Welcome, everybody, to the JP Morgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at JP Morgan. I'm joined by my squad: Malcolm Kuno, Priyanka Grover, and Ricki Pinhasi. Our first presenting company for the day is Cogent, and presenting on behalf of the company, we have CEO Andy Robbins. Andy?
Great, Anupam. Thanks very much for inviting us. It's always good to be here to kick off the beginning of the year and sort of reset and talk about the year ahead, so my name is, as Anupam said, Andy Robbins. I'm the CEO of Cogent Biosciences, and I'll probably spend 15 minutes , 20 minutes walking through a few slides, reviewing where we're at predominantly with our lead program, bezuclastinib, before we open up to some questions from Anupam and the audience, so before I get started, just to remind folks, I'm going to be likely making a good number of forward-looking statements. So we would ask you to carefully review our recent SEC filings for a full characterization of the risk associated with the company.
All right, with that said, for folks who are new to the story or sort of re-interesting themselves in the story, Cogent is a small molecule company focused on developing products for patients with rare genetically driven diseases. As I mentioned before, we're probably best known for our lead asset. It's a molecule known as bezuclastinib. It's a selective and potent KIT inhibitor that's in development for two large groups of patients: patients with systemic mastocytosis split into a couple of subgroups, and then patients with gastrointestinal stromal tumors. We are currently running three pivotal studies, each of which are on track to read out results in 2025. So sort of a unique situation as a small cap biotech company to have three pivotal trial top-line result card flips during the calendar year. So very excited to have gotten to 2025.
We'll go through some of the data that we believe support a high probability of success across these trials in a minute. In addition to bezuclastinib, we've assembled an exceptional research team comprised of just really, really strong chemists, but along with the chemists, biologists, pharmacologists, enzymologists, the entire sort of suite of a full integrated research team. That team was put together about three years ago, and now we are actively enrolling the first molecule that they invented themselves. It's known as CGT4859. It's a selective and potent FGFR2 inhibitor. That trial is currently underway, focused on patients with confirmed FGFR mutations. We would expect a lot of those patients to be cholangiocarcinoma patients.
In addition to that compound, which is our first Cogent-invented drug to go into the clinic, we are guiding this week for the first time that we plan to have two additional compounds make it to IND by the end of the year. That would be our highly CNS-penetrant ErbB2 inhibitor, as well as our H1047R mutant PI3K alpha inhibitor. In addition to those products, so now we're down to the fourth drug in our portfolio. The fifth program that we've announced publicly is a pan-KRAS inhibitor, a RAS (ON). And while that compound is still in the research stage, we've already presented data at a major research meeting that shows picomolar activity across the KRAS mutants.
If you believe in sparing H and NRAS to potentially alleviate some of the toxicity associated with those isoforms, we think we have a pretty good program that we're very excited about. We have a very strong balance sheet. I can show you on the next slide at the bottom, about $345 million as of the end of Q3. We will announce the end-of-year cash balance in February, but we're in a very strong position to have at least a year of cash and probably more deep into 2026 after the pivotal trial readouts begin. You can see here on this slide, slide four, that bezuclastinib, again, has these three pivotal studies sort of going from top to bottom: the SUMMIT trial in the non-advanced systemic mastocytosis population.
This is a trial that we announced around ASH in December of 2024 that is fully accrued and over-accrued with nearly 180 patients. That was enrolled in about 10 months, which is an exceptional job by the team, but also a credit to the data we've presented in this patient population. The patients and the investigators are very excited about the potential of bezuclastinib to help resolve their symptoms. We're announcing that the top-line results from that trial will be released in July of this coming year, so literally right around the corner. Very excited about that. Kind of going down to the next one, the blue row, that's the PEAK study, the global phase III study of bezuclastinib and sunitinib as a combination in imatinib-resistant GIST patients. That trial finished enrolling 413 patients around the world back at the beginning of August.
We are excited to say that based on the rate of event accrual, the primary endpoint is a progression-free survival endpoint, so we're waiting for the PFS events to accrue. Based on that implied rate that we're seeing in the blinded data, we're looking towards the end of this year, 2025, to take a look and unblind that study and look at the top-line results, and then sort of rounding it out with the advanced systemic mastocytosis population known as the APEX study. That trial is now formally closed to screening. We did that a couple of weeks ago, and so now we're just waiting for that last cohort of patients who screened and consented into the study to make it through the screening process. We expect to complete enrollment within the coming weeks as that last group of patients gets through.
