive, and we'll have final data next year. You can read the rest of the slide, including data coming out of the phase 2 trial from our partner in Greater China, which is on the Fast Track for registration in China under the innovation pathway there. This slide just shows a number of the milestones that we've achieved, and this is a living document, and you can see that the remainder of this year into 2026 is a data-rich environment for us. A good chance for value creation as we continue to report. This slide also does not list business development opportunities, but we've done three licenses in the last nine months, and most recently the Catalent license that we announced last week. There'll be data coming out from those collaborations on a timeframe similar to this as well. Financially, we have cash until the first quarter of 2027. We are debt-free, and we have about a little more than $20 million of cash on the balance sheet right now and a relatively clean cap table. This is just reminding you of what I said. We are a company that has strong management. We're very prudent with our capital, lots of development experience. We know how to get products done with big pharma rigor on small pharma budgets. Our products are protected for a long time going forward. We have value-creating milestones, which should be very interesting to investors, capital to keep our programs running, and the ability to continue to partner based upon already a solid foundation of partnering. With that, I have a couple of minutes to answer some questions, and I'd be happy to take questions from the audience. Yes, sir. Great presentation. Thank you. Question is, does SERTEPATIDE, if you look at the NRP-1 biomarker, do you see a higher response in any of the cohorts with NRP-1 or higher thresholds? We actually haven't done that specifically. We know from preclinical and some early-stage screening in humans that we've done that basically all of these solid tumors present with a sufficiently upregulated concentration of both the integrins and Neuropilin 1 that it's the concentration of SERTEPATIDE that is limiting, not the concentration of the receptors. We really don't have to screen in that fashion. What we will be doing, though, is because tumors from patient to patient are not always homogeneous in terms of size and comorbidities, and that's the premise of one of the diagnostic licenses that we have. They're looking to demonstrate that in combination with SERTEPATIDE, they can use an MRI imaging agent with very high resolution to define the boundaries of those tumors and to measure its progression or lack thereof. That's only done these days with CAT scans, and most insurance companies don't allow you to get multiple CAT scans. They'll let you get one, but they'll let you get multiple MRIs. I know that my sister-in-law, unfortunately, just passed from pancreatic cancer four months ago, and it was a devil of a time getting the insurance companies to pay for a CAT scan to measure progression. That could be a very interesting way to determine which patients might be more susceptible to treatment with SERTEPATIDE. Are there opportunities with small molecules for increased scale? Absolutely. The size of the co-administered moiety has no impact on SERTEPATIDE's ability. In fact, in some respects, smaller is better. We have demonstrated that SERTEPATIDE opens pores and vesicles large enough to actually transport whole cells, cell therapy. Yes, sir. I'll answer the question. From an administration perspective, how I saw your cohorts were pushed too pushed. It looks like you have a confusion protocol. Can you comment on administration challenges and maybe a brief comment on PK? Sure. Administration challenges really don't present themselves. Almost, frankly, all the chemotherapeutics and checkpoint inhibitors are given intravenously, and SERTEPATIDE is given—it's not co-mixed, but it's used as the same line. In the case of GemNab, you administer gemcitabine, and it's a roughly 30-minute infusion. We give a bolus of SERTEPATIDE that's infused over 30 seconds, and then we hang nab-paclitaxel. The only difference there is that 30-minute break. Otherwise, it's standard-of-care infusion. From a practical and patient perspective, they really see no difference in how drugs are treated. From a PK perspective, the half-life of SERTEPATIDE in humans is about 90 minutes, which is why we gave the four-hour other dosing. PD has been very difficult to determine in humans. In mice, we know it's about 24 hours, but we can't sacrifice humans to determine PD. I'm being told I have to leave, so I appreciate it. I may have a minute or two. I unfortunately have to run to catch a plane, but if anyone has a question, I'll step outside for just a moment. Thank you for your attention.