Okay, I think we can get started then. So today, I'm Adam Vogel, with Wells Fargo's Biotech team, and today we have ORIC Pharmaceuticals on the stage. We have Dominic Piscitelli, CFO, and then CBO, Matt Panuwat. Gentlemen, welcome. Thank you for joining us today.
Yeah, thank you for having us.
So maybe we can start with just having you run us through, like, the high-level introduction of what ORIC's long-term vision is, and what sets you apart in the oncology space.
Yeah. So just a little background. So, ORIC is a clinical-stage oncology company, and our name really encapsulates our overall mission, which stands for Overcoming Resistance in Cancer. We've got a broad pipeline of potentially first-in-class and best-in-class clinical programs, which we'll talk about a little bit later today. And we actually have three ongoing Phase I-B studies, which we're expecting data over the next two quarters. And well, again, we'll get into a little more details on that as well. We've assembled a top-notch team. Our CSO, Lori Friedman, used to run Translational Oncology at Genentech. Our CMO, Pratik Multani, was the Head of Clinical Development at Ignyta, was responsible for the development and regulatory filings for entrectinib.
And then we have kind of a finance strategy BD team that came from the likes of both Ignyta and Medivation. So the overall strategy, obviously, is to bring new drugs to patients. Our key areas of focus, based on the team that we've assembled, is really around three main tumors: breast cancer, prostate cancer, and lung cancer, and we'll talk about, again, our clinical program. So just real quickly, I'll just hit on the three Phase I-B studies we have ongoing. The first one is ORIC-114. This is a brain-penetrant EGFR exon 20 program. This is primarily being studied in non-small cell lung cancer. We will have a presentation in October at ESMO, so next month. The second program, ORIC-533, this is an orally bioavailable CD73 inhibitor. Here we're taking a different approach.
We're actually studying this as a single agent in multiple myeloma, and the current guidance on this is to have initial data in the fourth quarter of this year. And then the third program, ORIC-944, this is a PRC2 inhibitor, an allosteric PRC2 inhibitor, that we're studying in prostate cancer, and we said we'd have our initial data in, in the first quarter of 2024. One thing from a strategy standpoint, based on the team that we've put together, the capabilities we've built out in-house, we kind of take a two-pronged approach to building the pipeline, which really comprises of both internal research and discovery, as well as BD, which Matt heads up the BD department here. So when we look at our pipeline today, you know, we've got four programs, three are in the clinic, one is preclinical.
Two of those, ORIC-533 and PLK4, are the results of our internal research and discovery, and then ORIC-114 and ORIC-944 are the results of business development opportunities.
Wonderful. All right. So maybe, yeah, we can dive in a little bit more in your clinical programs. If you wanna start maybe with the EGFR inhibitor, ORIC-114. Maybe if you could summarize where you're at, where it's differentiated as far as EGFR inhibitors and exon 20 mutations, for example, against Blueprint's BLU-451.
Yeah, sure. So when you look at the EGFR exon 20 space, there's two approved agents, amivantamab and mobocertinib, and then there's a number of other competitors in the clinic. I think the key factor here, there's a gap in the sense that there's not any CNS-active agents. BLU-451 that you mentioned is one that we believe claims to be CNS-active. They did have some data at ASCO in June, so we're watching them closely. But the two approved agents, as well as a number of other agents that are in the clinic, just are not CNS-active. And the reason this is important in this patient population is, when you look at the demographics of these patients, about 35%-40% of these patients will have brain mets.
So that is an underserved, underserved patient population right now, and so that's kind of where we're focused on. This ORIC-114 was specifically designed to be selective against both EGFR exon 20 and HER2 exon 20, but most importantly, it's the brain-penetrant aspect that we think we want to differentiate on. So that's kind of the initial proof of concept data that we want to show in October, in that ESMO.
Gotcha. Okay, so maybe diving a little bit deeper into that, maybe you can walk us through the trial design and how you manage patients with brain metastases.
Yeah. Matt, want to take that one?
Sure. Yeah, so the phase I is a typical dose-escalation study. We are enrolling patients with exon 20, both in the EGFR and HER2 side. You know, our enrollment criteria is pretty broad, so we're allowing patients that have previously been treated with exon 20 inhibitors. We are enrolling patients with active brain mets, and so those are features you typically don't see in the other studies in exon 20. What we will be sharing next month at ESMO, it is dose-escalation data. We're expecting about 30-35 patients' worth of data. We expect about half of those, so call it 15-18 patients at clinically effective doses.
