Without any additional side effects and with an approach that's patient-friendly and pharmacoeconomically beneficial or attractive. You'll notice, as I go through this in a moment, that there have been very few advances in the treatment of solid tumors over the last several decades. We are a company that has a very seasoned management team with successful international development experience and expertise, proprietary field-leading technology with intellectual property protection out into the 2040s. Importantly for investors, we have multiple business development and clinical execution milestones that are projected over the next 12-18 months, and we have a platform technology that we believe has already been validated by external parties because we have a number of existing partnerships. Importantly, in these times of very difficult financing for small companies or, in fact, for all companies, we have cash that's projected to run our operation into 2026, funding all of our current development programs through to data. So, as I mentioned, we have a very experienced management team. Collectively, we have about two centuries of development experience. Personally, I've been in the pharmaceutical business since 1983, and for most of that time was an executive in R&D at Big Pharma. Collectively, also, as individuals and throughout our career, we have all contributed to approximately 75 international products that have been marketed, many of them in the oncology space. So, let's talk about why we focused on solid tumor oncology. It remains a vital and growing global need. Over the next 30 years, cancers of this type will cost the world about $25 trillion. 90% of newly diagnosed cancers here in the United States are solid tumor cancers. And by the end of this decade, pancreatic cancer will be the second leading cause of cancer death. And as you can see along the bottom of the slide, solid tumors represent all those cancers that people really dread being diagnosed because, in many cases, they carry very poor outcomes, very short lifespans, and a very difficult death. And the reason is that the tumors themselves present, rather, both a challenging morphology and a microenvironment. These are obstacles to optimized outcomes. First of all, the tumor creates a stroma, a barrier of cells around it that acts as a physical obstacle to the penetration of anti-cancer agents. Also, the tumor microenvironment that it presents is immunosuppressive, and that contributes to tumor resistance as well as tumor metastases. Really, up until now, the most commonly used approach to overcoming these obstacles was brute force, simply prolonged or escalated dosing of non-targeted agents, which almost in every case leads to intolerable off-target side effects and eventually the cessation of treatment. Now, we have taken an approach that mirrors rational drug design to identify an agent that helps overcome these obstacles. So, when you have a dense stromal barrier, what we need to do is find a way to traverse that barrier. And we do that using a technology that employs internalizing RGD peptides. Now, RGD peptides have been long known to be effective targeting agents for solid tumor stroma, but using a technology that internalizes or transports materials across the stroma is important, and that's an iRGD. When you have an immunosuppressive TME, then it's important then to design your iRGD with traits and characteristics that reduce the immunosuppressive nature of the microenvironment and actually recruit cytotoxic T cells to the tumor. And finally, when you have frequent metastases of these tumors, which often is actually the cause of death, not the primary tumor itself, if you design your iRGD to inhibit the metastatic cascade, then you have effectively an agent that will attack all three of the problems associated with that. And the solution that we've come up with is our agent called certepetide, which is in late-stage clinical development now in several solid tumors. Certepetide converts the tumor stroma to a conduit from a barrier, and it actually selectively reduces the immunosuppressive T cells in the microenvironment and increases the concentration of cytotoxic T cells while inhibiting the metastatic cascade. Interestingly as well, certepetide is agnostic to the modality of the companion agents with which it is dosed. And so, we can combine it with chemo, immuno, radio, RNA, and other types of anti-cancer therapies. So, as I mentioned, we do have a number of partnerships, and we believe that they've already validated the potential as seen by others. On the R&D side, we just announced an alliance yesterday with the University of Cincinnati working in a preclinical model for endometriosis, which I'll speak about in just a moment. But we have R&D alliances with clinical trial groups and with foundations around the world who provide resources with little to no commercial interest in our product. We also have a strategic commercial partner in China called Qilu Pharmaceutical. It's a typical Biobucks kind of deal for the license that they took for the Greater China Territory. We've already collected about $15 million in milestones, and there's up to $200 plus million of milestones and commercial royalties available on that transaction as they move forward. And because we can combine certepetide with so many different things, we can create new partnerships by indication, by the modality of the companion agent, and/or by geography. So, let me tell you a bit more about what certepetide is and how it works. So, certepetide is a nine-amino acid cyclic internalizing RGD peptide that has a very high affinity and specificity of binding to alpha-v beta-3 and alpha-v beta-5 integrins. And these are integrins which are significantly upregulated on the cells that comprise the stroma of these solid tumors. Once certepetide is bound to these integrins, it's subjected to proteolytic cleavage by proteases such as furin, which exist naturally in the tumor microenvironment. You cleave those disulfide bonds on the cyclic peptide, leaving behind a five-amino acid C-end rule linear peptide. That linear peptide dissociates from the integrins and almost instantaneously binds with a high degree of selectivity and affinity to an adjacent receptor called neuropilin-1. When neuropilin-1 is activated, it actually initiates the C-end rule active transport mechanism, which is a naturally occurring active transport mechanism that most normal cells use to transport nutrients across the cell wall and into the cytoplasm. Here, we've