Thank you for standing by, and welcome to the BBOT Clinical Data Update call. Today's program is being recorded. At this time, all participants are in a listen-only mode. We ask that, due to a full queue in program today, you limit yourself to one question and one follow-up. You may get back in the queue as time allows. I'd now like to introduce your host for today's program, Heather Armstrong, Head of Investor Relations. Please go ahead. Thank you for joining us today. For today's prepared remarks, I am joined by Dr. Eli Wallace, CEO, and Dr. Ben Yang, Chief Medical and Development Officer. Also joining for the Q&A section are Dr. Pedro Beltran, Chief Scientific Officer; Uneek Mehra, CFO; and Dr. Adrian Sacher, Thoracic Oncologist and Affiliate Scientist at the Princess Margaret Cancer Center and an Associate Professor in the Departments of Medicine and Immunology at the University of Toronto. As we begin our presentation, I would ask that you review our legal disclaimer on slide two. With that, I'll turn the call over to Eli Wallace, CEO. Eli? Thank you, Heather, and thank you for everyone who has joined us today. I'll begin on slide three. We at BBOT are advancing a next generation of small molecule therapies targeting the RAS pathway, one of the most important and historically difficult areas in oncology. Our mission is to accelerate meaningful scientific and medical breakthroughs and to deliver medicines that are not only more effective but also better tolerated for patients facing the deadliest cancers. We've designed our inhibitors with the goal of optimized target coverage for patients with tumors driven by RAS and PI3K alpha, positioning us to address key resistance and durability challenges. Importantly, our portfolio is designed to be synergistic, enabling targeted KRAS combination strategies both with standard of care therapies as well as within our own pipeline. With multiple clinical stage assets, we expect several meaningful value inflection points in 2026. With our strong financial position, we are well-funded to execute on this strategy and support operations into 2028. Moving on to slide four, today's data, which Ben will walk you through shortly, underscore the strength of our precision oncology portfolio. By focusing on the active, on-state of RAS and leveraging differentiated chemistry, we are delivering on the promise of innovative RAS PI3K alpha inhibition through direct effector blockade. We believe our differentiated direct KRAS G12C on-off inhibition may position BBO-8520 as the combination agent of choice with immune checkpoint inhibitors in early line non-small cell lung cancers. Ben will provide more details on the data, but in short, BBO-8520 monotherapy in patients with KRAS G12C non-small cell lung cancer showed a 65% overall response rate, with 83% of patients with at least six-month follow-up remaining on treatment greater than six months. It also showed a favorable safety profile, particularly as it relates to liver enzyme elevations compared to what has previously been shown with off inhibitors. We believe the improved therapeutic index observed with 8520 is a direct result of the on-state hit-and-run mechanism, as we observed promising efficacy signals at substantially lower exposures than off inhibitors. As has been well documented, all off inhibitors are plagued by varying degrees of liver toxicity, including grade three, which we believe is likely due to the high exposures required for off-only inhibition. Combination therapy with pembrolizumab at a potentially optimally active dose of 8520 also showed early efficacy signals with a distinct tolerable safety profile without increased liver enzyme elevations compared with pembrolizumab alone. This contrasts with off inhibitor combinations, all of which have had to reduce their dose to suboptimal levels and nevertheless still experience significantly increased toxicities, particularly liver toxicity. Taken together, the encouraging early safety and efficacy data positions BBO-8520 as a compelling combination partner with pembrolizumab in earlier line non-small cell lung cancer patients. Additionally, we have also observed encouraging early efficacy signals in STK11 KEAP1 co-mutant tumors. This is a highly resistant patient population for which there is currently no effective therapy, and we are working to confirm this finding in additional patients. Moving on to BBO-11818, where dose escalation data demonstrate the potential of direct pan-KRAS inhibition in patients with KRAS mutant tumors, showing anti-tumor activity with a favorable and differentiated safety profile. This includes a partial response in a pretreated pancreatic ductal adenocarcinoma patient. To our knowledge, this represents the first publicly disclosed monotherapy pan-KRAS response in a patient with PDAC. BBO-11818 is a close cousin of BBO-8520 and incorporates key learnings from that molecule into a reversible pan-KRAS inhibitor. It is designed to be a highly potent, orally bioavailable inhibitor that targets both the on and off stage of KRAS. We believe this approach has the potential