Greetings and welcome to the Nuvectis Pharma investor call to discuss the NXP900 phase 1b program in advanced solid tumors, including the combination with osimertinib in non-small cell lung cancer. At this time, all participants are in a listen-only mode, and this call is being recorded. Joining me on today's call will be Ron Bentsur, Chairman, Chief Executive Officer, and President of Nuvectis Pharma; Dr. Asier Unciti-Broceta, Professor of Chemistry at the University of Edinburgh; Dr. Alexander Spira, Chief Scientific Officer of Next Oncology. Also joining us for Q&A will be Dr. Enrique Poradosu, Nuvectis' Executive Vice President, Chief Scientific and Business Officer. Before we begin, I'd like to remind everyone that on this call, we'll be making forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements within the meaning of the federal securities laws are subject to substantial risks and uncertainties. During this call, all statements other than statements of historical fact are considered forward-looking statements and are based on our interpretations of past events, as well as current expectations, estimates, and projections about future events, including expectations for the timing and data for the NXP900 phase 1b study. These and other risks and uncertainties are subject to market and other conditions and described more fully in the section titled Risk Factors in our Form 10-Q for the quarter ended September 30th, 2025, and our other public filings with the Securities and Exchange Commission. However, these risks are not exhaustive, and new risks and uncertainties emerge from time to time, and it is not possible for us to predict all risks and uncertainties that could have an impact on the forward-looking statements made on this call or other filings with the SEC. It is now my pleasure to turn the call over to Ron Bentsur, Chairman and Chief Executive Officer of Nuvectis Pharma. Ron? Thank you, Tara, and good morning, everyone. We appreciate you joining our call today. We believe that NXP900 provides a unique opportunity to address unmet medical needs across large oncology indications where new treatments are urgently needed. The target addressable population for NXP900, as a single agent and in combination in non-small cell lung cancer alone, is estimated to be approximately 45,000 patients. This is one of the largest opportunities within non-small cell lung cancer development today. This morning, we're here to discuss the ongoing NXP900 phase 1b program in advanced solid tumors, including the combination arm with osimertinib in non-small cell lung cancer, which will start soon. To go through the agenda, we are joined by Professor Asier Unciti-Broceta from the University of Edinburgh and Dr. Alexander Spira. Dr. Unciti-Broceta is a highly respected medicinal chemist and drug developer. He received his PhD in medicinal chemistry from the University of Granada and completed his postdoctoral training in cell delivery and chemical biology at the University of Edinburgh. Dr. Asier Unciti-Broceta established the Innovative Therapeutics Lab at the University of Edinburgh, and he's the director of the Edinburgh Cancer Discovery Unit. He is the discoverer of NXP900. Dr. Spira is Chief Scientific Officer for Next Oncology, the largest private oncology practice in the U.S. Dr. Spira also serves as Chair of the U.S. Oncology Research Executive Committee. He's an experienced clinical oncologist and scientist specializing in thoracic cancer and phase I development. As an accomplished principal investigator, Dr. Spira participated in important studies in the development of EGFR inhibitors for non-small cell lung cancer. We have invited Professor Asier Unciti-Broceta, as I mentioned, to review the mechanism of action and preclinical data to date. We believe that these data provide a compelling strategic rationale to evaluate NXP900 as a monotherapy and in combination with other EGFR and ALK inhibitors for the treatment of non-small cell lung cancer and other solid tumors. After Dr. Unciti-Broceta will speak, he will hand over the baton to Dr. Alexander Spira, who will discuss the clinical program for NXP900, including the planned combination for osimertinib in non-small cell lung cancer, and we expect to initiate the combination segment of the phase 1b program by year-end. We will then open the call up for Q&A. I will now turn the call over to Dr. Unciti-Broceta to review the mechanism of action and preclinical data to date. Dr. Unciti-Broceta, please. Thank you very much, Ron. And good morning to everybody. Brief disclosure: I am co-inventor of NXP900, and I led the medicinal chemistry and preclinical development of NXP900 until the University of Edinburgh licensed it to Nuvectis Pharma. The race for the development of Src inhibitors is a fascinating story because it cannot be told apart from the history of cancer research itself. After the discovery that the Rous sarcoma virus was inducing cancers in chickens in the first half of the 20th century, in 1970, the gene responsible for the chicken sarcoma was isolated, called viral Src, the very first oncogene discovered. In 1976, it was found that the genome of the chicken had a longer version of that viral oncogene, which was called c-Src, the very first proto-oncogene discovered. This discovery changed the field forever. Most cancers are not transmitted by viruses, but by mutations happening in our cells. The enemy is inside us. In 1980, the human version of the gene was identified, and its protein characterized. The human Src protein was the first tyrosine kinase discovered, launching the search for more cancer targets and for targeted therapies in cancer. One of these discoveries led to the discovery of YES1, which is a family member