All right, great. Well, good afternoon, everyone. Thanks for being with us for the Baird Global Healthcare Conference. My name is Colleen Kusy. I'm one of the senior analysts covering biotech here, and it is my pleasure to have with me ORIC Pharmaceuticals, with us, Jacob Chacko, CEO, and Dominic Piscitelli, CFO. So thanks for being with us, guys. If you want to kick it off with a corporate overview.
Sure thing. Thanks for having us, Colleen. ORIC stands for Overcoming Resistance in Cancer, and that, in a nutshell, is the mission of the company. It describes the pipeline of programs that we've put together over the years. We have three different small molecules that are in phase Ib dose escalation right now for various tumor types. ORIC-533 is a small molecule oral inhibitor of CD73, which we're developing in multiple myeloma initially. ORIC-944 is a PRC2 inhibitor, which is a complex that is relevant to a number of different tumors. We are focused on prostate cancer specifically, and then ORIC-114, which is, again, a small molecule. It's an inhibitor of EGFR and HER2 exon 20, which is a brain-penetrant compound, which is what differentiates that molecule.
Maybe taking a step back, 'cause I know we're gonna dive in on each of the three programs specifically here for the rest of the talk. I'll just talk a little bit at a high level about how we've put the company and the pipeline together, which I think are quite unique. First of all, we have a management team that's worked together for years, even prior to ORIC, so a very long-dated management team that's known each other for a long, long time. That's enabled us to put together the pipeline in a unique way, which is that we have both internal discovery, but we also complement that with opportunistic business development, as is the case with ORIC-944, the PRC2 inhibitor, and ORIC-114, the EGFR exon 20 inhibitor.
So the pipeline really has been put together from both of those sources. It allows us to take a path of best molecule wins, which essentially means we pick the targets that we like. We are focused exclusively on small molecule drug development, and if we have a way to develop a, a compound against one of those targets that we like internally, we'll do it, but if someone else externally has a better or more advanced approach, we're happy to take that as well, if we can in-license the compound, and so that is what's led to the pipeline that we have today. We have 3 readouts coming in the next 6 months or so, so I think a lot of activity that I'm sure we'll dive into later today.
Awesome.
But back over to you.
Well, thank you. Great, great broad overview. Let's start with ORIC-944, a drug we've been doing a lot more work on recently. Maybe just start with the background of the target, PRC2, and what makes it an attractive target in prostate cancer?
Sure. So PRC2, the first reaction we get from some people is they're not as familiar with the target.
Yeah.
And we always tell them: "You actually are familiar with the target - you just don't know." So PRC2 is a complex that's composed of three different subunits. The one that almost everybody in oncology knows is EZH2.
Mm-hmm.
That's where all the first generation of compounds have focused, is on EZH2, which is the catalytic subunit of PRC2. Our compound, ORIC-944, which we in-licensed from Mirati Therapeutics back in 2020, is an allosteric inhibitor of EED, which is a second subunit of the PRC2 complex. It's really just two different ways to drug the PRC2 complex. Now, PRC2 dysregulation shows up in a lot of different cancers. I would argue, we would argue that it is a validated target, in general in oncology, not specifically yet in prostate cancer, and the reason I say that is because tazemetostat is an EZH2 inhibitor, so therefore, the broader class, it's a PRC2 inhibitor, which is approved in two different indications, though not in prostate cancer.
The reason why we and everybody else with a PRC2 inhibitor is looking at prostate cancer is because the strongest biological rationale for PRC2 dysregulation leading to cancer is in prostate. And so it's no surprise, therefore, that everybody, with no exceptions that I'm aware of, who's got a PRC2 inhibitor, prostate is on their list of areas that they're developing.
Great. And so I wanna spend some time talking about the read-through from Pfizer's EZH2 program.
Mm-hmm.
You know, yeah, prior, prior generations of EZH2 inhibitors haven't worked that well in prostate cancer yet, but Pfizer highlighted some really interesting data recently on an earnings call for their EZH2 inhibitor, PF-06821497, in combination with enzalutamide. So for those that are unless familiar with the data, maybe run us through what Pfizer has shown for their EZH2 combo.
