Good morning, everyone, and thank you for joining us for today's Inhibrx Presents phase II Randomized Data for INBRX-106 in First Line HNSCC." As a reminder, today's conference is being recorded, and all lines are in a muted or listen-only mode to prevent any background noise. Later, you will have the opportunity to ask questions during our question and answer session. To get us started with opening remarks, I'm pleased to turn the floor over to Co-Founder and CEO, Mr. Mark Lappe. Good morning, sir. Good morning, everyone. I'm Mark Lappe, CEO and Co-Founder of Inhibrx. Throughout today's presentation, I'll be referencing a set of slides. These are accessible directly through the webcast window or available under the investor relations tab of our website. Before proceeding, I would like to remind you that during our call today, we will be making forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These statements and other risks associated with our business can be found in our filings made with the SEC. These statements are based on our current beliefs and expectations, and we assume no obligation to update or revise these forward-looking statements as circumstances change, except as required by law. With those disclosures noted, let's get started. Today, I'm very excited to share what we believe is the most important clinical update we've had on INBRX-106. We started this program with a very specific thesis. OX40 is an extraordinarily compelling target, but previous molecules were not able to activate it effectively enough in patients. We designed INBRX-106 to solve that problem, and today we believe the clinical data show that we have. What we're going to share is what we believe to be the first clear clinical validation of OX40 co-stimulation with an exceptional opportunity emerging in HPV-positive head and neck cancer and a much broader opportunity beyond it. Let me start with the key takeaways on slide three. First, we believe we've clinically validated OX40 as a therapeutic mechanism. INBRX-106 is the first OX40 agonist to demonstrate clear clinical activity as T-cell co-stimulatory therapy. In the randomized HexAgon head and neck study, INBRX-106 plus pembrolizumab achieved a confirmed objective response rate of 48.3%, compared with 26.5% for pembro alone, a 21.8 percentage point improvement. We also see deeper responses, including four complete responses that we did not see with pembro alone and a meaningful improvement in six-month progression-free survival at 72.4% versus 42.8%. Second, the HPV-positive data are exceptional. We see an 80% confirmed objective response rate versus 33% and a 30% complete response rate versus zero, 90% progression-free survival at six months versus 33%, and the median progression-free survival that has not yet been reached versus 4.6 months. We are expanding the phase II study, which we believe can support a potential accelerated regulatory path and a potential launch by the end of 2028 to early 2029. Third, we believe the HPV-positive data are the first clinical expression of a much broader biological opportunity for INBRX-106. The biology points us toward expansion in highly immunogenic tumors, and our ongoing perioperative lung cancer study is an important clinical test of that broader thesis. Lastly, combining with individualized cancer vaccines could ultimately become one of the largest opportunities for INBRX-106. This is supported by our HPV-positive data demonstrating INBRX-106 is driven by antigenic recognition, not PD-L1 expression, and more than 20 years of academic research demonstrating that OX40 agonism can enhance vaccine-driven immune responses. As you think about INBRX-106, we see HPV-positive head and neck cancer as the fastest path to market, but we believe it is only the beginning of the opportunity. Before we dive deeper into the clinical data, I want to spend a minute on the biology of INBRX-106 found on slide four because it explains both what we are seeing today and where we believe we are headed. The simplest way to think about this is effective T-cell activation requires both recognition of the tumor and a strong co-stimulatory signal. The first step is what we call signal 1. The T-cell recognizes an antigen being presented by the tumor or an antigen-presenting cell. But antigen recognition alone is not enough. The T-cell also needs a second signal, co-stimulation, to drive a strong, sustained immune response. That is where OX40 comes in. OX40 co-stimulation is designed to amplify the T-cells that already recognize the tumor, increasing their proliferation, improving their survival, and promoting the formation of immune memory. At the same time, PD-1 signaling suppresses that response, so the combination is very intuitive. Pembro releases the brake and INBRX-106 steps on the accelerator. A number of major pharmaceutical companies have invested heavily in the OX40 target in the past, but all of those attempts were conventional bivalent antibodies. However, OX40 is a receptor that depends on higher order clustering to generate a strong co-stimulatory signal. A bivalent antibody can engage the receptor, but it does not effectively bring