All right. Good afternoon, everyone. I'm Stephen Willey, one of the Senior Biotech Analysts here at Stifel. Glad to have with us in the next session, the CEO of SELLAS Life Sciences Group, Dr. Angelos Stergiou. He's gonna be going through an overview of the company, using some slides. We'll have an opportunity for some Q&A, following his presentation. Angelos, really appreciate the time today and I'm gonna hand it over to you. Great. Thanks so much for having us, Steve. You know, as a reminder, today's presentation includes forward-looking statements that reflect current expectations and assumptions. I encourage you to review the company's SEC filings, which identify the specific risk factors. With that, let me begin by saying that our core mission at SELLAS is to prolong patients' lives, to develop and deliver innovative treatments for patients battling cancer. We're a late-stage oncology company with focus on the development of galinpepimut-S or GPS, an innovative and potentially first-in-class Wilms' tumor 1 or WT1 targeting heteroclitic immunotherapy, which is in phase III study, as well as our highly selective CDK9 inhibitor, SLS009 in phase II. We're currently focusing on acute myeloid leukemia with both of our assets, and quite exciting, we may be able to shift the AML treatment paradigm, among others, from induction, if you will, all the way through maintenance with SLS009 and GPS respectively. As for GPS, we licensed this exciting technology from Memorial Sloan Kettering Cancer Center, and we're in a pivotal phase III trial in acute myeloid leukemia, the REGAL trial in patients after the second complete remission, and expecting data very soon. The study was based on previous AML work in the CR1 as well as CR2 settings, with exciting data which I will discuss shortly. We recently announced 78, or 78 out of 80 events or deaths in the study, and the 80th event is the trigger point really towards analyzing the data. With orphan drug status for the asset by the FDA and EMA, as well as Fast Track designation by the FDA. SLS009 is a selective CDK9 inhibitor, which gives us an opportunity to potentially be first and best in class. We're currently in the phase II study in frontline AML and utilizing our extensive transcriptomics, genomics, proteomics work down the path really of precision medicine to identify patients most likely to benefit and respond with our treatment. This is on the heels of exciting data we saw in our previous relapse refractory AML study with highly promising response rates in patients with myelodysplasia-related changes up to 50%, and median overall survival of 8.9 months, where the expected survival with standard of care is around 2.5 months. Here we have received orphan drug designations by FDA and EMA, as well as Fast Track and Rare Pediatric Disease designations by the FDA. Really, this diversification and complementary nature of both assets from frontline treatment with SLS009 to maintenance with GPS and AML, as I mentioned earlier, really positions SELLAS as an emerging leader in targeted cancer therapeutics. GPS targets the number one ranked cancer antigen, Cancer Institute Wilms' tumor 1. Wilms' tumor 1 or WT1 in the fetal state is responsible for kidney formation, among other functions it has. Once we are born, it disappears and then comes back again when it causes cancer. It's a fetal oncoprotein that functions as a nuclear transcription factor. It's a validated target and overexpressed in about 20 tumor types. We truly have a differentiated immunotherapy with GPS. GPS was precisely and deliberately designed to select the right cancer target, WT1, and it consists of a mixture of four peptides, which are fragments derived from the entire WT1 whole length protein. You know, what we have done is we've utilized the heteroclitic concept in two of the four peptides by design, engineered mutation of amino acid sequences to further enhance immunogenicity and to break tolerance to allow for booster injections. That really allows us to treat patients over a long period of time through booster inoculations. This substitution alone with the heteroclitic concept allows and leads us to a 70-fold stronger binding of the peptide to MHC class I pocket versus the native sequence. The multivalent approach of GPS, again, targets 25 carefully selected WT1 epitopes, and they're predicted to have an optimal MHC class I presentation and really were via the design to be immunogenic, and it targets both CD4 and CD8 cells. They're much more prone to elicit antigen-specific immune responses, including cell immunity based memory and helper function via CD4 and cytotoxic immune response through the CD8 cells. Our GPS monotherapy studies are in patients with low burden of residual disease. In AML, for example, those in complete remission, because the tumor microenvironment could be a barrier. Nonetheless, we have done studies in combination with PD-1 blockers, where we administer GPS both frontline as well as a maintenance setting. In the former scenario, it's attacking measurable microscopic metastatic disease. In the phase II AML trial in patients after first complete remission or CR1, which included 22 patients and about 65% of them with unfavorable cytogenetics, we actually showed a median overall survival of 67.6 months, with a median follow-up of around 45 months. This activity is indeed unprecedented. The study was positive for its primary endpoint, which was obviously our priority find. According to the pre-specified efficacy threshold. This study would be deemed positive if the actual overall survival rate would exceed 34% at three years after first GPS administration. Indeed, the total number of patients at three years surpassed this landmark analysis significantly. It was close