That would put us on track to have top-line results sometime in the second half of 2025. So again, just sort of summarizing three pivotal trial readouts starting in July and ending by the end of the year. So a very, very data-rich, busy year for the company. I mentioned the FGFR program. That phase one trial is up and running. We're actively enrolling patients. And then while I'm not going to spend a lot of time on it today, as we move through the year and we get to some of these earlier stage conferences, we will take the opportunity to highlight some of these programs in our pipeline as they move towards IND and clinical development. So when we take a really deeper look at bezuclastinib, what will this product, what could this product become?
We think that it has the profile based on its selectivity, sparing the other commonly hit class three receptor tyrosine kinases like PDGFR, CSF1R, FLT3, et cetera, et cetera, that many of the earlier generation KIT inhibitors implicate, as well as its inability to penetrate the CNS, again, differentiating it from one of the most notable KIT inhibitors on the market. That gives it the potential to be dosed at its clinically relevant exposure based on the safety profile and tolerability profile that we're seeing across our studies. So the SUMMIT study, as I mentioned before, we, based on patient demand, investigator interest, enrolled six months earlier than we thought. So lickety-split , over-enrolled by a significant amount. And that trial, if successful, we're pegging that market as a $2 billion+ U.S. total available market.
Our colleagues at a different company that are interested in this disease just, I think yesterday, called it a $4 billion opportunity. We're still trying to make math work on that, but whichever number you want to pick, there's essentially two companies developing drugs for this one indication that somewhere between a $2 billion -$4 billion opportunity. We think we have a better profile. We'll get into the data in a little bit. From a peak perspective, again, six months earlier than we thought, from a historical benchmark of enrolling these studies, very excited about that based on investigator and patient interest around the world. Just in the U.S. alone, we think that the total available market, based on the number of patients that develop resistance to imatinib on an annual basis, could potentially exceed $1 billion.
And with no new drugs approved in the last 20 years in second-line GIST, we're positioned to be the first new advancement if the PEAK study wins later this year. As you are aware, when you show survival advantages in oncology indications, the adoption of that new treatment is relatively rapid as a standard of care. So we're excited about that. And then kind of rounding out with ASM, a smaller commercial opportunity, but not trivial. And I think you'll see later from a PD effect and a balance of really, really strong efficacy with a safety profile that is clearly different than the incumbent that is dosed at a clinically relevant dose, but has a lot of toxicity associated with it at that level. We believe that later this year, we'll be able to show data that is clearly differentiated for that patient population as well.
So in aggregate, bezuclastinib is teed up for somewhere clearly north of a $3 billion commercial opportunity across these three studies, all of which will be shown this calendar year. So I want to do a quick review of some of the data. I'm going to start with the SUMMIT study. We presented these data at ASH just literally a month ago. So you can see here on the left side, the line chart. This represents what the primary endpoint of this study will be, both for our predecessor and for SUMMIT in part two, which is a measure of symptomatic improvement based on total symptom score at 24 weeks for the population. You can see here we got to nearly 56% mean improvement at 24 weeks with nearly a 28-point reduction.
Historical benchmarks suggest that placebo does around a 9-point reduction, and the currently approved active standard of care did a 15-point reduction at their 24-week benchmark. If you look at the right side, what we show is for individual patients on the waterfall, the depth of symptomatic improvement that they experienced at 24 weeks. And so what we're showing here is a 50% improvement is, I think, widely accepted by investigators, patients, the FDA, our competitor company, ourselves as a clinically relevant benchmark of, let's call it, "a response in a patient." So if you see a patient have at least a 50% improvement in symptoms, that's considered clinically relevant. We show here in our data set at the recommended phase II dose, 76% of patients achieve that benchmark by 24 weeks, which was very impressive to the investigators.
One thing that we hear quite often from folks is, well, the company that came before you and has a drug approved, they developed a questionnaire that's called ISM-SAF, and you guys developed a different questionnaire called MS2D2, and how can I possibly compare these two? So what we've done here on the left, you can see the green line is literally a copy-paste from the prior slide of our data from our phase one trial scored on total symptom score using the MS2D2 tool, which outlines the symptoms in the column with the green at the bottom. What we've done for the benefit of folks who asked that question is we've rescored the data from our phase one trial using the items from the ISM-SAF tool, which is listed there on the right with the pink boxes at the bottom.
