I'm Eli Wallace. I'm the CEO of BBOT, BridgeBio Oncology Therapeutics. It's a pleasure to be here with you today. I'm going to give you an overview of our pipeline. I'll start with just this slide that's a brief history of who we are. In 2019, I left Peloton Therapeutics, where I was the Chief Scientific Officer, and I moved to BridgeBio. At the time, I led the affiliate within BridgeBio that focused on oncology research. I built a team that discovered and is now developing all the assets that I'll highlight today. From 2020 to 2024, we really focused on intense research. In 2024, May of that year, we separated from BridgeBio to become an independent biotech, a private company. We raised $200 million in private capital, and we started functioning as an independent company. Very soon thereafter, we started dosing our assets. In June, we dosed our G12C inhibitor. In October, our RAS PI3Kα breaker. In February 2025, we raised a pipe of about $260 million and announced our intention to merge with Helix II, Cormorant SPAC. In March of that year, we dosed our third program, our Pan-KRAS inhibitor. In August, we closed the de-SPAC transaction. We raised over $380 million. We had only 39% redemption in that de-SPAC. A very successful fundraising for us. Between the February and August timeframe, there was not a single IPO. This was a very good transaction for us and gave us the capital to advance our programs. All of our programs are focused on RAS. We do two types of inhibitors, direct RAS inhibitors, but also we inhibit PI3Kα signaling that's dependent on RAS. We have three assets in the clinic. All will have readouts over the next 6-18 months. Basically, all three will read out next year. Our programs, and I've been in the industry for over 30 years, are really optimized to drive target inhibition. We think that's ultimately really important for patient benefit, particularly those driven by these two most prevalent oncogenes, PI3Kα and RAS. Through that fundraising I described, we have runway into 2028. We know there's been a lot of advances for therapeutics that target both RAS and PI3Kα, but we truly believe there's a lot of room for improvement in both spaces. For KRAS, the two approved inhibitors are well-known, sotorasib and adagrasib. Both are G12C inhibitors that only target the off-state. Their data, while they have accelerated approval, we believe, you know, leaves quite a bit of room for improvement. Response rates of about 30% in those phase III studies and PFS around six months. For the kinase inhibitors of PI3Kα, of course, it's well-known that they have a difficult time separating from glucose homeostasis. All of those, from our perspective, really suffer from limited therapeutic index. Our approach is to hopefully fully unlock the potential of inhibiting both RAS and PI3Kα. We do this in two ways. Our KRAS inhibitors are able to inhibit KRAS directly by binding to the known switch II pocket, but do it in a way that inhibits both the on and off-state. We think for patient benefit is ultimately you have to inhibit the on-state, the one that actually drives tumorigenesis. For PI3Kα, we inhibit it in a very novel way in which we only inhibit the signaling where it's activated by RAS. That enables us to separate the effects on glucose homeostasis from tumor genesis. Finally, we can also combine within our own portfolio these two approaches, and we think we can give even greater benefit for patients with KRAS mutant tumors. Here is an overview of our pipeline. All three programs are in phase I clinical studies. Our first program to enter the clinic is BBO -8520. This is our KRAS -G12C on-off inhibitor. It binds directly to the switch II pocket that was first described over 10 years ago by Kevan Shokat and colleagues. What we did there is we did structure-based design and used our medicinal chemistry to bind with really high affinity within the switch II pocket that enables us to bind in the presence of the trinucleotide. That is a very unique feature of our compound that distinguishes it from most everyone else in this space. The data I'll share a little bit today. We presented early data in January of this year. I'll show you some phase one monotherapy data. The compound is focused in KRAS -G12C lung cancer, looking both at monotherapy and combination with pembrolizumab. The second program, BBO -10203, is a RAS PI3Kα breaker. This is a very novel approach to inhibit signaling from the second most mutated oncogene. It distinguishes from, has two key differentiating points from everyone else in this space. First, because RAS activation of PI3Kα is very important in tumor genesis, but does not play a role in glucose homeostasis, we can inhibit this pathway to a large extent without risk of hyperglycemia. The other important point of differentiation comes to addressable patients. Our mechanism here is agnostic to the mutational status of RAS or PI3Kα. We can inhibit the signaling where PI3Kα is wild type and RAS is mutated. There are some approaches out there that are in development that bind