Okay. It's noon now, let's get started. Welcome, everybody. I am Boris Peaker. I'm a Senior Biotech Analyst here at Titan Partners, and I'm delighted to host Genelux today. We have the senior management team with us on the webcast. We have Thomas Zindrick, who's President and CEO, Matt Pulisic, the CFO, and Jason Litten, Chief Medical Officer. Many investors are probably familiar with Thomas and Matt, Jason is a new team member. Perhaps, Jason, give us a quick overview of your background before we jump into specific questions. Yeah. Thanks, Boris, hi to our audience. My name's Jason Litten, chief medical officer. I'm a pediatric oncologist by training. I've been in oncology drug development for the past 20 years. For the past 10 years of that, I have been focused on immuno-oncology. The opportunity to join the Genelux team and advance Olvi-Vec in advanced ovarian cancer and other indications was something I didn't want to pass up. I joined the team just a couple of weeks ago and really excited about the journey we're taking in 2026. Great. Fantastic. Before we jump into the specific question, maybe, I don't know who the best person will be, just to give us a one-to-two minute brief overview of Genelux's technology. Yes, thanks, Boris. Genelux is a late-stage clinical development company focused in oncology. Our lead asset, Olvi-Vec, is an oncolytic immunotherapy, which has a multimodal mechanism of action, which gives it opportunities in a wide variety of cancers and also with a wide variety of combinations, which is really important in oncology because the field has certainly learned that there is no magic bullet, and it really requires a differentiated attack against the various defense mechanisms of a tumor to really overwhelm those defense mechanisms. We think Olvi-Vec is really positioned to be potentially a backbone with a number of therapies. Our lead asset, our lead clinical programs are really following the theme of platinum resensitization. Platinum is one of the most commonly administered chemotherapies, and when it works, it works very well. Unfortunately, in many, in fact, in ovarian cancer, our lead indication, it ends up not working for the vast majority of patients. Being able to resensitize a tumor to platinum to make it more responsive to what it might otherwise be is really something that we're excited about. We're definitely not limited to combining with platinum, but we're positioning our program to follow our most mature science. Great. Let's jump into just general questions, maybe. The first oncolytic virus approved was IMLYGIC. That was about a decade ago. What have we learned about oncolytic viruses over that decade, and what have been the challenges in getting other oncolytic viruses really approved? Yeah, I think one thing we've learned is coming out of animal models, certainly not all oncolytic viruses are created equally, and we're very pleased with Olvi-Vec and its unique backbone. Olvi-Vec is derived from vaccinia virus. Vaccinia, for context, is a lab-derived virus developed to really help combat smallpox in the most successful vaccination program in history. To be clear, it's not a natural human pathogen. It creates cross-reactive antibodies to smallpox. In that vaccination setting, it was demonstrated to be very safe in the millions of patients to whom it was administered. We knew going into the program that we were working with a really ideal agent for an immunotherapy, in the sense that it was designed as a vaccine. It's designed to light up the immune system, and we've subsequently modified the backbone to form Olvi-Vec, to help attenuate or ensure a good safety profile, while also adding some really unique characteristics that we, as I mentioned, think really definitely positions it well. In terms of the space generally, in addition to the standard questions that need to be overcome, such as safety and therapeutic efficacy relative to standards of care. What the field has learned is that as a live agent, there's a multitude of aspects that need to be evaluated, host clearance, tumor targeting, immune presentation, and a variety of aspects in terms of how best to administer the virus and how best to combine it, if necessary, to potentiate its effect and the effect of other combination therapies. What we've seen over the last 10 years is the field has advanced in significant ways, and we're very excited. There are some other late-stage oncolytic programs that are demonstrating the power of oncolytic viral therapy. Those programs are limited to more local delivery. In one case, direct delivery into tumor lesions. We think to ultimately unlock the full potential of the oncolytic virus space really requires the ability to have all the characteristics I just alluded to for Olvi-Vec. One that we're very excited about is the ability to administer it through physician-preferred routes. That really opens up the field, we believe, and positions Olvi-Vec in a great spot to really build on this emerging development in the space and take it to the next level. Your route of administration for ovarian cancer, intraperitoneal. Can you describe the logistics of that, how the catheter installed, and also what that implies in terms of virus detectability in the blood after intraperitoneal administration? Yeah, great question. In our case, in all of the current clinical studies are really focused on a speed to market strategy. We're dealing with a very difficult to treat patient population in all of our clinical studies. We're going after high bars, but we're confident that we can clear it. In the case of the ovarian cancer study, patients will have a catheter implanted and receive Olvi-Vec, a single dose on two consecutive days. They receive a total of two doses. That's the entire exposure they have to Olvi-Vec. The catheter is removed in less than two weeks, so there's not the risk that you see in long-term catheter implantation, such as adhesions or infections that can often occur. In the ovarian cancer setting, gynecologic oncologists are surgeons by training. The delivery of chemotherapy by intraperitoneal administration is not at all uncommon for them. It goes back to, as I mentioned, we're working within and not trying to change the practice of medicine with this particular approach. In terms of your question about the virus being detected in the blood, we look for, to be clear, because we think it's the most relevant metric, we look for live virus through a viral plaque assay. In our studies, we've not found live virus in the bloodstream. We've found it certainly in the abdomen as we evaluate ascites. We've certainly also seen