I'm a technology analyst at Cantor. Thank you all for coming out to day two of our conference. We're delighted to host our next presenting company, BridgeBio Oncology Therapeutics, or BBOT. This is a momentous occasion, as this is the very first time, I believe, that BBOT has presented at an investor forum as a public company. We're delighted to have with us today the company's CEO, Eli Wallace. Eli is going to give a quick overview using some slides because this is an inaugural presentation. We've also got Uneek Mehra, who is the recently appointed company's Chief Financial Officer. Idan Elmelech is the company's Senior Vice President of Strategy. Uneek, Idan, and Eli will all be joining me for a fireside chat after the slide presentation. Thank you, Eric. Yeah, it's a real honor to be here. As Eric mentioned, our first investor conference as a public company. I'm going to give you a little introduction to BBOT. I'll skip that. A brief history of who we are. You know, we're not really a new company in a way. We've been around since the end of 2019. This is when I left Peloton Therapeutics, which was acquired by Merck, to join BridgeBio and lead the affiliate focused on oncology within the BridgeBio spoke and hub model. That was the very end of 2019. We started our internal research programs in 2020. It's important to note all of the programs you're going to hear about today were discovered in-house through our own research team. That is kind of an abbreviated little timeline there from 2020 - 2024. A lot of research, of course, goes into discovering these novel assets. What we then did in May of 2024 is we separated from BridgeBio as we were progressing all of our assets towards the clinic, and BridgeBio was focused on its late-stage portfolio. We agreed that the best way for each to progress from there was to be an independent private company. We were fortunate enough at that time to raise $200 million in private capital, and BBOT was formed and born as a private company. Very soon thereafter, as you can see, in very rapid succession, we moved three programs into phase I clinical studies. The first is BBO-8520. That was first dosed in May of 2024, followed closely thereafter in October with BBO-10203, our RAS PI3K alpha breaker. In March of this year, we dosed our third program, BBO-11818, our pan-KRAS on/off inhibitor. Between dosing of the second and the third program, we announced our plans to combine with Helix II, Cormorant SPAC, and at the same time, we announced a closing of a $261 million PIPE. Just last month, on August 12th, we initiated trading on NASDAQ as we closed our business combination with Helix 2. We were very fortunate to have, I think, a very successful transaction there. Between the PIPE and the D-SPAC, we had gross proceeds of $380 million and a relatively low final redemption rate of only 39%, which is like the second lowest redemption rate for a biotech D-SPAC in probably the last five years. What we're focused on is the RAS pathway. We focus on both KRAS and PI3K alpha, the two most mutated oncogenes in human cancer. We have a pipeline of three assets moving into the clinic that we believe will have important inflection points over the next 6 - 18 months. We have a very proven research engine. That is, my background is research. We continue to work on additional programs in-house. Our mechanisms and our inhibitors are designed to provide patients with these mutated oncogenes optimal target coverage. These are patients both with KRAS and PI3K alpha-driven tumors. Importantly, we believe we have a unique opportunity to combine our assets within our portfolio to give patients with KRAS mutant disease even greater benefit. On the finance side, I just mentioned we did a PIPE and a D-SPAC. Together with that, we have funds to get us into 2028. I'll just be very brief. I'm sure this audience knows very well the space. Of course, there have been advances on both RAS and PI3K alpha recently. We think there's a lot of room for improvement. The approved inhibitors for KRAS are in the G12C space. We think these off-only inhibitors leave room to be improved both from efficacy and a safety perspective. In the PI3K alpha space, there are kinase inhibitors approved, but these inhibitors have been plagued with side effects that really limit their efficacy. We really think that is driven a lot by the effects they have on hyperglycemia. Our approach to hopefully fully unlock the potential of targeting these important oncogenes is to optimize for target coverage. We do this on the KRAS space by inhibiting the on-state, and we do that by directly binding to the protein. We're able to inhibit KRAS G12C on and off by binding directly with very high affinity. We're also able to do that in a pan-KRAS approach by binding directly. We inhibit the PI3K pathway in a very novel approach. You can think of this as a pan-RAS inhibitor of PI3K alpha, where we only inhibit the signaling where it's driven by RAS. That is a very unique approach that gives you a therapeutic index that derives from the biology of where RAS activates the target. As I mentioned, we are uniquely positioned to combine these approaches