Thank you for standing by. At this time, I would like to welcome everyone to Inhibrx Reports Interim phase II Data for INBRX-106 in first-line HNSCC. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question and answer session. If you would like to ask a question during this time, simply press star followed by the number one on your telephone keypad. I would now like to turn the conference over to Mark Lappe, CEO. The floor is yours. Thank you, everyone, for joining the call this morning. This is Mark Lappe, the CEO and one of the co-founders of Inhibrx. We're excited to share these compelling interim data from the randomized phase II po rtion of the HexAgon study for INBRX-106 in combination with KEYTRUDA for the treatment of first-line PD-L1-positive head and neck cancer released today. These data show the promise of INBRX-106 to become the first costimulatory agonist in the field. Before proceeding, you know, I would like to remind you that during our call today, we'll be making several 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, expectations, and we assume no obligation to update or revise these forward-looking statements as circumstances change, except as required by law. As many of you know, OX40 agonism has been a highly validated target that many pharmaceutical companies have pursued, but no one has been able to develop an effective drug targeting it. The popularity of this target stems from the significant opportunity of having costimulatory T-cell therapeutics that can raise the efficacy bar across all indications where checkpoint inhibitors are used. Earlier generation bivalent antibodies generally demonstrated limited receptor agonism and minimal clinical activity, which we believe reflected the challenges in effectively clustering and activating the OX40 receptor. Through our hexavalent design of INBRX-106, we are able to drive robust OX40 receptor activation and downstream signaling. Importantly, earlier clinical experience with INBRX-106 showed encouraging signals of antitumor activity, which we previously presented in both head and neck cancer and CPI refractory non-small cell lung cancer with preliminary evidence of immune activation. Together, these findings strengthened our confidence in the therapeutic potential of robust OX40 agonism and informed our decision to pursue the randomized study in head and neck cancer. Head and neck cancer was selected as our initial proof of concept indication as PD-1 monotherapy is active in this tumor type but leaves, you know, significant room for improvement, particularly in achieving deeper and more durable responses. Given the encouraging activity previously observed with INBRX-106 in combination in this setting, we believe head and neck cancer represented an efficient and biologically rational opportunity to evaluate whether robust OX40 agonism could meaningfully augment the efficacy of checkpoint inhibitors. This trial was modeled after KEYNOTE-048, testing INBRX-106 in combination with pembrolizumab versus pembrolizumab alone in patients with high PD-L1 expression CPS, you know, greater or equal to 20 in order to detect a treatment effect above checkpoint inhibition alone. A clear signal of added benefit in this study design would support Inhibrx's potential to enhance checkpoint inhibitor efficacy across checkpoint inhibitor sensitive indications. Today, we are presenting preliminary data from 53 patients, 25 in the INBRX-106 combination arm and 28 in the control arm with a data cutoff of May 7th of this year, representing the evaluable population for confirmed response defined as patients who had either experienced confirmed disease progression or death or completed at least two on study tumor assessments. The first tumor assessment in this study is at nine weeks, and the second is at 15 weeks. There are 15 remaining patients in the overall population across both arms that have not yet reached the maturity threshold for response confirmation or were not evaluable at the time of this data cut and were therefore not included in this analysis. Active unconfirmed responses and ongoing tumor increases and/or reductions are present in both arms, and these patients are expected to contribute to the final efficacy data set, which we will provide in a subsequent update with the progression-free survival data. Additionally, baseline prognostic factors are balanced between both arms of this study, and this study was conducted in over 80 sites across the U.S., Europe, and Asia. HPV positive status is about 30% in each arm, and the CPS scores per patient are on the depth of response slide in our corporate deck that was updated this morning. In the evaluable population, 11 out of 25 patients, 44% in the INBRX-106 combination arm achieved a confirmed objective response compared with six out of 28 patients, 21.4% in the KEYTRUDA arm. This represents a 22.6 absolute increase in confirmed responses. Three complete responses were observed in the INBRX-106 combination arm reflecting tumor clearance, while no complete responses were observed with pembrolizumab alone. Complete responses in first-line head and neck remain uncommon and are generally associated with more durable outcomes. Importantly, these clinical findings were supported by pharmacodynamic data, which showed up to a 15-fold increase in peripheral CD8 and CD4 T cell proliferation and up to a four-fold increase in activation in INBRX-106 combination treated patients compared with up to a 2.5-fold and 1.5-fold increase respectively in those receiving pembrolizumab alone. These observations of robust systemic T cell expansion and activation in combination treatment patients alongside the clinical activity observed in this arm supports the activity of INBRX-106 as a potent T cell co-stimulator. More