enough OX40 molecules together to produce the level of signaling required for robust T-cell activation. In other words, the field may have had the right target, but the wrong molecular architecture. INBRX-106 is a hexavalent OX40 agonist, meaning it can engage multiple OX40 receptors simultaneously and drive the higher order clustering that we believe is required for potent co-stimulatory signaling. That distinction is fundamental to the INBRX-106 story. On the right side of slide five, you can see the higher order clustering generated by INBRX-106 compared with the lower order clustering produced by a conventional bivalent format on the left. That matters particularly in T-cell populations where OX40 expression may be relatively low, including CD8+ T-cells, which are central to direct tumor cell killing. The HexAgon head and neck study was designed to test whether the biology we just discussed actually translates into meaningful clinical activity. On slide six, we present the trial design. In the phase II portion, patients with first-line recurrent or metastatic head and neck cancer were randomized one to one between the combination arm and pembro alone. A head-to-head study gives us a very clean way to answer: what is the contribution of benefit from INBRX-106? What does INBRX-106 actually do, add? The primary endpoint is objective response rate with duration of response, six-month progression-free survival, and safety among the key secondary measures. This study was also built from the beginning as a seamless phase II/III program, so we can move directly into the confirmatory portion without having to stop and start a completely new trial. Before we get into the efficacy results, I wanted to quickly discuss the baseline characteristics on slide seven. We had 33 patients randomized to INBRX-106 plus pembro and 35 to pembro alone. The key point here is the two randomized treatment arms were well-balanced across the major disease characteristics, including HPV status, disease status, ECOG performance status, and PD-L1 expression. Next, let's move on to safety found on slide eight. Given that INBRX-106 is designed to actively costimulate the immune system, we would expect to see some incremental immune-related toxicity when we add it to pembro. The most common treatment-related adverse events with the combination were rash, fatigue, and diarrhea, and importantly, these events were predominantly grade 1 or grade 2. There were no grade 5 adverse events in the INBRX-106 plus pembro arm. There was no increase in pembro-induced pneumonitis and no meaningful increase in CRS. We do see a higher rate of treatment discontinuation with the combination, and these events were varied, with no single adverse event accounting for the difference. Importantly, after patients came off treatment, most either maintained their tumor response or remained stable. In some cases, we continue to see tumor reduction even after dosing had stopped. This also includes a few patients whose first response was documented after discontinuation. It's also important to mention that we did not see the same pattern in the patients that discontinued pembro. Overall, we believe the combination has demonstrated a generally manageable and well-tolerated safety profile, supporting continued development of INBRX-106 in combination with pembro. Slide nine gives us direct biological validation in patients that INBRX-106 is doing exactly what it was designed to do. When we add INBRX-106 to pembro, we see up to a 15-fold increase in T- cell proliferation and up to a four-fold increase in T- cell activation compared with pembro alone. The magnitude of that separation is striking. Remember what we discussed earlier. Pembro releases the brake on the immune response, INBRX-106 is designed to step on the accelerator. This is the clinical evidence that the accelerator is working. INBRX-106 is not simply adding another antibody to pembro, it's materially changing the biology of the T- cell response. Importantly, we see this in both CD4+ and CD8+ T cells. CD8 T cells are particularly important because they are the effector cells responsible for directly recognizing and killing tumor cells. So before we even look at tumor response, we have direct pharmacodynamic evidence in patients that INBRX-106 is producing the costimulatory biology that we engineered the molecule to deliver. The next question is whether that substantial increase in T cell activity translates into better outcome for patients, and that is exactly what we see on the next slide. On slide 10, we see that the biological activity translates directly into clinical benefit. The primary endpoint of the phase II study was confirmed objective response, or cORR. INBRX-106 plus pembro achieved a cORR of 48.3% compared to 26.5% for pembro alone. A 21.8% point improvement. So we are seeing substantially more patients respond when INBRX-106 is added to pembro. Importantly, it's not just the number of responses that is different. When you look at the waterfall plot, you can see greater depth of tumor reduction in the combination arm. We observed four complete responses in the INBRX-106 plus pembro arm