to a cryptic pocket of PI3Kα and have some level of selectivity for some of the mutants, for example, H1047 mutants of PI3Kα. Those compounds cannot work in KRAS mutants because 90% of KRAS mutants are wild type for PI3Kα. This mechanism will address both the PI3Kα signaling if it is driven by mutants or the KRAS mutant space. The third program is BBO -11818. This is our pan-KRAS on-off inhibitor. It is selective for KRAS, so it has high selectivity over H and N. You can think of it as a close cousin of 8520. We took the learnings from 8520 and applied that to a pan-KRAS inhibitor. Very potent inhibitor that inhibits both the on and off-state. Really focused on KRAS G12D and G12 V, figuring we have G12C covered with our 8520 inhibitor. That's also in phase one clinical studies. As I mentioned briefly, we have this unique opportunity to combine our agents within our own portfolio. On the right side of the slide here are arguably the two most important oncogenic signaling pathways in human tumors, MAPK or phospho or PI3Kα AKT. We, as a field and myself personally, have tried to co-inhibit these pathways for about 25 years, but unfortunately, tolerability over the years was not acceptable. That's because the tools we had to inhibit these two pathways really did not have the specificity or the selectivity required. We first tried to do this with MEK inhibitors and non-selective PI3K inhibitors, and it was very poorly tolerated in mice and some tried to take it in the clinic, and it did not go very far. We think now we are positioned to do this optimally. It is really based both on our selective RAS inhibitors, but also on our breaker, which only inhibits the PI3Kα signal where it is driven by RAS. You can think of our breaker 203 as a pan-RAS inhibitor of PI3Kα. As I mentioned, we have three data readouts next year. They are laid out on this slide, and we also have runway into 2028. In the first quarter, we will release updated data on 8520 to include dose escalation and some combination data with pembrolizumab. In the first half, we will release data on 203, LB monotherapy, and some early combination data. Then in the second half, we'll share data on our pan-KRAS inhibitor, what we call 818. Next year will be a big year for BBOT. Okay, when we think about G12C, I think, you know, many in the audience are probably familiar with this signaling pathway. It's been well described. You know, we differ because we bind directly and are able to inhibit both the on and off-states of KRAS-G12C. We think this brings two very important points. One is the ability to prevent adaptive resistance. Unlike a lot of mechanisms, when you're only an off-inhibitor of KRAS-G12C, you can overcome that pressure just by making more protein. That can come from receptor tyrosine kinase flux, or that can come from synthesis of new protein. You don't need a genomic alteration to develop resistance to an off-inhibitor. An on-inhibitor should prevent that. The other thing, and it's very important from a medicinal chemistry drug property perspective, when you're a covalent inhibitor of the on-state, you can take advantage of the covalent mechanism. What I mean by that, you can have a disconnect between PK and PD. That means you can have resonance time on the protein and inhibit it, but you can clear circulation. That's important when you're giving a reactive species to the body, a covalent inhibitor. That should lead to a better therapeutic index, both from an efficacy and a safety perspective. That can be very important when you combine with an immune checkpoint inhibitor. Here is some of the differentiation. I won't go into all the details here, but you can see on this slide, we can modify the protein to a high degree in both the on and off-state. We are very potent by Kianct/KI, the best measure of potency for a covalent inhibitor. Importantly, shown on the graph on the right, our mechanism is different than an off-inhibitor. An off-inhibitor traps it in the off-state. An on-off inhibitor actually inhibits signaling. We block effector binding. That is shown on the right where you look at RAS activation of RAS, we can inhibit that very potently. Importantly, our structure is a normal acrylamide warhead. We published this about a year ago in Cancer Discovery. It is not an esoteric compound that is highly reactive. We optimize the compound for binding deep into the pocket with extremely high efficiency and affinity. That can then lead to very good efficacy. Here is a comparison of efficacy in a mouse model compared to sotorasib, adagrasib, and divarasib. You could argue that the efficacy here is similar. Possibly we are a little better. They were not head-to-head studies, but in each case, we get regressions. Really, the difference is that middle row there, we can do it in a fraction of the concentration. That is the power of hitting the on-state, that you can get very good efficacy with very low levels of compound, and that should lead to better safety. Our phase one study, as I mentioned, is focused on KRAS-G12C lung cancer. Here