Good afternoon, everyone. Giving the platform a moment for everyone to join. I see the number is getting higher right now. Okay. I'm going to kick it off now that we have a lot of people. I'm Allison Soss from KCSA Strategic Communications, and I would like to welcome you all to the SELLAS Investor Symposium on GPS. All right. Before we begin, I would like to remind you that SELLAS will be making statements on today's call relating to future expectations regarding the further development of and regulatory plans for GPS. These statements constitute forward-looking statements for purposes of the Safe Harbor Provisions under the Private Securities Litigation Reform Act of 1995, and by their nature, involve estimates, projections, goals, forecasts, and assumptions, and are subject to risks and uncertainties, which include, without limitation, risks and uncertainties associated with the COVID-19 pandemic and its impact on the company's clinical plans. Risks and uncertainties associated with immunotherapy product development and clinical success thereof. The uncertainty of regulatory approval and other risks and uncertainties affecting SELLAS and its development programs that could cause actual results or the outcomes to differ materially from those expressed in the forward-looking statements. These forward-looking statements speak only as of the date of this conference call and should not be relied upon as predictions of future events. While SELLAS may elect to update these forward-looking statements at some point in the future, the company disclaims any obligation to do so, even if the company's views change. Additional information about the material factors and assumptions forming the basis of the forward-looking statements and risk factors can be found under the caption Risk Factors in the SELLAS annual report on Form 10-K, filed on March 23rd, 2021, and in other SEC filings. The focus of today's symposium is SELLAS' lead clinical program, GPS. Dr. Angelos Stergiou, the company's President and Chief Executive Officer, will begin today's program with remarks around today's event and then introduce our two additional speakers, Dr. Yair Levy of Baylor University Medical Center, and Dr. Dragan Cicic of SELLAS. Following the presentations, we will hold a Q&A session with all of today's speakers. Please submit your questions at any time during today's program using the Q&A prompt in the webinar. We will hold all questions until the dedicated Q&A section, where the team will answer as many as they can in the time permitted. We kindly ask you that your questions be addressed only to the subject of GPS, the subject of today's call. With that, I would like to turn the call over to Angelos Stergiou. Thank you, Allison, Hello everyone, and welcome to SELLAS' Investor Symposium on our lead asset, galinpepimut-S, or GPS. First, I want to thank you for the participation and support in joining today's virtual symposium. We're very excited to take this time to focus on GPS to further discuss our clinical program, including additional details on our recently released data. As well as the significant unmet need in acute myeloid leukemia, or AML, the indication being studied in our GPS phase III REGAL study. It's my pleasure to introduce our two expert speakers today, Dr. Yair Levy and Dr. Dragan Cicic. Dr. Yair Levy is the Director of Hematologic Malignancies at the Baylor University Medical Center, specializing in lymphoma, myeloma, and leukemia, among other hematological malignancies, and focused on novel research endeavors. We're grateful that he has agreed to join us today to provide insight on the current landscape of AML, available treatment modalities, and the challenges and opportunities faced. Dr. Levy is an expert in the space, and we're also pleased that he's a member of our REGAL study steering committee. Following Dr. Levy, we will hear from SELLAS' Dr. Dragan Cicic, our Senior Vice President of Clinical Development. There's really no better person than Dragan to provide the deep dive into our science and greater clarity in our recent promising data readouts. Before I turn it over to those exceptional gentlemen, I'd like to quickly touch upon why we are hosting the symposium on GPS now. At SELLAS, we believe that GPS has the potential to change the face of treatment for leukemia and other WT1-expressing tumors. We believe that it has the potential not only to help cancer patients in remission to live significantly longer, but also to provide patients with the opportunity for a more tolerable, continuous treatment. We are pleased with the progress of our GPS programs in 2021. Real exciting. Earlier this summer, we reported the encouraging data seen to date in the checkpoint blockade combination studies for GPS, and we're eager to continue to advance these studies and further our analyses of the data. Also, we have advanced our registrational phase III REGAL study for GPS and have continued and enhanced patient enrollment and opening additional sites in the U.S. and in Europe, and we plan on opening sites outside of the U.S. and Europe as well. As you are aware, we plan to accrue 116 patients in approximately 100 centers globally. We are fortunate to be working with one of the top global CROs, PPD, on the REGAL study. At this time, we expect the interim analysis to occur in the first half of next year, first half of 2022, provided that the ongoing COVID-19 pandemic does not significantly adversely impact our projected timeline for enrollment. Assuming we receive positive data at the interim analysis, we will then prepare the BLA regulatory submission and submit it to the FDA on a rolling basis due to our Fast Track designation, with potential approval and commencement of commercialization in late 2023. I'd like to speak briefly about the overall landscape of the AML market, a question that many of you have asked, which is one of the themes of today's call. The annual incidence rate of AML is around 80,000 patients in the U.S., Europe, Japan, and China. We estimate that approximately 15% of all new patients with an AML diagnosis eventually are eligible for entry into our REGAL study, and this also represents the total addressable market in the AML CR2 indication. That is patients who have achieved the second remission. This is the indication of our REGAL study. If GPS is approved in the AML CR2 setting, this would allow for GPS to enter the AML market, and we will then consider potential label expansion for patients who have achieved their first remission, the CR1 setting. It is absolutely feasible and strategically sensible to consider a GPS study in patients older than 60 years in the AML CR1 space. Again, assuming positive data in the AML CR2 study, we believe that there is significant opportunity for GPS to be the key anti-leukemic vaccine immunotherapy in various other settings in AML, such as maintenance after allogeneic stem cell transplant, whereby GPS could potentially sensitize, if you will, the donor's successfully grafted T cells to prevent post-transplant leukemia relapse. This is a key topic Drs. Levy and Cicic will touch upon today. We believe that it's crucial for us to