to deliver a superior therapeutic index relative to many existing strategies by maintaining selectivity for KRAS over HRAS and NRAS while capturing multiple KRAS mutants as well as wild type. For those who have been following the BBOT story, you may notice that we have moved 818 earlier in the sequence. This reflects our decision to group our KRAS inhibitors together, given their similarities and their large potential when combined with our breaker. We are encouraged by these findings as these data support continued dose escalation and progression into expansion cohorts. Next, clinical data support the approach we're taking on our novel RAS PI3K alpha breaker, BBO-10203, in KRAS mutant and breast cancers. We have achieved our objectives in monotherapy dose escalation, and the data align closely with our expectations and preclinical findings. Even without any restrictions on HbA1c status, we observed no hyperglycemia at dose levels that fully engage the target, and we rapidly established a recommended dose for expansion studies. It is important to note, to our knowledge, 203 is the only inhibitor of PI3K alpha activity to both treat patients without HbA1c restrictions and observe no hyperglycemia. As has been reported, other inhibitors in this space have restrictions and still observe varying degrees of hyperglycemia. The observed monotherapy safety profile of 203 to date may portend well for our planned combination approaches. As a reminder, all inhibitors of this pathway have been developed in combination. Notably, because its mechanism is agnostic to mutational status, 203 has the potential to be effective whether RAS or PI3K alpha is wild type or mutated, significantly extending the population of patients who may benefit. Moreover, combination studies with standard of care therapies in KRAS mutant colorectal and breast cancers have been initiated, and we expect to open internal combination studies with 8520 and 818 later this year. Slide five shows a high-level view of BBOT's portfolio of clinical stage RAS pathway inhibitors designed to enable direct dual inhibition of KRAS on and off states and pan-RAS inhibition of PI3K alpha activation. We believe our portfolio uniquely positions us to safely achieve concurrent high-level inhibition of PI3K alpha and MAPK through internal combinations for the first time. This strategy provides us the potential opportunity to treat a large number of patients with some of the most aggressive cancers. In fact, we estimate an annual incidence of approximately 250,000 patients in the U.S. across multiple indications. We are very pleased with these data and look forward to the next steps. I'll now turn it over to Ben to review the data in more detail. Ben. Thank you, Eli. Starting on slide seven with BBO-8520, which is designed with a differentiated mechanism of action binding directly to both the on- and off-state of KRAS G12C. By targeting the active oncogene and directly blocking effector binding, this approach may help prevent adaptive resistance mechanism. It also fully leverages the covalent mechanism of action that allows for sustained pathway inhibition even as systemic drug levels decline, creating a favorable PK/PD profile. Together, these features support the potential for favorable safety and efficacy profile in combination with pembrolizumab in patients with KRAS G12C non-small cell lung cancer. As you can see on slide eight, ONCRAS- 101 is an open-label multicenter global phase one study designed to evaluate the safety, tolerability, preliminary anti-tumor activity, and pharmacokinetics of BBO-8520 as a single agent and in combination with pembrolizumab in patients with KRAS G12C mutant non-small cell lung cancer. Patients have been enrolled across dose levels ranging from 100 to 700 milligrams once daily as monotherapy. Monotherapy and the pembrolizumab combination cohort expansions are currently enrolling. Moving on to slide nine, 8520 demonstrated robust monotherapy activity across those levels in previously treated patients with KRAS G12C non-small cell lung cancer who had not received a prior G12C inhibitor. As of November 15, an objective response rate of 65%, 11 out of 17 patients was observed across all those levels, including 10 partial responses and one complete response. We also saw a disease control rate of 100%. As you can see on slide 10, responses appear durable, with 83%, 10 out of 12 patients who were eligible for six months follow-up remaining on treatment for at least six months and a six-month progression-free survival rate of 66%. Moving on to slide 11, 8520 monotherapy has demonstrated a generally favorable safety profile with a differentiated liver safety profile compared with off-state inhibitors characterized by a low frequency and low grade of AST or ALT elevations that have been transient and asymptomatic. Gastrointestinal events were the most commonly observed AEs and were mostly grade one or two and manageable. Importantly, there have been no dose-limiting toxicities, no grade four or higher treatment-related adverse events, and no treatment-related serious