to inhibit both the MAPK pathway and the PI3K alpha pathway in human tumors, we think, for the first time in a really safe manner. Here's a snapshot of our programs. BBO-8520 is our KRAS G12C on/off inhibitor. It is the first direct inhibitor of KRAS G12C in the on-state. It binds in the same pocket as sotorasib and adagrasib. It just does so in a manner that is designed with very high affinity that allows it to also inhibit in the on-state. That differentiates it from almost everybody else in this space. We have programs in phase I dose escalation monotherapy, as well as in combination with pembrolizumab. Here we're focused on KRAS G12C lung cancer, where KRAS G12C makes up about 15% of non-small cell lung cancer patients. The second program, which entered the clinic last fall, is BBO-10203. This is our RAS PI3K alpha breaker. This is a very novel approach to inhibit the second most mutated oncogene in human cancer. It's a protein-protein interaction inhibitor. It's important to note it is not a kinase inhibitor. It binds to the RAS binding domain of PI3K alpha and blocks the ability of RAS to activate the pathway. We believe this is differentiated in two very important ways. One is the therapeutic index is driven by the biology. RAS activation of PI3K alpha is very important in tumor settings, but does not play an important role in normal adult physiology. RAS activation of PI3K alpha does not play a role in glucose homeostasis. The therapeutic index here is driven by the biology. We don't believe we will have any risk of hyperglycemia. Our phase I study for this program has no restriction on HbA1c status. The second differentiating point is we can drive this therapeutic index, both the safety and the efficacy, in a manner that's agnostic to the mutational status of either RAS or PI3K alpha. That's important when you think about addressable patient population. If you are an inhibitor of mutant PI3K alpha, let's say a kinase mutant, you will not really be able to address KRAS mutant population because 90% of KRAS mutants are wild type for PI3K alpha. Our mechanism will work where RAS is mutant or wild type or PI3K alpha is mutant or wild type. That program is in phase I monotherapy dose escalation. You can see the tumor types we're looking at there. Two types of breast cancer: HER2 amplified breast cancer, hormone receptor positive breast cancer, and then KRAS mutants. The third program, which entered the clinic at the very end of March, is BBO-11818. This is our PAN-KRAS on/off inhibitor. Again, a direct inhibitor, very potent for KRAS G12D and KRAS G12V. It binds directly in the Switch-II Pocket. That's in phase I dose escalation, focused really on KRAS G12X tumors of lung, pancreas, and colon cancer. Very briefly, then, I just want to dig in just a little deeper on the therapeutic opportunities here. Let's just focus on 203 there, those tumors in red. This is where we think we're uniquely positioned to inhibit both the MAPK pathway and the PI3K pathway, driving to high levels of target inhibition in a safe manner. This is not a novel concept. This is something that myself has tried over 25 years ago. At the time, the tools we had didn't allow this to happen to really translate in a safe manner. It's because we had inhibitors that couldn't distinguish between normal tissue and tumors. We tried MEK inhibitors, PI3K inhibitors, and the tolerability even in mice was suboptimal. Of course, in patients, it was not a tolerable combination. We believe now with our RAS PI3K alpha breaker, 203, we can do this in a safe manner. We're going to inhibit the left side of the pathway only where it's derived from RAS. That really only is driving in tumors. Then we inhibit the MAPK pathway with our mutant selective RAS inhibitors. We're very excited to try this combination in patients. We think if we're able to do this, it should be very beneficial for patients with KRAS mutant tumors. Here is our expected upcoming catalyst. First quarter of 2026 will be 8520, both monotherapy and combination with Pembro data. First half of 2026 will be 203 clinical data from the phase I study. The second half of 2026 will be our pan-KRAS inhibitor readouts from the phase I. Onwards will be additional data on 8520 and 203. You can see next year is a very data-rich year for us with readouts from the first quarter throughout the rest of the year. I believe large patient populations, we have opportunities across all of these with our compounds. Certainly, 8520 in KRAS G12C lung cancer. 