And then what we have seen from other studies in exon 20, you know, approximately a third of those patients should have some history of brain metastases, so in the mid-single digits. And that's where we really think the differentiation of our molecule, what it's designed to do, is to be brain-penetrant and have intracranial activity, and so that's what we're aiming to show. We think that would be a promising feature of our molecule. It is early data. You know, this will be the first time we're presenting, and so, you know, we don't wanna focus too much on ORR, given it's a small number of patients at a number of different doses, so it'll be a little bit early to make those comparisons. And then also durability. We won't be able to make.
You know, we won't have a long follow-up period for our patients. And so those will be focuses of, of future updates.
Yeah, and maybe just add one other point, that's a great summary, Matt, is when we look at the patients here, and you compare it to the patients that were in, you know, with amivantamab, with mobocertinib, and even Cullinan, we think these, the, the patient population that we'll have will be more in line with what Blueprint shows. If you look at the Blueprint poster, I think about 75% of those patients had seen a prior exon 20. The point being that just now that the, the landscape is out there, there's more available treatment for these patients. The patients that we're enrolling in our study are gonna be more heavily pretreated than the ones that I just previously mentioned.
Gotcha. Okay. Looking forward to the data. So maybe then just on that 50% population that you're expecting to have clinically relevant doses, one-third you expect will have CNS metastases, then I assume you're— will you be breaking out the data for that too, or will that just be presented all in one cohort?
Yeah, we'll provide sufficient detail. Obviously, we think, you know, providing clarity and transparency around the CNS aspect is key. That's the key differentiator here. If you look back—y ou know, again, we think, first of all, we think, you know, if we demonstrate this, we think there's an accelerated approval path going forward here as a single agent, because it still is a severe unmet medical need. And I think that's our key area of differentiation here. So that's the area we need to focus on, and we want to be as transparent as possible on the data that we have. But to Matt's point, again, this is early POC data. We want to prove the hypothesis that we do have intracranial evidence of intracranial activity in these patients, along with systemic.
And then, you know, the later data would be more about what is the OR, what is the duration of therapy. You know, longer term, the benchmark probably is more in a 35%-40% response rate. But again, given the early nature of this data, that's not the intent of this.
Okay. So what—o verall, then, what would be a win for you, with this?
Yeah, I mean, a win, I guess a win for us is if you see a couple patients out of the, you know, the five or six that Matt kind of broke down for us, that you do see evidence of intracranial activity, right? True intracranial activity, you're seeing responses, not systemic responses in patients with CNS Mets, but responses in the brain.
Gotcha. Okay.
I'd probably add in safety profile, I think will be important too. A lot of the other EGFR exon 20 inhibitors are limited by a number of toxicities. So I think establishing that the safety profile is trending, you're seeing some activity, especially in these difficult to treat patients with brain metastases. I think that would be important proof of concept.
Got it. Okay, yeah, and that kind of leads into my next question, just kind of pulling back and looking at it again, like, what are the challenges of developing an exon 20, inhibitor in this space?
Yeah, I don't think it's anything different than any other drug. I think, again, here, it's a matter of making sure you get the right patient population. Obviously, as I said before, you're getting more, later line patients because the treatment paradigm has changed. But no, enrollment is going well. We're excited about the program, and, you know, we'll present the data next month.
Wonderful. Looking forward to that. Then maybe moving on to your CD73 inhibitor, ORIC-533. Maybe for everyone, if you want to just maybe walk through the rationale behind targeting CD73 in multiple myeloma.
Yeah. Matt, you want to take that one?
Sure. So CD73 is a target in the adenosine pathway. And so it has been a target that has been studied by mostly the big pharmaceutical companies for the last 5-1 0 years. The most advanced program is AstraZeneca. They have oleclumab that has positive Phase II randomized data that they presented. It's now in a Phase III study. So that's really the proof of concept in the field so far. A number of other companies also have antibodies to CD73 that they are developing in a similar way. It's primarily solid tumors. It's primarily in combination with PD-1. And so that's where the field is going, has been going. So our ORIC-533, it's differentiated in that it is highly potent.
We have actually published a lot on this, but it seems to have more potent adenosine inhibition than the antibodies do. It seems to have more, adenosine inhibition than the A2A receptors do. And so we think we have a really nice profile preclinically. What's also differentiated about our molecule is that it's orally bioavailable, and so we are the first CD73 inhibitor that is orally bioavailable. And so we think that's a unique feature. And then, as you mentioned, you know, we are the first to go after multiple myeloma, and so that is also. We have a unique clinical development path. We have been working on this program, in collaboration with the Dana-Farber Cancer Institute, with Ken Anderson. He's one of the leading KOLs in multiple myeloma.
