All right, everyone, I think we'll get started here with our next buyer side. My name is Derek Archila. I'm one of the Senior Biotech Analysts here at Wells . I'm very excited to have our next company, ORIC Pharmaceuticals. From the company we have Jacob Chacko, CEO, and as well as Dominic Piscitelli, CFO. Gentlemen, thank you so much for joining and look forward to the discussion here.
Thanks for having us, Derek.
Awesome. Maybe just give us the thousand-foot view, Jacob, in terms of what ORIC is all about, what you guys are working on, and then we can kind of dig into the Q&A.
Sure. I'll keep it short because I know we want to get into the 50-foot view pretty quickly. ORIC stands for Overcoming Resistance in Cancer. In a nutshell, that's the mission of the company. Obviously, oncology is a very large area in which to do drug development. We tend to specifically focus on small molecule drug development within solid tumors, specifically prostate cancer and lung cancer. Our two lead programs are ORIC-944, which is a small molecule inhibitor of the PRC2 complex that we're developing in prostate cancer in combination with two different androgen receptor inhibitors, and ORIC-114, a brain-penetrant, selective TKI that's being developed in three different targeted therapy populations within non-small cell lung cancer. Both of those programs are in dose optimization right now, and both are headed to a potential start of phase III studies next year.
A clinical stage pipeline that is increasingly getting later stage development.
Gotcha. Maybe let's start with ORIC-944. Maybe if you provide a little bit of background on that program and I guess why PRC2 is kind of an interesting target within prostate cancer.
Yeah. PRC2 is a target that's been kicking around in prostate cancer for the last half dozen years or so. The therapeutic potential, at least preclinically, has always been that if you combine a PRC2 inhibitor with an androgen receptor inhibitor, you ought to generate even longer, more meaningful durations of therapy on those androgen receptor inhibitors than is already the case today. Maybe taking a step back from there, Derek, as you look at the state of play within prostate cancer today, the androgen receptor inhibitors, of which there are three major ones, one is called enzalutamide, one is apalutamide, and one is darolutamide. Those three drugs collectively have transformed the way that prostate care takes place today. They're small molecules, they're pills. They've led to dramatically better outcomes for those patients with prostate cancer. They have spread across the prostate cancer landscape.
Whether it be castration-resistant prostate cancer or even in much earlier lines of prostate cancer, they're well-tolerated drugs. Patients do well as a class commercially. They are incredibly successful. They collectively do more than $10 billion of sales globally each year, and that is continuing to grow at solid double-digit rates. Like almost any cancer therapeutic, patients eventually develop resistance. The problem is that these tumors, which start out exquisitely dependent on the androgen receptor, and therefore you give an androgen receptor inhibitor and effectively squelch that connection, and that's what leads to the good outcomes that those drugs have. Eventually, the tumors become AR-independent, androgen receptor-independent, at which point an AR inhibitor doesn't work as it was intended. Without getting into all the minutia of the biology, essentially PRC2 is an epigenetic modifier. By inhibiting PRC2, you're effectively able to push those tumors back into an androgen receptor-dependent state.
That's why a PRC2 inhibitor ought to work to increase the durability of an androgen receptor inhibitor. I mentioned the preclinical rationale has been well-characterized, well-studied, no disputing that. What has been problematic is that testing PRC2 inhibitors in the clinic, the first several PRC2 inhibitors that were tested in the clinic had very, very poor drug properties. Half-lives on the order of one to two hours. CYP autoinduction, meaning that the drugs would rev up the CYP enzymes, but themselves were also metabolized by the CYP enzymes. You would literally get phenomena like dose-dependent decreases in exposure. The more drug you give, the less exposure you get. The field is littered with PRC2 inhibitors that have not really proven out the case in the clinic, namely because they had such poor drug properties.
Along comes Pfizer, which is our main competitor in this space, with a drug called Mevrometostat that has now shown in two different castration-resistant prostate cancer settings in the phase one setting, phenomenally long PFS outcomes, much longer than you'd expect with enzalutamide or with an AR inhibitor alone. Earlier this year, they presented some data that showed in a randomized setting within CRPC, again, much better outcomes, much longer durability than what you'd expect with enzalutamide alone. In that case, their control arm was enzalutamide, and they far outperformed enzalutamide. That's the kind of initial proof of the thesis in the clinic. Of course, with ORIC-944, we think we have a drug that's got even better drug properties. In contrast to Pfizer's drug that looks like it has about four or five hours half-life, is dosed BID in quite large doses, ORIC-944 has a 20-hour clinical half-life.