that through its mechanism of action, where Olvi-Vec not only directly kills tumor cells but also stimulates the immune system. We've seen evidence of that immune response against distant metastases. No evidence of virus, but evidence of a holistic whole body attack against the tumor, wherever it may be in the body. Got it. That's helpful. Maybe let's better understand the virus itself. Interesting you mention, obviously, that this is a vaccinia, and we know that it was used as an immunization for smallpox, which was stopped in roughly early 1970s in the U.S., which implies that some of the patients you're going to see probably were immunized. Maybe some of the other patients were not immunized. How does the prior immunization impact your oncolytic virus? We're pleased to say it doesn't. We've spent a lot of time, obviously, as I mentioned, as the field has learned more about host clearance and the like. We were trying to sort that out ourselves. We've definitely treated patients. In ovarian, when you consider many of the patients are 60+ years old and would have had prior exposure, you will have some minimal baseline of the neutralizing antibodies to prior administration. We have not seen any impact on efficacy with those patients. We believe we're dosing, first at a safe dose, but one that, given our dosing regimen and the size of the dose, that we can evade that natural immunity to have a very effective delivery of Olvi-Vec against the tumors. Great. Then mechanistically, how does Olvi-Vec sensitize tumor to platinum? Obviously, there is a focus. I guess maybe even a broader question is platinum is the key focus because that's what you're working on right now in ovarian cancer. Just a general question, how that expands to potentially other chemotherapy mechanisms as well. Yeah. Pre-clinically, we've shown that Olvi-Vec can combine with a variety of very common chemotherapies. It's something we're definitely interested in pursuing. Even then, we're not limited to just combining with chemotherapies, as we'll talk about with one of our ongoing lung cancer studies. We're also combining, in addition to platinum, with a checkpoint inhibitor. There's very good pre-clinical data, and we have some encouraging translational data from our clinical studies that suggest that Olvi-Vec will be very effective when combining with the checkpoint inhibitor, but could also very similarly with cell therapies and the like. We think, as I mentioned, we're following our most mature science, but we think we're only starting to kind of scratch the surface. The reason I say that is, again, in some of our translational data in our monotherapy trial in ovarian cancer, before we moved to phase II and combined with chemo, we were getting some paired tumor biopsies. What we demonstrated consistently was that in patients that were being treated, we could generate an anti-tumor T cell response, that we saw an influx of effector T cells or killer T cells into the tumor epithelium, and a modification of a number of pro-therapeutic genes as we turn the tumor so-called cold to hot. What was interesting is in almost all instances, the virus seemed to be doing what we were asking it to do. Interestingly, not all patients, though, responded equivalently to that platinum rechallenge. What that I think informs us is we believe that, hey, if it doesn't work with platinum, there could be other combinations as we think about how to optimize treatment in patients, whether it's layering a checkpoint inhibitor or a different chemo combination. I think that, again, underpins why we believe Olvi-Vec would be such an important backbone in that regard. In terms of your question about how it works, so as I mentioned, it's a multimodal approach. The first and most important aspect, really a catalyzing event, is it will selectively replicate and kill tumor cells, so you get direct cell killing. In the course of that cell killing or lysis event. The tumor antigens, those specific biomarkers that can flag for the immune system that the tumor needs to be attacked, which in a typical tumor-suppressed microenvironment, the immune system is blunted and unable to oftentimes amount that attack. We can unravel that defense mechanism to create an anti-tumor T-cell response. The third point I mentioned in terms of the positive aspect on pro-therapeutic genes, one of those has been shown to be implicated in tumor resistance. We reverse or upregulate that gene, enabling the tumor cell to retain, or causing the tumor cell to retain platinum and not have it expunged as quickly. In the context of turning the cold tumor hot, it's a variety of mechanisms that are all suggestive of a very pro-therapeutic effect. There's immunogenic cell death. There's a transition from M2 to M1 macrophages. Significantly, we've shown that we can kill cancer stem cells, which have also been shown to be chemo-resistant. What gives us great confidence is both clinically and translationally in human clinical studies, we see a consistent story, all of which points to the ability of Olvi-Vec to be successful. As we look at mechanistically, as we look at our clinical data, it all aligns, which again, gives us great confidence as we expand the program. We're not having to explain away any kind of anomalies. This is all very consistent, starting with a wealth of preclinical data and now translating into clinical data. Great. Well, speaking of clinical data, let's zoom in on ovarian cancer. As we mentioned in our discussion earlier, the focus is on platinum-refractory patients. What we normally observe in ovarian cancer patients is that a high response rate to a first line of platinum, and then a diminishing response rate durability of response on further retreatments. What's interesting, if we look at your phase II VIRO-15 study, we saw essentially the same response rates in mid-50% range duration response around 7.5-8 months, both in platinum-resistant and platinum-refractory patients. What can we extrapolate from that? Yeah, I think at a high level, it suggests that the general mechanism of action of Olvi-Vec in terms of at the cellular level that I touched on can be effective across a variety of different tumor types, including the most difficult to treat, platinum-refractory. Which, to your point, the NCCN guidelines specifically contraindicate the use of platinum for refractory patients. It would, in its own right, not be seen as being very effective. In our phase II study in ovarian, we have some great case studies. You pointed out, across the board, we saw 54% objective response rate where you'd expect something in maybe the 15%-25% range. These