bring the investment community along as we prepare for upcoming milestones for GPS. As you will hopefully appreciate by the end of today's symposium, GPS has a potential market opportunity in AML alone, not only in the AML CR2 setting, but also in the CR1 setting, as well as in the post-allogeneic stem cell transplant setting. We hope you enjoy the following presentations and will welcome your questions during the Q&A session towards the end of the symposium. With that, it is my pleasure to pass the call on to Dr. Levy. Welcome, everyone. Thank you for your time and for listening. My name is Yair Levy, and I'm the Director of Hematologic Malignancies Research over at Baylor University Medical Center. I'm going to give some background on the current treatment of acute myeloid leukemia, as well as the residual unmet needs that we certainly have in this aggressive cancer. The treatment of acute myeloid leukemia is rapidly evolving. Treatment of acute myeloid leukemia, or AML for short, has been and continues to be a rapidly evolving one over the past decade. Traditionally, when a patient is diagnosed with Acute Myeloid Leukemia and they're considered fit for induction, in other words, that they're healthy without a lot of comorbidities, they typically receive a chemotherapy regimen called 7+3, or something very similar to it, in which we give combinations of a chemotherapy called cytarabine with another chemotherapy called an anthracycline. This regimen is referred to as an induction regimen. In other words, it's intended to really rapidly reduce the amount of leukemia burden that they have and to allow the bone marrow to regain normal function. When people present with acute myelogenous leukemia, oftentimes they can present with a low red blood cell count, anemia, low platelet count, thrombocytopenia, and a low white count, called leukopenia, and therefore, they are susceptible to infections as well as complications of bleeding and all the complications of anemia with a low red blood cell count. The goal with the initial therapy is to put people into what's called a complete remission, in which when we look in their bone marrow, we don't see a lot of these leukemia cells and allow the bone marrow to restore its normal function. When we give this induction therapy, if we don't give any further therapy after people achieve a remission with their induction therapy, typically the leukemia comes back within a few months. Clearly, just getting to a remission is not enough. Therefore, this induction therapy is often followed by what's called consolidation therapy. Again, in folks who are fit, who are able to tolerate a lot of chemotherapy, we typically give something called high doses of cytarabine. Not everyone can tolerate high doses of cytarabine, in which case, we'll often have to use something else. What's typically used are these drugs called hypomethylating agents, as both a consolidation and a maintenance strategy. We know that this treatment will not be curative. When we take a look at leukemia, we often risk stratify people based on the chromosomes of their cancer cell. We stratify people into what's called favorable disease, intermediate disease, and unfavorable disease. Even favorable disease appears to be sort of an oxymoron, because even with favorable disease, when people receive chemotherapy, about half the people are going to relapse. Once leukemia reappears, patients are often treated with a different chemotherapy regimen. We call that salvage therapy or reinduction therapy. Again, they have to receive something else because their leukemia grew through the initial therapy. The definition of insanity is doing the same thing, expecting different results. There is no consensus on a standard of care of how to give salvage therapy or reinduction therapy. Like I said, typically we give something different than they've received before. The hope is that they'll enter a second remission. Typically, the first remissions are the ones that last the longest, and the second remissions tend to be much shorter. After a second relapse, that's if we're fortunate enough to get a second remission, most patients will unfortunately pass away from their disease. A third remission is usually considered to be quite rare. The end result is that the vast majority of patients would usually succumb to their disease by the second anniversary of their initial diagnosis. Even though we think of Acute Myeloid Leukemia as a cancer that we try to cure, oftentimes we are unable to cure the patient. The primary goal is still cure, so we treat with curative intent. Unless people have what we call favorable risk disease, then curative therapy often involves consolidation with an allogeneic bone marrow transplant. In other words, a transplant from another donor. In AML with high-risk features, chemotherapy alone is very unlikely to offer a durable response, i.e., cure. This is why we do consolidation with an allogeneic bone marrow transplant to greatly increase the likelihood of having this durable response or a cure. In many cases, it's the only treatment that will actually lead to a lasting remission and a potential cure. Not everybody can get a transplant. There are issues that can limit the ability of patients to receive a transplant. In the past, people actually had to have either a complete match or a very close genetic match to their tissue typing. If that wasn't the case, then they could develop something called graft-versus-host disease, in which these transplanted cells from the donor not only attack their leukemia cells, but can also attack their normal cells. These complete matches were not always available. Secondly, a transplant is also a very rigorous procedure, and not all patients can tolerate this rigorous procedure. As we know, many cancers, and leukemia is certainly no exception, occur more often in people who are older as opposed to people who are younger. These older folks may have some compromised organ function and other comorbidities that make it very difficult for them to tolerate. Because of this rigorous procedure, not all patients can tolerate it well, and it's typically reserved for patients who are in good condition. We also usually have an upper age limit of about 75 for what we call mini or non-myeloablative allogeneic transplants. This is not because we want to deny anybody therapy, it's just because we know we do more harm than good when people are older. We can give transplants to people who are older, and by that I mean people between the ages of 60 and 75. Oftentimes, those patients are treated with much lower doses of therapy for conditioning. If people can't tolerate a transplant, we can certainly give them some other treatments in lieu of a transplant, clearly, these are not curative therapies. We have made some advances in bone marrow transplantation over the past decade or so. Now we also have the ability to transplant partial match patients, almost everybody has at least a partial match. We're also able to use umbilical cord blood as a source for the transplanted cells. It certainly made finding a donor a lot easier than it was maybe a decade ago. Clearly, with