It's dosed QD. The importance of that QD dosing versus BID is not just the convenience, obviously, of QD versus BID dosing, but rather, as you think about what wins the day from a drug profile, you want to be able to cover Cmin for 24 hours, and you want to be able to do that without pushing your exposure so high that you hit Cmax-driven toxicities. With ORIC-944, we think we've kind of threaded that needle just right in terms of the profile of the drug. We've presented some initial data earlier this year, which we can review. Long story short, it looks very promising in terms of the differentiation of that drug right out of the gate.
Gotcha. Maybe before we get to the data, just knowing that Mevrometostat is out there, how do you think ORIC-944 is kind of differentiated, and what have you done to obviously improve those properties or lead to potentially better data down the road?
Yeah. It looks like Pfizer has done a nice job of differentiating from all the first-generation inhibitors that came across as PRC2 inhibitors. ORIC-944 seems to have done an even better job of that differentiation. It really fundamentally comes down to the drug properties themselves. Having that long half-life, both drugs are very potent, equally potent, in fact, and much more potent than the first-generation compounds that came across. Neither drug looks like it has, certainly we know our drug does not have CYP autoinduction. We don't think their drug has CYP autoinduction. That's a good thing. You're not revving up the CYP enzymes and then metabolize the drug. It fundamentally comes down to things like the half-life and the much longer half-life of ORIC-944 at 20 hours, like I said, which just gives you better target coverage.
Gotcha. I mean, is there anything specific to how you engineered that drug relative to Mevrometostat? Ultimately, I'm sure the IP is all solidified on that, but maybe you can walk us through there.
Yeah. We can't take credit for engineering the drug originally because it was really the chemists at Marathi that engineered this drug, came up with the compound. Judging based off of the Pfizer structure, based off of our structure, both drugs were made off of different chemical scaffolds than the first-generation compounds that came across. All hats off and kudos to the Marathi chemists that came up with ORIC-944 because essentially they looked at this PRC2 field, and they had the exact same observation we did, which is that all the promise on the therapeutic side of things in terms of combining with an AR inhibitor was not being properly tested in the clinic because you had these substandard drugs that were PRC2 inhibitors that were being tested in the clinic. Marathi looked at the PRC2 complex. They basically said there's two different units that you can drug.
You can either drug the catalytic subunit, which is called EZH2, or you can approach it through allosteric inhibition by drugging the EED subunit. Marathi's chemists said they don't care which subunit they drug. They're just going to make a bunch of EZH2 inhibitors and a bunch of EED inhibitors and then put them all through the preclinical paces and be very pragmatic about the selection of the eventual candidate. What ended up winning the day was what is now known as ORIC-944, which happens to be an EED inhibitor. It drugs the EED subunit of PRC2. I love that it was just an empirical experiment they ran to figure out how do you optimize the drug properties, and they were clearly able to do that.
Gotcha. Maybe walk us through kind of the phase one data that you guys have reported for ORIC-944, and what gets you excited based on some early comparisons to Mevrometostat.
Yeah. I always hesitate a little bit to do the comparisons to Mevrometostat, only just out of fairness to the stages of the programs and the fact that Pfizer has now initiated two different phase III studies with Mevrometostat. They're about to initiate a third phase III with Mevrometostat. Clearly, Mevrometostat is just further along than where we are. With that caveat, I would say that the early data we generated, which we shared in the first half this year in a group of 17 patients where I mentioned earlier that we're doing our dosing, I mentioned three big androgen receptor inhibitors that are approved, enzalutamide, which is Pfizer's drug that came to them by way of their acquisition of Medivation. That drug is accompanied by apalutamide, which is Janssen's drug that came through an acquisition of a company, and then finally darolutamide, which is Bayer's drug.