patients had an expected life of probably less than one year, and we had a progression-free survival period across as a median of 11 months. So very, very encouraging as we look at that. Specifically, when we think about the refractory patients, the couple of case studies which I think are most compelling when using women as their own control as we think about this study. The first instance, the data I just shared with you is really in a representative population. There was nothing unusual. Our patients, in their immediate preceding line of therapy, had a progression-free period of 4.5 months. You'd typically expect on the subsequent line of therapy to be even less, call it four months or less. As I mentioned, we reversed that negative trend and converted that to 11 months. When you drill down into some specific patients, we had a couple of refractory patients who on their immediate preceding line. By definition, refractory patients are those that when exposed to platinum progress while on drug or a short period of time after that. These patients had a very short response to platinum. They joined our study, received that single cycle, only those two doses of Olvi-Vec, and were rechallenged with platinum in a relatively short period of time. You wouldn't expect there to be a response to platinum at that point. In fact, we demonstrated very impressive durability in those patients, suggesting that it was definitely Olvi-Vec, in our belief, that was the cause for that reversion of platinum refractoriness. Are there any other drugs that we could look at as reference that you have in ovarian cancer that show similar efficacy in both platinum-resistant and platinum-refractory patients? Yeah. Putting our data into context in this space, I think is really critical. We are differentiated in, I think, a number of ways. The emerging therapies, more often than not, end up segmenting the population. Whether it's by capping the number of prior lines, by requiring a biomarker, or in many instances, excluding refractory patients because they are so difficult to treat for all the reasons I just mentioned. There has been work that is very encouraging in earlier lines of therapy. When we look at our data, and in fairness, we're looking at our phase II data against some relative later-stage studies, we don't see any therapies right now that match our PFS. In fact, when you look at the PFS of a recently approved therapy in an earlier line of treatment, we doubled the PFS of that therapy. Again, putting into context, we believe we're taking on the most difficult to treat population in almost an all-comers basis. We don't require a biomarker. We treat refractory patients, and we don't cap the number of prior lines. In our phase II study, we had a median of four prior lines with an N, meaning patients had any ranging from two prior lines to nine prior lines. I think the most important aspect here is for the reasons I mentioned about Olvi-Vec potentially being a backbone therapy, by and large, we don't necessarily see those other agents as competitors. We see them as potential combination partners where we believe we can help potentiate their effect even beyond what they've been able to achieve to date. Again, we're moving into a space where we don't believe the current standards of care or even the later-stage emerging assets can competitively shift to where we are. We're confident that we can move forward, and ultimately our plan is to move to frontline and effectively bracket the space, and then combine with those newer agents in somewhat earlier lines of recurrent therapy. Great. Heading into the top-line data readout, and we'll probe more into the OnPrime phase III study shortly. Help us understand a little more about the unmet medical need for these patients and how could Olvi-Vec change the landscape for these patients as well as physicians? Yeah, I'll take this one, if you don't mind, Tom. Absolutely, Jason. Yeah, thanks. As Tom's already suggested, platinum's the most important agent that's used for women with advanced ovarian cancer. Everyone in frontline treatment receives a platinum-based doublet, and it's actually quite effective. Once patients progress on or after platinum, there are lots of different treatment options. Now, there are an increasing number of treatment options, as Tom's described, many of which are biomarker-directed. Unfortunately, none of these work as well as platinum, so they will not be displacing platinum for upfront treatment anytime soon. None of them provide a curative opportunity. I was speaking with a gynecologic oncologist earlier this morning, and he was telling me that he continues to try to reintroduce platinum in multiple lines of therapy really as much as he can. It continues to be the most effective agent in his armamentarium. With Olvi-Vec, the opportunity to reinitiate sensitivity to platinum is really something that's potentially practice-changing and is something that I think could not only be used in that platinum-resistant and refractory population, but potentially, as Tom suggested earlier, turn these cold tumors hot and provide an opportunity for combination with lots of other agents that are already used in later lines of therapy. Great. Let's zoom in on your OnPrime phase III study, which is probably of greatest interest to investors here. Ovarian cancer trials often include fallopian and peritoneal cancers, even though people don't mention it, typically that's part of the study. You're allowing those tumor types into phase III as well. How do these tumors differ from primary ovarian tumors? Is there any phase II data in these tumor types or just address any concerns investors may have in the potential patient heterogeneity by including these tumor types? Yeah, thanks, Boris. Again, great question. In terms of those tumor types relative to primary, biologically, pathologically, clinically, they're pretty similar, even though they're identified by somewhat different sites of origin. The treatment tends to be similar as well. To your point about how we do include those, as I mentioned, we effectively take on and don't limit the potential patient population. In fact, there are a couple of other tumor types that we take on that are also frequently excluded that would include clear cell and mixed histology tumor types. We had a couple of those in our phase I-B monotherapy trial. In the clear cell case, we were able to get a stable disease and have a PFS for eight months, which was very encouraging. The mixed histology patient actually became, as a monotherapy, so on virus alone, was a PR with a PFS of 13.8 months. Again, very