of Src and is involved also in cancer. It's a proto-oncogene, very important proto-oncogene. In 2006, the first inhibitor that inhibits Src and the protein Abl, the saracatinib, was approved for the treatment of chronic myeloid leukemia. It was approved because it inhibits the protein Abl; the BCR-ABL is the oncogene driving chronic myeloid leukemia. In 2012, the Src-Abl inhibitor bosutinib was approved also for chronic myeloid leukemia. Decades of research have validated the role of Src and Yes and all many family members in cancer survival, proliferation, and angiogenesis metastasis in many different cancers. Src is a master regulator of extracellular and cell-to-cell communications, and because of that, it's used by multiple oncogenic pathways and proteins, including receptor tyrosine kinases like EGFR, to drive survival, proliferation, and migration. Yes is also very important; it's very important in many different cancers, including lung cancer, as it affects one of the key tumor suppressor pathways, the Hippo pathway. However, despite all this evidence, many much, much evidence of the role of Yes, Src, and many family members of Src in cancer progression, metastasis, and resistance to therapies, still there is no current clinical Src-Abl inhibitors approved for the treatment of Src or Yes-driven cancers, which is a paradox. Why is that? The unique mode of inhibition of NXP900 has the explanation. What we have here is the sequence of how Src is activated. On the left, you see the closed conformation of the protein Src. An oncogenic signal is going to activate the protein, open it, and this open conformation is going to be able to form complexes with other substrates or protein complexes that are going to be phosphorylated by the protein Src. That is, as a consequence, what is going to drive survival, proliferation, and migration. All Src inhibitors, including bosutinib, saracatinib, dasatinib, that have been tested in the clinic, all of them inhibit in the active conformation of the protein when the protein is forming a complex with a substrate. This is why we see here in the middle dasatinib inhibiting in that conformation. This has two problems. One of them is that this active conformation is very, very common in many, many different kinases, and therefore these drugs are less selective. The most important thing, in my opinion, is that it is stopping the protein in a conformation that when the drug is cleared, the protein is already in an active conformation to reactivate and lead to survivor proliferation. NXP900, the big thing about NXP900 is that it's inhibiting earlier. It's inhibiting in this native inactive conformation. One of the consequences is that the NXP900 is more selective because of that, because this conformation is the active conformation, the ATP conformation of the inactive conformation of Src is very different from other kinases. That is the reason why it's more selective. The most important thing for the mode of action of NXP900 is that it's inhibiting in an earlier conformation. When the drug is cleared, the protein is inactive and therefore requires an activation from an oncogenic signal to reactivate and lead to the reactivation of the pathway. What is the consequence of that? Really important. We have shown that preclinically. Here we have a PD study. Basically, it is the inhibition of Src in a xenograft model in mice. What we have studied is what is the Src inhibition after three hours of giving the dose and after 24 hours. Here on the left, you can see the results after three hours. If you see, dasatinib is inhibiting very well because it is inhibiting relative to the control, and NXP900 is inhibiting dose-dependent effect, which is a beautiful effect giving at 20, 40, and 80 milligrams. I have to point out here that we can give to mice NXP900 up to 200 milligrams per kilogram, while 30 milligrams per kilogram is the maximum that we can do daily to mice for dasatinib because it's very toxic. We are working with the maximum tolerated dose of dasatinib while we are not working with the maximum tolerated dose of NXP900. What you can see is after three hours, dasatinib is doing the job. It's inhibiting the phosphorylation of Src, which is the way that we measure the activity of Src. You see that basically our drug is working, NXP900 is working well. The important thing is what happened after 24 hours. We need to imagine now that after 24 hours, the drug has been cleared and the protein can, in the case of dasatinib, reactivate. You can see on your right very clearly that the mice treated with dasatinib have completely reactivated the protein activity of Src, while with NXP900, you see a prolonged inhibition effect. In fact, you can look at the 20 milligrams per kilogram dose with NXP900 that before at three hours was not as potent as dasatinib, but at 24 hours is more potent than inhibition of Src. This correlates perfectly with the mode of inhibition, which is the unique thing that NXP900 is bringing to this field. Besides this, which is preclinical information, I'm really excited to pass to Dr. Spira to hear more about the clinical development, which is the really exciting thing. Thank you very much. Great. Thank you. Thank you very much for that great scientific discussion. I'm going to talk, excuse me, I'm going to talk briefly about the status of lung cancer and why it's very important that we continue to develop novel therapeutics. I know this is old hat for some, but I think it's always worthwhile revisiting. To remind us where we are right now, we can break it down into two categories: those patients without actionable genomic alterations, which is all squamous cell, and between here it says about 37% of lung adenocarcinoma. When you think