you can see our schema, dose escalating from 100 mg QD up forward, and also escalating with pembrolizumab. I think another difference from off-inhibitors, if all data that we have seen with off-inhibitors with pembrolizumab have had to reduce the dose from their monotherapy, generally because of liver toxicity, we are escalating. Here is our early clinical data that we did a data extraction last year, or actually this year in January. You can see very good response rate across doses here from 100, 200, and 300 mg QD, where we get 60% confirmed responses. We also have responses in patients that have been previously treated with off-inhibitors. Importantly, we'll release the PK data in the next data set, but what I can tell you here is that this thesis of getting efficacy with lower levels is translating into the clinic. Free concentrations of compound here through 300 mg are about 1% of sotorasib. Arguably better efficacy, early data, much, much lower levels. We think that's why that really then translates to a differentiated safety package or profile. Here you can see that through 300 mg, we had no liver tox of any grade and no grade three toxicities at all. We're very excited to escalate with pembrolizumab, see how that safety performs, and then see, obviously, with better safety and a higher dose, you should get better efficacy. Okay, let's move to the second program, BBO -10203, what we refer to as our RAS PI3Kα breaker. This is really a program that drives its specificity and selectivity from the biology. Here, the key here is a difference between the normal context and the malignant context. On the left, you can imagine that's a muscle cell or adipocyte. You can activate PI3Kα directly from growth factor signaling. That can be insulin receptor activating directly. Okay, on the right is the malignant context. Here, a RAS is involved in activation. We are really going to take advantage of the unique or the specific role of RAS driving PI3Kα in tumors as opposed to in the normal context where RAS does not play a role. I should mention we published this preclinical work in Science in June this year. You can find that publication on our website. Some earlier work actually from Francis Crick Institute right here in London showed that blocking this interaction could be efficacious in several mouse models and could avoid hyperglycemia. What they did is they made two point mutations in the RAS binding domain of PI3Kα. Those two point mutations blocked the ability of RAS to activate PI3Kα. That led to good efficacy in many settings. I am just showing you one here. This is a gem model of KRAS G12D driven lung cancer. You can see that in the RAS binding domain mutants have very good efficacy, but importantly, they did not observe any hyperglycemia. This is really one of the first examples to separate the efficacy of the pathway from the hyperglycemia that is observed with the kinase inhibitors. What we did is we designed a small molecule. This is BBO -10203 that binds specifically and selectively to the RAS binding domain of PI3Kα. It is a covalent inhibitor, and it blocks the ability of RAS to activate PI3Kα. Importantly, it can block that signaling without affecting the kinase. The kinase can function fine in the presence of our compound. If you are signaling through insulin in an adipocyte or muscle cell, that functions fine. It only inhibits where RAS is activating the pathway. The biology here is really driving the selectivity and the specificity. As I mentioned earlier, the mechanism is agnostic to the mutational status. So it can work where RAS is wild type or mutated, or where PI3Kα is wild type or mutated. I'll show you some of the data there that supports the efficacy and the safety in the next slide. You can see here in this KYSE -410 xenograft model, this is a KRAS-G12C mutant with a HER2 amplified, very good PK/PD on the left-hand side. By dosing the compound and increasing doses, you have increased exposure, and you can inhibit the signaling looking at phospho AKT in tumors. In the next panel, you can see very good activity where you can get regressions, dose response efficacy with regressions at 30 mg per kg. At the right-hand side, the gold standard model for hyperglycemia in a mouse where you have an oral glucose tolerance test. We're comparing 203 at 100 mg per kg QD, so three times the dose for which we get regressions, and comparing that to alpelisib at its maximum tolerated dose versus its clinically relevant dose. You can see a big difference between Alpelisib and the breaker, where we have no change from vehicle with the breaker, so glucose metabolism can occur normally, as opposed to a kinase inhibitor where you can see you cannot clear glucose, and that's exactly what you observe in patients as well. There are three real populations that pop out when you look at the mechanism and look for genotypes that are responsive to the breaker. The three are listed here, HER2-amplified tumors, where PI3Kα is a key dependency of that signaling. We believe that this is, it's also a resistance