encouraging results from that patient. With respect to your question about the fallopian and the peritoneal cancers, we had about six patients of the 27 were in our phase II study where they received Olvi-Vec-primed immunochemotherapy, so Olvi-Vec plus the platinum chemotherapy. Generally speaking, their responses were equivalent to the broader population. That comes back to my earlier point about as we've cut the data, whether it's by prior therapies, by genomic markers, tumor subtypes, what have you, we're seeing a consistency of benefit through this, which is one of the reasons why we think we're so differentiated and have such great potential. Got it. PARPs have obviously been used to improve platinum sensitivity as well in ovarian cancer, and there is pros and cons and things that have happened over PARP therapy over the last several years. Does prior PARP use impact Olvi-Vec? Is there any PARP or any data specifically you could share on that from the data to date? Yes. To your point, there has been data out there that prior PARP exposure can actually have a negative effect on subsequent platinum rechallenge in the recurrent population. It's notable that in our case, it did not show any negative impact. In fact, we had total of 20 of our 27 patients had had prior PARP exposure, and 11% actually were responders, 11 of the 20 were responders. That's very encouraging, 55% consistent with our broader population going forward. Where you would think that because of that prior PARP exposure, if Olvi-Vec wasn't having that remodeling effect, that you would expect a lower response rate in those patients that had prior PARPs. That's not something we saw. Across the board, it comes back to my earlier statement that Olvi-Vec seems to be doing what we want it to do in a broad swath of patients, and then it's just combining it with the best possible therapies to optimize its effectiveness. Got it. Another question that comes up with investors is, are brain metastases allowed, or patients with brain metastases allowed to enroll? Because that was viewed as an issue for ovarian cancer drug that failed not too long ago. Curious, kind of your take on that. No, we don't allow brain metastases. I will say, in looking at the available data, it's a fairly small percentage of the population, but I can appreciate that, given the randomness of enrollment, and depending on whether brain metastases patients were geared to a trial because they permitted it. They could certainly end up with a higher percentage of brain met patients than you would find in the general population. It's a relatively small percentage. Got it. That's good to clarify. I think the investor concern sometimes is like, yeah, it's a small population, but if you're the only study that's allowing it and everybody's not, then all of a sudden you find yourself in a very different position. Focusing on OnPrime, what are the statistical power assumptions? How should we think about it, and what are your expectations just for the PFS and the control arm and the active arm? In looking at historical data, in this population, I think it would be fair to assume something on the four to four and a half month PFS. We took very conservative assumptions when we designed the study, and we expect a 10-month PFS minimum on the experimental arm. Remember, in phase II we had an 11-month PFS. Instead of that four to four and a half months, we estimated five and a half months of PFS in the active comparator arm. We believe we have very conservative assumptions, but even with that, it's a relatively small trial because in ovarian cancer, anything north of a three-month—and especially recurrent ovarian, anything north of about a three-month improvement in PFS is considered clinically significant. In our case, we're powered to 90%, and it's powered to have a hazard ratio point of 0.55. We believe we have very strong biostats behind this trial and are confident in being able to clear the bar. Great. Now question, maybe looking at the competitive landscape. There's a number of other drugs being developed, obviously in ovarian cancer. This includes ADCs, checkpoint inhibitor. We have a cortisol modulator with a PDUFA in about, what, six months or so. How do you think these agents will impact the standard of care in general ovarian cancer, and how would that fit in with Olvi-Vec, assuming that it meets roughly the targets that we just talked about in terms of study design? Yeah. First and foremost, we're really excited about the advances in ovarian cancer, and Jason can certainly speak to this. For far too long, there weren't any new emerging agents that could help patients. The PARPs came along, and then for the reasons we talked about, their labels were restricted, and it really sent tremors through the industry or the field. We're really excited about that. In terms of its direct impact on our development program, we think it'll be minimal. Those other therapies cap the number of prior lines. In the case of ADCs, they segment it by a biomarker, for example. When you look at some earlier data on those later stage assets in populations with greater number of prior lines, kind of where we're playing, you actually start to see a pretty significant fall-off in efficacy. We don't see there being the opportunity for those agents to necessarily shift into where we are. We do think that in a population for which there's really not much after second or third line, that if they are able to develop effectively a healthier population for us, it will actually lead to more patients that would be able to benefit from Olvi-Vec because they'll be coming to us in larger numbers and in a healthier position. We hope to then create what will ultimately be longer term survivals, building on this paradigm. As Jason Litten touched on earlier, our long-term goal, and he can certainly speak to this in greater detail, is to move into frontline, where we can really start having significant impact on patients, getting them when their immune systems are not beaten down by chemotherapy, their tumors are not hostile to therapy. I'll say that that's actually something that the FDA has approached us on a couple of times during our discussions with them. It's not something we have been focused on. It was something they brought up because they know this space better than anybody. Given our results in this most difficult to treat population, their point was how excited it could be to be able to work in a population that might even be more responsive to Olvi-Vec in combination with platinum. Again, we see this as a very broad opportunity, and we really don't look