818, you can see, obviously, in the other KRAS spaces, KRAS G12D and G12 V. 203 goes across all of these areas, whether it's in the breast cancer space in combinations with standard of care or in the KRAS space in combinations with our own inhibitors. This is the team, a very strong board of directors that supports us and a very experienced management team. Thank you. OK, thanks, Eli. Very efficient overview and presentation. We'll start with the fireside chat portion of the discussion. Maybe just to put a finer point on that last market slide, Eli, we're all aware that there are a lot of patients out there who could be served by RAS pathway inhibitors. Why this pathway and not others? From a macro standpoint, what drove you to becoming a RAS company? Secondarily, why BridgeBio Oncology Therapeutics? What do you bring special to the equation here? Yeah. I think when you think about RAS and the journey on RAS for over 40 years, it's really the holy grail for patients with cancer. We're targeting the two most mutated oncogenes in human cancer. If we can do that in a way that can drive to high levels of target inhibition, I think that's going to give the best benefit for patients. When I left Peloton Therapeutics, where we did the HIF2 antagonists, at the time, of course, very validated from biology, but really no approach to inhibit it. We took on that challenge and were able to accomplish that. When Professor McCormick and Neil Kumar reached out to me to come to BridgeBio, it really felt very similar. Here is the RAS space, but how do we target it? When we did BBO-8520, and I remember the first time I presented it, there were a lot of leaders in the field in the audience, including Professor Shokat. People didn't think we could bind to the Switch-II Pocket and inhibit the on-state. That's certainly a challenge from the research perspective from my career that we love to take that on. When you can mirror that with the opportunity to give patients the benefit that have these very important oncogenic targets, it just really made sense. For the breaker here, it's really a novel approach. PI3K alpha has obviously been a target for almost 30 years. You really challenge separating it from hyperglycemia. When Professor McCormick pitched this idea to me of breaking that interaction and then completely separating it from the side effects that plague the inhibition of the kinase function, it was the opportunity I couldn't pass up and tried to execute on that type of approach. You bring both chemical and potentially biological insights in a new fashion to this old problem. Maybe we'll get into each of the three clinical candidates. I'll do them in order that you have here on the slide, starting with BBO-8520, the KRAS G12C on/off inhibitor. Obviously, this compound is differentiated by its on properties in addition to off. What does that mean in terms of clinical profile? What can we expect to be different? Safety, efficacy, both? Yeah, when you inhibit the on-state. Certainly, first off, that's the protein that signals. The off-state has no biological consequence, so you would expect better efficacy at number one. Number two, you're going to address at least some of the resistance pathways to the first-generation off inhibitors, those at least that function to increase the on-state. That would be our receptor tyrosine kinase flux or synthesis of new protein. Both of those increase the on-state. The third one, which I think is a little underappreciated, and I'll talk about what we've observed so far in the clinic, is that when you're a covalent inhibitor of the on-state, you can get this efficacy with very low levels of covalent inhibitor. I think this is very important when you think about clinical profiles. Just give me 30 seconds on this. When you're a covalent inhibitor of a protein that signals, you can act as a hit-and-run mechanism. You get resonance time of the protein of interest, but you can clear the circulation. You don't have high levels of a covalent reactive warhead in the body. If you're an off-only inhibitor, you have to wait for cycline, so you're there at large levels. We certainly see that preclinically. Our early clinical data supports that as well, that we can get efficacy with very low levels of compound. What have we seen clinically? Through the first three cohorts, we've released early data. You can find this on our website. From a PK perspective, which we'll share when we do the more robust data set, we're getting our efficacy through the first cohorts at about 1/100 of the levels of sodoinib. What does that translate to? First, we'll start with safety. In about the first 16 patients, we have no liver tox of any grade. All the off inhibitors have significant grade 3. We have no liver tox. Through those first three cohorts, we had no grade 3 toxicities reported either. I think that's very much related to the ability to hit the on-state. From an efficacy perspective, in the early data through the first few cohorts, we had 6 of 10 confirmed partial responses. Very promising early efficacy. I think very differentiated safety profile, particularly on the very important endpoint of the liver toxicity. Great start to the phase I dose escalation, as you mentioned. What do you want to see or need to see in terms of safety or efficacy benchmarks to be convinced of the differentiation before, say, putting further resources behind the construct for the compound? Yeah, I think what that profile as monotherapy that we've started to generate really sets us up well to combine with checkpoint inhibitor. I think that's really where you need to go in the field. If we're able to combine with active doses from a monotherapy and be differentiated in liver tox, I think that's going to give the best benefit to patients. We have opened the pembrolizumab combination. We