about those with KRAS or others that are not yet actionable, it's probably a little bit higher than that. How do we break it down as oncologists? If your PD-L1 score is low, it's platinum-based therapy with an immune checkpoint inhibitor. Greater than 50%, it's still hotly debated, and everybody uses something different. It's either a checkpoint inhibitor alone versus triple therapy. I won't go into why one picks another one for this conversation today, but I'll just leave it be that it still varies among physicians. Surprisingly, and I think for this population here, everybody is still well aware that the second-line therapy is still docetaxel, with a median survival of about 12 months and a PFS that's less than that, which has somehow managed to beat all the other drugs in this area, mostly at this point antibody-drug conjugates. We'll now talk about actionable genomic alterations, and I'll really focus today on those with just EGFR mutations because I think that's the big focus, which, depending on where you live, is about 17% of lung cancers. For us, it's actually higher than that. We have a very high non-smoking Asian population here outside Washington, D.C., so we actually see more EGFR mutated than wild-type at this point, which seems kind of crazy. There has been a lot of headway, and the field has gotten very complicated over the last couple of years. Suffice to say, for first-line, there are still some choices: either the FLAURA2 regimen, which is osimertinib with chemotherapy, or just osimertinib by itself. If you look at the patient population because of the toxicity that is seen either with chemo or with the MARIPOSA regimen that I will mention in a second, a lot of patients still get and will continue to get osimertinib as single-line therapy. It is either FLAURA2, which is chemo + osimertinib, or the MARIPOSA regimen, amivantamab, lazertinib. Although it's a non-chemotherapy regimen and solely a targeted regimen, one cannot underestimate or under-describe the side effects of the rash and cutaneous toxicity from that. Second-line, it does get a little bit messy. One thing to remind everybody is that only about three-quarters of our patients get to second-line because of progressive disease, and that's borne out in all the randomized studies as well. Still a bad disease, as we remind it. What we give in that situation is a little bit depending on what you get in the front-line situation as well, and I'll discuss that as well. To remind everybody, this is a very diverse and very challenging patient population with a lot of needs because obviously they're young and they want to live well and do well, but they also want to maximize quality of life because when these patients will live for a few years and you have young children, which is not uncommon in the EGFR-mutated population, it becomes very important for maximizing the quality of life despite the overall survival. We need drugs, but we need more benign drugs as well. To remind everybody, here's the FLAURA2 survival, and this is one of the regimens we now use, which has clearly shown improvements in outcomes. We still are seeing people not live as long as we like. Despite the improvements, about a 12% or so improvement in overall survival at year three, 8% at year four, we still need better drugs. To remind everybody of MARIPOSA study, this is amivantamab versus Osi. As you can see, the improvement in amivantamab was still not yet reached. It was estimated to be at least a year at the time of the final data cutoff. It's probably still going to be further information despite being called final. We estimate it to be about a year with a hazard ratio of 0.75. Great results. Again, we still need to do better. This is just to remind us that what do you do after MARIPOSA? If you look at the studies here, it's a little bit all over the map as to what people are getting. This will change a little bit with some of the antibody-drug conjugates. Two ways of looking at it: we still need to do better early on because only about three-quarters of patients get to second-line therapy, but still there's a huge unmet need post this as well. A lot of patients, a lot of young patients as well. We'll now talk, and this is a little bit all over the map. This is just one of the regimens and one of the studies looking at docetaxel versus Dato-DXd. Although a better drug in terms of progression-free survival, this is an all-comers population. Dato-DXd versus docetaxel, again, not fOsiusing on EGFR-mutated. Although we had improvement in PFS, the overall survival here was not statistically significant. Hence, despite a lot of money in the TROPION-Lung protocols, Dato-DXd was not FDA approved. However, we did see an improvement in TROPION-Lung01 in this patient population. We saw a slight improvement in efficacy here. It was a little bit of a gift by the FDA in that Dato-DXd, patritumab deruxtecan was approved, both the TROPION-Lung01 and TROPION-Lung05 as they looked at the subsets and combined them at all for approval here right now. To kind of look at where we stand and what is the opportunity, right? I mean, that's the ultimate question why we're having this phone call and webinar today. What is the opportunity? If we look at patients without actionable genomic alterations, the standard of care is docetaxel, which is still a large unmet need. Why the antibody-drug conjugates did not improve outcomes is largely unknown. I view it there's clearly a signal of activity with patients responding. I kind of view it as the drugs work, but they're still pretty toxic. ADCs, as I like to describe, and they're not going away, and something is going to get approved over time for multiple different cancers, but it's still chemotherapy on a stick. There's