hijacked that to transport cytokines, immunotherapies, and other anti-cancer agents. That's done because when the C-end rule is activated, you see this formation of microvesicles at the surface of the cells that encapsulate these agents that are in the circulatory system and percolate them through the stroma, depositing them deeper into the tumor, giving greater access to the actual target. At the same time, the presence of certepetide and the C-end rule linear fragment in the microenvironment suppresses the immunosuppressive nature of the TME, and it actually recruits cytotoxic T cells to the tumor and stops the metastatic cascade. So, in simple terms, depending upon what generation you come from, it removes the Romulan cloaking device or Harry Potter's invisibility cape from the tumor and allows your immune system to actually recognize it. And I have a couple of slides here to demonstrate how effective that is. Again, agnostic to the modality of the agent with which it is co-administered. So, in this particular case, this is an experiment using nude mice with a human pancreatic ductal adenocarcinoma implanted. And we're dosing fluorescent quantum dots. Now, when FQDs are in the system, they would fluoresce entirely in the circulatory system. If you apply an etching solution, any of the FQDs in circulation would be quenched, and you'll see nothing. That's what you see in the mouse on the left side, or I guess that's my right. When you add certepetide to the experiment, all of the fluorescent quantum dots end up transported into the tumor, and it's the tumor that selectively lights up. It shows you the high degree of selectivity that certepetide brings to the experiment. We also have here a sampling of more than 350 peer-reviewed publications from around the world that show the consistent improvement in efficacy of anti-cancer agents of all types when dosed in validated solid tumor models with certepetide. You can see we have here cytokines, we have immunotherapies, we even have an adaptive cell therapy example. That's really important, again, to demonstrate the breadth of applicability of the compound. What's really become very interesting of late is that certepetide consistently improves immunotherapy outcomes in multiple preclinical solid tumor models. I think if you've done any work in this area, you'll know that immunotherapies on their own have a very, very low impact in solid tumors. For example, it's between 3% and 5% response rate in pancreatic tumors, as an example. Here, you can see we have across a wide variety of different solid tumor types, including cholangiocarcinoma, which is bile duct tumor, of course, pancreatic cancer, prostate, breast, non-small cell lung, gastric, and even hepatocellular carcinomas. We see an improvement in overall survival and improvement in tumor uptake, a reduction in tumor volume, and a significant reduction in metastases across the board. Just to give you two examples, this is a trial that was done preclinically in mice. These are mice with cholangiocarcinoma, which is an aggressive tumor type that has very limited treatment success. In this tumor type, the standard of care for humans was established by the TOPAZ-1 trial, and that is the combination of gemcitabine, cisplatin, and durvalumab. You can see here that, in fact, when we add certepetide to the various experiments, and I apologize, the color schemes aren't consistent from one panel to the next. So, on the left, it's the green line that you want to look at that shows a significant improvement in survival for the treatment with certepetide. On the right, it's the dark purple, which shows a significant, almost a complete elimination of metastases to the lung in the same experiment. And then similarly, in pancreatic cancer, this is with a PD-L1, you can see that we have a much greater recruitment of the immunotherapy to the tissues, a very, very high specificity of sequestration of the IO in the target tissue, which in this case is the tumor, and then ultimately an enormous improvement in efficacy by a treatment survival improvement. So, very high results here that we have corroborated in multiple other experiments preclinically, and as you'll see in a moment with some early clinical data as well. So, based upon this, we have a development strategy that is composed of two pillars. On the one hand, we're working toward a rapid global registration in metastatic pancreatic ductal adenocarcinoma in combination with gemcitabine nab-paclitaxel standard of care. For that, we've completed our phase II-B enrollment, and we're waiting on data from that trial very, very soon, and we're actually in phase III preparation. In parallel with that, we have a number of proof of concept phase II- A trials combining certepetide with a variety of different regimens in multiple different tumor types to demonstrate, again, its broad applicability. And some of the results from our early trials are shown in the next several slides. Here, you see the trials from our phase I-A to phase I-B/II-A trial that was done in multiple centers in Australia. That's the center fuchsia bar. And then the companion bar, the darker color bar to its right, is in fact the results from our partner's trial in China, the Qilu trial, which was a replica trial in that. Then the dark bar all the way over to the left is for reference. Those are the results from the Von Hoff trial from 2013, which established gemcitabine nab-paclitaxel as a standard of care. You can see a consistent and almost groundbreaking improvement here in overall survival in these metastatic patients. What's also important, though, is that there's internal clinical consistency within these trials. That in almost every case, you see an improvement in the efficacy measures in the presence of certepetide. That was very, very encouraging, and that allowed us to move into phase II-A in pancreatic cancer, phase II-B. As another example here, we have a case study that we published earlier this year for a gentleman who had metastatic gastroesophageal adenocarcinoma, a hideous disease. This person had actually several months to live when we finally were asked to provide certepetide to add to their treatment regimen under compassionate use. He had been treated with FOLFIRINOX, radiotherapy, pembrolizumab, and immunotherapy, and really only received a partial response and was not given a very good prognosis. As I mentioned, under compassionate use, we added certepetide to that regimen, and after several more treatments, he actually had a complete remission, and