compared to none with pembro alone. That degree of depth is particularly encouraging, and it begins to connect all the pieces we've shown you so far. We engineered INBRX-106 to generate stronger OX40 signaling. We showed you direct evidence that it dramatically increases T cell proliferation and activation in patients. Now in a randomized study, we see that translate into substantial improvement in confirmed response rate and deeper tumor responses. The next question, of course, is whether those responses are durable, which we will look at on slide 11. This is where the data become even more compelling. At six months, 72.4% of patients receiving INBRX-106 plus pembro were progression-free, compared to 42.8% on pembro alone. This is a substantial separation between the two treatment arms. We are also seeing a meaningful difference in median progression-free survival. Median PFS is currently 9.6 months and still maturing with INBRX-106 plus pembro, compared to 4.9 months with pembro alone. We are seeing more responses, we are seeing deeper responses, and now we are seeing those responses translate into longer disease control. That consistency across response rate, depth of response, and progression-free survival gives us increasing confidence that INBRX-106 is adding meaningful clinical benefit to pembro. When we start to look at the data by HPV status, the magnitude of the benefit becomes even more interesting. Before we get to the HPV-positive population, I want to spend a moment on what we're seeing in the HPV-negative patients found on slide 12. The key observation here is durability. At six months, 63% of the patients receiving INBRX-106 plus pembro were progression-free, compared to 46.8% with pembro alone. Median progression-free survival is seven and half months in the combination arm and still maturing, versus 5.1 months progression-free survival with pembro alone. The swimmer plots are particularly informative. When you look across the individual patients, you can see more patients in the combination arm are continuing on study with ongoing progression-free responses. Based on the pattern we are seeing in these swimmer plots, we expect the difference in durability and progression-free survival between the two arms to become more evident as these data continue to mature. Even in HPV-negative disease, a low immunogenicity tumor, we are seeing an encouraging durability signal that supports activity for INBRX-106 across the broader head and neck cancer population. Now on slide 13, we come to the HPV-positive population, a high immunogenicity tumor where the magnitude of benefit becomes truly remarkable. INBRX-106 plus pembro achieved a confirmed objective response rate of 80%, compared with 33.3% for pembro alone. A 46.7 percentage points differential. Eight out of 10 patients responded to the combination. Importantly, we're not just seeing more response, we are seeing very deep responses. Three of the 10 patients treated with INBRX-106 plus pembro achieved a complete response, compared to none in the pembro arm. When you look at the waterfall plot, the depth and consistency of tumor reduction in the combination arm are striking. On slide 14, we see that depth of response we just showed you is being accompanied by very strong durability. At six months, 90% of the HPV-positive patients receiving INBRX-106 plus pembro were progression-free, compared with 33% on pembro alone. Median progression-free survival has not yet been reached with the combination, compared with 4.6 months for pembro. When you look at the swimmer plots, the difference is visually very clear. Almost all patients in the combination arm remain ongoing and progression-free, while those in the pembro arm show substantially earlier progression. Now in HPV-positive disease, we are seeing the full picture. The consistency across response rate, depth of response, and durability is what gives us a strong conviction in the HPV-positive opportunity. The next question is why the effect appears to be so pronounced in HPV-positive disease. When we look at the biology of HPV and the mechanism of OX40 illustrated on slide 15, we believe there's a compelling explanation. The effect is driven by greater antigen recognition. HPV-driven tumors consistently express the viral E6 and E7 antigens. These are foreign antigens, exactly the type of strong, persistent immune signal that can generate antigen-experienced T cells. Those T cells have already recognized the tumor. INBRX-106 is designed to provide the second signal, OX40 co-stimulation, that amplifies their proliferation, survival, and memory. The enhanced activity we are seeing in HPV-positive disease is exactly the type of setting where we would expect OX40 co-stimulation to have its greatest effect. That gives us greater conviction in both the HPV-positive development strategy and the broader biological thesis for INBRX-106. There are also two important strategic implications. First, we believe this gives us an opportunity to establish a leadership position in HPV-positive head and neck cancer, particularly because the emerging EGFR bispecific class appears to have its greatest activity predominantly