All right, so we're gonna go ahead and get started. I'm Stephen Willey, one of the senior biotech analysts here at Stifel. I'm glad to have with us, presenting in the next session, Viracta Therapeutics. We have the CEO, Mark Rothera. He's gonna be giving an overview of the company. Also in attendance is Darrel Cohen, who is the Chief Medical Officer. Mark, I'm gonna hand it over to you. I think there'll probably be some time for Q&A at the end, and thanks for coming. Thank you very much, Steve, and good morning. I appreciate the invitation by Stifel Healthcare to join the conference and present Viracta today. During the course of my presentation, I may make some forward-looking statements. So Viracta is a clinical stage precision oncology company that's focused on the treatment and prevention of virus-associated cancers, and for today's presentation, I'm gonna be focusing on our lead program, Nana-val. And Nana-val is directed at specifically EBV-associated cancers, and it is an all-oral combination that's comprised of our proprietary nanatinostat and also an antiviral, valganciclovir. And right now, as a company with this program, we're aiming to develop a tumor-agnostic approach to treating EBV-associated cancers. But in order to get there, we're conducting studies in both relapse refractory EBV-positive lymphoma, as well as advanced solid tumors with EBV. In the lymphoma program, we're now in a pivotal phase 2 study that we call NAVAL-1, and I'll tell you a bit more about that in a minute. We're also a long way down the track in a dose-ranging study in the advanced solid tumor setting. As you'll see later on in the presentation, we have a lot of milestones ahead of us as we turn the corner into 2024. About 2% of cancers worldwide are EBV-associated, and that's likely an underrepresentation, given that it's not systematically tested for. What we've done is we've we've decided to focus on some of the most important subtypes, both on the lymphoma side and in the solid tumor side, to start with, as part of our development program. So on the lymphoma side, we're focused on PTCL, DLBCL, and PTLD, and you can see their associated EBV positivity rates. And then, on the solid tumor side, we're focused on nasopharyngeal carcinoma and gastric cancer, and you can see the EBV positivity rates for those as well on the right. The reason we're here, though, is when you look at those patients that do have EBV associated with their condition compared to those that are EBV negative, for the most part, you see a very, very significant difference in survival rates. So, for example, if you look at PTCL on the left in this chart and DLBCL on the right, there is a very dramatic difference in survival, and that's why we're here because there is a lack today of targeted treatment options for this population. Our approach to targeting and killing EBV-associated cancer cells is demonstrated here in our mechanism of action. So in the presence of latent EBV, valganciclovir is inactive. But then, if you add nanatinostat, which we've selected because it is a potent and selective EBV protein kinase expression inducer, that enables the conversion of valganciclovir to its cytotoxic form through phosphorylation. And then, your activated ganciclovir inhibits DNA replication, leading to cell death. So this mechanism has been very well documented in the literature. What is important, though, is how does this translate into the clinic? So, in my next slide, I'm gonna introduce you to our lymphoma program and show you the data that we've generated so far in those key indications. Before I show you the data, let me just remind you of the design of our pivotal Phase 2 trial in relapsed/refractory EBV-positive lymphomas. This is a Simon two-stage design study that was one that we discussed and aligned on with the FDA at our end of Phase 2 study discussion. What you can see, it's multistage. We're in Stage 1, where we're looking to enroll 10 patients into the PTCL cohorts, as well as DLBCL and PTLD. Now, if you hit an efficacy threshold in Stage 1, you then automatically advance that indication to Stage 2 for a further 11 patients, and our goal is to then discuss with the FDA the route forward for an accelerated approval with data from those first 21 patients. We announced in June that the PTCL cohort is advancing on the basis of the data that was generated, which I'll share with you in a moment. But I would like to just point out that for PTCL, we have two, if you like, cohorts for PTCL, one for Nana-val and one for nanatinostat alone, and this was a requirement by the FDA so that you could look at the distinction between nanatinostat alone in PTCL and Nana-val, that mechanism that I showed you in action. And so we're looking forward to completing enrollment into those two groups before the end of this year and having data early next year to share with you. Now, in addition, you may have noticed, some of you who would have seen in our recent Q3 press release, that we have recently adjusted enrollment criteria for DLBCL and PTLD to enroll second line, previously third line. We believe that we can do this without adjusting the possibility of an accelerated approval, but also, I think in doing so, it enhances enrollment rate and increases market potential. So let's dive into PTCL. This is our most advanced cohort and our most advanced part of the Nana-val program. So PTCL is an area of very high unmet medical need. In the relapsed-refractory PTCL population, there