that was demonstrated both laparoscopically and radiographically that there is no discernible disease, and that person remains cancer-free now for the last two years. Now, again, an N of one, so you have to take that with a bit of a grain of salt, but it does demonstrate the consistent improvement that certepetide brings to almost any treatment regimen in almost any solid tumor cancer. We have an accumulation of data that demonstrates certepetide's ability to augment anti-cancer efficacy with cytokines alone or cytokines plus immunotherapies. I've shown you the phase 1b, excuse me, phase 1b/2a trials that were done in Australia and China independently. We've demonstrated that the dose-limiting toxicity cannot be discerned for certepetide in humans and that the adverse event profile in combination with standard of care is the same as standard of care alone, meaning we don't increase the adverse events. We also have the sustained complete response that I demonstrated, but importantly, we have the first results coming out of our iLSTA trial, which is a combination in non-resectable pancreatic cancer, gemcitabine nab-paclitaxel in combination with durvalumab and immunotherapy. Here, with about two-thirds of the patients treated, we're already seeing a clinical improvement in outcomes and using paired biopsies, a much greater increase in cytotoxic T-cell concentrations in the tumors in the presence of certepetide, sort of corroborating what we've seen in murine models. While we've been doing a lot of work preclinically and clinically, we haven't neglected the regulatory development aspects, and we have achieved quite a few regulatory special designations with their concomitant benefits. On the far side, you see that we have fast-track designation from the United States FDA in pancreatic cancer, and the benefits are listed, and I'm not going to read them to you, but you can see there are substantial benefits in accelerating approval and review. On the far right, we have a long list of orphan drug designations that we received from FDA and EMA, including pancreatic cancer, malignant glioma, which is brain cancer, osteosarcoma, bone cancer, and cholangiocarcinoma, bile duct cancer. And those orphan drug designations bring tax credits, market exclusivity, and fee waivers as we move forward through development. And then in the middle, we also have received a rare pediatric disease designation from FDA in osteosarcoma. And that, among other things, brings with it the eligibility for priority review voucher, which, upon approval in osteosarcoma, we can actually use to get a priority review for another indication, or we can sell to another party who can use that. And those vouchers have sold for up to $350 million historically, more recently more in the $100 million range, but they bring with them a very substantial financial benefit. Here's the table of our ongoing clinical trials. As I mentioned earlier, all of these trials are funded through data with our current capital, and most of them are either enrolling and nearing completion of enrollment or beginning to enroll very, very soon. All of these are projected to have data in the course of 2025. I also mentioned earlier we have a couple of new preclinical collaborations, one of which we just announced yesterday, and that is with the University of Cincinnati, looking at the ability to combine a VEGF inhibitor with certepetide in the treatment of endometriosis. Now, you may say, well, endometriosis is not a cancer. It isn't, but it actually behaves like a cancer. It hijacks the angiogenic mechanisms of the body to grow these uncontrolled tissues inside the uterus, and it actually exhibits the integrins and the neuropilin receptors that are necessary for certepetide to demonstrate its activity. So, we're very excited about the possibility of being able to enhance treatment of endometriosis. It's an enormous market for women and very, very poor treatment options today, many of which include surgery. And we also have a collaboration with Valo Therapeutics, a Finnish company, which has a very interesting oncolytic virus, looking at combining their oncolytic virus with certepetide and a checkpoint inhibitor to see if we can augment T-cell responses in melanoma, another cancer, solid tumor-like, where outcomes are not always, especially metastatic melanoma, the outcomes are not very good. As I mentioned, lots of milestones over the next 12 to 18 months. You can see data milestones, execution milestones, and there are business development milestones that are not projected on this slide, but we expect to see some of those coming to pass already. We have top-line cohort A data from our phase II-B trial, expected sometime later this quarter or into early next year. Financially, the company remains very stable. We have not had to raise money since 2021, and we still have about $38 million. We have no debt, and that will allow us to operate the company and run all of our programs through into 2026. As you can imagine, we have a very capital-efficient structure and a very capital-efficient clinical development program in order to make things work along these lines. So, in the end, we think we're a very attractive investment opportunity. We have a very promising asset that's based on a body of compelling and growing data, both preclinically and, most importantly, clinically. A rational and focused development program, highly experienced management team with success in bringing products through to commercialization, and a company that has a long history of being good stewards of our capital, financially credible. So, this is just a summary again of what I just said, but we would be very interested in seeing people join us on our journey and become investors in Lisata Therapeutics. With that, I will stop and take any questions, and I thank you for your attention this morning. Any questions? Yes, sir. What has been the issue when the product hasn't worked? Where is it not binding? Well, candidly, in all the experiments that we've done, the product has worked. So, I don't have an example of where it hasn't worked. And that's partly because we've chosen those areas where it should work, tumors that display a dense stromal barrier and exhibit these integrins and neuropilin-1. And so, you know, it's somewhat of a rigged game, but every place we go, we kind of expect it to work because of that. As in only solid tumors? Only in solid tumors so far, yep. Anyone else? Questions? Well, thank you again for your attention. Hope you have a good conference.