Apalutamide and darolutamide are the two androgen receptor inhibitors that we are working with. We're partnered with both Janssen and with Bayer in terms of giving us free drugs to do our dose exploration, dose finding, and dose optimization. What we showed in the first half this year is that regardless of whether we combined our drug with apalutamide or with darolutamide, we saw pretty profound PSA activity in terms of both PSA 50s and PSA 90s. As you look at Pfizer in their randomized data set that I quoted earlier, where they had the much longer PFS than the control arm, they had a 14+ month PFS versus the control arm of enzalutamide alone that had a six-month PFS.
They also more than doubled the various other metrics they looked at in the treatment arm versus the control arm, including PSA 50, PSA 90, some of these other key metrics. They had a 34% confirmed rate of PSA 50s. They had a 12% confirmed rate of PSA 90s. In our early data set with 17 patients, in contrast to Pfizer's 34% rate of PSA 50s, we had a 47% rate of PSA 50s. In contrast to their 12% rate of PSA 90s, we had a 24% rate of PSA 90s. Even right here early out of the gates, across two different potential combo partners for us, whether it was apalutamide or darolutamide, in the aggregate, you see really nice PSA 50s, really nice PSA 90s.
Importantly, just as we had suspected, because of the better drug properties, likely of the drug, the ability to cover Cmin without getting that Cmax driven toxicity, we saw fewer AEs and a lower intensity, lower incidence rate of AEs than what Pfizer saw in their experience as well. With PRC2 inhibitors, you expect really two large classes of AEs. That should be GI toxicities and heme toxicities. You can just look at the Tazemetostat label, which is an approved PRC2 inhibitor, and you can get a sense of what that ought to look like. Clearly, we and Pfizer both see those on-target toxicities, but as I mentioned, we see it at a lower incidence, lower severity than what Pfizer sees.
That should bode well for us because as you think about the long-term development plans, obviously, the initial flag in the ground in terms of later stage development for both Pfizer and us will be in the castration-resistant prostate cancer setting. Clearly, there's a lot of other settings within prostate cancer in which we would want to develop this drug. As you go earlier and earlier in prostate cancer, you're going to want a drug that is very well tolerated. That tolerability profile is going to become increasingly important.
Gotcha. When you make those comparisons, Mevrometostat, I mean, obviously, it's not apples to apples, but are these patient populations fairly similar? I guess, how do you think about that and whether or not one population from one trial is more advanced? Does that also speak to kind of some of the efficacy we're seeing?
Very good question. It is something that we look closely at. The patient populations between the two data sets were very similar, with one exception, which is that our patients were more heavily pretreated than their patients. If anything, that actually helps make the case that despite us having a more heavily pretreated population, we were able to generate the results that we did. Both drugs were being studied in a castration-resistant prostate cancer setting where all of the patients had already progressed on abiraterone, which is one of the abiraterone, along with those three AR inhibitors, are collectively known as ARPIs. Those are kind of the mainstay of therapy in prostate cancer. Every patient had progressed on abiraterone. Prior chemotherapy was allowed in both studies.
The reason I say that our patient population was more heavily pretreated was in Pfizer's case, that was kind of the sum total of the inclusion and exclusions in terms of prior therapies for the patients. Whereas us, just being at an earlier stage development, we allowed a whole plethora of other therapies as well. We had three median lines of therapies for our patients, whereas in the case of Pfizer, I think it was technically one prior median line of therapy that they had before those patients had come onto the study.
Gotcha. Maybe we can talk about the update we expect in 4Q. Also, you have a 1Q or first half 2026 update. Just maybe uncover for us what we should expect in these updates and really what we should be kind of comparing them to relative to some of the Mevrometostat data as well.
Sure. I'm chuckling a little bit because we had an update in May, which was fairly substantial this year. We have another update in the second half this year in the next four-ish months, and then yet another update in Q1 next year. It seems like that's the cadence you have to be on these days as a public company. What I would say is that the next update for ORIC-944, that one coming in the second half this year, I'd characterize as more incremental in nature. If anything, it's more of an operational update. The reason I say that, Derek, is essentially the point of that update is to lay out the rationale for people to understand why it is that we chose the provisional RP2Ds that we chose to optimize in the dose optimization portion of the study.