at the emerging therapies as necessarily competitive for us, but actually complementary to what we're doing. Great. If approved, obviously you mentioned that you're enrolling a wide range of prior line of therapy patients. Let's say you get a broad label for platinum-resistant or platinum refractory. What line of therapy do you think you'd get be used right now, and how would that translate to the specific commercial opportunity for the drug? Putting aside the front line that you just mentioned, a kind of a longer-term goal, just based on the current study. In our phase III study, we require a minimum of three prior lines. We had thought about that quite significantly. In talking with our key opinion leaders, there was a push to move into these earlier lines of therapy where these other agents are, and certainly welcome that opportunity eventually. As we evaluated our phase II data, what we noted, and again, very significantly, when you look at patients that had in our trial, a phase II trial, who had two to three prior lines versus those that had four to nine, there was no drop-off in progression-free survival. There was no drop-off in overall survival. When we thought about the patient population that was in most need, and one that frankly we felt was not only underserved but would continue to be underserved unless we developed Olvi-Vec in this population, we decided that's where we're going to pursue our lead. The bar is very low. We expect to clear it pretty handily, as we mentioned with our biostats. We believe that our label will mirror our clinical trial design, so it would be for patients with 3 or more prior lines with a very wide variety of eligible patients as we move forward. That's where we're starting. That's only the beginning of where we're going to go. Great. Maybe a longer-term strategy question. I don't know if this is for Jason or for Thomas. You've mentioned, Thomas, plans to go into early line of therapy, maybe even front line is something the FDA discussed. I understand that's not the current focus, what would it take to get there? How long, how big would these studies have to be? What are your general thoughts on future expansion to that front-line indication? Yeah. I'll let Jason speak to this. One thing I do want to note, and you touched on it earlier, Boris. Matt and I are somewhat familiar to many of the investors. Over the last year, we've really been building out the management team. We also hired Eric Groen as our General Counsel and Head of Business Development. Jason is just another tremendous hire for us. He didn't go into a lot of his detail of his experience, he has experience in the ovarian cancer setting as well as a number of others. He's just an ideal candidate as we think about getting into these questions about where do we go next as a clinical strategist. Jason is absolutely the right individual for us at the right time. We couldn't be more excited for him to join. With that big build-up, Jason, I'll let you speak to Boris's question. Yeah. Thanks for the question, and thanks for the intro, Tom. That's very kind. Yeah, I am excited about the opportunity for Olvi-Vec in frontline ovarian cancer. As I said before, platinum is the standard of care for all patients with advanced ovarian cancer globally. What we're starting to see and what Tom, I think, was suggesting, saying that we're demonstrating activity even in the very latest lines of therapy, is that Olvi-Vec is doing something fundamental to the biology of these tumors. As I said earlier, turning potentially cold tumors hot. Whatever it is, it's changing the biology in a way that's taking a tumor that was previously not receptive to therapy or not fully receptive to therapy, and molding it in a way that it can potentially demonstrate activity. In my mind, the opportunity truly is in frontline, when patients are getting their best and first opportunity at cure and delivering that, and really trying to introduce the plateau that we've seen that so many immunotherapies have provided and so many indications of a prolonged and durable response from frontline therapy. Really when we do see it, a complete response in ovarian cancer, it's relatively rare. I want to introduce Olvi-Vec to hopefully introduce the rate of complete responses. Maybe more importantly is really impact that durability, and provide something practice-changing and transformative for patients who are receiving upfront therapy. Your question about what it would take, Boris, though, getting all the way back to the beginning, is it would take a study with several hundred patients, and it would take probably several years before it could report out. I think our opportunity in 2026 is to demonstrate the benefit that Olvi-Vec provides to ovarian cancers broadly beyond that frontline therapy and really start to drive clinical usage and start to think about what it would take, as you said, to deliver on that opportunity for frontline patients. Great. Maybe, I guess, Thomas, back to you. You mentioned about building out the team as you're kind of rounding out the major pivotal study. What about the commercial side of the organizations? Where are you right now? What kind of preparations are you making to the potential commercial launch? Yeah, we've always developed Olvi-Vec in this indication with an expectation of commercial launch. There's some great examples in the recurrent setting, again, not necessarily in this population, of small to mid-size companies being able to successfully launch, most recent of which was ImmunoGen for ELAHERE, which was subsequently acquired by AbbVie for over $10 billion. The reason for that is it's a highly concentrated set of clinical sites. A significant number of ovarian cancer patients are identified and initially diagnosed at a relatively small number of sites, and there's a limited number of gynecologic oncologists. We believe we have the ability, as a smaller biotech, to be able to develop a very effective sales and marketing organization that can take advantage of that. In that regard, we have begun preparations with respect to not only what it would take to commercialize, we have a very good idea about that and just hired another clinical science liaison. As you think about how we would advance this, the science, this is really a science story, given we're doing something different in a population that for which there is no standard of care. We think, ultimately, a medical science liaison force will be significant. We're starting to build out that capability currently. We're also, and Matt will speak about this when he speaks to finance, but we are also building