compelling than the ORR data is the depth of response observed, which can be seen in the waterfall plot posted to our corporate investor deck earlier this morning. We know that deeper responses are what ultimately translate to more durable long-term outcomes. We believe we don't just have more responders, but better responders, with the majority of responders in the combination arm exceeding 50% in tumor shrinkage, with three patients achieving complete response so far. If I'm a patient, it's clear from the depth of response data which arm of the study, you know, I'd want to be in. The combination of INBRX-106 and pembrolizumab was generally manageable, with a safety profile consistent with immune activation in the setting of checkpoint blockade. The most common treatment-related adverse events were rash, diarrhea, fatigue, and infusion reaction, which were predominantly low grade. No treatment-related deaths were reported in either arm. Based on these promising early results, we plan to evaluate INBRX-106 across broader indications to potentially improve the efficacy of checkpoint inhibitors. This strategy includes initiating a study in perioperative non-small cell lung cancer setting later this quarter. We believe OX40 agonism has the greatest potential to drive cure in earlier stage disease settings where patients typically retain a more active and responsive immune system. We are beginning to plan for expansion into frontline metastatic non-small cell lung cancer settings, with studies expected to begin next year. Outside of the combination with checkpoint inhibitors, we plan to explore combinations with agents that could benefit from T cell co-stimulation, such as vaccines, T cell engagers and CAR-Ts. We also plan to begin the phase III portion of the HexAgon study in head and neck cancer during the third quarter of this year. I would like to, you know, 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 also want to thank the entire Inhibrx team for their relentless dedication over the last decade to drive the INBRX-106 program from inception to where we are today. I believe that this team has achieved in drug discovery and development is truly remarkable. You know, potentially the first and only recombinant alpha-1 antitrypsin that Sanofi expects approval for next year, a clinically successful DR5 agonist that we expect to receive FDA approval for its initial indication later this year, and now potentially the first OX40 agonist to demonstrate effective T cell co-stimulation. We believe we've finally overcome the challenges of effectively agonizing OX40, which could unlock the broad therapeutic potential of T cell co-stimulation for cancer patients. INBRX-106 in combination with KEYTRUDA has the potential to be the first co-stimulatory therapy to reach the market, and we are incredibly excited and hopeful about the profound impact this could have on the lives of so many patients. Thank you for taking the time to listen to this call, and we'll now open up the line for questions. Thank you. We will now begin the question and answer session. If you would like to ask a question, please press star, then the number one on your telephone keypad to raise your hand and join the queue. If you would like to withdraw your question, simply press star one again. Your first question comes from Dara Azar with Stifel. Your line is open. Hi. Congrats on this consequential randomized proof of concept update with several complete and high-quality responses. I think I should start exactly there. It looks like OX40 is dragging the entire waterfall plot towards deeper responses with just more force. We're seeing multiple complete responses, several deep partial responses. I mean, the lowest quality partial response is 53% lesion reduction, and even stable diseases are creeping towards responses. When you look at this chart, this picture, and put it next to your learnings from phase I and your knowledge of this mechanism, do you see an investable signal that deserves to be studied in large phase III studies across multiple indications? Hi, Dara. Yeah, thanks for the question. The interim data we are presenting today, you know, are highly consistent with the observations, you know, from our, you know, phase I, phase II studies. You know, across multiple indications and in more, you know, heavily pre-treated populations, you know, we've observed deep and durable tumor responses. This interim readout, you know, reinforces that pattern. I think importantly, the clinical activity is supported by clear pharmacodynamic signal. You know, we are seeing meaningful expansion and activation of T cell populations in the periphery, which is consistent with the proposed, you know, mechanism of OX40-mediated immune activation. The alignment between the biological activity and the clinical responses, you know, increases our confidence that this signal is real and potentially reproducible across indications. You know, we believe the consistency of the efficacy and translational findings, you know, supports the continued development, you know, into larger, you know, phase III programs. Makes sense. Mark, what supports your confidence in durability of these high-quality responses that patients would be able to maintain their deep PRs and CRs out to one year, two years or longer? Yeah. The data from this randomized study are still maturing, and, you know, longer follow-up will be required to fully assess, you know, durability and the translation into progression-free survival. That said, I think what gives us confidence is the quality and the depth of the responses we are already observing, along with what we saw in the phase I/II. You know, historically, immune-mediated responses that achieve deep tumor progression, particularly complete