That rationale, a substantial amount of that rationale has already been presented in the May update we gave where we had the 17 patients. What we've said is that we would have at most a handful of additional patients beyond the 17, the patients that the street has already seen. The rationale for why we picked the provisional recommended phase II doses that we picked would include things like efficacy measures like PSA 50s and PSA 90s. Again, you've seen that for the vast majority of that data set already. We could include actually as new data ctDNA. ctDNA is something that we're happy to talk about.
It's something that has come up in various conversations of people saying, "Hey, it would be nice to also get a look at ctDNA because in addition to PSA 50s and PSA 90s, that has been shown, in fact, even more so than PSA 50s and PSA 90s, ctDNA has been shown to be an early marker of long-term durability measures like PFS and OS." Obviously, long-term, you care about those kind of durability markers. We may talk about ctDNA as part of that update. We might have PK or PD be part of that update, and clearly, we'll have safety be part of that update as part of the second half update. It's kind of meant to sort of set up the Q1 update of next year.
The Q1 update for next year is really where you're going to see some meaningful new data because that'll be dose optimization data that we share as part of the Q1 update. Obviously, there's a lot of moving parts right now in terms of a study. What I mean by that is in dose optimization, we have two different AR inhibitor combo partners, apalutamide and darolutamide. We are studying two different CRPC populations. One of them is a population that is post-abiraterone. The other is a population that is post-AR inhibitor, meaning you've had either enza, appa, or daro and then progressed. Two different populations. Within each of those, we're studying at least two different doses for Project Optimus purposes. In terms of what to expect from that Q1 update, at this point, Q1 feels like an eternity away. It's a little hard to predict.
The most I can commit to at this point is that we will certainly share data on at least one combo partner, either combo data with apalutamide or combo with darolutamide, at least one population, either the post-abiraterone population or the post-AR inhibitor population, and at least two doses within one of those populations. Each of those doses ought to have roughly, call it 10- 12 patients' worth of data, which means that folks will get to see at least 20- 25 patients' worth of data across two different doses within one population and with one combo partner.
The reason that that's kind of the most I'm willing to or we're willing to commit to at this point is just we've got to make some selections and try to figure out in pretty short order here which combo drug we're going to take into the first phase III study. We've already said that the first phase III study will start first half next year. We may end up tailoring that Q1 update to sort of just lay the groundwork for that first phase III study. The population that is going to be the subject of that first phase III study and the combo drug that's going to be the subject of that first phase III study could potentially give more than that. At this point, I think it's probably safe to just leave it to the guidance I gave.
Gotcha. Can you maybe expand on ctDNA and just what should the expectation be? I mean, obviously, this seems like it's a new data point, as you pointed out, tends to correlate with real true outcomes measures in these patients. What would we hope to see in the data set on that biomarker?
Yeah. It's a great question. ctDNA is something that is increasingly getting looked at within prostate cancer and some of the other tumor types. In particular, in prostate cancer, I think there's papers, there's literature now that shows that ctDNA correlates even more highly with long-term durability outcomes like radiographic PFS than PSA 50s and PSA 90s. I think for that reason, people are increasingly starting to look at ctDNA within prostate cancer studies. To my knowledge, it's not become a primary endpoint in any of the phase III studies, but it certainly is an exploratory endpoint in some of the phase III studies. It is something that we've been looking at from day one. I think in terms of what you'd want to see, you want to see the bars go down. You want to see them go down deep and fast.
I think in general, what people generally quote is they want to see what portion of the patients have substantial decreases in ctDNA. Substantial can be defined differently, but I think most often what people tend to gravitate towards, you want to see at least 50% reduction in the ctDNA across a wide swath of the patients. The other stat that people tend to quote is what percent of patients had complete molecular clearance of the ctDNA. Those are things obviously we'll be looking at and will be quite instructive as we kind of try to help understand the activity of the compound. Of course, that's a data point we do not have from our competition. I'm not sure we'll be able to do any side-by-side benchmarking there. Clearly, even in absolute terms, you can see is the drug doing what it should be doing by reducing ctDNA.
Gotcha. You said you've been looking at that since the beginning, so we should expect that for all patients?