We've plotted that line using the score from the items in the ISM-SAF and the dotted line. I think I can convince you that the green line and the dotted line look very similar, nearly identical. We're hopeful that as we continue to build larger sample sizes in this patient population and continue sharing this data, that it becomes less and less confusing about whether these tools are completely different and hard to compare. More what we in the investigator community feel is they're both highly representative of symptomatic improvement in this patient population. Just kind of rounding this out from an efficacy perspective, you can see here individual items.
So if you don't want to look at the composite blended total symptom score, you can actually drill down into the data and see how bezuclastinib performs for individual symptoms, starting with skin, then moving to fatigue, cognitive GI, and pain. We also include the additional symptoms like diarrhea, severity, brain fog, and dizziness that are not part of our composite tool, but are part of the competitive tool just to demonstrate that we also have significant benefit on those symptoms for patients. And then finally, if you take your eyes all the way back to the left here on slide nine to the most severe symptom at baseline, on a scale of zero to 10, with a baseline severity of about 7.7 at 24 weeks, we're dropping that severity by almost four points.
Moving it from very, very severe to very mild, which is exciting again for the investigators who and the patients that don't care about necessarily the composite in a population. They care about the thing that is bothering me the most. How good is your drug at helping that? Turning now to the safety and tolerability, you can see here the slide that we presented at ASH.
Our drug, and we now know this by looking not just at the SUMMIT trial, which is dosed at 100 milligrams once a day, but also at the APEX study, which is at 150 milligrams once a day, and the PEAK study, including blinded safety data from patients who are receiving 600 milligrams of bezuclastinib once a day, that we believe very strongly the safety and tolerability profile of bezuclastinib will be largely characterized as probably causes patients' hair to turn white, which is an on-target effect of hitting wild-type KIT, and probably causes a low incidence of asymptomatic and reversible transaminases, so AST and ALT fluctuations. What we can tell you is looking across all these patients from the different studies, these changes are asymptomatic and reversible. We have no Hy's law. We have no serious clinical consequences, no liver toxicity, and no irreversible lab abnormalities.
So we believe that that profile, if you want to sign up for it, is highly potent, hits the target hard, just very impressive PD data, translates to very impressive symptomatic improvement. And the trade-off is your hair might turn white, and you may have numbers on a piece of paper that are reversible. We think that that's a very compelling profile for investigators and patients fighting this disease. Just to kind of summarize again where we are with our already presented data, what we've done here in the pink and the gray columns is put up the results of the only other drug that's run a pivotal study in the non-advanced mastocytosis population. And you can see their scores relative to placebo. And then in the green column, again, this is cross-trial comparison. So take that little gray vertical word. You can see the results of the SUMMIT.
So somewhere between a doubling and tripling of effect size, depending on if you're looking at mean reductions, if you're looking at threshold responder analysis, if you're looking at improvement of most severe symptom at baseline. And then if you look at the very bottom, what's even more encouraging to us is when you think about a 56% improvement at 26 weeks for the patients that have now made it out to 46, that continues to deepen. Those patients have a 65% mean improvement. When you think about three-quarters of patients getting a 50% threshold at 24 weeks, nearly 90% of patients get there by 48 weeks. So not only do we have rapid and deep responses, they continue to be sustained and improve over time, which is very encouraging again for the patients that are looking at how do I resolve these severe symptoms.
Okay, I'll try to hustle a little bit so we can get to some questions. Looking at the PEAK study, so first of all, for those who aren't familiar with GIST, the first-line therapy for GIST, a drug known as Gleevec, we're all familiar with it. It's amazing. High response rates, very durable, revolutionized the treatment of this disease. But after that, the three approved drugs are all less than 10% response rate in mid-single-digit months of progression-free survival. So patients progress rapidly through lines of treatment. So this is a patient population that is in desperate need of new active therapies, especially in that second-line patient population. The reason you want to put our drug together with a drug like Sutent, which is already approved in the standard of care in the second line, is we hit different resistance mutations.
While Sutent is quite good at covering resistance mutations that occur in exon 13/14 in the KIT gene, they do not work on patients that have 17/18 mutations. We're the opposite. We work very very well on patients that have exon 17/18 mutations, but not so well on exon 13/14. And because of our selectivity and our inability to get into the CNS, that allows us to combine with Sutent. You'll see the safety profile and not be additive on toxicity. That combination you can see in the bottom row provides us pan-mutational coverage, which is exactly what you want in this disease. Back at ASCO last summer, we presented data from a 42-patient run-in or a part one where we were trying to get to the right dose for our phase 3 trial that's now fully accrued.