is no current standard of care, and if you look on the right, the survival rate, the five-year survival for EBV-positive PTCL is around 11%, so it's a very, very poor prognosis. And so we're hoping to really address that unmet need, and ultimately, we believe that, Nana-val should be also a first-line treatment to help patients with EBV PTCL. So in this slide, I'm showing you data from the first 5 patients enrolled in the NAVAL-1 study in Stage 1, and as you can see, we saw 2 complete responses in those first 5 patients, so, a 40% ORR and a 40% complete response rate, and this was at the cutoff date at the end of June of this year. So that immediately met the threshold of 2 patients in Stage 1 for advancement, so that it would automatically go to Stage 2. It's a little too early to say anything about duration of response since it's still relatively early post-treatment, but as I say, we are close to completing enrollment of Stage 1 and anticipate moving into Stage 2 next year. Now in this slide, what we're doing is juxtaposing the NAVAL-1 data with a new cut of the 201 data from the prior study at a cutoff of May 4 of this year, so with much longer follow-up than in previous cuts. What you can see there is, you know, excellent congruence between the 201 study data and the NAVAL-1 data, with approximately similar complete response rates and ORR rates. But what was very important from the 201 study data was a sense of the median duration of response, and as you can see on the right, we saw a median duration response of 17.3 months as of the cutoff date. So I think that's a very attractive median duration of response. It means that, you know, patients are clearly benefiting, both in terms of continuing efficacy as well as safety and tolerability. And talking about safety, this is actually the total safety database from the 201 study of 64 patients worth of data, showing that from a serious adverse event perspective, really, the key point is cytopenias that are mostly uncomplicated and generally reversible. So we think that this profile really lends itself to combining with other chemo or immunotherapies. So the goal, as I mentioned, is to take data from the 21 patients worth of Stage 2 in this study and have a conversation with the FDA about how many more patients we need to add for an accelerated approval. We think that the profile of Nana-val in PTCL really lends itself to an accelerated approval because it... you know, in our view, it really meets the criteria for an accelerated approval. It's a high unmet medical need. As you see, 5-year survival rates of relapsed refractory PTCL being around 11%. We're seeing attractive ORR and PR rates and complete response rates, and we've also seen a very good duration of response in the data generated so far, and it's generally well-tolerated. So in many respects, I think, this lends itself to an accelerated approval, and our best estimate today is that we're likely to need a total of 60-90 patients to complete this study for accelerated approval. That obviously is to be discussed with the FDA, and that's total, by the way, includes then the 21 patients up to Stage Two. So in terms of milestones, as we look to turn the year into 2024, we're looking to present Stage One data, complete the enrollment of Stage Two, and I should say that by closing Stage One nanatinostat alone, we're gonna be concentrating our enrollment firepower. Those two, if you like, arms become one in a Nana-val arm, so we expect enrollment of Stage Two to be relatively rapid. We'll then meet with the FDA to discuss the data and continue then the enrollment into Stage 2 expansion for accelerated approval, and towards the back end of the year, share Stage 2 data. So a lot's happening with our lead cohort. Now, I'd like to spend a few minutes on our second cohort, which is EBV DLBCL. Now, I'm sure you're all aware that, you know, DLBCL is generally a crowded area. However, we believe that DLBCL is a very unique subtype, a unique entity. It has its own WHO classification. It is associated with distinct biological features and a distinct mutational landscape, and as you can see in the survival curve on the right, you can see that the prognosis of EBV DLBCL is substantially worse, you know, despite standard of care. And what we're gonna be doing, beyond what you see in this graph, is collecting real world evidence in a structured way that will continue to demonstrate, we believe, you know, the poorer outcome seen in this particular subtype with EBV. And so we think we're setting ourselves up for an accelerated approval pathway to target and treat EBV DLBCL. And the data that was generated in the 201 study, and again, this is a cut on the fourth of May, 2023, with longer follow-up, you know, is very encouraging in this, you know, difficult prognosis patient population. You know, these are patients that have failed R-CHOP, and you can see that, we're seeing a 67% overall response rate, and half of those are complete responses. And on the right, we haven't yet been able to determine a median duration of response because, as of the cutoff date, half the patients were still ongoing on treatment, so some as long as more than 4 years on treatment. So again, I think that's very encouraging in terms of both continuing efficacy and safety. So to complete the milestone picture for the lymphoma program, following the advancement of PTCL, we have for DLBCL and PTLD the potential advancement into Stage Two next year, as well as