As many patients as it's available. There's always sort of like a pre and post measure of things like that, and you don't always get it on every patient, but we should have it for most patients.
Gotcha. For the first quarter 2026 update, I know you've said in the past that you might share landmark PFS. Is that still potentially on the table, or how are you thinking about communicating that?
Yes. Thank you for raising it, Derek. In the 1Q 2026 update, we will certainly show things like PSA 50s, PSA 90s, probably also ctDNA for all the reasons we've highlighted earlier. We'll show safety. I think the thing that people, ourselves included, care most about out of that update will be durability. I think we've continued to guide people to that Q1 2026 update being the one that we ought to start to look at durability, namely because at that point you have as clean a data set as you're going to get in a pre-phase III study. What I mean by that is you'll have a substantial number of patients, 10- 12 patients at a given dose. You'll have at least two provisional RP2D doses, which we would be taking into a phase III study, and it'll be with one drug.
It'll be as clean as you can get with as large an N as you can get to be able to get a sense of how does durability look. It will not be a mature PFS number just by definition. It cannot be given where the timelines are. At a minimum, we ought to be able to lay out the data in such a way that you can start to calculate three months landmark PFS, or four months landmark PFS, just some kind of landmark analysis of what percent of patients are on at three months or four months, whatever the right cutoff is at that time. Obviously, there are stats that folks are well familiar with where you can start to do the extrapolation of what that ought to translate to in terms of PFS.
One thing I want to be clear on is we have said repeatedly that we intend to start the phase III study in the first half of next year. We are not going to wait to see phase III data from Pfizer. We are not going to wait to see our own mature PFS data from the current dose optimization work before we start that study. We just think that at this point, the evidence here is profound in terms of what they've shared, what we've shared. It would be, I think, a little foolish for us to just delay timelines to wait for those data points.
Maybe just a couple of follow-up questions on what would be your expectation for what Pfizer can show in phase III relative to, obviously, we've seen in the phase II that leaves the door open enough for ORIC-944, right? I think from a safety perspective, you've got them. In terms of an efficacy perspective, what would you think is like a good result for Mevrometostat but not so good?
Yeah, next time we should invite Pfizer to come up here.
They can say.
Yeah. They can say what their expectations are. I guess just given, the randomized data that they shared earlier this year, they had a control arm with enzalutamide alone in that post-abiraterone setting that achieved six months PFS, which is exactly what you would expect from enzalutamide in that setting. You always like it when the control arm performs as expected. The treatment arm got 14.3 months of PFS, and that was a very good result. It was more than doubling of the control arm. I believe that the way they have powered their phase III study is such that they're expecting a control arm performance of 6.75 months PFS. That's a physician's choice control arm that includes both enzalutamide and chemotherapy. That 6.75 months seems like some kind of blend of the PFS you'd expect from enzalutamide and chemotherapy.
I believe they're powering it for a 10-month PFS on the treatment arm. Clearly, they far exceeded that in the randomized data we've already seen. I think you see anything in that 10-month to 14-month range, it would be a great result for patients. It would be a great result for Pfizer. Frankly, it'd be a great result for us because we think that, you know, to use that old cliché, anything they can do, we can do better with a drug that we think has optimized drug properties. One thing to be clear on is we very much believe that this is such a large indication. There's such a large unmet need here for all the reasons I mentioned earlier that we don't need to be heroes here and have a PFS that ultimately beats whatever PFS they put up. It's always hard anyway to do these cross-trial comparisons.
We just need to beat our control arm and hopefully do it in kind of the same manner, same magnitude that they do versus their control arm, and then ultimately have a toxicity profile that hopefully looks better tolerated than theirs. That'll be easily win the day. For all the reasons I mentioned earlier on what we've already seen from the data, as well as the drug properties, the long half-life, that is fully our expectation.
Got it. Last question on the ORIC-944.
I guess just in terms of, like, you'll be probably launching maybe two years behind Pfizer. I guess as you were just mentioning, it's a large market. You'll have some differentiation on safety for sure. I guess, how do you think that informs potentially your combo of choice? Ultimately, obviously, we'll see some of the data in the first quarter. How do you kind of take together all these things in terms of, like, ultimately what you want to be at launch and the value proposition at launch relative to the incumbent who would have been there for a couple of years?