are escalating from our 200 mg and going up. I think that's the exciting opportunity. If we can combine safely or well-tolerated profile with doses of monotherapy that are active, I think if we're able to do that, that can give patients across the TPS scores really a potential benefit, particularly in earlier lines of therapy. Could you frame what exactly we might see in terms of size of cohort for both of the next two updates? Yeah, so we're enrolling patients in the U.S., Canada, and Australia, both monotherapy and combination. We're going to give that data readout in the first quarter. We'll have monotherapy efficacy as well as efficacy and safety with pembrolizumab. The exact number of patients, we'll just have to see when the readout comes out. That'll be one readout with both the combination and the monotherapy as well. Yes. Let's move on then to the breaker, which maybe by some metrics is your most innovative and exciting compound. I don't know if you feel that way about your three children here, but certainly. I have three children, and I love all of them, just as I love all three of these. Yeah, that program we're really excited about. Both our CMO and myself have many years of experience, but we've never had a program where every PI we talk to wants to be on this program. The excitement level is off the charts. Really, it's because how often do you get the opportunity to tackle the second most mutated oncogene in a completely novel approach? The selectivity here is the biology, right? We feel very good about that selectivity in the therapeutic index. As I mentioned, our phase I study has no restriction on HbA1c status. There's no other inhibitor of PI3K alpha that does that. The opportunity here to be able to do either mutations or drivers on the PI3K alpha side or on the RAS side means the addressable patient population here could be very large. We're very excited about this program. As I mentioned, we're looking at a first clinical update on data in the first half of next year. Does the ability to navigate around hyperglycemia mean that you can have better PI3K alpha inhibition as well as just a better safety profile? Are you looking for better efficacy as well? I think they always go hand in hand. Really, a thesis for us has always been to drive the high levels of inhibition. I started my career on wild type targets, which you just couldn't really achieve. I think the thesis here will be able to drive the high levels of inhibition in a safe manner. You're in a phase I dose escalation study here as well. Would we expect this candidate to work well as a monotherapy? We'll see what we see. I think traditionally, inhibitors of this pathway have needed combinations. Our strategy here is to go monotherapy as quickly as possible to get to our dose and then open up our combinations. We have three combinations that we'll start with. All these are standard of care combinations. In the HER2 amplified space, we'll combine with trastuzumab. Very interestingly, this is a very sensitive genotype for the RAS breaker, which is a novel finding that RAS is involved in HER2 signaling. We have very good activity there in preclinical models. The second combination is with fulvestrant in the hormone receptor positive. In KRAS mutant CRC, combinations with FOLFOX. Those will be our first three combinations that we'll do. Preclinically, you had some interesting findings in breast cancer. Do you want to speak to that a little bit more? Yeah, so in the breast cancer space, I think it's well established that about 30% - 40% have PI3K alpha mutations. That includes both the hormone receptor positive and the HER2 amplified setting. We do work very well there, particularly in combinations with standard of care. In the HER2 space, we work even in the absence of those mutations. In HER2 amplified space, RAS plays an important role. I think it's interesting the most mutated oncogene in human cancer, in breast cancer for many years, for maybe a long time, people hadn't thought RAS plays a role. I get 203 is a very specific selective compound. When we see activity there, we're very confident that that's the effects of RAS activation of PI3K alpha. We think that really RAS does play an important role in breast cancer. I think that's further supported that you're now starting to see in CDK4 resistant hormone receptor positive patients, you're starting to see RAS mutations pop up, as well as NF1 deletions up to about 15%. I think RAS's role in breast cancer is underappreciated. We're going to fully explore that opportunity. Remind us, are you enrolling HER2 positive patients in the phase I? We are. When might we see the first clinical data on BBO-10203? Yeah, we're projecting the first half of next year. Can you give us a sense of how many dose cohorts, numbers of patients, any combination data at that time? Certainly, we'll do the full monotherapy at that time. We should have early clinical, early combination data as well. Have you begun dosing in combination? Yeah, at that readout, we will have combination data. Have you begun dosing in combination? OK, that's great. Sounds like that program is proceeding very rapidly