these novel sources of cells for the transplant, there can be some additional complications, these are certainly amplified in older folks. There are still some folks that, even with the availability of a donor, may still not be able to undergo a transplant. Even if people can't undergo a transplant, they still have some treatment options. Actually, let me even back up. For people who can't be transplanted, even if they have a match, there are many reasons for this that I forgot to disclose. There are some patients who can qualify for a transplant but just decline a transplant. Whenever we consent people for transplant, we talk about everything that can potentially happen, and there are certainly very real considerations for morbidity and mortality with a transplant. Some people, when they hear about this, decline a transplant. Some people also may not be able to get it due to the need for having a 24/7 caregiver, as well as the need to locate themselves, at least for the first month or two, near a transplant center, which are usually housed in major metropolitan areas. We know that not everybody has a family member or a friend who can devote that 24/7 time to be a caregiver. For patients that can't get a transplant, there are certainly new drugs that have been approved recently that have demonstrated some response rates and some benefit in patients who have relapsed and refractory Acute Myeloid Leukemia and can't get a transplant. Unfortunately, these are also not curative therapies. Despite the fact that they have efficacy, the efficacy tends to be quite modest. There have been new developments and improvements in AML, but unfortunately, they have not really demonstrated a very significant overall survival extension. We were hoping with some of these newer therapies that for patients with AML, both newly diagnosed and relapsed, that we would see a significant extension of remissions and survival. Unfortunately, this disease has proven to be quite difficult. What we saw over the last few years is these important new advances didn't entirely live up to our expectations. Even patients who undergo a transplant are still at very high risk for morbidity and mortality. It turns out that their median survival remains just a little bit above two years if they have any meaningful trace of remaining leukemia cells after induction. We can actually get these very sensitive assays looking for one cancer cell, even in 1 million. This is what we call measurable residual disease. If people have measurable residual disease after their treatments, clearly they don't do as well as if we can't find any residual disease left. As a result, there's a large subset of transplant patients in whom transplant is not working great. Actually, if you take a look at deaths after bone marrow transplantation, they're usually not due to complications of the treatment. They're not due to morbidity and mortality of the treatment, but they're frequently due to failure of these allogeneic cells, these cells from the donor, to completely eradicate the leukemia. As we mentioned before, there are patients who can't get a transplant for the various factors that we discussed. While in a recent trial, the new less toxic therapy did bring response rates close to the level of response rates with intensive chemotherapy, the survival was not increased correspondingly among all these patients. The average survival of these patients who are considered less fit and cannot get what we call these intensive inductions, tends to be a little bit more than eight months. In general, the patients who do achieve a complete remission after induction live an average of about a year and a half. In patients treated with targeted therapies, survival was significantly extended when they were combined with this intensive, heavy duty chemotherapy. However, many of those patients still relapse as well. Just to point out, all of these estimates refer to newly diagnosed patients in whom we're hoping to achieve first remission. As we mentioned earlier on, survival is certainly much worse for patients who relapse and then achieve a second remission. Those patients survive an average of less than a year, and typically it's much closer to half a year. Even with targeted agents, if they're administered in the second-line setting, survival is usually measured in months. Paradoxically, the improvements that we've achieved in Acute Myeloid Leukemia in general over the last few years may make treatment of relapsed patients more challenging and not less challenging. Because of their efficacy in leading to complete remissions and a relatively lower toxicity profile that allows them to be used for an extended period of time, these new drugs and treatments tend to be used immediately in the upfront setting. Since these drugs are rarely curative, and we know that transplant doesn't have great success if people still have residual disease, as measured by that measurable residual disease assay, clearly these results are suboptimal. What that means is those patients progress while they're already receiving new drugs and procedures, that limits our ability to offer these newer treatments in the second-line setting because clearly this leukemia has progressed through those therapies already. Even the transplant is used, even allogeneic transplant is used much less in second line than it is in first line. With transplant, we like to take our best shot up front, in the second-line setting, it's much like all of the other therapies. It certainly tends to be less effective. A patient who relapsed after a transplant stands much less of a chance to significantly benefit from another transplant, given that the first transplant failed. At the same time, the cumulative risk of dying from the toxicity of the procedure also increase if you were to consider a second transplant. This is not something that we utilize usually outside of a clinical trial setting. There's still a very large unmet medical need in acute myeloid leukemia. For those reasons, it's still an urgent unmet medical need to find a way to extend survival for relapsed acute myeloid leukemia patients. I'm very glad that galinpepimut-S is actually targeting exactly that. They're targeting extension of survival in patients who achieve the second complete remission after suffering a disease relapse. This Phase III REGAL study will exclude transplant patients. As I mentioned earlier, patients in their second remission, on average, live about a 0.5 year. What we've previously seen with galinpepimut-S is that they've had an unprecedented 21-month median overall survival for those patients who receive galinpepimut-S. Best available therapy was right in line with what we had seen historically, about 5.5 months. The REGAL study is expected to have interim data available by around summer of next year, and we're all very excited with the prospects of the study, especially for patients in need and for physicians to hopefully use this safe and effective immunotherapy to treat this disease with a high unmet need. At the same time, as I pointed out, there are additional patient groups in the frontline setting that still need to