in HPV-negative disease. Second, the magnitude and consistency of the efficacy signal create the potential for a faster path to market. The 80% response rate, the complete responses, and the durability we just showed you provide a compelling basis to pursue an accelerated regulatory strategy. HPV-positive disease brings together a compelling clinical activity, a mechanism that explains the activity, and a highly differentiated development and commercial opportunity, and that is why we're moving quickly to expand the HPV-positive program. We plan to amend the HexAgon study to add approximately 50 additional HPV-positive PD-L1 CPS equal to or greater than one patients to the phase II portion of the study, and this is illustrated on slide 16. These patients will be randomized one to one between INBRX-106 plus pembro versus pembro alone. Based on the magnitude of the preliminary signal, we believe this expansion opens the door to an accelerated regulatory path. That includes the opportunity to pursue breakthrough therapy designation and to engage regulators around the use of objective response rate as an accelerating approval strategy supported by the durability data we are generating. Importantly, there's a regulatory precedent in head and neck for accelerated approval strategies using objective response rate, including a development path for the EGFR bispecifics. Because the confirmatory phase III is already built into our seamless design, we can pursue an accelerated path with a potential clear route to full approval. The commercial significance of that potential accelerated path is substantial, which is outlined on slide 17. HPV-positive head and neck cancer is a large and rapidly growing market. We estimate the U.S. HPV-positive population is growing at approximately 2.6% annually and expect it to reach roughly 30,000 patients in 2029. That timing aligns closely with our targeted launch window of the end of 2028 to early 2029. The numbers on this slide are intended to represent the potential market opportunity around launch. Our initial opportunity is in recurrent and metastatic disease. With the 2029 population, we estimate approximately 6,000 are first-line recurrent or metastatic patients. That population alone represents a $1 billion annual U.S. sales commercial opportunity. Recurrent and metastatic disease is only the starting point. If we move into earlier stage HPV-positive disease, the opportunity becomes substantially larger. Additionally, we estimate approximately 16,000 stage 1 through 3 nonsurgical patients and 8,000 stage 1 through 3 surgical patients. Taken together, that expands the estimated U.S. HPV-positive opportunity to more than $4 billion. There are several qualitative factors that make this market particularly attractive. Current therapy can carry substantial morbidity, particularly from surgery and radiation, and clinicians are actively looking for opportunities to deescalate treatment in HPV-positive patients. There is also significant unmet need for a therapy developed for the HPV-positive population, since, as I noted earlier, the emerging EGFR bispecific class appears to have its greatest activity predominantly in HPV-negative disease. We believe the magnitude of the clinical benefit we are seeing, combined with a relatively concentrated patient population, also creates an opportunity for premium pricing. Given the depth and durability of responses observed to date, we expect meaningful duration of therapy. The key takeaway is simple. We believe the recurrent metastatic disease gives us approximately $1 billion near-term beachhead, with expansion into earlier stage disease taking us to the overall U.S. opportunity to more than $4 billion. On slide 18, we widen the lens because we believe the opportunity for 106 extends substantially beyond HPV-positive head and neck cancer. The common biological thread across the opportunities on this slide is ongoing antigen-driven T cell co-stimulation, exactly the setting where we believe OX40 co-stimulation can have the greatest impact. The first category is highly immunogenic tumors. That includes large indications such as non-small cell lung cancer, melanoma, renal cell carcinoma, triple-negative breast cancer, and bladder cancer. These are tumors with substantial pre-existing immune engagement, making them very logical settings in which to test whether INBRX-106 can amplify an existing anti-tumor immune response. This category also includes tumors with high neoantigen burden, including MSI-high, mismatch repair disease, as well as TMB-high tumors. We believe our ongoing perioperative lung study is intended to provide a relatively fast clinical proof point for this category. We also have work underway in perioperative triple-negative breast cancer that can contribute to the broader immunogenic tumor thesis. The second category is virally antigen-driven cancer. Here, HPV-positive head and neck is our first clinical example, but the opportunity extends into HPV-driven cancers outside of head and neck and other virally linked malignancies. This is a distinct expansion path driven by the same principle we just discussed in HPV-positive