mucositis here. There's dose interruptions. There's a question of CNS activity. In my mind, these drugs failed not because of a lack of efficacy, but because of an overall lack of efficacy balanced with toxicity. If you look at the EGFR-mutated population, it's still an area of unmet need. Where things are going to fall out in terms of first-line is going to be very complicated depending upon the physician, their level of comfort. Amivantamab has clearly taken a share of the market, but if you talk to Janssen, it has not met what they had estimated that they thought they were going to get. Why is that? It's very complicated. They're saying it's because of subcutaneous formulation. My saying is that it's because it's still a pretty toxic regimen, having treated probably at this point, at least on clinical studies, more patients than anybody in the United States. It works, but it's pretty toxic. Osimertinib will still be given, and I think that's still going to dominate it for ease of being given, tolerability, toxicity. It's a pill. Patients can have the best quality of life on it. There will be a patient population that gets the FLAURA2 regimen. What you do in the second-line setting is still up for grabs. It's a little messy because it really depends what you get in the front line. You can get even off-label use, right? I mean, amivantamab, lazertinib is not approved. You can try giving off-label. You can try giving the MARIPOSA-2 regimen. You can try giving Dato-DXd, but there's still an area of unmet need because, again, focusing on this webinar today, NXP900 as an orally administered combination is likely to be much better tolerated than what's in there and can overcome some of the resistance patterns as well, as well as offer a regimen for those in the third and the fourth line also. I'll take a break right now and pass it back to my colleagues to talk about the clinical progress and where we stand. In terms of the phase 1a, that has been completed, as many of you know, we tested a broad range of doses, 20 all the way up to 300. We did not reach a dose-limiting toxicity. The reason we stopped is because starting at 150 and obviously higher, we were able to achieve over 90% Src inhibition in humans. Obviously, we did not feel that there was any need to go higher than 300. The starting dose for the monotherapy program is 200, which we feel gives us a fair amount of flexibility to titrate up or down as needed. Also, of course, the ability to titrate up or down is going to be very important for the combination studies, which are about to start. In terms of the programs or the arms that are being conducted in the phase 1b, we actually have five monotherapy arms, two of them in lung, adenocarcinoma and squamous. We have renal, mesothelioma, and then kind of a basket group that's going to catch hopefully a lot of patients that fall under these different mutations that you see listed there. It is a very ambitious, very broad program and started about two or three months ago. The combinations that we're going to have, the first one out of the gate will be the EGFR combination with Tagrisso with osimertinib. That will start by year-end, and the second one will be ALK where we want to combine with lorlatinib. Of course, we'll be looking for patients who are starting to progress on these respective medications. Obviously, the goal would be to try to reverse that resistance in these patients. Just a few takeaways that I think are very important, a couple of take-home points before we turn it over to Q&A. First of all, I want to thank Dr. Spira and Dr. Unciti-Broceta for joining us on this call. Thank you very much. I think the information that you provided is invaluable. With respect to the program, I think the key takeaway points are that NXP900 provides truly a unique opportunity. We're talking about large unmet medical needs where we know the treatments are urgently needed. This is, in terms of the size of the opportunity and the ability potentially to transcend different disease states, I think is quite unique. We also know that, generally speaking, in the targeted therapy precision oncology space, we've seen multiple times that companies that basically have compelling phase 1b data can generate significant interest from the investment community as well as obviously the pharmaceutical community. What's very encouraging from the phase 1a, the dose escalation, is that the drug appears to be well tolerated. Again, the Src inhibition that we've seen is rather unprecedented. As I mentioned, greater than 90% starting at 150 milligrams per day. The drug-drug interaction study that we did in healthy volunteers is also very important because it rules out all these different concerns that are mentioned in the package inserts for lorlatinib in particular, but also for osimertinib. It is very nice to be able to kind of clear the table from that. The phase 1b program is underway. Again, looking specifically at these genetic alterations that were mentioned, the YES1 overexpression, YAP, FAT1, and all those. We are going to be very meticulous about the patients that are going to be coming in. Obviously, that is key to being able to enrich the patient population appropriately in these studies. We also have a lot of high hopes for the combination program, which is set to begin. Dr. Spira gave you an overview of what is going on in non-small cell lung cancer, where osimertinib obviously plays a critical role in the EGFR component. Obviously, when patients start to progress on osimertinib, that is when troubles begin, and that is when there is a lot of uncertainty. That is where we hope that NXP900 can play an important role. In general, we are talking about, with NXP900, an opportunity that we believe