given the physician interest. Congrats on that. Let's move on to your third child and the pan-KRAS on/off inhibitor, BBO-11818. There are others in this space. Maybe you could just provide us a quick lay of the land and talk about what you've got that's differentiated. Yeah, it's important to note that BBO-11818 really grew out of BBO-8520. As I mentioned, when we started BBO-8520, people didn't think you could inhibit the on-state and switch to pocket. Clearly, you can. Our compound is really derived in the structure-based design program, really grew out of BBO-8520. We think we have a very good handle on how to inhibit the on-state there. We think from preclinical data, the way to drive the high levels of inhibition, again, the theme here of KRAS, is to be selective for KRAS and to spare H and N RAS. We think that will allow us to drive to higher levels of inhibition, where in the wild type setting, H and N will compensate to enable you to drive to high levels of inhibition. That is a different approach than a RAS multi approach. As compared to some other approaches, we think if you can do that safely, it will give the better commercial opportunity to hit more than one KRAS mutant in that setting. I think also bringing some wild type KRAS activity could help you in some resistance that could develop if you were a specific inhibitor of that pathway. OK, so you're a little bit more selective for KRAS versus other isoforms. You also are potentially differentiated with off activity in addition to on activity. Is that an important feature to inhibit off, or is that unlikely to be additive relative to on? Yeah, I mean, the key is the on activity. When you bind to the Switch-II Pocket, you're going to inhibit the off. That does have activity. Clearly, sotorasib and adagrasib show that. Bringing the on is really, I think, going to be the differentiator. It is very important as a KRAS inhibitor from our perspective to bring on-state activity. What type of clinical profile might you expect to see in terms of differentiation versus those KRAS multis or KRAS on-onlys? I think we'll have to see. I don't believe there's been any data out from a pan-KRAS inhibitor yet. We'll see what the profile looks like. I think we would expect it to be different than a RAS multi approach from a therapeutic index perspective. We'll just have to wait till the clinical data emerges. OK, when will we see the first data on BBO-11818? Yeah, I think it will be the second half of next year is what we're projecting. That should at least be the phase I monotherapy. Are there tumor types or benchmarks that you think are most relevant? I think for a pan-KRAS inhibitor, you're going to look at the big three, right? CRC, pancreas, and lung cancer. We'll just have to see how the data matures. That program just started at the very end of March. We'll see how the data progresses as we move into the new year. OK, let's just start with a couple of broader corporate overview questions. You do have a lot on your plate for a newly public and still somewhat younger biopharmaceutical company, three wholly owned candidates, all progressing through the clinic, and then other candidates coming behind that. Any thoughts on partnership considerations or collaborations or how to best resource some of these intriguing candidates? Thanks, Eric. I mean, as Eli mentioned, I think we love the three children we've got right now, but we'll be data-driven. With the last capital raise, now we're going as a part of the D-SPAC transaction. We believe we have sufficient cash to prosecute all three candidates to proof of concept, get the data, and then we'll be data-driven into any opportunistic partnering decisions. Remind us how much cash you have. I know that was mentioned by Eli and the cash runway exactly. Yeah, as of June 30, by the time we close the transaction, $480 million in the bank, that should take us into 2028, including all of the preregistrational programs for all three programs. Beyond what we've talked about here in terms of the research engine, is that continuing to fire on all cylinders and be resourced as well? What's next coming? Yeah, we do continue to do active research. We haven't really disclosed what we're working on. We do think we have first mover status in breaker, and we continue to invest in that. We're looking at some other interesting approaches that we haven't yet disclosed. When's the right time to talk about what's coming next? Is it IND stage, or would you do something a little sooner than that? Yeah, I think probably IND stage is probably the right time to talk about those next things. This is a very competitive space. Is this the sort of thing that you at some point are going to require help with in collaboration? Do you need a partner to conduct multiple phase IIIs? I think in the early stages right now, our decision is to go alone. As we move forward, let the data define us, and then we will make those decisions. We're just about out of time. It sounds like 2026 is going to be a really important year for you in terms of data readouts and turning cards over. We'll be paying close attention. Thanks very much, team. Thank you so much.