Sure, sure thing, and I'll actually start, Colleen, even a level higher, which is just what has been the issue with PRC2 inhibitors.
Yeah
... thus far, and what, therefore, why the Pfizer data set was so meaningful for the space. So PRC2 inhibitors in general, and this applies even to tazemetostat, which is the approved PRC2 inhibitor, have terrible drug properties. So tazemetostat and most of the first generation that has come through before of PRC2 inhibitors have very short half-lives. You're talking 2-hour, 3-hour, 4-hour half-lives. They often have CYP liabilities, autoinduction issues, essentially a multitude of issues that lead to poor drug exposure. And as an example of this, this is well documented from the time that Epizyme was developing tazemetostat. Tazemetostat, the approved agent in the space, has dose-dependent decrease in exposure. You literally give more drug to the patient, and you get worse exposure. That's a problem.
Yeah.
The first-gen compound from Constellation, same kind of thing. It had short half-life, it had CYP liabilities, it was dosed TID with a CYP modifier. This is just kind of what's been par for the course for the space. Now, the Pfizer compound seems to be a bit different. Best we can tell, it's got a half-life that may be closer to four hours. They haven't said officially what their half-life is, but staring at the PK curves, it looks like still quite a short half-life, though maybe a little longer than what's come before. And it seems that because they're dosing at hi- such high doses, they're getting to decent exposures.
Now, the data set that you referenced, I think, has really drawn a lot of attention to a space that we've been following for a while, which is in May of this year on Pfizer's Q1 earnings call... their earnings call, keep in mind, it's Pfizer's earnings call, they highlighted four programs that are in development stage that are of high strategic priority for them. One of them was this PRC2 program. What they highlighted was profound, which was that they took a cohort, two different cohorts actually, of patients with prostate cancer. Some of those patients had not ever received enzalutamide, others had received enzalutamide in the past. In both cases, they blew out of the water in a single arm setting, albeit, and with small N, they blew out of the water the PFS expectations you would've had.
So more specifically, the enzalutamide-treated population, so you're giving them enzalutamide for a second time, but in this case, they were doing it in combo with their EZH2 inhibitor. In that population, you would expect, on just redosing of enzalutamide, a radiographic PFS of 2-3 months. Instead, they were seeing 8.7 months. So 3x the PFS you should have seen, 6+ months, what you should have seen. In the enza-naive population, you should, given that all of those patients had received prior abiraterone and progressed, and in that population, again, it's very well known, in that case, you should get about 5 months of radiographic PFS, and they got 17.1 months of radiographic PFS. So by all measures, with the caveats of obviously single-arm studies and small N, the data were quite compelling.
What they also announced on that call is that they have a randomized study that is already ongoing, and they'll have data from that randomized study in the enza-naive population early next year.
Great.
And so all of that, I think, has really led to probably the first, what I'll call validated data set in prostate cancer for PRC2.
Awesome. And so talk to us a little bit about the design of the phase Ib study that you're running for ORIC-944. What type of patients are you enrolling, and what sort of dosing schedules are you exploring?
Yeah. So as is typical of a phase I dose-escalation study in this late-line prostate cancer population, it is an all-comer study, standard 3 + 3 dose escalation. The intent here is for us to escalate and pick a couple of different potential RP2D doses that could be taken forward into a phase II or into combination studies. And so, you know, nothing out of the ordinary there. I think in terms of what we are hoping to see out of that study, given that Pfizer and every other company with a PRC2 inhibitor has never shown single-agent activity-
Mm-hmm
... in prostate cancer, you know, we want to temper expectations-
Yep
... that, you know, it's not really about the single-agent activity here. It really is about the potential to combine with a potential AR modulator. But what will be crucial for us to show in that first update is exactly the sort of the counterpoint of what I just told you about the class, which is we are hoping to show good drug properties. I know people in oncology like to skip straight past the phase I development and jump straight to efficacy.
Yep.