could be truly transformational for Nuvectis. We are very happy to be in this position to be able to potentially unlock the true value of the drug and obviously to provide benefit to the patients. That is obviously the key goal for every study that any of us do in this industry. Hopefully, we will be able to deliver that to patients and caregivers. With that, I will stop and hand it over to Tara for the Q&A session. Thank you very much. Great. Thank you so much, Ron. As mentioned, we will be conducting a question-and-answer session with our speakers. Please hold for a brief moment while we pull for questions. Our first question comes from Jonathan Aschoff at Roth. Please go ahead, Jonathan. Thank you very much. I was kind of wondering, what are the potential advantages of an oral combination in EGFR resistance versus all the other options, which I believe are IV? I mean, as far as I know, this is the only oral regimen of which I'm aware. Dr. Spira, if you can answer that question, please. Yeah. This is the only oral regimen that I know that's currently advancing into clinical studies. I think most of the other energy has been spent on antibody-drug conjugates, which is really where I think the field has gone right now. Obviously, those are interesting drugs. There's a couple of different approaches there. Some of them are, most of them now, looking at EGFR-MET ADCs, kind of super amivantamabs, although there's other mechanisms of action as well. Obviously, we know that patritumab deruxtecan didn't work, but I think this is the only clear one I think that's making its headway as an oral option. There was one other question, and I may have missed it, so I think I got the second part first. Oh, no, no, that pretty much does that one. I was curious. If you look back at the poster from several weeks ago, there's four cases of grade 3 hypoxia. I was kind of wondering, what doses was that hypoxia at? Do you think it's dose-related? Do you care about it at all? Is it not something that concerns you? Yeah. I can answer that. It was in several doses, and we're not concerned by it. All those were deemed to be not drug-related. The study was done over the winter. It was a nasty flu season. Obviously, these are fragile patients. We ran into some of those cases, but they were all not drug-related. For example, the patient that ended up passing away from that was off drug for two to three weeks, actually, before passing away. We know for sure that that's not drug-related. We saw it, but I'm pleased to say that it's not drug-related. Okay. Lastly, what are some key patient restriction criteria that you're talking about that you'll be implementing most likely in the near future? Maybe what does that mean for the market size using those criteria? Yeah. In terms of, obviously, you want certain ECOG scores and things like that. You want patients with kind of a natural expected life expectancy with a threshold to go into the study. All those are kind of typical things when you run these types of studies. I don't think there's anything unusual in the inclusion-exclusion criteria. Obviously, in the monotherapy, we're looking for all these different mutations. We can do the math of what that size is up to be. On the EGFR side and also on the lorlatinib side, we're not looking for any specific mutations for patient entry. I think that opens up a pretty wide gamut in terms of the patients that can come into those combination studies. Yeah, it sounds like it does. Thank you very much, guys. Thank you. Thanks for the questions, Jonathan. Our next question comes from Christopher Liu at Lucid Capital Markets. Please go ahead. Hey, guys. Thanks for the question. Maybe one for Dr. Spira. Just following on the topic of safety profiles, you mentioned some of the assets being used today might not have as much market penetration because of their safety profile. Could you just elaborate on what kind of toxicities we're seeing? In addition, just curious, what's the tox profile of some of the ALK inhibitors and EGFR inhibitors just so we can get a sense of how NXP900 could potentially avoid overlapping toxicities? Sure. There are two parts here. The first part, are you talking about ones in trial or the approved ones or both? Both. Okay. Just Google me, number one. I've given a whole bunch of online stuff about the merits of amivantamab versus chemotherapy in the frontline setting. The biggest toxicity of amivantamab is cutaneous and rash. While they're great drugs, the toxicity cannot be underdescribed. There are some patients that do fine, but the majority have some. It's largely limited by skin rash and cutaneous toxicity and hair stuff, which you can say is benign and it's not a big deal, but it's a huge deal. I mean, these patients have clear effects and quality of life and largely describes why the market penetration has been less than I think that Janssen anticipated. If you ask any doctors that have given it, there's also the infusion-related reactions, which are being mitigated by subcutaneous formulation, but it's still a real deal. I'll just give you one example that if you go to some institutions, including the Dana-Farber Cancer Institute, which has multiple branches throughout the entire state of Massachusetts and beyond, they only allow amivantamab to be given at its mothership because of the risk of infusion-related reactions. I think that's an overkill. They're not trusting their doctors. Just to give you a sense, it has some clear logistical issues on multiple fronts. When you combine it with chemo, it's chemo. Some argue that chemo is actually better tolerated than amivantamab, despite the fact that it's chemo, with the traditional fatigue and tiredness and nausea and blood count effects. Where the