He has been studying adenosine, being a driver of resistance in multiple myeloma. It has been observed that as patients progress with multiple myeloma, they have increasing levels of adenosine. He has been working with our CD73 inhibitor. He has developed an ex vivo assay, where he actually takes bone marrow samples from patients that are treated at the Dana-Farber, and basically puts therapeutics in this assay. When he uses a CD73 inhibitor, he actually sees lysis of multiple myeloma cells as a single agent. And so we found that pretty compelling. Obviously, he has been leading the charge. He is a proponent of this target in multiple myeloma, and that was really the foundation for us to go into multiple myeloma. And so we initiated that study early last year.
We will be presenting initial phase I data for this program in the fourth quarter of this year.
Will that be as, like, a PR or a company event, or a conference?
Yeah, it's. You know, our. We typically like to target major medical conferences, if possible. But again, that's if possible. If it doesn't work, we could always pivot and do a company-sponsored event, but similar to what we're doing with 114, we'd like to use ESMO for that. We haven't specifically said which conference it would be at in Q4, but obviously that's, that's kind of the current thinking. We'll probably try to target that if, if it works out.
Okay. Can you elaborate then on how your thinking has progressed with 533 in combination, and specifically your partnership with Pfizer?
Yeah, a couple things on that. I think, I think, you know, I think it's fair to say that the data on CD73 inhibitors has been mixed, right? There's been no single agent activity with any CD73 inhibitor that we're aware of. There has been some interesting data in combination with PD-1 from AZ, where they showed, in lung, they showed the COAST data, they showed a hazard ratio, I think it was 0.44. So there has been some interesting data, but overall has not been overwhelmingly positive. I think the bar for monotherapy here is extremely high in this in that sense. And also, you think about the competitive landscape. If you look at, you know, these BCMA-targeted agents, whether it's CAR T or bispecifics, they're showing really great response rates, 60%-70%.
So the more likely scenario here from a mechanistic standpoint, from a commercial standpoint, if this goes forward, is more in combination to your point. As you mentioned, we did sign an agreement with Pfizer late last year, and it's really two components to that agreement. There was, you know, one component was very, very straightforward. It was a $25 million investment from Pfizer. You know, they have this Pfizer Breakthrough Growth Initiative Fund. They invested $25 million at a premium. Jeff Settleman, their oncology CSO, joined our SAB as well. And then the other component, which is actually really, probably more interesting to us, right? There's a collaboration agreement that Matt was able to strike with Pfizer, which basically gave us the right to start a phase II study combining our CD73 inhibitor with their BCMA bispecific.
The beauty of that is we would basically get to use Pfizer's global infrastructure to operationalize the study. We would pay them for this study, they would supply free drug, which is a big component of the cost, but we get to leverage their, their knowledge of the multiple myeloma space, their network in operationalizing this study. So, again, that is totally at our discretion, to do that or not to do that. You know, that we are not—we didn't give up any economics on the deal, and we're not restricted from, you know, obviously speaking to other strategics about potential combinations as well. So, whether or not we move forward, obviously, will be our decision.
It'll be, you know, based on the totality of the data that, you know, we show later this year, as that kind of continues to mature.
Okay. Maybe can we dive into the scientific rationale of combining their BCMA bispecific with your CD73 inhibitor?
Yeah. So I think a couple things. I think, one, you know, adenosine, high levels of adenosine, you seem to wear out T cell function, and so T cells get exhausted, they lose, lose their activity. And so if you can reduce adenosine, at least what you can show pre-clinically, you preserve T cell function. And so T cells are kind of key in multiple myeloma. And as you think about the mechanism of Pfizer's BCMA, it's a BCMA CD3 bispecific antibody. So that is basically taking T cells and attacking the multiple myeloma cells. So if you have something complementary to that, where you can actually increase the function of T cells in the microenvironment, I think it makes strong scientific rationale to combine that with, with BCMA. So I think that's, you know, what Pfizer was excited about that potential combination.
The other thing is the BCMA bispecific antibodies obviously have a lot of toxicities that they're dealing with, and so they're very difficult to administer. We know that, so it is important to have a very strong safety profile. I think there are limitations on what you can combine with BCMA therapies. And so, again, having a safe profile, you know, is what we hope to show with our molecule, to make sure it's safe to combine, not only with the BCMA therapy, but other therapies as well. And as we look at the field, other companies with CD73 inhibitors seem to be actually relatively clean from a safety standpoint. There's no, you know, on-target toxicities that people generally are concerned about with CD73, so I think that's another benefit of the target.