Yeah. Maybe to go contrary to Ricky Bobby, this is not a situation where if you're not first, you're last. It's just really what it's all about is if you look at the commercial data, it's well studied that if you have a first mover, first to market in any given indication, and then you have a second program that comes along two years later with a completely undifferentiated profile, which is a big assumption, completely undifferentiated profile, the commercial data would suggest that that second mover will get anywhere from 30%- 40% of the overall market. In markets as large as the ones we're talking about, if that is all we can achieve is a completely undifferentiated profile that launches two years after Pfizer and we get 30%- 40% of the market, it's still a blockbuster many times over.
For all the reasons I highlighted to you earlier, we think that we will, in fact, be better than the profile that they ultimately end up delivering. There's only upside to those numbers that I just quoted to you. I think the name of the game for us, Derek, is go fast. Just keep that timeline gap as small as possible. That's exactly the reason why I mentioned that we're not going to sit on our hands and sort of wait for either phase III data from them or mature PFS data from ourselves. We've seen enough from them and from us that it's time to go. We're moving as fast as we possibly can to get that first phase III study started.
Gotcha.
We are thinking actively about everything that comes after that first phase III study as well.
Got it. Okay. Maybe move to ORIC-114 and just kind of we expect some updates there. Maybe you can just walk us through what to expect there. Also, I guess what's the strategy with this asset now with so much focus on ORIC-944?
Yeah, so much external focus on ORIC-944, internally focused on both programs. Go ahead, Dominic.
Yeah. We've got a couple of updates on ORIC-114 and ORIC-533. It's called six to nine months. In the second half of this year, we'll share some second line and later data for three patient cohorts: EGFR exon 20, HER2 exon 20, and atypicals. There'll be about 25 patients' worth of data in each of those cohorts as well. It's a pretty sizable update as well. We did actually update one of our milestones. We brought forward the first line EGFR exon 20 data. This is in monotherapy for exon 20. We'll share that data as well. There, we'll have about 10- 15 patients' worth of data. Earlier this year, we made a strategic decision not to pursue the second line setting for both commercial reasons and cost of capital reasons. The focus is really on first line.
From the second line setting, you should have some insight into how the profile of the drug and how that looks potentially in the first line as well. Jumping to mid next year, we'll have two more updates. These are both in the first line setting. This is first line EGFR atypical, and again, that'll be mid 2026. Then we'll have the first line EGFR exon 20. This will be in combination with Amivantamab. As you know, most people are taking one of two approaches in the first line EGFR exon 20. It's either a monotherapy or it's in combination with chemo. We've kind of taken a different approach given our profile. I think the key areas for differentiation for ORIC-114 are around the safety and tolerability and potentially CNS.
The reason that's really important is a lot of these drugs have some off-target toxicities in the form of QTC prolongation, elevated liver enzymes, and elevated ALTs as well. CNS is actually equally important. If you look at the data, and this is well documented, about a third of these patients present with baseline brain mets. The second thing is it's a point of first progression for a number of these patients as well. Having a CNS active agent could be significantly differentiated here as well.
Gotcha. I guess where do you think the bar is for efficacy that you want to show in some of these cohorts? Ultimately, again, I guess going back to the data for first line with Amivantamab, what do we want to see in these updates?
That's a great question. I think for the monotherapy first line EGFR exon 20, the bar for us is probably in the 55% range for the top line ORR. With the combination with Amivantamab, that probably goes to about 65% top line response rate. Obviously, we want to see good safety and CNS activity along that.
Gotcha. Maybe after these data sets, what's kind of the development plan, and how fast are you able to kind of gear up potential pivotal trials?
Yeah. Great question, Derek. We're set up to basically start our first Phase III study for ORIC-114 in 2026. That is in our plans right now. Whether that's EGFR exon 20 or atypicals, we'll kind of wait and see on that.
Okay. Gotcha. Maybe just on the cash runway, you guys are in a pretty enviable position among biotech land. Maybe just walk us through where you're at and ultimately what you're funded through.