field has largely moved in terms of drug development are twofold. One is novel TKIs, which are largely limited because they're going to be limited to only patients that have new mutations, which is relatively small. I'm on many of those clinical studies. Again, you can AI or Google me and figure which ones those are out. Those are going to be largely limited to certain patient populations where the field has really moved into the antibody-drug conjugate world. As I like to say, another day, another antibody-drug conjugate, if you follow that at all. It's another antibody, another linker, and another warhead. While those drugs clearly do work, they are limited by their toxicity. I describe it as chemo on a stick. You're balancing both, can you give those drugs for a duration, number one, and what's the toxicity and what's the discontinuation rate because patients have clear toxicity there. There's that balance where a drug like NXP900 doesn't have because it's just a completely different MOA. The major side effects of the EGFR inhibitors are actually skin toxicity and rash. Osimertinib is an incredibly well-tolerated drug. It should be easy to combine, but its mild cutaneous toxicity, rare interstitial lung disease side effects, but it is one of the most well-tolerated drugs. If you look at the ALK inhibitors, either completely benign, some mild nausea, hypercholesterolemia are the biggest ones that you can see. Overall, there should be no overlapping toxicities and should be able to combine. Thank you very much. Thanks for the questions, Christopher. Our next question comes from Yale Jen at Laidlaw. Please go ahead, Yale. Good morning, and thanks for taking the questions. I've got two here. The first one is for Dr. Spira. You mentioned earlier that the Amy + Laza has been used in the second line, although it's not approved. Just curious, what was the efficacy and the safety of that study being done? Maybe offer a benchmark for NXP900, and then I have a follow-up. Thank you. I think the benchmark response rates, and you have to remember it's a little bit all over the map, but I think you were talking about 20% or so. I think that's from, I forget which, 20%-25%, and I forget which butterfly study it was. It was not MARIPOSA, but that's kind of where we are. The toxicity is the same as the frontline setting. It's rash. It's all skin rash. In that study, because it was second and third line, there was a little bit less side effects because patients were not on as long in the second line in advanced setting. The first line setting, they're on for a lot longer. In the second line and third line setting, where the data exists for that, they were not on for that long a period. You will see less side effects because they just didn't have the time to be on there. It's just one of the statistical, we have to look at the statistics of that study. It is not approved. If you look at the data, the only approval is with chemo and amivantamab. Amivantamab was not approved in the second line setting. Some people are using it off-label, but I've tried it a couple of times, and it's been very challenging because insurance companies have not reimbursed it. Okay. Great. Maybe one question for Ron. Mostly, we are talking about the combo study at this moment. Just curious, what's the longer-term development for the monotherapy? I know you have the first study done, but what should we anticipate over the next 12 months- 24 months in terms of monotherapy? Thanks. Yeah. Thanks, Yale. In terms of the monotherapy, that component started a few months ago. The data should start reading out probably in the second quarter of 2026. Obviously, whenever there will be some critical, maybe two arms, we will report it, whether it is at a medical conference if the timelines align or through a press release or one of these different forms of news dissemination. I think starting in the second quarter throughout 2026, there will be multiple data readouts. Also from the combination, by the way, as that starts accumulating patients. I think certainly the second year should be very exciting with multiple data readouts. We have these seven arms. I do not know which one is going to win the race, which one is going to recruit faster. I have no idea at the moment. We also have the basket arm, which catches everyone else that carries the mutations. We really try to cast a wide net here, but without overextending and doing stuff that we think is very reasonable and very rational, without trying to find the cure for death for the entire world because we know that's not feasible. I think that the approach that we're applying here makes a lot of sense. The goal is to have lots of opportunities up in the air, and hopefully, several of them will hit. Then we'll figure out what to do in terms of next steps vis-à-vis discussions with the FDA. Hopefully, that makes sense. Thank you. Great. Thanks a lot. Congrats on taking off. The program is taking off soon with combo. Great. Thanks for the questions, Yale. Our next question comes from Naz Rahman at Maxim. Please go ahead, Naz. Hi everyone. Thanks for taking my questions. My question is for Dr. Spira. Based on everything you've seen thus far, what do you think of as the ideal patient population or ideal patient characteristic for 900? Also, do you think it may make sense to evaluate it in first-line patients or, I guess, wait for first-line failure prior to initiation? Sure. An ideal patient population, which there's still tons of, as you heard my discussion, would be those that just get amivantamab. I'm sorry, that just get osimertinib for the frontline setting, right? Not heavily pretreated, very early on, that would be ideal. The reality is you'll probably get some of those. You'll get