Gotcha. Okay, then maybe coming back to your decision-making on moving forward on a phase II combo with that then, what goes into that? You kind of alluded to it, the data package and things like that, but, yeah, what remains, and is there a timeline that you're working on, you're working within?
Yeah, we haven't committed to a specific timeline. Again, it's totally at our discretion. I think, you know, in selecting combinations, I think Matt kind of hit the key points, right? One, you want to make sure you have strong scientific rationale. Two, you want to make sure you want to have a clean side effect profile. As Matt said, you know, some of these agents, you do have pretty harsh side effects, so you want to make sure that what you're combining is not going to compound that. Ideally, you want to see some level of activity. Now, I'm using the word activity versus responses more broadly. You know, it doesn't necessarily have to be, you know, X number of responses.
If we were to see, you know, a drop in paraprotein in both the urine or the plasma in these patients as a single agent, I think that would be pretty interesting, you know, clinical activity in our minds, and that could get us excited to move forward or not. And obviously, we, you know, we could also discuss that with Pfizer as well. So it really depends on what we see as a result of the kind of the monotherapy study that we're doing.
Great. So looking forward to that in the fourth quarter. Okay, then maybe moving on to your PRC2 inhibitor ORIC-944, do you want to walk us through the rationale of that and why you chose to focus in prostate cancer?
Yeah. So maybe a little background on this. This is an asset that we in-licensed from Mirati in 2020. And most people, when you say PRC2, aren't necessarily familiar with the complex. When you kind of explain to them EZH2, which obviously there is a number of drugs against EZH2, there's actually approved drugs, tazemetostat, against EZH2 as well, they get more familiar with it. So when you look at the PRC2 complex, it has two druggable subunits, both EED and EZH2. So this is really shutting down that complex via the EED subunit.
And what we did here was we licensed from Mirati, and Mirati did that we really like here, they really profiled a number of both EZH2 inhibitors and EED inhibitors, and based on that profiling, looking at drug properties, looking at the, you know, the potency that they saw, they decided that this was their, their lead molecule. So we took that under MTA, we ran it through a number of difficult-to-treat prostate cancer models, and we saw a tumor growth inhibition in these in vivo models for about 80%-90%. If you look back and see what the, kind of the first generation EZH2 inhibitors showed here, was more along the 40%-50%. So that's what really got us excited here. So, I will say that people have been-...
exploring EZH2 inhibitors in prostate for a long time, and the data has been mixed. And I think some of the reasons for that is one is drug properties. I think some of the first generation EZH2 inhibitors had really, really poor drug properties. You're talking about a half-life of 2-3 hours. You're talking about a decrease in exposure or repeat dosing. So we think that contributed to the poor results that I've seen. Late last year, we saw some interesting data, both from Pfizer and from Ipsen. Their data was in combination with enzalutamide, which is an AR modulator, in these patients. And Pfizer showed a PFS, radiographic PFS benefit of 8.7 months, and Ipsen actually showed a benefit of about 11 months. So we thought that was really, really interesting.
What really caught our eye was on the Q1 earnings call in May. Pfizer kind of highlighted the data again. What they did here, they kind of broke out the patients that had previously seen Xtandi and those that had not. So we'll talk about both these subgroups separately. So the first group, which were patients that had seen and failed Xtandi. So they failed Xtandi, then they went on to the combination of Xtandi plus their PRC2 inhibitor, which is referred to as PF-06821497, and they showed a radiographic PFS of 8.7 months. So both Matt and I worked at Medivation. We know the prostate space well. If you go back and look at historical benchmarks there, you probably see a 2- 3 month benefit in that patient population.
Even more interesting, if you look at the patients that were Xtandi naive, these are patients that had failed abiraterone and then went on to the combination of Xtandi plus PF-06821497, their PRC2 inhibitor, and here they showed a benefit of 17 months. Two caveats. These are single-arm studies, and, you know, this is the n of 12 for regards to the, the Xtandi-naive patients. 17 months on the study, their CSO actually referenced the historical benchmark here, which is known as the CARD study, and that benchmark is about 5 months, 4.8 to be exact. That's a tripling of the expected PFS benefit in this patient population. We thought that was really, really interesting, kind of validates kind of what we thought of the potential of PRC2s in prostate cancer.