We showed, I think, very impressive durability, including many patients achieving response. Those are the patients with the blue dots and the darker bars. When you drill down just into the patients who are the classic second-line patients that only received imatinib prior, we have a 40% objective response rate. Those responses are quite durable, lasting out to a median progression-free survival estimate in the second-line population from our trials of 19.4 months. You remember Sutent per label in the second line as a monotherapy has about a six-month PFS. In a more recent phase three trial run by our colleagues at Deciphera called the INTRIGUE study, the control arm of Sutent monotherapy did just over eight months.
So with a combination that showed an admittedly small number of second-line patients and 19.4-month PFS, we believe we have some room to develop a very active and successful clinical trial. Again, I'm not going to go through row by row, but if you're familiar with Sutent, Sutent has its own set of tolerability issues associated with it, mostly low-grade nuisance tolerability like diarrhea, fatigue, nausea, again, for metastatic cancer patients. This has not been a barrier to use. It is the standard of care around the world. When we add bezuclastinib to it, we don't noticeably increase the discontinuation rate. We don't noticeably increase the dose reduction rate. We don't noticeably increase the rate of any grade 3/4 tox. So this profile of being a selective agent and a good combination partner is really going to help us, we believe, win the PEAK study.
And then just finally to wrap up in the ASM population, we presented this data again also at ASH data from our dose escalation phase one or part one study of APEX, where we showed very robust response rates. You can sort of see in that if you take your eye to the CR plus PR row, looking across at if you use the historical gold standard criteria called modified IWG, about a 56% response rate in patients that are classic first-line patients. If you use the newer emerging criteria that the investigators like to judge drugs and their activity in this disease called pure pathological response or PPR, we have about an 88% ORR. I'll show you in a minute the PD data too. You essentially give this drug, it's going to work in every patient. It's going to have a dramatic effect.
It's a very active drug for this population. You can see the Kaplan-Meier curve for our patients. Very rarely do you see Kaplan-Meier curves that are horizontal lines at 30 months at 100%, no progressions. So very encouraging, durable drug for these patients. Here's the PD data I spoke about. Whether you look at tryptase levels, whether you look at mast cell aggregates in the bone marrow, whether you look at variant allele fraction in peripheral blood. On the waterfall charts, essentially with the exception of one or two patients here and there, every patient getting a very deep response is well below 50% improvement, with all of the open symbols at the bottom denoting essentially complete response per PD on those measures. So again, a very, very active drug in this patient population.
And then just wrapping it up, similar to what I showed you for SUMMIT, the profile of this drug is it will turn patients' hair white. That is an on-target effect of inhibiting KIT and wild-type KIT at clinically relevant exposures. And it will have asymptomatic reversible AST, ALT elevations. Many of the other preferred terms there in a single-arm trial in a very severe blood disorder are going to be hard to tease apart from underlying biology of the disease versus related to drug. But we think that this profile of not having intracranial hemorrhage, not having 40% cognitive impairment, not having 80% peripheral edema, not having 30% rates of grade four heme tox is going to be very competitive with, again, the incumbent.
So just wrapping up, and I'll ask Anupam Rama to turn to some questions, reminding folks that bezuclastinib, in these three indications, we have an opportunity within the next 12 months to have pivotal data, which would lead us to a greater than $3 billion commercial potential. There's very limited competition. There's one other company in mastocytosis that we're competing against, and we are by far the leader in second-line GIST, the only other drug that's currently used as a 25-year-old generic drug in the second line that we combine with.
So from a setup position, if these trials show positive results, and I think we have some very compelling data from our part ones of each of these studies that de-risk not to 100%, but to a very high level of confidence that this drug is active and is going to be important for patients, we're well on our way to commercial success. So with that, I'll ask Anupam to see if he has any questions. Thanks, Andy. I just want to remind folks that there's three ways to ask a question. You can do it the old school way and raise your hand, and I'll call on you. You can submit a question in the question portal, and I can read it on your behalf, or you can just email me and I'll do it.
So, Andy, just thinking about the most recent ASH updates that you reviewed in your presentations in both ASM and ISM, what do you think are the kind of top two or three most misunderstood points coming out of ASH for the street?
Yeah, it's a good question because one of the things we struggle with is this sort of confusing disconnect between the reaction of, I'm going to call it the broad biotech buy-side investment community and the reaction of the mastocytosis investigator community, who when we showed these data, remember the data that we just reviewed that were at ASH is from the part one of the study. We showed these data to investigators in the early fall in an attempt to ensure we were going to enroll the pivotal part of summit in Q1 of 2025.