some beyond that as well. Even though there's data on FLAURA2 and amivantamab, most patients were treated with single agent, and we still have a ton of those before patients migrate over. That's number one. There will be some second or third-line setting. Yes, I think obviously a frontline setting is a way for the team to go. I will not tell them how to, on this phone call, how to spend their money and to design a frontline study. The challenge with that is that's only really doable in a randomized study. I mean, you have to remember the duration of response from first-line Osi is incredibly high. Doing a study right now is not going to give you adequate information because those patients will respond. How are you going to know if you have a better drug? You have to look in the refractory population and then take it to a frontline situation, which is obviously a very big, very large study, but it should be done over time. There have been some debates right now, and I'll just get a little bit of a high horse here as to, as we design new frontline options, which obviously there's going to be frontline things coming down the pike, Osi data, pick one right now, what is your control arm? Because there are three valid control arms. I think right now we all feel comfortable, and I think the FDA will likely buy in that osimertinib as a single agent is still a valid frontline control arm because people are using that right now because of the toxicity concerns, and people will still continue to use that as well, especially XUS. Thank you. That was very insightful. Thanks for the questions, Naz. Our next question comes from Joseph Pantginis at H.C. Wainwright & Co. Please go ahead, Joseph. Thank you, everybody. Two questions, please. First, obviously, there is a lot of great historical perspective given with regard to Src inhibitors and what have you. I guess there is going to be a lot of hypervigilance with regard to going into establishing the safety profile for 900. Obviously, you have some great data so far. What do you feel the clinical community will be hypervigilant for with regard to AEs or not, and how they may look to handle them? The second question that I have is, as the lung cancer program moves. Joe, you're cut off a little bit. We heard the first question, did not hear the second one. Oh, sorry. The second question was, what do you feel the minimum clinical benefit might need to be seen for physicians to get excited in the combo arms going forward? Yeah. Dr. Spira, if you can answer the first question. The first question is regarding the toxicity. I think the class effects of toxicity have been nausea, some GI side effects. It's been pretty well tolerated so far. I think those are the things that'll get people concerned about, especially as you think about combination profiles as well. To me, those are the things that are limiting. We should not be seeing significant cytopenias, skin toxicity that have plagued, I think, some of the other effects, some of the other drugs as well, or in the case of datopotamab, some of the mucositis that's been seen as well. I'll let you guys comment on other things that you've seen early on as well. Your second question. The clinical threshold that would make physicians pleased. Yeah. Thank you. I think in any clinical study, I mean, this is, I think, no matter what you're doing, a 20%-30% response rate is a good benchmark of seeing some efficacy right now. I think if you ask that of anybody in a very heavily pretreated population, that's kind of what we like to see. If it's a little bit less than that, looking at prolonged stable disease is never a bad thing. I think a benchmark around 20% or so is always a good number in a large patient population. I always question, when you see two out of 10 patients respond and everybody gets excited, is that really enough? You'd want to see it in a sufficient number of patients. Thank you. Thanks, Joe. Great. Thanks for the questions, Joe. Ron, I believe we had a few questions you may want to address, so I'll turn it back to you. Yeah. I just need to find the question. Bear with me for one second. I'll read out the question. Every targeted therapy in non-small cell lung cancer eventually fails because persister cells reactivate Src family-driven bypass signaling. If NXP900 can fully shut down this network, including YES1, FAK, YAP, TAZ, etc., do you see a path forward eliminating that persister cell reservoir and moving the field toward true functional solid tumor cures for a subset of patients? Asier, maybe you want to take an initial crack, and then we'll hand it over to Dr. Spira. Yes, that is a very good question. The persister cells are difficult to handle. That is very clear. Of course, if they are depending on Src family kinases, our NXP900 is going to do the job. I wonder also what we have seen before in other preclinical studies. We have been seeing that in some preclinical studies with breast cancer, and recently it has been published with glioblastoma multiforme in a preclinical study, that there is a clear effect on the immune system. The immune system somehow helps to kill those persister cells. This has been seen only preclinical. That is, of course, what has happened so far. I think this is a very interesting aspect that we do not know yet, this proimmune effect of NXP900, which can be very relevant for those persister cells that are there and then regrow. Hopefully, NXP900 could handle that, either just directly inhibiting the Src family kinases or having this extra effect that we do not know yet how it is happening. There are some clues about that, and there are some important papers that are going to come up on that, but we do not know yet the answer to that, how the immune system is