Pfizer does have a randomized study ongoing, where they're comparing the combination of Xtandi plus their PRC2 versus Xtandi alone. This is an open-label, phase II randomized study, and they're expected to report data early 2024. So we're keeping a close eye on that. Based on this data, if they're able to replicate that, this is really, really fascinating data for prostate cancer.
So when you look forward to that data readout, how will that shape your thinking about your own program with ORIC-944 and its combination potential?
Yeah, again, I'd say that similar to 533 , with PRC2 inhibitors, nobody has shown single-agent activity. So maybe the more likely path here is in combination. So for us to move forward in combination, I think we need to see a couple of things. One, we want to make sure we have good drug properties. As I said before, the first generation EZH2 inhibitors did not have good drug properties. The second, we need one of two things to happen. We need to see good single-agent activity with 944 in the ongoing study, or we want to see confirmatory data from Pfizer or from Ipsen in this patient population. That would be enough for us to move forward in combination.
Okay, great. So, any other items on 944 you'd like to hit on before maybe moving on to your preclinical?
No, again, the readout here is pretty consistent with, you know, the other two we're saying about. So this will be in Q1. Again, we'll target a major medical conference if it makes sense. The patients, we're talking about 30-35 patients. Again, half of those will be at a clinically relevant dose. Again, here, we're going to look at safety. We want to look at PK, we want to look at PD, and any early, preliminary antitumor activity that we see.
Okay. Then again, what would be a win there for you guys?
Yeah. So the monotherapy is a high bar here, again, because we haven't seen anything. For a combination, we haven't given specifics, so look at the totality of the data. But again, if we see some level of activity there, that could be enough for us to move forward. That could be responses, you know, RECIST response or PSA declines, that could interest us to move along. But again, if even if we didn't see that, but we do see the Pfizer data, I think that would be compelling enough for us to move forward.
Got you. So maybe a go or no-go decision for a combo is going to be differentiated on, on how you see the data in combined with Pfizer's readout?
Yeah, we're looking at Pfizer's data and our drug properties.
Okay.
Yeah, we think our, you know, the monotherapy data from us could be interesting. You know, really looking at these drug properties, which we think is important. So establishing a good half-life, having nice bioavailability, having good PK, good PD. I think we can look at all of that in phase I and hopefully make comparisons to others. If we look at the Pfizer molecule, it does appear to have a pretty short half-life. Their RP2D is 1,250 BID, plus in combination enzalutamide, so it doesn't seem to be an optimal therapy. So we think that, again, if we have the strong drug properties that we see pre-clinically. We think we can show some, you know, hopefully some nice data as a phase I monotherapy. That would give us confidence to combine going forward.
Interesting. Okay, so how much juice is being left on the table then, with that shorter half-life, do you think?
Yeah, that's TBD.
TBD.
We don't know. We need to see it.
Fair enough.
You know, they haven't disclosed a lot of it. This is Pfizer, so they don't need to disclose as much as smaller companies, so.
Yeah, they haven't put out as much data. If we go back, what's interesting, one of the earlier generation molecules is tazemetostat from a company Epizyme, now Ipsen. They're approved in sarcoma and follicular lymphoma. They're also being studied in prostate cancer, so in a randomized study. But I point that out, if we go back and look at their phase I data, it's a drug with really poor drug properties, a really short half-life, about three hours, and they dose that molecule BID. But when you look at their phase I publication and they show you PD activity, there's some pretty good PD assays you can use to measure activity in the clinic, they're only inhibiting target about 30%-40% if they're RP2D. And so again, we think that is important.
If you kind of think about leaving stuff on the table, as you mentioned, we think that all the drugs that came before us just aren't effectively inhibiting the target enough in the clinic. We think that that has been a flaw that has been plagued a lot of the earlier generation molecules.
Okay. Can you remind us, too, the percent you're hitting with your molecule?
Yeah, we haven't disclosed that. That'll. Well, that'll be some of the information we include in the poster early next year.
Okay.
Yeah, similar to our other 2 programs, that'll be the first time presenting initial phase II data in Q1 next year.
Okay, great. And then I guess diving into your, yeah, preclinical assets, PLK4, do you wanna maybe walk us through the significance of that program and what the developmental timeline is there?