sharing data from Stage One for both of these indications. So the idea was these would be follow-on indications for PTCL. Now, let's move on to the solid tumor program. So again, this is an exciting new frontier because now we're talking about the solid tumor setting. We're talking about advanced EBV-positive solid tumors, and in the study 301, we're in the phase I-b dose-ranging portion of that study, and I'm gonna show you data in a minute from that study. The goal is to establish the optimal dose for this setting, which we think is distinctly different from the lymphoma setting, and then go into a phase II study and explore other EBV-positive solid tumors, particularly gastric cancer. So the dose-ranging work that's ongoing is in EBV-positive recurrent metastatic NPC. This is data from the first 17 patients in 5 dose levels from the NPC dose escalation work. In the first part of this... and note that at dose level 1, this was the dose that we're currently using in the lymphoma program. So we started there, but we've been working our way upwards from there. You can see that we escalated nanatinostat in Phase III, and at 40 milligrams, we saw our first partial response. We then introduced split dosing of nanatinostat, and I'll explain that in a minute, and tried two additional doses, and as you can see, at 20-10 milligram split dose, that's the fifth dose level, there we saw a partial response as well as an ongoing stable disease response and a further shorter stable disease response. So this was very encouraging, and what it has, and by the way, all these have been confirmed. And what this has really encouraged us to do is to go a little further in our dose escalation work because we think we can do even better. And the safety profile in this population is distinctly different from lymphoma, and these patients seem to be tolerating Nana-val very well. So there's no dose-limiting toxicities to date, and the majority of treatment-related adverse events were mild and moderate in severity, and manageable. So as we dose escalate from here, there are a few very important insights that we gained from some preclinical work that was recently conducted. Firstly, I've mentioned split dosing of nanatinostat. That's nanatinostat four hours apart. What that does is extends the kick in the mechanism, and we see increased antitumor activity in the EBV-positive gastric cancer xenograft model when we do that. The second thing that we're doing is we're introducing daily dosing. So it was for lymphoma, four days on, three days off for Nana-val, but in for nanatinostat. But in this setting, where it's very well-tolerated, we're actually going to daily dosing, so seven days a week. And finally, we're going to higher doses. And again, these are insights that came from preclinical work. By allowing 3 days off in the gastric cancer model, we saw some tumor regrowth in those 3 days. But by now doing it daily, and this is, again, was borne out in the preclinical work, we saw it really control the tumor very, very well. So that's why we're going to 7 days a week and to higher doses, and we have additional IP that we've filed on the back of these insights. So we have 3 dose cohorts up to 3 ahead to find that recommended Phase II dose. We will be enrolling patients in dose level 6 before the end of this year. So then, as you look across the Nana-val program, there are a lot of milestones as we turn the corner into 2024. So as you can see, we're going to complete the phase Ib dose-ranging work with these new SDD regimens. As shown, we intend to determine the recommended phase II dose. We'll present data from the dose escalation work with the new SDD formulation and initiate our phase II study. So that's the plan for next year. So to summarize, really, our number one priority as a company is to maximize the Nana-val opportunity. We think it's a unique medicine that we're bringing to fulfill an unmet need in a unique area, EBV-associated cancers. Our goal ultimately is to bring to the world a tumor-agnostic medicine for EBV cancer, both solid tumors and lymphomas, and I think we're well on that track. This would be great news for patients, and I think will create value for shareholders in the process. Thank you very much. All right. Very good. If anyone has a question, feel free to ask one. But, so the NAVAL-1 trial, I guess, what's your expectation around what you're gonna see with monotherapy nanatinostat in that PTCL cohort, just kinda given what we know about the HDACs in that setting? Yeah. And do you think that 10 patients will be kinda sufficient and enough from a sample size perspective to really kind of to really demonstrate attribution of benefit when it comes to the Nana-val treatment system? Right. I'll start, and if you wanna add any comments, feel free, Darrel. So firstly, this is what we aligned with the FDA on. Okay. This is what they asked us to do, and that's why we're doing it. The second thing is, just to remind you, we're using nanatinostat at 25% of the maximum tolerated dose. So we're not using it as a typical HDAC inhibitor. Mm-hmm. We're using it to express EBV protein kinase. That's why we selected... It took two years to select nanatinostat for that purpose. So when we're looking at the activity of nanatinostat in that monotherapy arm, our expectation is, you know, you'll get minimal effect in that arm, and that really what we're looking to see is, you know, the effect of Nana-val, which is, you know, deploying a different