have an extension of survival. We discussed these MRD-positive post-transplant patients who live maybe one-two years after transplant on average. What about those even MRD-negative post-transplant patients? We can achieve a cure in about half of those patients, but about half of them are not cured and will die within a few months to maybe even several years after. Even in these measurable residual disease positive patients in their first complete remission, galinpepimut-S showed pretty impressive data of 67.6-month median overall survival from diagnosis, or greater than four years from time of enrollment. In patients 60 years or older, a median overall survival of 35 months, so almost three years, which is way higher than anything we had seen with our other best available treatments. There's clearly a potential for an expanded role of galinpepimut-S in AML. For all the reasons that I noted so far, a new therapy that specifically aims to extend survival rather than primarily increase the response rate is needed. Remember, we said in the way beginning that even if we achieve a remission doesn't mean cure. These remissions can often not last very long. What I find particularly interesting is that the latest survival data after the first-line transplant highlight the role of this measurable residual disease as potentially the most important predictor of survival, even in a transplant setting. Think about that. If we are able to eradicate the disease effectively, people are clearly going to do better than if we don't. It appears to be even more important than the quality of the response, which was traditionally considered the strongest predictor of survival, to the point that a complete remission with incomplete hematologic recovery. In other words, we don't see any of these leukemia cells in the bone marrow, but the blood counts maybe did not come all the way back. Now we're getting stronger and stronger signal that even an incomplete response can lead to a lasting benefit if we don't see any evidence of this measurable residual disease. The fact that the same principle appears to apply in both transplant and non-transplant settings really opens up a new space for drug development, indicating drugs targeting minimal residual disease specifically can play a major role in improving the outcomes of AML patients. Clearly, we've seen this in other acute leukemias, in which there has actually been a drug that's been FDA-approved to treat that measurable residual disease positivity and has actually led to better outcomes. Our traditional approach has been to ensure that a drug can affect a complete response and then see whether or not it has an impact on survival. Now that we have even stronger indications of what impacts survival most, which is its measurable residual disease status, we can start addressing it directly. Galinpepimut-S might be on the forefront of this new trend. In other words, it can play a key role in a variety of settings, including the transplant setting. As we mentioned before, traditionally, we divided new AML drugs into those that help on the path towards a transplant and those that help patients who can't get a transplant. Right now we're making big distinctions between first remission and second remission with good reason, because the prognosis is vastly different. All of these lines are starting to blur as we better understand the biology of disease, as well as the diagnostic and prognostic information that we are receiving. That's why I find galinpepimut-S so interesting because of its potential to transcend the historical classifications of AML and target directly the major remaining unmet medical need, including in many transplant patients, and that is to really try to eradicate all minimal traces of the disease. I'm going to turn this over to Dragan, who's going to talk more about how galinpepimut-S works, as well as the scientific rationale for this. Thanks, Dr. Levy. Thank you for your introduction. Okay. Starting slideshow. Okay. The target for our lead clinical candidate, GPS, is Wilms' tumor 1 protein, or WT1. The National Institutes of Health considers it to be one of the best, if not the best, cancer targets due to its properties. Those properties are that WT1 is found in almost all human tissues during fetal development, but its expression abates and eventually ceases almost completely in adults. The only time WT1 reappears in meaningful quantities is when the cells become cancerous. It is present in many cancers, most notably in the three indications that we are currently studying in clinical trials: acute myeloid leukemia, malignant pleural mesothelioma, and ovarian cancer. In acute myeloid leukemia, WT1 expression is in fact considered a hallmark of the disease due to its near universal presence in acute myeloid leukemia stem cells, so the cells that actually fuel and propagate leukemia. Presence of WT1 in cancer cells and its virtual absence in normal cells provides an opportunity for targeting cancer cells without affecting normal cells, which is an approach that is a holy grail of oncology drug development because it could potentially allow killing of cancer cells without causing toxicities that limit the amount of the drug that can be administered.However, WT1 is a strictly intracellular protein, so it cannot be targeted by monoclonal antibodies as the whole protein never appears on the cell surface. Only small pieces of protein called peptides appear on the cell surface, and they're embedded in a natural carrier called MHC complex. The depiction of a WT1 peptide embedded in an MHC molecule is shown in the right bottom panel. At the same time, WT1 is not known to trigger an important physiologically active intracellular pathway, it cannot be targeted by small molecules either. That's why we are developing a peptide vaccine. Peptide vaccine allows us to generate T cells that can target and kill cancer cells harboring WT1 inside them and displaying pieces of WT1, peptides that I mentioned before, on the cancer cell surface. Next slide. GPS is very carefully designed, we believe much more sophisticated than most anti-cancer peptide vaccines. Firstly, in GPS, we are not using just a single peptide, rather four of them. You can see in the circle in the middle, there are these four peptides in boxes. Further, because of some overlap and combinatorial potential, we are targeting not one peptide and not four peptides, but actually 25 carefully selected and distinct different ones, which are called epitopes. Greatly enhancing the probability of generating a T-cell clone that will effectively recognize at least one peptide on any given cancer cell. Most other cancer vaccines recognize only one peptide molecule. GPS is designed to work with multiple HLA types, thus enabling us to use the vaccine in almost any patient, not only patients with a certain type of cell markers. Another major obstacle that GPS is designed to overcome is immunotolerance. WT1, like almost all cancer markers, is recognized by the body as its normal part. There is little immune response to it, and that's why cancer is such a big problem. We have therefore synthesized a peptide