But in this case, it really is about the basics-
Mm-hmm
... of good dose proportional increase in exposure. So we'll look at the, what the PK looks like, what the PD, the pharmacodynamic measures in a number of different ways look like, what the safety and the tox profile looks like. If you're going to really dose patients in a chronic setting, the way that with those kind of PFS numbers that Pfizer generated, you're going to want to have a tox profile for these, somewhat frail, older men, to be able to handle for over a year and a half. So it's some of those basics that we'll be looking for in that first data update. If nothing else, you know, half-life is going to be critical here. So our preclinical prediction of our clinical half-life is 10+ hours.
We'll want to see whether that validates in the clinic, and obviously, that would set us apart, dramatically apart from Pfizer and the other compounds that have come before.
Great. And so in that update, in 1 Q, would you expect that at a medical meeting or a company-sponsored event? And kind of how much data can we expect in that initial readout?
Yeah. Our general philosophy is to try to target medical meetings where possible and when things line up with when we are ready to present data on a program. In the case of Q1, there's obviously ASCO GU-
Mm-hmm
... which is the most high-profile, probably, medical meeting that's targeted towards prostate, so that's one option for us. But we also reserve the right to hold a separate company-sponsored call. In terms of total data and expectations there, we anticipate we'll have approximately 30 patients' worth of data. At least half those patients ought to be what should be a clinically active dose. And then we'll run through some of the basics, like I just mentioned, in terms of, you know, PK/PD and target engagement, efficacy, if there is any. And we'll kind of go from there as we think about what the path forward would be.
Great. Yeah, and so depending on what your data show, and probably with some read-through from what Pfizer shows, what are the next steps you'd be considering in prostate cancer?
Yeah. So there are three phenomenal AR modulators, second-gen AR modulators, that are used today in prostate cancer. Enzalutamide is one of them. There's also apalutamide from Janssen and darolutamide from Bayer. And so, really, the solution set for us would be if Pfizer's randomized data set looks, you know, quite positive, as we anticipate it would, but also just based on, you know, some of our own work and our own profiling, there's a lot of rationale of combining with an AR modulator. And so, you know, at that point, the next steps would be assuming that there's a positive signal, and that we take the drug forward, we'd want to do some dose finding in combo with, you know, one or more of the AR modulators, and then eventually run a combo study of our own.
Great. And any potential differences you would expect with targeting PRC2 via the EZH2 subunit versus the EED subunit that you're going after?
... Yeah, so if there's any theoretical advantage to targeting one or the other of those subunits, the advantage should go to targeting EED. And the reason for that is that, EZH2 inhibition could be susceptible to bypass resistance from EZH1. It could also be susceptible to acquired resistance mutations to EZH2. So for both of those, both of those are resistance pathways or mechanisms that are not relevant to allosteric inhibition of EED. So if you gotta target one or the other, EED would be better than targeting EZH2. And then apart from that, it, I kinda, it just comes right back to the drug property. So, and that's not really target specific-
Mm-hmm.
It's just which drug compound has better drug properties.
Great. So let's move to-
So in other words-
I'm sorry.
... anything, anything Pfizer shows or can show, we should be able to do better.
Great. So moving to ORIC-114, your EGFR HER2 exon 20 inhibitor, another exciting asset there. You'll have first-in-human data, in just a number of weeks. It's a fairly competitive space, so let's maybe start there. You know, you have two drugs approved for EGFR and HER2, and, a couple drugs for EGFR exon 20 specifically. So where do you see the unmet need that ORIC-114 would try to address?
Yeah, I wouldn't say it's a fairly competitive space. I'd say it's a highly, highly competitive space.
Yeah, thank you.
Yeah. But I think it's the first-order analysis is that it is highly competitive, and that's because if you just list off every EGFR exon 20 inhibitor out there, like you said, there's two agents that are approved. And then there's multiple agents that are in later-stage development. The problem is, and this is where you need to do the second-order analysis, nearly every single one of those compounds is not brain-penetrant, and has been proven time and time again in the lung cancer space with these TKIs. You need a brain-penetrant compound to have a best-in-class profile, and the reason for that is because 35% of patients at initial presentation have brain metastases. Even if patients don't have brain metastases at initial presentation, they will all, given enough time, develop brain metastases.