adverse events to date. The most common treatment-related adverse events were nausea, vomiting, and diarrhea, with few instances of grade three diarrhea being mostly associated with suboptimal management. Slide 12 shows encouraging combination data with pembrolizumab in treatment naive non-small cell lung cancer patients, as well as in patients previously treated with G12C inhibitors, where it shows three PRs out of three patients and two PRs out of five patients, respectively. It's worth noting that all patients remain on study treatment, except for one patient who withdrew consent despite achieving a partial response. I show on slide 13, in terms of safety in combination with pembrolizumab, 8520 has demonstrated a generally favorable safety profile with largely low-grade treatment-related adverse events, mainly GI-related. In terms of AEs of interest, the only AST/ALT elevation was reported as a grade three in a patient treated at a dose of 200 milligrams of 8520 in combination with pembrolizumab and was assessed by the principal investigator as primarily related to concomitant medications, and the AST/ALT do not appear to be dose-dependent. This patient previously treated with sotorasib, olomorasib, and pembrolizumab achieved a confirmed partial response and has remained on study for more than 36 weeks, with the AST/ALT levels having resolved. As of this cutoff, about half of the patients have been on treatment for over 12 weeks. On slide 14, 8520 exposure is approximately dose proportional, achieving predicted efficacious dose levels at the 200 milligram and above. Importantly, as we can see, 8520's on-state inhibition enables efficacy at a low systemic exposure, which we believe is why we observe superior therapeutic index compared with off-state inhibitors. Relative to 8520 at 500 milligrams once daily, exposures with adagrasib and sotorasib are more than 700-fold higher. MK-1084 and D3S-001 are more than 150-fold higher, olomorasib and divarasib are more than 10-fold higher. 8520's markedly lower exposure compared with what has previously been reported with off-state inhibitors is consistent with an on-state mechanism that creates a favorable PK/PD profile. We believe these attributes of 8520 may enable its combination with pembrolizumab at active dose levels to differentiate in earlier settings of the disease, as shown on slide 50. Off-stage inhibitors have had to significantly reduce their dose to suboptimal levels when combined with pembrolizumab due to liver toxicity. Even at the suboptimal dose levels, patients experience grade 3 toxicities from 30% to 70%. In comparison, we believe 8520 is well positioned to potentially differentiate in earlier settings where safety is critical. Lastly, as shown on slide 16, early 8520 monotherapy data in patients with STK11 and/or KEAP1 mutations demonstrate encouraging efficacy signals, with all five initial patients showing a partial response, which appears favorable relative to standard of care and off-state inhibitor benchmarks. We're very pleased with these results and look forward to future updates on this program. Now moving on to BBO-11818 on slide 18. As Eli mentioned earlier, BBO-11818 is a close cousin of BBO-8520. It's an orally bioavailable reversible pan-KRAS inhibitor with activity against both the on- and off-state designed to deliver an optimal therapeutic index. BBO-11818 is mechanistically differentiated in that it targets KRAS, the active oncogene, in the majority of RAS mutant tumors and directly blocks effector binding. In addition, it's highly selective for KRAS, whereas in HRAS and NRAS. We have also seen strong monotherapy activity and promising combination potential with anti-EGFR monoclonal antibody and BBOT's RAS/PI3K alpha breaker, BBO-10203 in mouse models. As you can see on slide 19, CONCUR 101 is evaluating the safety and preliminary anti-tumor activity of BBO-11818 in subjects with locally advanced or metastatic KRAS mutant solid tumors. Monotherapy dose escalation is ongoing, and expansions and combination cohorts are planned in patients with pancreatic cancer, non-small cell lung cancer, and colorectal cancers. Slide 20 shows efficacy data to date. We are pleased with the encouraging early anti-tumor activity. Of note, one patient with pancreatic cancer previously treated demonstrated a PR. We also saw tumor reductions at the predicted efficacy dose levels across tumor types. Slide 21 shows that BBO-11818 monotherapy treatment in 13 patients appears generally tolerable and manageable with no DLTs. Treatment-related AEs were largely GI-related, including two grade three GI events of diarrhea and nausea in patients with pre-existing GI conditions. Lastly, on slide 22, BBO-11818 PK exposure was approximately dose proportional with 600 BID covering G12D and G12V mutant alleles. We are encouraged by the early anti-tumor activity and tolerability of BBO-11818 and look forward to future updates. Next, I will discuss BBO-10203 starting on slide 24. As Eli mentioned, BBO-10203 employs a novel mechanism of action designed to inhibit the physical interaction between