to be very similar to the native one, to the naturally occurring one, but deliberately introduce the small difference that makes the immune system recognize WT1 as a foreign marker. GPS consists of a mixture of four peptides, which are fragments derived from the WT1 whole length protein. Two of the four peptides have, by design, single amino acid mutation embedded, which increases their immunogenicity and is helping to overcome tolerance. The so-called heteroclitic technology, which allows treatment over a potentially long period of time through administration of booster inoculations. The peptides in our vaccine are designed to cause an immune reaction from both the immune cells that kill cancer cells, so-called CD8 cytotoxic cells, and the immune cells that provide long-term memory and help to cytotoxic cells, CD4 cells, which extends efficacy of GPS. Next slide. This is a brief overview of our previous study in the exact same patient population that we are addressing in our REGAL trial. In our previous AML phase II study, again, the exact same patient population as our phase III trial, that is patients who achieved secondary remission or as we call them, CR2 patients. We have this debilitating disease where patients typically relapse and die on average within five-six months. We observed a striking clinical and statistically significant survival benefit in patients who received GPS. You can see here an almost 16 months differential survival benefit, 21 months versus 5.4 months. You can see that we also had more than a two-fold increase in disease-free survival, in leukemia-free survival, which was statistically significant. Next slide. The key with our GPS therapy in AML is monotherapy indeed seems to be the fact that patients are in remission. As we saw in CR2 patients, similarly, patients who achieve their first remission or CR1, have the survival benefit. This is another trial which was conducted in CR1 patients, and we treated 32 patients in this study, and these patients had a very prolonged median overall survival. As you see here, their survival was 67.6 months from time of the enrollment, and it was observed across all ages with strong CD4 and CD8 immune responses. If we separate out the patients 60 years and older, who are most of the AML patients currently, the median overall survival was 32.2 months in phase I and 35.3 months in the phase II trial, which was much better than the best standard treatment for this patient population, which is typically about 12-15 months. Across all our studies in CR1 and CR2, we have two-three -fold survival benefit versus best available treatment. Next slide. Our most advanced study is our ongoing phase III pivotal trial in AML patients who achieved second complete remission. That's the REGAL study. As you've heard from Dr. Levy, those are patients with the worst prognosis, typically expected to live around sx months. We plan to enroll 116 adult AML patients in second remission and randomize them into a study group and control group. In the study group, patients will receive only GPS over a 1-year period. During the first 10 weeks, patients will be receiving a GPS vaccination every two weeks, then once a month for six months, and during the final vaccination period, once in a one month and a half for the remainder of the year. Patients randomized to the control group will be treated per investigator's choice because there is no standard of care, and there is a great variability in how these patients are treated in the clinic. I will touch upon that again later, but the very important point is that all approved available treatments cause, sooner or later, as Dr. Levy pointed out, significant levels of toxicity, primarily by suppressing production of immune cells and platelets, which is the same effect that leukemia has. These patients really are between a rock and a hard place. GPS, on the other hand, does not cause suppression of the production of immune cells and blood elements. Patients on the trial will be treated with GPS for up to a year and followed up closely for approximately two years altogether. The main outcome of the trial will be a comparison between the length of survival in the GPS-treated patients and in the control group. Next slide. As Yair Levy pointed out, there are many treatment modalities for AML, and how the patient is treated depends on many factors, including whether the patient is newly diagnosed or relapsed, the patient's age, how healthy they are in general, the genetic makeup of their leukemia cells, and more. Without getting into a long and complex review, I'd just like to point out that although there are many treatment options for both newly diagnosed and relapsed patients to put them into a remission, there is a relative paucity of options that extend the survival after remission. In fact, you may notice that observation is a major option for patients in remission. As you will see, GPS is targeting that space where patients have the highest unmet medical need, post-remission state to extend survival. Next slide. Let me give you a high-level overview of how GPS fits into the current treatment paradigm. As I said before, the REGAL trial patients are patients in the second remission, they already had leukemia. They're treated, they relapsed, achieve the second remission. We are here focusing only on relapsed AML patients in this slide. Basically, patients younger than 75, as Dr. Levy pointed out, and who are in good shape, meaning good overall condition without major comorbidities, will be put on a pathway to transplant. They will get high-intensity chemotherapy with the goal of putting them into a remission. Once they are in remission, they will be assessed again for feasibility of bone marrow transplant. Some patients will have a deteriorating condition due to the toxicities of the intensive therapy and will no longer qualify for transplant. Many of those patients will have already had a transplant in the first complete remission, and most physicians, like Dr. Levy, see no benefit in attempting the same very high-risk procedure that has already failed once. For some patients, their insurance will require that patients meet very stringent medical requirements and will not cover the cost of their transplant. Some patients will not be able to go through with the transplant due to socioeconomic conditions that Dr. Levy described. Finally, some patients will decide not to go through with the transplant due to personal preferences. As a result, fewer than around a quarter of the patients who qualify for a transplant in second remission will go through with it. All patients who can't proceed with the transplant are candidates for the REGAL trial. If you look at the right-hand side where we describe patients older than 75 and those who are younger but have significant comorbidities, you will see that they're not considered for a transplant, and they will receive less intensive therapies because of their general condition. Those less intensive therapies have less toxicities, so they can be treated repeatedly, these patients. However, as Dr. Levy explained, less toxicities does not mean no toxicities. With