out our commercial manufacturing facility. We expect to be fully integrated in this space ultimately and are making significant tangible steps to make that happen. Great. Remind us again when we should see the key pivotal data readout. We've guided to the second half of this year, after which time we have Fast Track designation and we'll seek rolling submission towards BLA. Maybe Matt could speak a little bit in terms of from a cost perspective, how we are thinking about fully building out that commercial organization, and how we think the adoption curve will ultimately play out very effectively from a finance perspective. Sure. As you can imagine, we've done a lot of work on what the addressable market looks like and how to commercialize the asset. As Tom mentioned, we remain laser-focused on getting the asset to its intended indication as the first commercial launch. Subsequently, we'll consider, of course, earlier lines of therapy. Even with respect to just commercializing the asset as it currently stands through the existing phase III trial that we have and the label that we expect, it's not a significant lift from a not only a capital perspective, but also a human personnel perspective. As Tom mentioned, the concentrated network allows us to build a sales force that'll be predominantly MSL or medical science liaisons. Think numbers somewhere between, call it 50 - 70 in totality. From an investment perspective, not a significant level as well. Pre-commercially should take approximately, call it $30 million-$40 million to prepare and get the asset into the launch phase. Then as we launch the product and it's generating commercial revenues, maintaining that product in the market will take approximately $30 million-$40 million per year as well. As Tom mentioned, it's tailor-made for a company of our size to commercialize the asset, and we remain laser-focused on executing against that goal. Great. That's helpful. We only have 20 minutes left, so let's move on to maybe lung cancer, which is a potentially bigger indication than ovarian in certain patient numbers, certainly. You recently presented updated data on both non-small cell lung and small cell lung cancer. Interestingly, lung cancer is your first foray into IV administration. Let's talk about that first. In a typical IV chemo, we generally think about IC50 and blood concentrations of drugs, if we think about basic chemotherapy, for example. Right. Since this is a replicating virus, how does dose work and optimization work? Do you focus on peak viral load? Should we be looking at some other way of optimizing dosing? Is there a minimum viral load required to trigger the immune system? Should we even anticipate a maximum tolerated dose? Yeah. All great questions, and it really goes back to your initial question around what's been happening since the IMLYGIC approval and the work that's been done in the field to really better understand this. You're right. IC50 isn't really applicable in the context of a live agent. It is more typical in a chemotherapy setting when you're trying to set Cmax. I completely agree that peak viral load is a very instructive component of that. What we've seen pre-clinically, for example, is that regardless of the initial dose, the peak viral load is shown about 48 - 72 hours after initial administration. It really doesn't necessarily tie to the initial dose. What will often then dictate it, and this comes back to how we think about developing and selecting a dose, is regardless of the dose, how effective is the virus in being able to infect and replicate within a tumor substrate? What's the immune microenvironment, and how quickly is it cleared? All of the things we talked about earlier in terms of helping to develop it. In pre-clinical experiments, we showed that, take lung, for example, that we were pulling out in blood over a lot more virus than the initial dose in pre-clinical models. Clinically, it would be very logistically challenging to try to run those kinds of experiments. We haven't done that, and are not doing that currently in the clinical studies. Ultimately, it comes back to the point you made, which is we believe there is a minimum effective dose to really convert the tumor microenvironment to be immunoreactive as opposed to immunosuppressive. As we're looking through and have the ability to dose escalate on a relatively safe agent, the goal is don't give too much and don't give more than you need. We're trying to figure out what that dose looks like that can have broad applicability across a variety of different tumor subtypes. Theoretically, yeah, we could certainly hit an MTD if we get enough dose-limiting toxicity events. I'm happy to report that in seven clinical studies, in 150 or so patients, variety of routes of administration, different cancer types, we've not hit an MTD. We believe we can continue to dose escalate in our current studies to find that proper dose for systemic administration, initially in lung cancer as we move forward. What's the virus half-life? We're just trying to understand the kinetics here. Maybe even more importantly, how much of the virus actually goes and remains in the lung versus how it partitions to maybe some other organs, and how quickly does the immune system end up basically clearing it? Yeah. We've done a fair amount of work in our clinical studies. One in particular, we had a translational study conducted in San Diego, and we showed a half-life of about two hours in the circulation. When you think about how frequently the blood circulates, that we believe we can deliver significant and important amount of virus to any organ. With respect to the lung, the pulmonary circulatory system's, I'll let Jason check my math on this, but about 10% of the overall blood in the body. We would assume maybe 10% of the virus would get into the pulmonary circulation, and then ultimately into the lung. Again, that's just a seeding dose. It's really what happens at once it infects tumor cells, because with vaccinia at least, much of the transmission from one cell to the other is through cell membranes. It can be, in significant ways, can evade immune system clearance as we move forward. Again, it comes back to what we had said earlier, which is to try to find that right dose that can be effective across the broadest population of lung cancer patients. You recently presented some updates from the study. Can you help us maybe recap the updates and help us understand the initial insights on tolerability and safety as you're escalating dosing? Absolutely. I'll start with the last point. What we're seeing is what we've seen in other