RAS and PI3K alpha, thereby disrupting RAS-driven PI3K alpha AKT signaling without inhibiting the kinase activity of PI3K alpha. It blocks binding of KRAS, HRAS, NRAS to PI3K alpha and is agnostic to the mutational status of either partner. In preclinical studies, BBO-10203 demonstrated tumor growth inhibition in multiple mouse tumor models and excellent brain penetration in mice with Kp,uu 0.468 was observed. Notably, no hyperglycemia was observed preclinically even at three times the efficacy dose level. Consistent with the broader PI3K alpha AKT inhibitor class, the clinical development plan for BBO-10203 will focus on combination strategies. You can see the study schema on slide 25. BRINCL-101 is a multicenter open-label phase 1 study evaluating the safety, tolerability, pharmacokinetics, and the preliminary anti-tumor activity of BBO-10203 as monotherapy and in combination with trastuzumab, fulvestrant, or FOLFOX plus pembrolizumab in patients with locally advanced or metastatic HER2-positive breast cancer, HR-positive, HER2-negative breast cancer, and KRAS mutant colorectal cancers. As we have completed monotherapy dose escalation, where 24 patients, the majority of whom were heavily previously treated colorectal cancer patients, were enrolled across dose levels from 150 to 750 QD. We have selected 500 milligrams QD as the recommended dose for expansion based on safety, PK, and target engagement, which we'll cover in the next two slides. With the selection of a recommended dose for expansion, we have initiated three combination cohorts with standard of care therapies and expect to open combination cohorts with BBO-8520 and BBO-11818 later this year. As shown on slide 26,10 203 achieved predicted efficacy exposure at the 500 milligram QD dose. Importantly, rapid target engagement was also observed across all dose levels with complete engagement across all dose levels at the steady state. Slide 27 shows 23 monotherapy had a highly differentiated safety profile compared to other PI3K alpha targeting agents. There were no DLTs and no treatment-related SAEs and no hyperglycemia, even with the unneeded restriction on HbA1c levels and glucose levels at study entry. All TRAEs were grade one or two, except for one instance of asymptomatic hypokalemia lab abnormality. Notably, there were no dose reductions. Similarly, in early combination with trastuzumab and FOLFOX pembrolizumab, it appears tolerable with no grade three or higher adverse events observed. As for efficacy, clinical benefit was observed in patients with CRC of which more than 80% were third-line or beyond patients and HR-positive breast cancer who were previously heavily treated, and tumor reductions were observed in some patients. As you can see on slide 28, 203 has shown robust tumor regression in combination with standard of care therapies, and importantly, with our direct KRAS on/off inhibitors across the panel for breast cancer and KRAS mutant CRC, non-small cell lung, and pancreatic cancer models. We are pleased with this early yet encouraging data, particularly that we saw no hyperglycemia, even with the unneeded restrictions on HbA1c and baseline glucose levels. Now I will turn it over to Eli for closing remarks. Eli. Thank you, Ben. As you can see on slide 29, we have rapidly advanced our programs and achieved significant progress to date. Building on this momentum, we expect to announce updated data across all of our programs in the second half of 2026. Starting with BBO-8520, we anticipate sharing additional efficacy and safety data from its combination with pembrolizumab. For BBO-11818, we plan to report further efficacy and safety data in both the monotherapy and combination settings, and for BBO-10203, we expect to announce combination data across multiple tumor types, including HER2-positive breast cancer, hormone receptor positive HER2-negative PI3K alpha mutant breast cancer, and KRAS mutant colorectal cancer. I will conclude our prepared remarks by sharing that we are encouraged by the data across all three of our innovative and differentiated programs. These data support our portfolio-wide thesis that achieving meaningful clinical benefit requires driving high levels of target inhibition. Despite significant advances, there remains substantial room for improvement in both RAS and PI3K alpha therapeutics. We believe we are well positioned to address this opportunity. Finally, I'd like to thank the patients and their families, as well as our investigators. Without their belief in and support of our mission, none of this progress would be possible. I'll now turn the call over to the operator for the Q&A session. Thank you. To ask a question, please press star 11 on your telephone and wait for your name to be announced. To withdraw your question, please press star 11 again. Ladies and gentlemen, as a reminder, we ask that you please limit yourself to one question and one follow-up. You may get back in the queue as time allows. Please stand by for our first question. Our first question today comes from the line of Andrew Berens with Leerink Partners. Your