to 50%. If we focus at patients 60 years and older from this phase II trial, which were 13 out of 22, we saw again an unparalleled median overall survival of 35.5 months, which was similar to our phase I study in the setting of 32.3 months. Again, we saw a strong more than 80% of patients had either a CD4 and/or a CD8 immune response. The group of patients that actually had sustained CD4 response after the sixth dose of GPS, none of those patients progressed. The phase II study in the second complete remission, or CR2 here, included patients who had already undergone frontline therapy, so they achieved CR1, were subsequently followed without having undergone a stem cell transplant, but eventually relapsed. These patients were then reinduced through the use of second-line therapy to get into the second complete remission, or CR2. This was a very opportune clinical scenario for testing the safety and activity of GPS. In this trial, and at a much more advanced setting of their malignancy, GPS was deemed safe and again demonstrated unprecedented activity. In more detail, the median age was 74 years old, and we saw clinically and statistically significant improvement in the GPS-treated patients of 21 versus 5.4 months in favor of GPS with a p-value of 0.02. The two study arms were very well-matched, both as it relates to demographics and patient and disease characteristics. I think the key with our GPS treatment in AML, used as a monotherapy in the maintenance setting, is the fact that patients to whom the vaccine is administered are in remission. GPS overall continues to demonstrate meaningful and clinical benefit across multiple hard-to-treat cancers, and we have done work in AML, mesothelioma, multiple myeloma, into ovarian cancer. Our most advanced program is the phase III REGAL trial here in acute myeloid leukemia, a global randomized study evaluating GPS in patients who have achieved remission but remain at high risk of relapse. The rationale is strong, the data to date are compelling, and unmet, a need, you know, clearly and strongly remains clear. The REGAL study enrolled 126 patients with a 1-to-1 randomization, thus roughly half of the patients received best available therapy, which is clinician's choice, with any of the treatment modalities that you see here on the slide, versus the other half of patients getting GPS, which is administered every other week for about 2.5 months, followed by monthly and quarterly booster injections thereafter. This is an event-driven study, and we as a sponsor are blinded to study outcomes. We expect our 80th event very soon, as we just recently announced the 78th event just last week. Survival times in REGAL indeed appear longer than expected. From a mathematical standpoint, current treatment landscape and published data and real-world evidence, and the fact that we administer GPS to patients even three years out at this point, every passing month may increase the probability of a successful study due to a potential GPS effect, as we have seen in the previous CR1 and CR2 studies. I think what's very important also to note is the fact that overall survival or the primary endpoint of overall survival will be met with a hazard ratio of at least 0.636, which corresponds to an overall survival of 12.6 months versus 8.1 months, GPS versus control. Again, when the 80th event materializes, we will inform the public, which represents a very important near-term catalyst for SELLAS. The subsequent positive outcome could indeed position GPS as the first-in-class maintenance therapy in this AML setting and unlock significant commercial potential. Furthermore, there's been significant interest in evaluating GPS in combination with bone marrow transplant in AML. I think depending on the data, the work that we have done in the CR1 setting, I think we can really move the treatment paradigm quite significantly with GPS. Turning to SLS009, also known as tambiciclib, our highly selective CDK9 inhibitor, it's a next-generation targeted therapy with broad applicability across hematologic and solid cancers. The activity is really quite astonishing. CDK9 is a major cancer target. It's well known that many cancers, they depend on rapid production of proteins that promote cancer growth, like MYC, and/or to protect cancer cells from shutting down once they're damaged, either by environmental factors or chemotherapy, you know, such as MCL-1. To rapidly forge those proteins, cancer cells crucially depend on the activity of certain factors, among which is CDK9, that really allows the elongation of RNA transcripts, which are necessary for the production of proteins to keep the cancer alive. By shutting down CDK9, SLS009 blocks production of cancer promoting and protecting proteins, resulting in death of cancer cells. Here, speed is of the essence for cancer cells, as some of their key stimulating and protecting proteins, importantly the aforementioned MYC and MCL-1, they have short lives and have to be constantly replenished for a cancer cell to survive. CDK9 is a member, as you see at the bottom of the slide, of a larger CDK family. Therefore, there's a high level of similarity between CDK9 and other kinome proteins, which play an important role in the survival of not only cancer cells but normal cells as well. Therefore really to avoid severe toxicities that can eventually curtail duration of treatment and therefore efficacy, the selectivity of a CDK9 inhibitor is crucially and really important, especially for the strongly binding new generation of molecules. AstraZeneca, so Bayer's drug, for example, who discontinued the development programs due to toxicity in particular, suppresses other kinome proteins, as you can see at the bottom of the slide with the red circles, whereas