pathway to HER2-directed therapies. We believe that 203 is really well positioned to be the small molecule of choice in this setting. It also has high blood-brain barrier penetration, so it should be very good for patients with HER2-amplified breast cancer. The other setting is PIK3CA mutants in the hormone receptor positive space, where, of course, that's where most of the kinase inhibitors of PI3Kα have been positioned. As I mentioned, we're uniquely positioned to address the KRAS mutant space, where signaling there is, we found, is also dependent on this breaker mechanism. Very large addressable patient population. Here I show you just a few xenograft models in the breast cancer space. On the left-hand side is HER2-amplified. It It happens to have a kinase mutant of PI3Kα. You can see very good monotherapy activity that gets better with trastuzumab. The middle panel is a kinase mutant model of hormone receptor or ER-positive breast cancer. Again, you can see regressions with monotherapy that gets better in combination with fulvestrant. We also have activity in a helical mutant, which is on the right-hand side there in combination, and this time with CDK4/6 inhibitor. We can also combine with KRAS inhibitors, and this is our own G12C inhibitor. You can see very good activity in three different models on this combination. This concept of inhibiting both these pathways is new. What we're bringing is more selective different mechanisms to this approach. I can tell you it's very well tolerated in all the models that we've observed, no weight loss whatsoever. You can see you can turn good activity into regressions in this combination. The mechanism is as well described. You get a large increase of apoptosis, and you get strong inhibition of proliferation. When you look at these tumors, they are in the combination mice. Here is our study schema. As I mentioned, we should have data on this the first half of next year. We're doing monotherapy dose escalation in HER2-amplified breast cancer, hormone receptor positive breast cancer, and also KRAS mutants, and then quickly pivoting to combinations in different settings, trastuzumab in the HER2-positive space, fulvestrant in the hormone receptor positive, and initially in the KRAS mutant CRC space with fulvestrant and bev. We will then add the triple later with ribociclib in the hormone receptor positive. We are excited to do our own internal combinations in the KRAS-G12C space with 8520, and in the KRAS G12X space with our pan-KRAS inhibitor 818. Our third program that is also in phase I studies is BBO -11818. This is our pan-KRAS inhibitor. It is an on-off inhibitor. You can think of it as a close cousin of BBO -8520, and it's highly potent for KRAS, but it is selective for KRAS over H and N. Here I'm showing you some biochemistry data, the binding to both the on and off state, as well as the ability to inhibit effector binding, which is, of course, a property that you only get from the on state. The compound has very good activity in cells. Here's a panel of mostly KRAS G12D and G12V. You can also see the selectivity at the bottom where we have selectivity against BRAF and NRAS. We also have selectivity against HRAS. What you can see here is very good potency mechanistically against phospho-ERK, but also in viability. We think that's a very important property for an inhibitor, to have small or no shift or even a reverse shift from the mechanistic to the viability assay. That's a very potent inhibitor. 818 is highly potent and has a very slow off rate from the protein. It has very good efficacy orally in models from left to right here. I'm showing you KRAS G12D colon cancer, KRAS G12D pancreatic cancer in the middle, and then KRAS G12D lung cancer. It's dosed orally twice daily. This is a non-covalent mechanism, but a very potent on-off inhibitor of KRAS G12X. Just like with 8520, you can combine 818 with 203. Here is a fairly high bar G12V model. You can see the combination with 818 gives you regression. Both compounds give respectable tumor growth inhibition by themselves, but you get regressions in combination. After a single dose, you can really see the power and the efficacy of this mechanism. You can see very profound increase or decrease in proliferation of the combination and increase in apoptosis. You can see the tolerability where it is very well tolerated. We are very excited to do this combination in patients. I have covered a lot, but it probably goes without saying the market opportunities for each of these assets is quite large. We have market opportunities as monotherapy for 8520 in lung cancer and KRAS-G12C, 818 lung cancer, breast, or lung cancer, colon cancer, and pancreatic cancer. Of course, we have the combination potentials of 203 with our own assets, but also in breast cancer with combinations of standard of care. We think that combination that we are uniquely positioned as far as we know, we're the only one with a breaker and selective KRAS inhibitors. With that, I think we have a few minutes for questions if there are any.