mechanism. Mm-hmm. So that's why we think that's probably ample patients for- And, and- - for this ... has that also been kind of the perception of investigators in the trial as well, that nanatinostat's probably not gonna yield much in the way of clinical benefit? And I guess because of that, has that been a little bit rate-limiting in terms of your ability to enroll this Stage I portion and then and then move into Phase or Stage II? No, we've not heard that feedback. I would only add that if you look at other HDAC inhibitors that were treated for or indicated for the treatment of relapsed refractory PTCL, which were treated, by the way, at their maximum tolerated doses- Mm-hmm ... you saw response rates on the order of 25% to 26%. ... and that included both EBV-positive and EBV-negative patient populations, including the EBV-negative patient populations, are easier to treat. So that's another piece of evidence suggesting that the response rate we anticipate from monotherapy should be relatively low. But that hasn't dissuaded enrollment. In fact, we're very near the completion of stage one, as indicated by those milestones. Okay. I guess the decision to pursue now second-line DLBCL- Mm. is interesting. I mean, you showed- Yeah ... the outcomes of patients who are EBV positive. And we know the historical R-CHOP data would suggest that these patients don't do well. But do we know how EBV positive patients with DLBCL respond to, I guess, CAR T, for instance, right? Which is now, I guess, kind of institutionalized second-line standard- Yeah ... of care. Do you have any real-world outcomes- Well- - for that data? We have anecdotal evidence- Mm-hmm ... they're not doing as well, but that's why we have a plan to collect real-world evidence in a systematic way that will enable us to really show what outcomes look like for patients that do or do not have EBV DLBCL, right? Because so far, the evidence points to a dramatic difference between outcomes, right? 'Cause standard immunochemotherapy up to date, and now we have to look at CAR T as well, would suggest that they really have very different prognoses. I don't know if you wanna add anything to that, Darrel? Yeah. Our hypothesis is that, just as you saw in the prognostic curve- Yeah ... in the slide there with the existing standard of care at the time, our hypothesis is that existing standards of care is equally do not work as well, if at all, in EBV positive DLBCL compared to EBV negative DLBCL. If we can gather the real-world evidence to confirm that hypothesis, that will, A, drive patient enrollment on the trial, and secondly, build our case that EBV positive DLBCL is a unique disease entity. And there's certainly nothing approved specifically for EBV positive- Mm-hmm ... DLBCL. And so that will enable us to preserve an accelerated approval pathway, even in the second-line treatment setting. Mm. Does the WHO classification of EBV positive DLBCL as kind of representing its own unique subtype facilitate that accelerated approval argument? I think it's helpful. I mean, you know, again, if you look at the biology and the mutational landscape compared to other DLBCL, it is its own unique type. Mm-hmm. Now, we just need the evidence from the real-world side that the clinical outcomes are exactly as we've seen prior to that in, you know, other studies that have shown clinical outcomes are distinctly worse. Okay. I think we've seen in other virally induced cancers, right? So things like HPV-positive head and neck cancer, that there tends to be a correlation between reduction in viral load or copy number and clinical outcomes. Is that something that you see here- Mm-hmm ... with respect to Nana-val and seeing a reduction in EBV transcripts, and then that corresponding to depth and breadth of response? Yeah. Yeah. We continue to collect and evaluate those data, but, so far, that seems to be tracking to be the case, yes. Okay. And then, you're guiding to having the PTCL data, I guess, H1 of next year? Is that correct? Yeah. How are you thinking about disclosing data from the additional cohorts within NAVAL- 1? And should we think about those disclosure formats as kind of taking on, you know, the "yes, we did" format that you used for PTCL? Or do you wanna have those cohorts fully enrolled and then provide a more granular look at the data? Well, I think we will likely announce the progression or advancement of a DLBCL or PTCL cohort once we hit the threshold. Mm-hmm. So that may or may not be before we get to 10. So if that happens before we get to 10, then I'm sure we will let the world know because that means we will automatically be moving forward into stage two. So, that'll be during the course of the year. We haven't specifically said when. I guess that depends on how the data rolls out. I think the PTCL data, then, you know, we'll be sharing the PTCL 10-patient data for the monotherapy and the Nana-val arm, you know, also in the H1. Okay. You had previously specified third-line DLBCL as part of- We had. as part of NAVAL-1, and so do you now stop enrolling third-line patients and shift your sights to second line, or are you gonna complete that third line and then use that to pivot into second? We'll allow either line. We do not, the protocol will not be requiring a minimum number of each. Okay. It'll be open-label, second or third, or onwards. Okay. There's no other questions. I think we're out of time. Mark and Darrel- Great ... really appreciate it. Thank you very much, Steve.