SLS009 is quite selective and specific to CDK9. Unsurprisingly, the other drugs, they could only be tolerated up to 30 mg. We went up to 100 mg, and even then we could go higher but chose not to as we have reached optimal efficacy long before that. Basically, SLS009 is in the body long enough to kill cancer cells but not long enough to cause severe toxicities as other CDK9 inhibitors have shown. Since we are focused on AML, there's an important point here. We're targeting arguably the most urgent and biggest unmet medical need in AML at this time, resistance to venetoclax-based regimens. There are virtually no AML patients in the U.S. who either do not get venetoclax now or at some point in the future. Unfortunately, there are also no patients who do not develop resistance to venetoclax at some point. When they become resistant, their median overall survival is around 2.5 months, which is well-documented. Venetoclax in combination with hypomethylating agents has really become a staple of AML treatments. SLS009 interestingly exhibits an extraordinary synergy with venetoclax and has the ability to both improve response to venetoclax or even convert complete resistance to venetoclax into a strong response. SLS009 leads really to suppression of MCL-1 expression and almost all AML patients, as we know, have heterogeneous cancer cells. Some cells will depend on BCL-2 and may be killed by venetoclax. Some will depend on MCL-1 and will potentially be killed by SLS009. Some will depend both on BCL-2 and MCL-1 and, you know, we have a twofold assault by both anti-apoptotic agents at the same time. In our AML studies with SLS009, the addition of azacitidine also allows for a NOXA release enhancement, thus it increases the pro-apoptotic effect, the triple hit if you will, which may potentially response rates in relapsed refractory AML patients. Our phase I and II trials have generated compelling clinical data and showed strong response rates as well as overall survival benefit in relapsed refractory AML and really positions SLS009 as a potential first and best-in-class CDK9 inhibitor. The phase II study expansion and the latest data that we presented at ASH last year, we showed a 44% overall response rate across all relapsed refractory AML patients with myelodysplastic-related changes or MR and a 58% overall response rate in patients with one prior line of therapy at our 30 mg twice-a-week dosing. Those response rates far exceed the targeted 20% benchmark. Furthermore, we showed a median overall survival of 8.9 months in patients with relapsed refractory to venetoclax-based treatment AML- MR and a median 8.8 months overall survival in all relapsed refractory to venetoclax-based treatment with a median of one prior line of treatment, which surpassed the historical benchmark of around 2.5 months survival. The results to date, again, have been very encouraging and represent really what I believe an important advancement for SLS009. Indeed, our current trial, with input by the FDA, focuses on newly diagnosed patients where we administer SLS009 in the frontline setting, truly frontline, as well as in patients who did not respond to the refractory to Aza-Ven after two cycles and we're utilizing our biomarker approach here. We have conducted and continue doing so extensive, as I mentioned before, omics work and analysis among others with esteemed academic centers in the U.S. and in Europe. We're utilizing our AI biomarker model to further predict patients that are most likely to benefit from our SLS009 treatment. We've really geared our clinical development program accordingly. As far as I'm aware, we're the leading company in this space with this level of work. We have two settings, groups four and five, and each group will enroll 40 patients, 1-to-1 randomized, to either Aza-Ven SLS009 or Aza-Ven alone. We enrolled our first patients in March, and we will add Europe into the study here very soon via the IMPACT-AML collaboration that we struck. We ought to have top-line data from this phase II study available later this year. Really the goal of the study, in addition to safety, it includes assessment of the efficacy of SLS009 as an add-on therapy, measured by substantial increase in complete response rates, increase in overall survival considerably compared to control arm, and also to confirm our predictive properties of our biomarkers that we've identified and to compare and confirm those further with our omics work. Again, we're extremely excited about the potential to use the data towards an accelerated approval path and/or quickly move into a registrational study with SLS009 based on the predictive biomarkers we have identified. In addition, not only in AML, but also to utilize that in other solid cancer indications as well. Here's the development pipeline and expected milestones overview. You know, we're very excited about the prospects for the GPS and SLS009 programs. We're also extremely pleased to be in a strong financial position, with around $110 million in cash as reported in the last Q, which enables us to reach all our important upcoming milestones and beyond. Again, when the 80th event in REGAL materializes, we'll inform the public, which represents a very important near-term catalyst for SELLAS. The disclosure of the top-line data shortly thereafter. With SLS009, we expect to have top-line data from this phase II study available later this year. You know, in close, we have placed great emphasis on bringing about the next stages of value creation on behalf of SELLAS' shareholders. You know, I like to say and, we all firmly believe that we're not just developing treatments here. We're creating hope for those who really need it most, and together, we really aim to transform lives. That's the