protracted use, toxicities accumulate, and eventually, most patients have to at least pause, if not completely stop, those less intensive treatments. Those patients are candidates for the REGAL trial also. Altogether, as we can see, majority of CR2 patients are candidates for our pivotal phase III trial. Next slide. This is something that we found very exciting and very interesting. We would like to share with you some insights from a major paper that has recently been published in the Journal of Bone Marrow Transplantation. As we said, almost all the patients should get bone marrow transplant, if at all possible, because that's the only potentially curative procedure for most of the AML patients. For that reason, we designed our pivotal trial to not include patients who are slated for a transplant. However, this new study that included 4,280 AML patients treated in more than 450 blood and marrow specialized transplant centers in the U.S. and around the world between 2007 and 2015, provides some key insights. This analysis has demonstrated that the benefit of transplant does not accrue equally to all AML patients who receive it. When AML patients enter into a remission, the quality of all remissions is not the same. Patients in remission do not have leukemia cells in their blood and bone marrow that can be observed under a microscope. Some patients have complete recovery of their normal blood elements and some don't. That's what Dr. Levy talked about, too. Those who have complete recovery of their normal blood cells are said to be in a complete remission or CR. Those who don't are said to be in a complete remission with incomplete peripheral blood recovery. That's referred to as CRI. It has been long known that patients with CRI have a worse prognosis than patients in CR. Beyond this, for those patients in remission, in more recent years, we developed technologies to identify the presence of small numbers of leukemia cells that can't be detected with a microscope, but they can be identified by their genetic material's presence in blood and other chemical characteristics, their specific metabolism. If those genetic and chemical elements are present in detectable amounts, patients are said to have minimal residual disease, or as Dr. Levy referred to, measurable residual disease. These are all the same terms, and the acronym is MRD. We have learned from the retrospective analysis that transplants cure about half of the patients only if they have no MRD. In cases of both patients with CR and CRI, but only a bit more than one-third of patients with MRD can be cured. Maybe even more importantly, median survival for patients with MRD is just about one year, and if they did not have complete peripheral blood recovery after the treatment, and just bit more than two years if they had complete peripheral blood recovery. Consider these results in the context of GPS results that we've shown a few slides before. GPS patients had complete responses, and they were MRD positives, but were not even eligible for transplant. Even without a transplant, their median survival was 48.5 months, about 2x longer than for the same category of patients who actually received the transplant. Next slide. The results from the retrospective data analysis described have very important implications for GPS clinical development in leukemia. They once again confirm that the GPS not only has potential for CR2 patients, but it could be equally important in the CR1 patient population. The pool of addressable patients is further enhanced by the fact that we can now identify CR1 patients who actually undergo a transplant, but who are less likely to benefit from it, and for whom GPS could potentially significantly extend survival. We are referring to MRD-positive patients here. Yet another avenue of expansion is patients with CRI as opposed to patients with CR only, and we are already including patients with a modified CRI into the REGAL trial, allowing us to study the potential for GPS in the CRI patient population as well. All in all, we believe that GPS has potential for an AML patient population that is several fold larger than what we initially focused on in the REGAL trial, and we are beginning to explore these further clinical development opportunities. Next slide. I will now briefly address our additional ongoing trials. We are conducting a trial in advanced ovarian cancer and another trial in malignant pleural mesothelioma. Both trials are in combination with checkpoint inhibitors. Expected potential synergy between GPS and checkpoint inhibitors is an important avenue of clinical research for us. T lymphocytes are known to perform immune surveillance for cancer by patrolling the body and killing cancer cells when they recognize them. They build molecular brakes that engage with molecular structures from T cells and order them to stop. Checkpoint inhibitors, drugs called checkpoint inhibitors, act by blocking those brakes. At the same time, as discussed earlier, GPS is specifically designed to teach T cells how to recognize cancer cells, and very successfully so. Thus, the immune system needs to meet two requirements. T cells need to be able to recognize cancer cells, which is provided by GPS, and once they recognize them, to proceed to killing them, meaning that the brakes need to be blocked, which is what checkpoint inhibitors do. In some cancers, there are few molecular brakes, so the main issue is that T cells don't recognize cancer cells. That's the case with acute myeloid leukemia, and that's why we don't need to combine GPS with checkpoint inhibitors for that disease. But in some, like ovarian cancer and mesothelioma, there are both problems. T cells recognize cancer cells poorly, and cancer cells have molecular brakes. In those cancers, GPS and checkpoint inhibitors will have limited efficacy on their own but may work much better as a combination. Thus, to summarize the scientific rationale here is the potential immunobiological and pharmacodynamic synergy between GPS and checkpoint inhibitors, whereby the negative influence of the tumor microenvironment is mitigated by checkpoint inhibitors, and thus allows the patient's own immune cells, specifically sensitized against WT1 by GPS, to invade and destroy cancer cells. To properly check that hypothesis, we first need to know that GPS and checkpoint inhibitors when combined are safe for patients. At this early stage of clinical development for the combination, our primary goal has been to ascertain whether GPS can be safely combined with the best-known checkpoint inhibitors, pembrolizumab and nivolumab. I'm happy to report that the answer so far has been a resounding yes. There appears to be no difference in toxicities between the patients who receive checkpoint inhibitors alone and those who receive checkpoint inhibitors in combination with GPS. In addition to safety, which is our primary goal in this study, we have also seen early indications of efficacy. In the ovarian cancer trial, we have treated to date 11 patients, all of whom were resistant to the standard of care therapy and very much so. All patients were also resistant to second-line treatments, and