head and neck cancer. Persistent foreign antigens creating antigen-experienced T cells that we believe are particularly responsive to OX40 co-stimulation. There is a third category, individualized neoantigen cancer vaccines. That opportunity is particularly exciting because a vaccine can deliberately generate tumor-specific antigen-experienced T cells, precisely the population of T cells that INBRX-106 is designed to co-stimulate and amplify. This has the potential to take a lower immunogenicity tumor like HPV-negative in head and neck and create an outcome like we are seeing in HPV-positive head and neck. The way we think about INBRX-106 is not as a drug tied to one tumor type. We believe HPV-positive disease is our first major clinical validation of a broader biological principle. If we validate that principle across these additional settings, the opportunity for INBRX-106 could expand dramatically. The next step is to test whether the biology we've demonstrated in head and neck cancer translates into another highly immunogenic tumor. Our perioperative non-small cell lung cancer program is designed to give us that proof point and importantly, to give it to us relatively quickly. In this setting, which we discuss on slide 19, we can measure pathologic complete response at the time of surgery in months, rather than waiting years for a survival endpoint. Pathologic complete response is an important clinical readout because it's strongly correlated with improved survival in perioperative lung cancer. For context, in KEYNOTE-671, pembro plus chemotherapy produced an 18% pathologic complete response rate, leaving substantial room for improvement. That creates a clear benchmark and a relatively fast opportunity to determine whether adding INBRX-106 can materially increase the rate of pathologic complete response. The study is enrolling approximately 40 patients with stage 2 and 3-B non-small cell lung cancer. The primary endpoints are pathologic complete response and safety, and we expect the study to read out by mid-2027. We believe we will see a strong pathologic complete response signal, which could provide important clinical validation for expanding INBRX-106 into other highly immunogenic tumors. The next opportunity takes the biology one step further, which we discuss on slide 20. So far, we focused on tumors where strong antigen-driven immunity already exists naturally. Individualized neoantigen cancer vaccines create an opportunity by deliberately priming tumor-specific immunity. We believe that creates a particularly compelling combination opportunity for INBRX-106 and potentially one of the largest long-term opportunities for the program. What makes the vaccine combination so compelling is how naturally the two mechanisms fit together. Cancer vaccines are designed to provide tumor-specific antigens and prime T cells that recognize them, signal one. INBRX-106 provides signal two, OX40 co-stimulation designed to expand and sustain those antigen-experienced T cells. HPV-positive data give us a clinical example of this biology. Persistent foreign viral antigen is continuously presented to the immune system, and we are seeing exceptionally strong activity when OX40 co-stimulation is added. An individualized neoantigen vaccine is designed to recreate that same fundamental condition, tumor-specific antigen-experienced T cells that INBRX-106 can amplify. This rationale is supported by more than 20 years of scientific literature showing that OX40 agonism can enhance vaccine-driven immune responses. What makes this opportunity particularly timely is that individualized neoantigen cancer vaccines are now demonstrating meaningful clinical validation. We discuss this in more detail on slide 21. The Moderna and Merck V940 program has shown that a personalized neoantigen cancer vaccine combined with pembro can improve outcomes in melanoma, and the market response has been remarkable. More than $25 billion of market value was created in a single day following the recent V940 update, underscoring the level of investor interest in this emerging class. INBRX-106 has independently demonstrated powerful T-cell amplification in patients, including up to a 15-fold increase in CD8 T-cell proliferation, and the strength of our HPV-positive clinical data provides additional support for OX40 co-stimulation in an antigen-rich setting. That creates a very compelling fit. The vaccine primes a tumor-specific T-cell response, and INBRX-106 is designed to expand and sustain it. We believe bringing these two powerful complementary mechanisms together could be transformative and create a new paradigm in cancer immunotherapy. That is why we view individualized cancer vaccine as a major strategic expansion opportunity for INBRX-106. Going to slide 22. Let me close with what we believe we have demonstrated with INBRX-106. First, we believe we have clinically validated OX40 as a therapeutic mechanism. INBRX-106 is the first clinically active OX40 agonist in T-cell co-stimulatory therapy, with randomized data showing substantially greater T-cell activity and improved clinical outcomes when added to pembro. Second, HPV-positive head