quick, corporate overview, Steve. All right. Thanks for the presentation. That was great. A few questions on GPS. As you intimated, right, you're just a couple of events here from triggering the OS analysis within the REGAL trial. I know the accumulation, as you mentioned, of these death events has taken longer than expected. I think investors sometimes struggle with, you know, assigning better outcomes in the treatment arm as kind of a default explanation for this. Can you comment on how the delayed event accrual timelines have changed just relative to your initial expectations? Just comment on your level of confidence in terms of what you should expect to see within the control arm specifically. Yeah. So the initial, you know, assumption was, once the last patient was enrolled, which happened around March of 2024, we expected between 12 to 15 months or so to hit the 80th event. Obviously, that has surpassed the timing. The reason we're quite excited is really two or three-fold. One is we know the treatment landscape and the behavior of those patients and how they do quite well, again, not only from published literature but from key opinion leaders and real-world evidence. Ordinarily, the median survival for those patients, it ranges anywhere between, on the low end, six, seven months, and on the high end, maybe around 10, 11 months. That has really not changed across academic centers, who tend to do better. That's sort of the 10, 11-month frame perhaps. You know, the other hospital centers where it's the ordinary around eight months. One, we really understand to the extent possible how the control arm behaves. As we have all seen in clinical phase III trials, patients go to the clinic more often. I expect the control arm to perhaps be a little better than that by the mere fact that it's a phase III trial, and patients go to the clinic more often. At the same time, you know, we obviously, as a company, know the enrollments when they happen. That's not disclosed publicly. As I mentioned before, mathematically, but also clinically and scientifically, we certainly believe and obviously hope that GPS is driving the effect similarly to what we had seen in the CR1 and CR2 settings. My personal belief is that there's a very good chance that GPS will mimic survival data, what we had seen in the phase II study, and potentially even better, which would be a great segue also into the CR1 setting where, as you know, ONUREG in their phase III, they showed a median survival, if memory serves me well, of around 21, 22 months. If we can show in the CR2 setting similar data to what we had seen in our phase II study, comparable to what ONUREG as a maintenance therapy did in the AML CR1 setting, I think it would be not only tremendous news for obviously us as a company, but more importantly to patients being administered an efficacious and a much more tolerable, safe drug. You know, we're not myelosuppressive. And in addition, Steve, we have administered GPS, so we're blinded to study outcomes. One thing we do know, because we amended the protocol based on physicians' request, we've administered GPS to patients three years out. We have done immune response testing of 10 patients randomly picked where we saw the same immune response data as we saw in the CR1 and CR2 settings. I think the totality of that and all the work that we have done, we're very optimistic that not only do we see a GPS effect here, but ultimately that patients will hopefully benefit from a treatment like GPS. Okay. Then can you just walk us through the next steps following the unblinding of the trial and, you know, maybe just an estimate of how long you think it might take to then subsequently provide a top-line data disclosure? Yeah, I think once we announce the eightieth event, again, we will provide and issue a press release with some more guidance. I would expect, once the 80th event happens with all the final clear resolutions and cleaning of the data, it's gonna be a few weeks. We will provide more guidance, when we put the press release out, once we have materialized the 80th event. Okay. Maybe just one question on SLS009 before we finish up here. Look, there's obviously a lot of interest in this target as a mechanism to address venetoclax-mediated resistance. I know you talked about that in the presentation. What are you hoping to see across the different cohorts that you're now enrolling in the frontline setting? How important is the biomarker work that you're doing in terms of trying to translate these results into any future development effort? I think on the former, ordinarily, those patients have CR rates somewhere between 10%-20% in the Group 4 in the first setting. In the second setting, because those are patients who are basically refractory to venetoclax, the CR rate is 0%. On the former, I would like to see a CR of at least 50% or higher. On the latter, where they, you know, they don't have any response, you know, even a 30% CR rate would be tremendous. I'm obviously hoping and pushing for a higher CR rate, as well as a survival benefit. To your question on the biomarker, because we are utilizing the biomarker work, we really hope to translate that into the fact that we know which patients will benefit. I think the study has been designed in a way to tell us exactly that. Equally importantly is that data to then also translate into solid cancer indications. We do know that indications such as non-small cell lung cancer, potentially pancreatic cancer, and liver cancer would be really great indications to go after, which I think, you know, patients are eagerly waiting for effective and safe drugs. Okay. That's all we have for time. Angelos, really appreciate it. Yeah, thank you. Thanks everyone for listening. Thanks so much.