one-third of them to third and fourth-line treatments. Patients of that type unfortunately die within 9- 12 months in average. In our trial, they are already alive more than nie months, and they are continuing with the trial, so we are looking forward to continuing to analyze them and keeping you updated. When treated with pembrolizumab alone, this type of patients typically rapidly progress within approximately 63 days. The addition of GPS has extended progression-free survival to approximately 83 days so far, and the trial continues. As I said before, the combination of safety and efficacy allows these patients to continue receiving both GPS and pembrolizumab longer, which hopefully translates into survival benefit, which we will see as the trial progresses. We have also confirmed another major point in this study. GPS really does teach T cells how to recognize cancer cells. In fact, the number of T cells that recognize cancer cells increased by as much as 200% or more. Again, 2.5 fold almost after GPS treatment. Next slide. We also have an ongoing trial of GPS in combination with nivolumab, another checkpoint inhibitor, which is an investigator-sponsored trial at Memorial Sloan Kettering Cancer Center. This trial is in malignant pleural mesothelioma, a disease defined in part by its expression of WT1 target. We have had four evaluable patients to date in this trial, so the data is mostly anecdotal at this point. We can again say that the combination is safe and there are early indications of efficacy and immune response as shown in this slide. The median overall survival so far has been 8.3 months for the GPS-treated patients. Interestingly, one of the four patients suffers from the worst subtype of sarcomatoid mesothelioma, and that patient is still alive after 25 months, which is several fold longer than expected. Next slide. In closing, SELLAS' lead product, GPS, is a highly differentiated immunotherapeutic that has been given to over 150 patients with good tolerability and has shown real clinical benefit in extending the lives of AML patients in remission, which is a growing unmet medical need as well as in other indications. Our ongoing phase III REGAL study has been progressing well, and we have world-class experts monitoring its progress, and we have full support from our prominent scientific advisory board. It is important to point out here that when it comes to the gold standard endpoint for oncology trials, which is overall survival, safety, and efficacy go hand in hand. As we have discussed, currently there are many cancer drugs that are very efficacious in eliciting responses, meaning killing cancer cells. Unfortunately, patients don't live that much longer because those drugs and procedures result in toxicities that mandate early stopping of their use, and the cancer then returns with a vengeance. Today, the main remaining challenge in oncology is to be able to keep the patients on treatment for an extended period of time, thus significantly extending their survival. GPS has been up to that task so far, and we are looking forward to amassing even more confirmation, hopefully a data outcome which could lead to an eventual approval. The truly urgent unmet need in AML has been confirmed once again by the largest respective data analysis of patients transplanted for their AML. The insights garnered from the publication underlines the additional opportunities for GPS. That's why we are performing a pivotal trial in acute myeloid leukemia, but it's just our first foray. As you have seen, GPS has multiple more opportunities, and there is a serious need for it in several more AML settings in addition to the one in the current REGAL trial. We are following the AML trial with two additional solid tumor cancer trials, which, although in early stages, have already demonstrated that GPS generates surveillance T cell, that it can be safely combined with other immunotherapeutics, and that it shows early indications of extending patient survival. We have also demonstrated our operational ability as a company to handle a large multinational trial, which is REGAL, across continents, and to satisfy requirements of multiple international regulatory agencies. With all of that, we are on a very good track. Thank you, Dragan, and we will now address the questions that have been submitted. For sake of time, I think I will answer a few of them, and I'll ask Dr. Levy to also take some of the other questions. One question is regarding the market size of CR1, CR2, and if the company intends to do a study in CR1 in post-transplant. The annual incidence rate, as I mentioned, in AML is roughly about 80,000 patients in the U.S., E.U., Japan, and China. In the U.S., the total number of newly diagnosed patients with AML is roughly 21,500 patients. We estimate that the number of adult patients of any age with AML in the U.S. per year who successfully enter the CR2 setting, conservatively, is around 2,000 patients. Typically, somewhere in the 15th percentile, and approximately close to 5,000 patients in the rest of the world outside of the U.S. We estimate the number of CR1 patients to be approximately 16,500 patients in the U.S. alone, and approximately 38,000 patients rest of the world. As long as patients are really in remission after initial treatment, patients may potentially be candidates to get our GPS. As far as a study design of CR1 or post-transplant, as I mentioned in my early remarks, we absolutely will expand in the CR1 setting. We're working internally with a Board Science Committee, which is led by Dr. David Scheinberg of Memorial Sloan Kettering, whose lab discovered GPS, on a life cycle plan for GPS. The recently published analysis of the data that Dr. Levy and Dragan Cicic talked about for AML patients is very intriguing, and we believe that it indicates that there's an opportunity for GPS in the AML market landscape beyond the indication of the REGAL study, which we definitely intend to explore. As I've been saying for some time now, it is my personal belief that there's significant opportunity for GPS to be the anti-leukemic vaccine immunotherapy in various other settings in AML, as I mentioned, such as in maintenance and allogeneic stem cell transplant or the CR1 setting. Obviously, we have done some pricing reimbursement work as well, so I cannot talk about the revenue potential, as we have not provided any guidance on that. Rest assured, we have been doing everything to ensure that GPS will ultimately be a successful immunotherapy. The next question is around if we can provide some guidance and updates on the REGAL study enrollment and the confidence on the interim data. As I've mentioned in the past, we do not provide updates on enrollment and we've indicated that we expect to get the interim data by the end of the first half of next year, so by the summer of 2022, subject to any delays due to the continuing COVID-19 pandemic. We will provide meaningful updates when appropriate, and it's going to be done in concert with the data monitoring and steering committees. I've mentioned many times in the past that the independent data monitoring committee in particular has a