The reaction from the 70 investigators around the world who got to see these data under confidentiality was a nearly doubling of the enrollment rate of systemic mastocytosis patients. Unlike the buy-side and maybe our competitor who saw the data and said, "Yeah, I don't see any difference," the investigators and the physicians who treat these patients, the KOLs saw the data and they said, "I need to figure out a way to get my patients onto this study before it closes." That was responsible for pulling back the enrollment by about three months within the three-month period. That's just one example where the reaction from the people who treat the patients and the people who invest in companies is almost the opposite. That's confusing to us.
And I think one of the things that continues to be confusing about this disease is that the primary endpoint, as I sort of tried to mention before, based on some trademarking that our competitor did, is going to inherently be judged on a different instrument, the Blueprint instrument and the Cogent instrument. But what we, I think, easily and quickly demonstrated to the investigator community is that there is no believable difference in how you can judge the performance of symptomatic improvement. If you try to say one drug had a 30% improvement and one had a 31% improvement, that's probably attributable to maybe different words and different adjectives and different questionnaires. But when you have one drug that has a 24% response rate and one drug has a 76% response rate, the investigators, I think, quickly got to that's not an artifact of different adjectives.
That's an artifact of the drug is working better. And I think what's compelling to them, and I didn't go through all the PD data, is that when you take a drug that has an IC90 of 200 milligrams and you reduce it to 25 milligrams to spare the risk of intracranial hemorrhage, to spare cognitive impairment, to spare edema, to spare grade four thrombocytopenia, you spare all those side effects, but you also spare a lot of the activity of that drug. And so what these patients are looking for, and again, another I'll add a third one, Anupam, I think there's a sort of a misunderstanding in the buy-side that we've heard from a lot of folks that this is called indolent systemic mastocytosis. So these are patients that are like eczema patients. They have a little bit of nuisance skin disorder.
That's not who these patients are. The moderate to severe non-advanced patients are patients that have severely impacted lifestyle, often can't leave their house, they can't hold jobs, they have difficulty interacting with society, they have anaphylactic risk every day from left and right and up and down. They have suicidal thoughts. They can't live a normal life. And so they are looking for something that's going to modify their disease to improve their symptoms and return them to a normal lifestyle. That's quite a bit different than a nuisance community allergist skin drug. And so I think over time we'll be able to demonstrate that. I think the profile of our drug as being powerful and potent and alleviating the symptoms is what the patients and the investigators are looking for.
And I think that we'll be able to help educate the buy-side community that it's not about who was there first. It's about who helps patients the most.
Andy, a couple of follow-ups to what you just said. In ISM specifically, along the lines of what you were saying, what % of patients have more moderate or severe disease versus, say, a milder form?
Yeah, the epidemiology question of ISM is really fascinating because it's a, I would say we can all agree it's a very underdiagnosed disease because the diagnosis of disease is a little bit complicated and probably involves confirmation of a diagnosis with a bone marrow biopsy, which is not something that a local dermatologist or community allergist is going to be familiar or comfortable with.
And so by the time a patient is severe enough in the U.S., at least in recent years, to get a confirmed diagnosis, they're almost certainly moderate to severe in nature. And so there are probably literally 15,000 patients , 20,000 patients with mild mastocytosis that don't know the name of the disease that causes their episodic symptoms. We estimate, and I think we in Blueprint would agree with this, there's probably somewhere between 5,000 patients and 10,000 patients with the moderate to severe form of the disease in the U.S. as a treatable population. I think there's various estimates for how many of those patients are diagnosed. It's definitely not all of them. But I think what our colleagues at Blueprint are suggesting is that this disease, as there are treatments approved, the awareness and the education campaigns that they're leading as an on-market drug are finding new patients.
We continue to encourage that. We're going to start helping with that effort. We think that these patients deserve to know what disease they have and why the symptoms that they're experiencing are happening and hopefully bring a product that is going to be more effective at solving their symptomatic problems.
And then, Andy, just also following up on what you just said, what portion of patients are actually treated by oncologists versus allergists?
Yeah, that's an excellent question as well. We actually were quite interested to see that Blueprint just put out a poster a couple of months ago at a conference in conjunction with Kaiser Permanente, where they suggested, based on the data review of the Kaiser network of patients on avapritinib, that about two-thirds of the Kaiser patients on Ava are treated by hematologists.