studies. Patients typically respond to mild to moderate flu-like symptoms, as you would expect from a viral infection. Because the virus is cleared through the liver, you'll get some asymptomatic lab analyses. I'm pleased to say in the two lung cancer studies we have ongoing, one small cell lung cancer and the other non-small cell lung cancer, each of the safety committees for those trials have recommended recent dose escalation. Very encouraging in terms of the safety profile that we've been generating. In terms of what we're seeing, as we've talked about, Boris, what we put out later this year was very consistent with what we had expected to put out earlier in the year. It's dose escalation starting at very low doses and in relatively small numbers of patients. We're very encouraged by what we're seeing. As I mentioned, we've got good tolerability, and we're starting to see some activity, which in its own right is very encouraging. When you pull out a little bit and put it in the context that our entire program, as I mentioned earlier, is thematically designed to follow our most mature science, notably platinum resensitization. In each of these lung cancer studies, these are patients that failed frontline platinum-based therapy, and we're re-challenging them with platinum once again. As you look at this emerging data set in the lung and contextualize it with what we saw in the phase II in ovarian, and even saw as we were starting to dose escalate in ovarian, contextually, we are very encouraged that the dynamics, again, small numbers, suggest some similarity. Because of the commonality of mechanism, that is not a surprise, but it's certainly very exciting for us as we think about what the future holds, even over the next, call it, 3- 12 months of the systemic program, let alone the top-line data that we have guided to towards the end of this year. Got it. How do you think or expect, kind of, this emerging lung data to contribute to understanding the overall systemic delivery and maybe thoughts about other tumor types, how that could translate to that? Yes. Pre-clinically, we showed that Olvi-Vec was effective against 20 major tumor types, many of which, as Jason mentioned, or most of which are treated with platinum, and many of which, or almost all, would be accessible by systemic administration. The thought here is to pursue. We have prior data, both pre-clinically and clinically, that suggests that as a first foray into registration path studies, lung is an ideal organ, right? The pulmonary circulatory system allows us to get a lot of virus into the lung. First-pass effect allows us to get a lot of virus in prior to clearance. We think that is a great place to start, always putting the program in the best possible position to succeed. We're also confident there are a number of other avenues or tumor types that we can pursue. Jason will be instrumental in helping guide us through it. If anything, it's a matter of making sure we retain our focus and continue to succeed. We haven't failed a clinical study to date. We don't intend to as we move forward, that's really where Jason's expertise can help guide us in that regard. Great. Let's talk a little about small cell lung cancer. This trial, I think you also provided an update, is conducted by a partner in China. One fundamental question people have is how is the small cell lung cancer treatment overall treatment paradigm differs in China, U.S., or patients themselves, potentially, if there's any kind of genetic differences, smoking differences or anything else to help us kind of extrapolate the data from China to the U.S. I'm happy to take this one, Tom. Thanks, Jason. Yeah. Yeah. Small cell lung cancer, it is a smoker's disease, as you mentioned, Boris Peaker. In the U.S. as well as in China, it's diagnosed predominantly in smokers, and the biology of which is similar across smokers, across nations. The treatment paradigm is similar, but there are some important distinctions. I think the first important distinction or first important similarity is that platinum is the most effective agent like it is in ovarian cancer and is used in both China and the U.S. up front for all patients. It tends to be very effective in frontline, but unfortunately, those responses are oftentimes not as durable as we'd like for them to be. Again, like ovarian cancer, platinum is the most effective agent, and so it's oftentimes used repeatedly, and if patients can tolerate more than one line of therapy. The other important distinctions that I'll just kind of mention quickly is, although checkpoint inhibitors are increasingly used for patients with small cell lung cancer in both China and the U.S., the actual checkpoint inhibitors that are available are different. There are Chinese-approved checkpoint inhibitors that are available there, and FDA-approved, U.S. FDA-approved ones here. The way that they work, generally, is thought to be the same, but the results and the patients that they're used in may be different. We don't necessarily know the details of that yet. The different checkpoint inhibitors used. The other point that I would mention is there are newly approved agents in the U.S. that are not yet approved in China. We think that may shift at least the early opportunity for us in the U.S. a little bit later. Again, it would be that opportunity to combine with platinum in that relapse setting initially to demonstrate activity and then have the opportunity, as we've already described, to go into frontline with platinum-based doublets. Again, leveraging the opportunity to demonstrate that synergy with checkpoint inhibitors. Makes a lot of sense. I guess there's a lot of investor interest in the PD-1, or that VEGF space right now on translatability of China to the U.S. data. I think everybody's going to be watching for that very closely. Maybe if we talk about the small cell lung opportunity. You mentioned that there are three responders in the press release, and there may be a dose response correlation. Will we be able to correlate efficacy to peak viral load in some of these patients? Is that even a meaningful metric to consider? Yeah. For the reasons I touched on earlier. We won't be measuring that. What we did see and what's encouraging, again, in the broader context of the program writ large, is that across all dose cohorts, starting at a very low dose, we had three of nine that were responders, two of whom had been on trial for an extended period of time. In those responders, we're seeing very encouraging durability. In the most recent dose cohort in small cell, we had two of three partial responders with deep tumor