and neck cancer gives us an exceptionally compelling path to market. The strength and consistency of the data have given us the confidence to expand the study by approximately 50 additional patients and pursue an accelerated regulatory strategy targeting a potential launch by the end of 2028 to early 2029. We believe HPV-positive head and neck cancer is the beginning of the opportunity, not the boundary of it. The same biology points us towards large, highly immunogenic tumor settings with our perioperative lung cancer study providing the next important clinical proof point. Beyond that, individualized neoantigen cancer vaccines could open an entirely new dimension of the program. Our HPV-positive clinical data driven by greater antigen recognition, the pharmacodynamic evidence in patients, and more than 20 years of OX40 vaccine biology provide a compelling mechanistic foundation for that opportunity. All of this combined is why we believe INBRX-106 is positioned to become a major oncology cornerstone therapy, starting with a potential accelerated path to market in HPV-positive head and neck cancer, with expansion opportunities across immunogenic tumors and into emerging cancer vaccine paradigm. We believe we have finally unlocked OX40, and we are very excited about how large this potential opportunity can become. I would like to extend my deepest gratitude to the patients and investigators whose participation has made this study possible and to those who will join us in our upcoming trials. I am happy to take questions now. Mr. Lappe, thank you. To our phone audience joining today, if you would like to ask a question, simply press star and one on your telephone keypad. That is star and one, ladies and gentlemen. We will hear first today from Dara Azar at Stifel. Let me get this question out of the way so I can get to questions that we are getting from investors. Did Inhibrx cut down to its strong population to report data from that population? Dara, I am not sure. Can you repeat the question again? Sure. Did Inhibrx report data from its strong HPV-positive population, or are you seeing effect in other populations as well? So yeah. It's really clear. We see nice data in HPV-negative, which is a low immunogenicity tumor, which is great to see. I think there, our PFS, our duration is showing better than KEYTRUDA, and it's still improving. So I think it's very likely that even from a PFS point of view, we go over eight months in HPV-negative, and it very well may turn out that the OS is as strong or stronger than what you see with the EGFR bispecifics. Because I think, again, with a drug like this, the strength is going to be OS. The more duration that this data gets, I think the stronger it will look. I think HPV-positive, it's super clear why HPV-positive is so strong. It's a high immunogenic tumor. It has much more antigen activity than a low immunogenicity tumor. Those antigens are creating that T cell response, a stronger type 1 signal, and OX40 agonism amplifies that to a much greater degree. Again, it gives us very good confidence that as we go into higher immunogenic tumors, we're going to see really great activity. I think the other part of it really shows is when you go into with cancer vaccines, you have the potential to go into lower immunogenicity tumors and really produce the results that you would see in a high immunogenicity tumor. Okay, that makes sense. Had to get that question out of the way. Could you help us understand now what you're seeing in your new data that points you to lung cancer and separately to cancer vaccine combinations specifically? Sure. We've already done some exploratory data in later line non-small cell lung, and we've seen nice activity there. Again, when we go up into the perioperative setting, now we're going to catch these patients where their immune system is fully intact. Lung is a high immunogenicity tumor, so we would expect to see a much better complete pathological response rate than what you see with KEYTRUDA by itself. I think we already have a hint too, because as we mentioned on last call, we're also running an investigator-sponsored study in triple-negative breast cancer. In triple-negative breast cancer, immunotherapy has never shown a complete pathological response in the perioperative setting. KEYTRUDA has no single-agent activity. As we touched on our last call, at that point we had treated three patients, and two of those patients had complete pathological response with the INBRX-106 plus pembro combination. Interesting too, in those patients, it mechanistically all correlated. The two patients that had complete pathological response had dramatic change in their T cell populations from baseline and also in their T cell activation from baseline. The patient who did not respond had no change in T cell populations from baseline, no change in activation. You could just tell obviously, that patient had no antigen-driven T cell response. They had no type 1 signal. Okay. What evidence is there for us to be reassured that going from CPS 20 plus to CPS 1 plus in head and neck with OX40 would not dilute the efficacy? Yeah. I think it is really clear from