That obviously doesn't take into account many of the large academic medical centers in the U.S. from a sort of a physician specialty split, which probably only increases the number of patients that are being managed by hematologists, so at least today, and we think for the foreseeable future, many of these patients with moderate to severe disease are probably going to be referred up to either hematologists. I think that's probably clear number one, or I'm going to call them academic or large practice allergists. These are trained allergists that are familiar with dealing with very severe diseases, not single practice community allergists that are in the suburbs. These patients are, in order to get effective therapy and confirmed diagnosis, almost always being referred up to tertiary or large academic hospital settings, so that setup, I think, is very favorable to a drug that has a profile like bezuclastinib.
Questions from the audience?
Maybe switching gears a little bit to GIST. Can you remind us the powering of the GIST study on PFS and kind of what gives you confidence in this update?
Yeah, I can tell you without getting into all the statistical details that the way that we set up the trial and with 90% power, we set it up assuming that the control arm, Sutent monotherapy in the PEAK study, would perform similarly to the control arm from the INTRIGUE study. And I'll remind you that in the INTRIGUE, Sutent had a median progression-free survival of 8.3 months.
And so what we've said publicly is that beating 8.3 months by about a three-month delta is sort of the minimum clinical effect size that would take to win the study on statistics that's consistent with talking to oncologists for clinical relevance for increased progression-free survival for diseases that have PFS in that kind of 8-month to 12-month neighborhood is adding another three months on would be seen as clinically relevant. We, of course, are very hopeful that the active arm of Bezu plus Sutent will do quite a bit more than that from an effect size. But that gives you sort of a ballpark estimate of what we're looking for.
And you talked a little bit about the TAM and peak sales potential for all the products. But in GIST specifically, how do you kind of get to those numbers in terms of duration, in terms of penetration? Because you're going after, obviously, a much bigger population than some competitors.
Sure. It's a good question, and the numbers that we quoted, just to be clear, are meant to be total available market. So not trying to call what our share is going to be. That's sort of the overall market size. In GIST, I think what we say is about 60% of patients annually develop resistance to imatinib. There's about 5,500-6,000 newly diagnosed metastatic GIST patients every year. So you're looking at around 3,000 new second-line patients each year, plus or minus 500 patients. If you consider a mean duration of about a year, then you can plug in your favorite price of a new oncology-approved agent and you can get easily to $1 billion.
We'll sort of politely point out that ripretinib, which is now owned by Ono Pharmaceutical, is a fourth-line approved agent in GIST. Let's call it, a new oncology drug in GIST, is, to the best of our knowledge, the most expensive oral drug in the world for any indication. I think it now has a wholesale price of over $40,000 a month. That's not to suggest that's part of our pricing strategy, but just to point out in the same disease, there is precedent for very high-priced oral therapies.
Questions from the audience?
Andy, we talked so much about some of the core pivotal programs that are reading out this year. But any milestones that we should be monitoring here for the sort of earlier stage discovery pipeline?
Yeah. So we mentioned in our sort of kickoff year beginning press release that we're now actively enrolling the first Cogent invented molecule, that FGFR2 selective and potent agent. It's a reversible agent. It hits all of the escape mutations that have been characterized. And we think it offers the opportunity to see a similar, very impressive response rate that was seen by another agent that was recently developed in cholangiocarcinoma, but with the addition of really strong durability that that agent, because it doesn't hit the molecular break and the gatekeeper resistance mutations, sort of patients easily progressed on that agent. If we can do that and turn cholangiocarcinoma patients that have an FGFR confirmed mutation into a more durable long-term treatment disease, I think that's very exciting, certainly for patients.
That phase I trial is ongoing and we'll see how quickly that accrues and where we can get to and is there an appropriate scientific meeting to report out results from. But certainly, we'll monitor that along the year. The other two milestones that we would expect, actually, I'll just say for all three, for the ErbB2 program, the alpha-selective PI3K, and the KRAS program, you can assume that we will provide scientific updates in the form of presentation at major research meetings throughout the year. We don't want to distract from the fact that we have a lead asset with a greater than $3 billion commercial opportunity with three pivotal trials, but we're also cognizant of building a successful company in the long term with a portfolio and a pipeline of best-in-class agents.
And so the research team and the early development team are working very hard on those assets. And as they continue to mature, we'll continue to provide updates at scientific meetings. Any final questions for?
All right. Thanks, everyone.
Awesome. Thanks, Anupam. Appreciate it.