responses and deep partial responses, you know, can translate into very durable clinical benefit over time. In our, you know, prior clinical experience with INBRX-106, you know, plus pembrolizumab, the responses have generally been both deep and durable, and the emerging data from this study appear consistent, you know, with that pattern. You know, ultimately, I think, you know, durability will need to be confirmed with additional follow-up, but the totality of the clinical and translational data gives us, you know, strong confidence at this stage. Thanks. I think that makes sense. The next natural question that comes to mind is, what is the safety cost of this profound efficacy? In other words, how well would you say you know your drug? What other experiments have you conducted to get comfortable with safety? What external trial analogs would you point us to think about safety and tolerability of the doublet here? Sure. I'd say across our clinical development program, you know, more than 200 patients have been exposed to INBRX-106. I think this enables us to build a meaningful understanding of the safety profile, you know, associated with this mechanism. I think overall, the tolerability profile has been consistent with what would be expected from immune-activating therapy. The most common treatment-related adverse events have generally been manageable, with rash representing the most frequent on-target finding associated with OX40 agonism. You know, on the overall safety data, we haven't QC'd all of it yet. What's interesting is when you look at that and from a top-line number perspective, and you pull up, you know, the KEYNOTE-048, you know, safety data, from single-agent, pembrolizumab, it looks incredibly similar from a percentage level. Okay. thanks for that response. What is the rationale for going after perioperative lung cancer as the next opportunity? Could you tell us more about the level of similarity in the setting that you're targeting to Merck's KEYNOTE-671 study? Yeah. We believe the perioperative setting is particularly well suited for immune-based therapies because earlier stage disease is generally associated with more intact and functional immune system, you know, kind of lower tumor heterogeneity and potential greater opportunity to generate, you know, durable antitumor immune responses. From a development perspective, the strong, you know, clinical precedent established in, you know, perioperative non-small cell lung cancer, particularly with KEYNOTE-671, you know, helps validate both the setting and the overall therapeutic approach. Our proof of concept study was intentionally designed to closely mirror the elements of KEYNOTE-671 framework, which provides an important historical benchmark, you know, for interpreting efficacy, safety, and translational findings. Also from a, you know, proof of concept perspective, this is a faster path to further validation of clinical activity as complete pathological response is highly correlated with improved survival. This is data, you know, we could have in the not too distant future that will unlock another, you know, major expansion opportunity, you know, for INBRX-106. In KEYNOTE-671, you know, complete pathological response was only about 18%, providing you kind of ample opportunity for improvement in a setting that can be, you know, most valuable to patients, you know, which is providing the potential for cure. Just, you know, to further expand on that as well, and, you know, just to preface this, we have a study right now going in perioperative triple negative breast cancer. This study is an investigator-sponsored study, and the N right now is very small. Just keep all those things in mind. What's interesting here in perioperative triple negative breast cancer is KEYTRUDA has no single agent activity. To, you know, have the potential to reach a pathological complete response in triple negative breast cancer, you have to use a chemotherapy backbone, and when you put KEYTRUDA on top of that, it improves it by about 10%. You know, in this study so far, you know, we have dosed three women. Two women achieved complete pathological response. One had no response. What was interesting, you know, in this setting too is when we looked at T cell populations, the two women that had complete pathological response, you know, had massive change in their T cell populations. The woman that had no response, you know, basically, we didn't see any change in T cell population. I think what this likely comes down to, again, is this is a drug that amplifies type 1 signal. It's very likely that the two women that we drove to complete pathological response, you know, had preexisting, you know, type 1 signal. They had some T cell level of response to their tumor, and it's likely that the third woman, you know, just did not have a type 1 signal. It was really encouraging in the perioperative setting there to really see a complete, you know, two complete pathological responses so far where, you know, KEYTRUDA has, you know, no activity as a single agent. That's very interesting. Do you feel ready in terms of combining INBRX-106 with two different chemo regimens for squamous and non-squamous lung cancer histologies? What are you looking to learn between now and perhaps next year when you're planning to start metastatic lung phase III? Yeah. As part of our ongoing phase I/II study, we've already generated the safety and tolerability data in heavily pretreated non-small cell lung cancer patients in combination, you know, with chemotherapy regimens commonly used for both squamous and non-squamous disease. To date, the combination of INBRX-106 with pembro and chemo has generally been well-tolerated. We've not observed new or unexpected safety signals beyond what would, you