question, please. Hi. Thanks for taking my question and congrats on all the progress. I think you guys had said, and I think we've heard the same thing from some experts, RAS experts, that with the breaker, you might see some monotherapy activity in HER2-positive patients. So just wondering what's the rationale for the greater activity in that subgroup, and were there any HER2-positive patients that were treated in this data set? Thanks. Thanks, Andy, for the question. And yeah, so for the phase one monotherapy study, we really hit our objectives of showing differentiated safety and achieving our exposure targets both from a PK perspective and then as well with target engagement. So we're very confident in the dose that we're fully targeting, inhibiting the target. As far as the HER2 patients, in the monotherapy dose escalation, there were no HER2-positive breast cancer patients enrolled. You are correct that our preclinical data does support that that is the most sensitive genotype that we've observed, and we're excited that the safety so far with trastuzumab looks very favorable. And I think where we're going to see that benefit in that patient population is in that expansion when we combine with trastuzumab. Okay. Thank you. Thank you. Our next question comes from the line of Imogen Mansfield with Cantor. Your line is now open. Thanks. Good morning, everyone, and congratulations on the data. Eli, it would be great to hear a bit more about how you expect the development path to look in first-line G12C mutant non-small cell lung cancer, and are you planning to combine with chemo and pembro? Thanks, Imogen. Yeah, so for 8520, we're very encouraged with the data we've seen. We think the very promising overall response rate, early signs of nice durability, and importantly, very differentiated safety profile, particularly, we're excited that the monotherapy safety profile translated very well in combination with pembrolizumab. Our belief in the molecule is that the profile will set us up very well for earlier line settings with patients with KRAS G12C non-small cell lung cancer. We'll have to see how the data matures going forward, but we would expect that with a very good G12C inhibitor, you should not need chemotherapy in that earlier line settings. But we'll continue to evaluate that as we generate more data into 2026. Thank you so much. Thank you. Our next question comes from the line of Matthew Biegler with Oppenheimer. You'll let us know. Hey, guys. Thanks so much for the encouraging updates here. I want to ask about 8520 and the combination data because I think other off-binders like adagrasib and sotorasib, they typically need to dose down by about a third due to LFTs and other safety issues. And it doesn't look like you're seeing that here with the 20-mg dose. Can you just talk about how that kind of supports the big thesis behind the on-off binder and the better exposures that you're getting there? Thanks. And also, if I could squeeze in a second one about TPS scores. Were you seeing activity across TPS scores, both TPS low and high? Thanks. Yeah. Thanks, Matt, for the question. Yeah. So I think this is a very important point about the power of on-off inhibition. When you are a covalent inhibitor against an active protein, you get the benefit of the hit-and-run mechanism. And that, I think, we've established preclinically, and now that has translated well into patients where you get very encouraging efficacy signals, 65% response rate at the fraction of the exposure of off-stage inhibitors. We think that's why we have this differentiated therapeutic index. And then that has played out very well in combination with pembrolizumab, where our immune-related AEs so far seem very minimal. So we think that that is really important for patients, not only to avoid those toxicities, but also that we're able to do it at a highly active dose. And as you're right, all the off-stage inhibitors have had to reduce their dose in combination with pembrolizumab. We highlighted that on slide 15 here. That response rate that I'm showing for the off-state inhibitors is at their monotherapy best dose level. So once they had to reduce, you can imagine they're combining with pembrolizumab at a much suboptimal dose level. We think that this really starts to show in the early data shown from off-state inhibitors when you look across TPS scores, particularly at TPS less than 50%, the activity of the off-state inhibitors with pembro are not better than what we're seeing as monotherapy in second-line alone. So we think there's an opportunity here to combine at a highly active dose, at the same time, see less toxicity, and potentially treat across TPS scores. It's early data, but we have activity and responses at very low TPS scores. If I may, now I'd like to help us put our data of 8520 in perspective in the landscape by asking Dr. Sacher to weigh in with his thoughts. Hi, Eli. So just to give you a sense of the landscape, I think right now our main challenges with the G12C on/off inhibitors in non-small cell lung cancer are that the autoimmune hepatitis that we