shrinkage. One had 85%, and that patient has over a year's worth of PFS and is ongoing. The other at a 10-week scan had a 55% reduction in PFS. We're hoping as we proceed through the year and are able to follow these patients longer and enroll patients at higher dose cohorts, we start to see even deeper tumor shrinkage, which will then result in even longer durability. Which is really what's so important in this patient population. Great. Interesting. You also had two patients, one with 19% tumor shrinkage and the other one with 23% tumor shrinkage. Can you comment if these patients had any new lesions? The obvious reason for investor interest in that is that if there's no new lesions, then there's a possibility of deepening tumor shrinkage so that those two patients could potentially hit the 30% threshold. Is that something that you could comment on right now? What I can say is, because I want to be careful that we are close to what we had put out publicly, is that we're hopeful as we move forward, we continue to see these deepening tumor shrinkage. We've seen that in small cell where over time and with successive scans that we saw continued deepening, which certainly gave us encouragement. For both studies through the course of this year, as I mentioned, we will be following them, the existing patients for durability and continued response. As well as reporting on new patients that are coming in at higher level. I'll say we're very encouraged by what we're seeing to date and expect and hope that the dynamics continue. Got it. Just to clarify, patients on non-small cell lung cancer, will they receive maintenance immunotherapy? If that's the case, what kind of synergy should we expect to see there longer term? Should deepening of responses potential, or is that just going to be more evident in terms of extending the tail, maybe the PFS in some of these patients only? Yeah. If you go back to even the original ipi and nivo results, it was really that Kaplan-Meier tail that was so critical. I'll say that from a translational perspective, in human paired biopsies, we've seen a significant expression of PD-L1 after virus administration. We do think there's good opportunity for that to translate into meaningful clinical benefit, and we've seen something similar pre-clinically. We're very encouraged by that. Notably, I should mention, despite, or I should say even with the very encouraging durability in the small cell lung cancer study, we are not using a maintenance therapy, an immunotherapy. As Jason said, that's an area of great interest in this space. You can imagine, as we advance in clinical studies, we think there's ways to further optimize that design to even get better results. Great. We just have a few minutes left, so maybe we'll switch to Matt. Just a standard question on cash balance, cash burn, and the associated runway. Of course. I want to start with thanking you, Boris, for this opportunity. We really value it. It's great to be here today and appreciate the opportunity to share all the progress the company's made, as well as the financial position and how we're going to allocate capital. To start with our balance sheet, as many of you know, we've recently completed a financing on a pro forma basis that leaves us with approximately $41 million of cash. This financing meaningfully strengthens our foundation and removes what we believe to have been an overhang. With this capital in place, the balance sheet is sufficient to provide the organization forward coverage through top-line clinical results in ovarian cancer, as well as the additional lung data that Tom and Jason have been alluding to throughout 2026. Now thinking about cash utilization, the operating profile of the company is very much in line with what we've previously communicated. Our average quarterly burn is approximately $7 million, and we expect to maintain those levels throughout 2026. As we progress our manufacturing project, specifically the transition of our existing clinical manufacturing facility to a commercial-ready and inspection-ready facility, we do expect a modest increase in capital expenditures. However, even with that incremental investment, our current cash resources extend beyond top line and into 2027, providing us that clear and stable runway. Finally, from a capital allocation perspective, it remains unchanged and highly disciplined. First and foremost, we're focusing on executing against the clinical deliverables. Those are the primary drivers of valuation for our organization. Secondly, we're continuously investing in our facility, shoring up operations to enable that commercial and inspection readiness that I alluded to earlier. Lastly, we're advancing the BLA preparatory activities so that we can move efficiently and rapidly post top line. In summary, we're entering this year from a phase of strength. We have a clear runway, we have a disciplined cost structure, and we have our capital deployed squarely in service of our clinical manufacturing and regulatory timelines. Great. We're just about out of time, so maybe in the last minute, Thomas, can you just recap the key milestones which we'd expect this year? Any publications, any major medical meeting where we might see data, things of that nature? Yeah. Throughout the year, prior to the top line, we've guided that we will provide additional updates on both of the lung cancer studies. Because of their interrelationship on platinum resensitization, we think it really helps build the entire program up, including the potential implications in ovarian. I think Matt summarized where we are. We are incredibly well-positioned. We've got a data-rich, call it 3- 18 months, including the longer-term plans for where we'll take lung cancer next. We've got the management team that can now execute on it. Jason was touching on all of the areas we can go to, and we're certainly giving that due thought. The message for this year is we have everything in place to succeed on that which is before us. We're hyper-focused on execution so that we can get to those meaningful data points, including top line, because we know with that, the entire space opens up for us. We need to get there, and so we're not at all losing our focus on what we need to accomplish this year. That's what we're going to be doing, and are very excited about that. Great. With that, I'd like to thank the Genelux team for joining us today as well as our audience. Yeah, we definitely look forward to particularly the top-line results later this year. Fantastic. Thank you, Boris. Thank you, Boris. Great. Thanks, everybody. Thank you, everyone. Thank you, Boris.