our data that mechanism here is driven by antigenic response. It is not driven by PD-L1 expression level. Because we had very similar PD-L1 expression levels in HPV-negative. The difference is there is just much more antigenic activity in HPV-positive because it is a high immunogenic tumor, and the response data that we see does not correlate with the CPS score. Okay. Last from us, how much internal work have you done ahead of going public with the idea of combining OX40 with cancer vaccines? More directly, how reactive is this to Moderna and Merck's recent headline with [audio distortion]? Thank you. No, it's a great question. We've been working on this for some time, and we've had discussions going on even before the Moderna and Merck data came out a few weeks ago. I think this is something clinically that we want to get started in the first half of next year. I think we really felt this is very compelling. We felt that before the Merck/Moderna results came out. I think this is going to be an area where you're going to see really exceptional synergy. I think you're going to see that to really make a cancer vaccine really effective, you need that OX40 co-stimulation. We see what that can look like from the HPV-positive data because it's a very similar antigen tumor activity that you see in HPV-positive disease that you see with a patient in their tumor that's been treated with a cancer vaccine. Thank you. We'll take our next question today. I'm sorry, did you have anything further, Mr. Azar? No, I was going to say thanks. Hey, thanks, Dara. Excellent. Thank you, sir. We'll move forward to Oliver McCammon at LifeSci Capital. Hi. Congrats on the data today, and thanks for taking my questions. One for me here, and then a follow-up as well. I know we delved into it a little bit, but can you explain some of the mechanistic rationale behind the efficacy profile we're seeing in HPV-positive versus negative patients here? More broadly, how do you think about the immunogenicity of HPV-positive head and neck tumors as compared to lung and additional indications of interest you've identified? Is there a way to potentially quantify this? Thank you. Sure. I think, as we discussed, slide 14 really walks through why that depth of response is as strong and the durability as strong as it is. I'm sorry, I think it's slide 15, I meant. It's basically the biology of HPV and the mechanism of OX40 really coming together, because the HPV-driven tumors consistently express that viral E6 and E7 antigens. The foreign antigens create that strong, persistent immune signal that can generate antigen-experienced cells. I think that what we really see between the HPV-negative, which is a low immunogenicity tumor, and HPV-positive, which is a high immunogenicity tumor, is it's that antigen level, which makes it high immunogenic, which drives additional type 1 signal, and OX40 co-stimulation is very effective in amplifying that. Got it. Just one follow-up. Can you remind us on the relative maturity of the HPV-negative PFS data we are seeing? Then how you would expect those top-line numbers to potentially change over time? Then on discontinuations, obviously during the call hearing that we are not seeing any particular factors driving that rate, but just curious how discontinued patients have performed durability-wise and anything else to say on the granular safety events. Sure. Just to take the first part of your question, this study is still maturing, and I think with this mechanism, it is only going to continue to look better with duration. I would expect overall in the study, I think it is very likely that we go over 10 months on PFS. I think it is very likely, and you can see it from the swimmers, even in HPV-negative, that we will go over eight months. It very well could turn out as it matures in HPV-positive that the PFS could end up being 14, 15 months or greater. I am really excited as we get into next year to see how the OS data plays out too, because I think that is going to be the strongest part of the story. Then, Oliver, if you can just refresh me on your second question. Oh, I agree. It is on discontinuation patients? Exactly. Yeah. It is really interesting. So one of the mechanistic pieces when you are co-stimulating OX40 is you impart immune memory. I think you can clearly see that in the discontinuation patients. Because what we are seeing on the patients that came off is they are either continuing their responses or maintaining. Some of the patients then are still going deeper, and we have had a couple patients that responded post-discontinuation. I think basically what that is telling you is that the immune memory piece is being imparted. That is very likely going to give us extremely strong OS. Because when you look at the discontinuations that are in the KEYTRUDA arm, all of those patients progressed upon discontinuation. Very helpful. Thanks for taking my questions. Ladies and gentlemen, this does conclude today's Inhibrx phase II Randomized Data for INBRX-106 and First Line conference call. We thank you all for your participation. You may now disconnect your lines. We hope that you enjoy the rest of your day.