encounter with these agents seems to correlate with activity. So the newer, more potent inhibitors like divarasib and olomorasib tend to cause higher rates of hepatitis and GI toxicity. And importantly, that does not bode well for future combinations. And I think my fear is that once we see these agents be evaluated in larger randomized studies where you're not conducting these studies at a small number of experienced phase one centers, you'll also see that toxicity will probably be amplified because you won't have experienced investigators micromanaging autoimmune hepatitis in these patients. So I think just the fact that we're seeing kind of best-in-class response rates with monotherapy with 8520 around kind of 65%, albeit in a small number of patients, and we're not seeing any signals of autoimmune hepatitis in monotherapy, which we clearly saw with the G12C off inhibitors, and that you're not seeing that with the combination is extremely encouraging. So you're kind of getting the best of both worlds whereby you are not encountering high rates of hepatotoxicity with the combination, but you still are maintaining that kind of best-in-class potency. With the G12C off inhibitors, you generally have to choose one or the other. You're either choosing less toxicity, but less active agents, or you're trying to combine pembro with higher potency, more toxic agents. And so I think there's great advantage here to this approach. So even though there are some older agents that are further along in development, like adagrasib, I suspect that in the end, the agents that will win out are potent ones that are non-toxic, like 8520. I would also say the fact that you're seeing responses in patients who have progressed on potent agents like olomorasib is uniquely encouraging here. I don't think most of us in the field anticipated to see that. And so that is a nice added benefit that I think also bodes well for this molecule. Thank you, Dr. Sacher. Thank you. Our next question comes from the line of Biren Amin with Piper Sandler. Your line is now open. Yeah. Hi, guys. Thanks for taking my questions, and congratulations on the data. Maybe on the breaker for BBO-10203 program, could you just maybe talk about the selection of the 500-milligram dose for dose expansion in terms of what drove that? Was it the target engagement? Was it efficacy or safety relative to the 750-milligram QD dose? And just to confirm, for the 500-milligram dose, that's also being used for the combination cohorts as well? Thank you. Thanks, Biren, for the question. Yeah, I think it's a combination of those characteristics that led to that dose selection. So we were very encouraged even at the first dose level. On day one, we saw very good target engagement. Now, we're not showing steady state at any of the dose levels of target engagement, but it's because it's a flat line. So we were very encouraged with that. We had mouse PK targets, and we achieved them in all patients at 500 and 700 milligrams QD. What you can see then, so we have a combination of full target engagement at steady state across those levels. We have achieved mouse efficacy targets at 500 milligrams QD and above, and then we don't see a difference in exposure from 700 to 500. Safety was not really differentiated between those doses, but the combination of those three led us to select 500. Combination, we are going forward at 500. That is the recommended dose for expansion, and so that is the dose that we will test in combinations with standard of care, and of course, I want to also highlight, give me an opportunity here, that we will open internal combinations with 203 with 8520 this year, and later this year, we will also open 203 with 818. Thank you. Our next question comes from the line of David Nierengarten with Wedbush. Your line is now open. Hey, thanks for taking the question. I had one on the STK11/KEAP1 mutant patients. Had any of those been treated previously with a RAS inhibitor? And if so, did they respond or not respond to those prior treatments? Thanks. Yeah. The data we're showing there, those initial five patients were all not treated with a KRAS G12C inhibitor. Okay. Thank you. And as a reminder, to ask a question at this time, please press star 11 on your touch-tone telephone. One moment, please. Once again, that's star 11 to ask a question at this time. Thank you. This does conclude the question-and-answer session of today's program. I'd like to hand the program back to Eli Wallace, CEO, for further remarks. Yeah. Thank you, everyone, for joining the call today. We are very excited about the progress we've made across our whole portfolio, hitting all of our objectives. And we really feel that we've meaningfully de-risked all of the approaches and molecules. And so we look forward, as we continue to progress our portfolio, the differentiated RAS PI3K alpha inhibitors into 2026, and look forward to giving you updates later in the year. Thank you very much. Thank you. Ladies and gentlemen, for your participation in today's conference. This does conclude the program. You may now disconnect. Good day.