lot of weight in the REGAL study. They will be able to independently and directly liaise with the FDA. We will be very careful what we will announce to the public. We'll be very careful to seek information from the data monitoring committee because we want that body to be independent and provide guidance, and we do not want to jeopardize the integrity and the hopeful success of the REGAL study by providing data and making announcements that could potentially harm the success of our REGAL trial. I really hope you can appreciate that. The other question is around the Delta variant and as we're opening sites, obviously, COVID-19 is still there. So far, we've been very careful to mitigate risk, and that's why we have opened up additional sites. Initially, as you may recall, we planned to open 50 clinical sites. That was pre-COVID-19 time, but we've gone now to 100 sites to really mitigate exactly that and the potential time delay. At this point, where I'm standing today, I can tell you that by summer of next year, we believe we will have interim data, which will hopefully allow us then to pursue the approval process for GPS in Acute Myeloid Leukemia. One more question for me is around the 3D Medicines agreement and the question where we stand there. We provided the most up-to-date information regarding milestones from the 3D Medicines license agreement in our earnings release last week. As you know, to date, we have received a total of $9.5 million, and we expect to receive further milestone payments this year and thereafter. The total deal is $202 million plus royalties. We have received close to $10 million, $9.5 million to be exact. The relationship is very strong, and I have to say, very collaborative and I think they're a fantastic partner. I think I'll turn over some questions that are intended for Dr. Levy. Dr. Levy. Dr. Levy, one question that has come up is sort of if you want to talk a little about your confidence on the GPS data in AML, but also in the solid tumors to date and sort of your feeling around that. Yeah, absolutely. Obviously, I am not qualified to speak about solid tumors. I'm just a heme doctor. I can tell you that the preliminary data that we see looks fantastic. Whenever you have three to four times the expected survival, even in a non-randomized manner in a uniformly deadly disease like Acute Myeloid Leukemia, you certainly take notice. Now, clearly, there's need for confirmatory trials that document this in a prospective manner, and certainly in a randomized manner, randomizing to best available therapy. What we've seen so far is certainly nothing short of spectacular, and hopefully that data can be maintained. I would have a lot more confidence in something that has extended the expected survival by three to four times than I would something that led to a 50% improvement in survival. Here we're talking 300%-400%. I feel like that difference is more likely to be maintained. Even if it gets whittled down, it's still a very meaningful difference. Dr. Levy, the other two questions are, assuming that galinpepimut-S does get approved for AML, would you administer the drug to all your AML patients to specific type? If you can just talk a little bit about. Well, again, we have to see what the final data looks like and what that patient population looks like, and then also what the FDA label would be. There's a lot of things that actually go into that. One of the things that I don't know how much this was stressed, but this is certainly a very important point to stress out, is the tolerability profile of this treatment is spectacular. The reason that oncology exists as its own field is because we use very toxic drugs in order to try to eradicate cancer. This is an extremely benign safety profile. As I mentioned early, most cancers occur in people who are older as opposed to people who are younger, and people who are older tend to have more comorbidities. To have a side effect and tolerability profile as benign as this would certainly lend itself to be used in just about any patient. There wouldn't necessarily be a patient that has performance status or the ability to tolerate treatment that's not very good that couldn't necessarily get this therapy. Great. Thank you, Dr. Levy. I think maybe one more comment I would like to make is that the questions on the symposium today are around galinpepimut-S. There was one question around nelipepimut-S and the update on the licensing. I think the only comment I want to make there is that please stay tuned and we should be having news here very soon on the nelipepimut-S front. Today's session is around galinpepimut-S. I think those were the questions that we have received. Again, I think I would like to thank everyone for your questions and for tuning into our investor symposium. Before we end today's webinar, I'd really like to reiterate our belief that galinpepimut-S has the potential to change the face of immunotherapy as we know it today. It has the potential not only to help cancer patients in remission, but to really not significantly live longer, but to also provide patients with the opportunity for a more tolerable, continuous treatment. As Dr. Levy mentioned, the safety profile, tolerability profile is really favorable. In conclusion, the clinical data and immune response profiles from the basket study of galinpepimut-S in combination with pembrolizumab for treating WT1-positive advanced ovarian cancer, as well as the phase I open-label investigator-sponsored clinical trial of galinpepimut-S in combination with Bristol Myers Squibb's anti-PD-1 therapy Opdivo in patients in MPM or mesothelioma are really encouraging. We're looking forward to continuing to analyze updated data from these studies. Furthermore, as you hopefully appreciated today, galinpepimut-S has a market potential not only in the AML CR2 setting, but also in the CR1 setting, as well as post-allogeneic stem cell transplant. We have not addressed all the other WT1 expressing tumor types. As you may recall, there are around 20 of them. Finally, I would like to emphasize how grateful we are to all our shareholders for the continued support bestowed upon SELLAS. This is not a sprint, it's a marathon, and I know you have stood by us, and I really hope that you have seen over the past months and years that we have really taken the ship, if you will, on a shore that's really going towards success. Our team has worked diligently and extremely hard to get to where we are today. Still, the Ithaca is still coming, and hopefully that's going to be in the summer of next year. We ended the second quarter with approximately $21 million in cash on hand and recorded further revenue from the 3D Medicines license agreement. We're a small but experienced team that is dedicated and committed to seeing our lead asset, our lead clinical candidate galinpepimut-S through development so that it may one day really make a difference in patients' lives. That's going to be the day that's going to make us indeed very proud, and I'm sure it's going to make you very proud as well to be part of the SELLAS shareholder base. With that, I really thank you very much for tuning in today.