Yeah. So that's another one we're excited about. So as Dominic said, we have full internal R&D capabilities. This is a first-in-class novel target that we can see. We see we're the only ones that we're aware of that are actually working on this target. This comes with one of our areas of focus, which is breast cancer. So our research team has strong expertise in breast cancer. And the target is interesting because it's a way to attack TRIM37 amplifications, and that's a specific marker, mostly found in breast cancer, but other tumors as well, neuroblastoma and other smaller tumor types. But breast cancer is what we're most excited about.
And so TRIM37 amplified tumors are dependent on PLK4, and so if you can inhibit PLK4, it is a synthetic lethality target that actually can prevent growth and prevent growth of TRIM37 amplified cancers. And so we have presented some interesting data there. We have selected a development candidate, and we are moving forward with that program. I think what's also exciting, we've been working on this target for a while. The mechanism, the target, has also been validated by independent labs. So there were two Nature publications that featured the target a couple of years ago. So we think, again, this is kind of an increasingly exciting target from a scientific mechanistic standpoint, and so we're excited to move that program forward.
We haven't given any specifics on the timeline, other than we have recently selected a development candidate. We did share some preclinical data at AACR, and so I think this is a program you'll hear, you'll hear more about.
Great. Looking forward to it. Then maybe in the last part of this segment, we can touch on the financial and business development aspect of ORIC. So maybe you can walk us through your cash runway, what milestones does it get you to? We have, as you said, multiple data presentations coming up in the next few quarters.
Yeah, I'll take the first one. I'll let Matt take the business development one. So we recently did complete a PIPE financing for about $85 million in late June. With that financing, that did extend our cash runway from the first half of 2025 until late 2025. And the way we give guidance, we kind of assume full success, so that does assume that all three programs move forward during that time period, and that assumes that we retain full rights. So if there was ever a scenario where one of the assets attrited, you know, or we you know, discontinue the program or we partnered a program, obviously, that would extend our cash runway into 2026 easily.
With regards to milestone, we haven't given long-term milestones, but the three milestones obviously go through Q1 of 2024, so we're well capitalized through those milestones at this point.
Great. And then maybe Matt, as Dominic mentioned, you can walk us through your approach in thinking about business development and what criteria you look at for potentially bringing in external assets.
Yeah, absolutely. So I mean, one of the things. I've been at ORIC almost five years, so one of the things that attracted me to ORIC was, one, the team, and then two, the strategy of the company, to actually have internal research to develop new drugs, but also doing business development from the beginning. And so we thought that was—I think that's somewhat of a unique approach, you know, to take from such an early standpoint. And so we have executed on that with the ORIC-114 program. We in-licensed the ORIC-944 program we brought in as well. And so we're very specific, I think, on what we bring in. I think thematically, we wanna bring in programs where we actually have areas of expertise.
Just to be specific on that, the ORIC-944 program was specifically brought in for prostate cancer. Prostate cancer, we didn't talk about our history too much, but our founder, Charles Sawyers, was the inventor of enzalutamide and apalutamide, so two of the standard of care in prostate cancer. We have a team that has executed clinical studies in prostate cancer, so we feel, anything there, we, you know, we know exactly how to execute, we know, you know, what, what interesting data looks like. That was an easy one for us that made a lot of sense, and again, we're looking forward to presenting that data.
Our ORIC-114 program, our exon 20 inhibitor, we brought that program in because our clinical team, the whole clinical team essentially comes from a company, Ignyta, as does our CEO. And so Ignyta was responsible for getting entrectinib approved, so it's a targeted therapy in lung cancer. And so we have a team that knows lung cancer extremely well. And so when we had the opportunity to bring in ORIC-114, that was something our clinical team knew exactly how to develop. And so I think anything within business development will be consistent with that. It'll be areas that we know, and I think the areas that we have flagged that are highly interesting to us is prostate cancer, breast cancer, and lung cancer. And so those are the areas.
We are focused right now on just small molecules. At least historically, our business development has been validated targets, but with some differentiation. And so we are always looking to bring in programs. And we brought in 114 and 944 very closely together. Similar timeline is when we brought them in. It was also on the same timeline as 533. And so, but we're always looking for new opportunities, and so we, you know, we are picky. We don't need anything because we have a pipeline today. We have an internal research program, but at the same time, you know, there are plenty of opportunities out there, and so, I would expect business development, you know, more business development from us in the future.
Okay, great. Well, on that note, gentlemen, I think we can leave it there. Any closing comments you'd like to leave the audience with?
No. Thanks again. I appreciate the opportunity to be at the conference, tell our story, and obviously, the great scheduled one-on-one meetings.
Wonderful to hear. Yeah. Thank you, Dominic. Thank you, Matt.