know, typically be anticipated from this therapeutic backbone. From a development perspective, I think these data give us, you know, increasing confidence that the regimen can be feasibly administered across the, you know, major non-small cell lung cancer treatment settings. Okay. Lastly from me, among your non-evaluable patients, are you seeing a similar response trend and archetype in your first scan data that you may have collected so far? Yeah. The data there is in non-evaluable patients, you know, are still maturing. We're continuing to await, you know, first scan assessments for a subset of patients. We expect to be in a position, you know, to present, you know, more complete mature data set, including, you know, the longer-term endpoints such as PFS, you know, in the fourth quarter of this year. Very helpful. Thanks so much for all the responses. Your next question comes from Oliver McCammon with LifeSci Capital. Your line is open. Congrats on today's data, and thanks for taking my questions. Maybe just to start, can you contextualize for us the response rate and T cell expansion data you've shared today for INBRX-106 plus pembrolizumab relative to prior attempts at developing OX40 agonist? As well as within the broader co-stimulation landscape. Sure. I think, you know, there's limited data on prior OX40 programs because none of them really ever made it out of phase I 'cause the data was so poor. From the available public data, they've shown modest, you know, T-cell expansion generally, you know, in the 2x-5x range, you know, in selected patients, but without any meaningful clinical responses. What differentiates, I think, INBRX-106 is that we're now seeing, you know, both in a, you know, approximately, you know, 15-time T-cell fold expansion and an early, you know, increase in confirmed responses, you know, with 44% in the combo arm with, you know, with 21% for pembro alone. In addition, you know, we're seeing much deeper responses in the INBRX-106 arm. You know, in our view, that's the clearest evidence to date that crossing the agonism threshold required, you know, for clinical activity in OX40. Very helpful. It looks like you can activate the phase III portion of HexAgon quite rapidly and be dosing patients in Q3. Are you giving any guidance on enrollment timelines for that study at this point? Yeah. We would expect to have, you know, completed enrollment, you know, by 2029 at the latest. That said, we believe the phase II data, you know, is gonna generate significant enthusiasm with the clinical community and support, you know, strong recruitment momentum. We also plan to expand the number of active sites, you know, which should then further enhance, you know, enrollment efficiency and speed. Final question for me is just given the number of indications where checkpoint inhibitors are approved, as well as the synergy with INBRX-106, it's obvious that INBRX-106 would be best developed by a larger pharma. With INBRX-106 in your hands today, can you walk us through what studies you're willing to initiate and complete as you wait for potential strategic interest? Yeah, sure, Oliver. I think as reflected in our press release, you know, we're initiating the phase III portion of HexAgon, as this is part of the seamless phase II/III, where all of our sites are active and ready to begin the phase III portion. We also announced that we are immediately moving to a proof of concept in the perioperative setting in non-small cell lung cancer, which is particularly well-suited for immune-based therapies, where a patient's immune system, you know, is most responsive to immunotherapy. I think this is the fastest path to further validation of clinical activity as complete, you know, pathological responses are highly, you know, correlated with improved survival. You know, this is the data we could have rather quickly that can generate the next major inflection point for the asset. I think in addition, we are working on the path for future potential registrational studies in the front line non-small cell lung cancer setting. By, you know, covering head and neck and especially non-small cell lung cancer, you know, we're addressing over 50% of the checkpoint inhibitor market, which is about a $25 billion market opportunity. Of our focus is to maximize the therapeutic potential of INBRX-106 as aggressively as possible, and we have, I think, the investors support to accomplish this, you know, kind of irrespective of strategic interest. You're correct in inferring that, you know, this is a really attractive asset for big pharma, is there are a few opportunities that come along that can be transformative as INBRX-106. Additionally, you know, this is the only hexavalent, you know, OX40 agonist in clinical development. Very helpful. Thanks again for taking my questions. All right. Thanks. That concludes our Q&A session. I will now turn the conference back over to Mark Lappe for closing remarks. Thank you everyone, for joining the call today. It is, you know, beyond exciting to see, you know, co-stimulation, you know, really, you know, start to prove itself clinically. I'm really excited as this data matures because I think, you know, if you look at that, depth of response graph that we posted today, I mean, this is a really, you know, significant and meaningful change for patients. It's not only that, you know, the patients achieving ORRs are much deeper. Even, even when you look at the stable disease patients, you know, they look completely different. We will, you know, move this program aggressively for patients, and I'm, you know, really excited to, you know, watch it unfold and reach its full potential. This concludes today's call. Thank you for attending. You may now disconnect and have a wonderful rest of your day.