helping. Yeah. From my standpoint, that was really well said, and I have little to add on top of that. I do think, just being a little humble here, cure is a gold standard. We would love to get there. While there is some mechanism of action, I think we would all be using the word cure for this patient population, I think would be a little bit of overstatement and unlikely. Of course, one never says never. Long-term disease-free survival would be great. Lots of different ways to do it. I know we can imagine historically, based on multiple mechanisms of resistance and the way things are, and just practical reality is cure is still unlikely. We need to get there, but just want to set everybody's expectations here. Great. Ron, I'm going to jump back in here. We have a follow-up from Aydin at Ladenburg. Please go ahead, Aydin. Yeah. Good morning, everyone. Thanks for taking questions. We talked a little bit about the frontline setting, but I wanted to ask a little bit deeper regarding that. We have Src inhibition and linked to osimertinib resistance. Do you think you can design sort of a trial in the frontline setting when you would avoid testing patients for too long? What do you think of a potential trial design in frontline setting that would not be as long and as large in order to show the benefit of NXP900 in the frontline setting? Want me to take a crack at that? Yeah, please. Sure. I think the reality is there's two ways of looking at it. One is a little bit of proof of concept. Two is what's the reality of what the bean counters and the FDA is going to like. I think you're not going to be able to shortcut this. I mean, at the end of the day, frontline is one thing. It's PFS, but it's really overall survival, but it's progression-free survival. There's really no way to shortcut that for the long term, despite everybody's interest. Without being critical of the FDA, that's actually a very fair assessment right now. I mean, you need to show improvements over the standard of care there. If you wanted to get some hints of activity, there's a few different ways of looking at that. Circulating tumor DNA has always been a great surrogate. Can you drop the circulating tumor DNA higher? I'm sorry, look to a lower number. Can you clear circulating tumor DNA faster? Can you take patients? One very intriguing trial that's been done at Memorial by my friend and colleague, Helena Yu, is taking those patients who don't clear their circulating tumor DNA after six weeks or so, and then you add on a second drug at that point to see if you can clear them. There are lots of different surrogates you can do, and I think that would be very interesting to do to get some hints of activity. At the end of the day, if the team decides to go to a frontline scenario, there is not going to be a long-term shortcut there. Right. Understood. If you want to think of potential pivotal trial design in any of the sub-indications, what do you think is, if you have to design a potential success scenario for NXP900, what do you think will be the breakthrough as a single agent, as a combination? Just to make our lives a little bit easier as analysts to understand, what is the potential path to success for NXP900? At first line, success is activity and PFS in the second-line situation, which is an area of unmet need. Whether or not, obviously, there's even paths for accelerated approval because you have a biomarker-driven study where there's very limited. How that's designed and what the comparison arm is a little bit up to debate. Most likely, it'll be a second or third-line scenario. An ideal would be a second-line versus chemo-Ami or third-line, just a single-agent response rates if you have an area of unmet need, which there still is an area of unmet need there in this EGFR-driven biomarker population. That's how I kind of think about it. Whether or not it's single-agent or a combination, I think it's going to bear upon solely the toxicity. Can you be giving these two drugs together? Single-agent is obviously a very easy path. There's been a lot of data to suggest that leaving patients on Osi in whatever you're giving them on does improve outcomes, probably due to CNS progression. Obviously, the data will need to bear out in terms of right now, I don't anticipate any toxicity tolerability issues in combination. Obviously, the data needs to bear that out. We need to see where that goes, number one. To me, that's kind of a more ideal approach as we think about it. That's borne out in everything except the MARIPOSA-2 regimen, where if you gave chemo, amivantamab, lazertinib, and docetaxel, the toxicity was too high, probably because of the combination and increased deaths due to AEs due to venothrombotic events. To me, that's how I kind of think about it. Okay. Thanks so much for taking questions. Great. Thanks for the follow-up questions, Aydin. I'll now turn it back over to Ron for some closing remarks. Thank you, Tara. I want to thank everyone for joining the call this morning, and in particular, to our two doctors on the call, Dr. Unciti-Broceta and Dr. Spira. Thank you very much for joining. We thank you for your continued support of the company. Obviously, we're very much looking forward to providing you updates as the NXP900 phase 1b program progresses over time. This is a very exciting program with tremendous potential, and we're all kind of chomping at the bit to get this thing moving. I think 2026 will be a very eventful year for the compound and for the program. With that, we'll close out all the remarks. Again, thank you all very much. I'll hand it back over to Tara. Thank you. Great. Thanks, Ron. Yes, this concludes today's presentation. We thank you once again for your participation, and you may now disconnect.