Yeah. Great question. As you guys know, we completed a PIPE financing in May of this year with about $125 million. Subsequent to that, we did access the ATM and we drew down another $119 million. On a pro forma basis, at the end of the second quarter, we have $436 million in cash. That does give us cash runway into the second half of 2028. It's a pretty considerable runway. More importantly, that does assume full success for us. That assumes we're moving forward with ORIC-114. That assumes we're moving forward with ORIC-944. That's a fully burdened cash runway number. That runway gets us through the top line phase III readout through both the ORIC-114 study and the ORIC-944 study. Probably equally important is it gets us basically runway one year post the top line phase III data readout for ORIC-944.
That readout, if we start the study in the first half of 2026, that top line readout should come in mid 2027. We've got cash runway through the second half of 2028.
Gotcha.
I think, you know, as I'm sure lots of your covered companies tell you, Derek, we don't love where our stock price is today. We didn't love where it was earlier this year. The reason to raise as much capital as we did earlier this year was really to have that cash, like Dominic said, to get past both programs for phase III data readouts. Most importantly, that gives us a ton of leverage also with potential partners as we start to think about, because as you think about the long-term plans for ORIC-944, obviously, you know, one, maybe even two CRPC studies are quite doable by a team with our capabilities and with our balance sheet. As you think about broader development, that would start to go earlier and earlier in, say, the castration-sensitive prostate cancer setting.
Those are bigger studies, and those are things that are going to be quite amenable to having a big BD partnership to get in place. Ahead of starting those kinds of conversations, we want to have a rock-solid balance sheet so that we have maximum leverage as we embark on that.
Got it. Maybe last question, Jacob. Basically, I've been asking a lot of companies this, but I guess what do you feel is underappreciated about the story right now? Do people kind of get the data? Is it hard for them to make the jump with Mevrometostat and you guys? Obviously, cash isn't the issue. Where do you think that the story is underappreciated? Is it more just that we need to see more data and get confident about doses and some of this biomarker stuff? What is it, do you think?
Yeah. I would say everything, all of the above seems to be underappreciated. As it relates to ORIC-944, what I would say that is underappreciated is just the strength of the data set that people have already seen from the competition. The early de-risking data that you've seen from us, I think, leads us to the conclusion. Look, biotech drug development is always a game of probabilities. The probabilities have increasingly stacked in our favor over the last six to nine months as it relates to PRC2 drug development within prostate cancer.
Importantly, I think people are missing the fact that if those probabilities play out the way we think they're going to play out, which would ultimately lead to a positive first phase III study from Pfizer, there are very few PRC2 inhibitors that are in clinical development these days, especially as late in development and with as fleshed out a package in prostate cancer as ORIC-944. There is going to be a huge scarcity value that I think people just are dramatically underappreciating today. That's with respect to ORIC-944. With respect to ORIC-114, I think what's underappreciated is I think people, it's funny, like you sometimes talk to some investors, you talk about EGFR exon 20, even EGFR atypicals, and eyes kind of roll right away because they just feel it's too crowded and there's too many players. I agree fully, there's a lot of players. It is very crowded.
I would urge people just go back and look at the playbook you've seen and all these different targeted therapy targets within non-small cell lung cancer. The drug that ends up winning the day is a CNS penetrant drug. The reason for that, and people should go back and do the homework to understand what happens because people try to tease out those differences in things like resist response rates early on, and you won't find those differences in resist response rates. Go look at alectinib in the ALK space. Its resist response rate is not dramatically different than the first, second, and third ALK inhibitors that came before alectinib. What's dramatically different is the PFS.
Where that difference in PFS comes from is if you look at the subset analysis of the PFS in patients with versus without brain mets, what you will see is for any non-brain penetrant drug, you'll see a dramatic difference in the PFS for patients with versus without brain mets. Because of the high incidence of CNS mets in all these populations, that drags the overall average down on the PFS. What you see in a brain-penetrant drug is very little difference in the PFS for patients with versus without brain mets, which is why you see such long PFS. That story remains to be written for ORIC-114, but we're confident that as long as we keep showing that CNS activity, that will play out in a long-term PFS difference versus the competition.
Got it. All right. Cool. Thanks, guys.
Perfect. Thanks, Derek.
All right, good to see you.