The brain is often the first site of progression for these patients. So in other words, not having a brain-penetrant compound is holding back the entire space. And as one example of this, the two approved agents you mentioned, both had accelerated approvals. Mobocertinib from Takeda just failed their confirmatory study. I think that is in part due to the fact that they've got such a toxic profile, but it is also in part due to the fact that they don't have a brain-penetrant compound. So there is only, that I'm aware of, us and one other compound that's at a similar stage of development from Blueprint, that have what are purported to be brain-penetrant compounds, and that is the entire crux of the differentiation here.
And then, like I said, you also have to have a safe and well-tolerated compound that avoids the toxicities of some of the compounds that have come before.
Got it. And so why has the field gravitated away from a brain-penetrant in the past?
Well, you mean... It's not that, in the exon 20 space, you mean?
Mm-hmm.
I don't, I wouldn't say it's gravitated away from a brain-penetrant compound. I would just say you also can't snap your fingers and have a brain-penetrant compound, so you've got to be able to design a brain-penetrant compound from the get-go. And I think a lot of these compounds were in development for many, many years, and, you know, maybe the companies hadn't prioritized it. I think now, if you look at ALK, ROS, classical EGFR, I mean, you can just run through the list of mutations in lung cancer, the best-in-class compound, if there, if one exists, it, it... The best-in-class compound is a brain-penetrant compound if there is one that's brain penetrant.
Mm-hmm. Got it. And so you're expecting to present your first data at ESMO-
Yep
... in late October. You've already hinted at some of the activity there, so maybe make sure we're all up to date on what you've said on the early data.
Sure. So, we at one of your competitor conferences in early June, because it was two days after ASCO-
Mm
... and because the other compound that I mentioned from Blueprint, that one that is purported to be brain penetrant, had just presented data, we did something that we don't typically do, which is we gave a little bit of a sneak peek-
Mm-hmm
... about the dataset, at least qualitatively. And what we said at the time was that, we had already dose escalated through multiple doses. We hadn't hit a maximum tolerated dose at that time, and we importantly mentioned that, we had already seen confirmed systemic responses at multiple dose levels. We also mentioned that we had seen evidence of intracranial activity at multiple dose levels, and that at the dose levels where we were seeing the systemic activity and the intracranial activity, the drug was well-tolerated in the patients. So that's what we had mentioned.
Mm-hmm.
Now, you referenced ESMO, which is where we've now said we'll have the official Phase Ib dataset for this compound. You know, I think in terms of what people ought to look for in that dataset and to set expectations, again, we'll have approximately 30 patients worth of data, at least half of those patients at what ought to be a clinically active dose. So very similar to the guidance I just provided you on the PRC2 inhibitor. I'll tell you, we're looking... We've been very consistent in this messaging, and a couple of your peer analysts from other banks, I'll leave unnamed, but have thrown out ORR thresholds.
Mm-hmm.
I'll tell you, we're not endorsing any ORR thresholds at this point. I just think it's foolish in this, for a Phase Ib dose escalation dataset, to start talking ORR thresholds. So there's two things, and two things only, that we've been looking for in this first dataset, and we've been very consistent about this messaging over the past year, which is, number one, the safety tox tolerability profile. And what I mean by that is, absence of untoward safety and tox, and I'd break that down in three different buckets. So number one is skin tox. You want to avoid the kind of skin tox that inhibitors like poziotinib have seen in the space. Number two is GI tox. You want to avoid the kind of GI tox that, say, mobocertinib, an approved drug in the space, has shown.
And number three, and this is an area that nobody in the space wants to talk about because a lot of off-target activity exists for the compounds in this space. You want to avoid non-EGFR related, but still drug related, tox.
Mm-hmm.
And so those are the three areas of tox that we want to show an absence of, because that means you've got a drug that can be well-tolerated, and dosed well, you know, for these patients in the space. And then the second thing that we want to show is preliminary evidence of intracranial activity. The reason I say preliminary is it's obviously an early phase I dataset. The N is not going to be large, but you will want to see, you know, at least a couple examples where we have intracranial activity.... And the reason for that is, back to your first question or your first premise, this is a very, very crowded space. So the way to differentiate ourselves, we have always said, is with the CNS activity.
If we can't even show some early evidence of CNS activity, then there's no point for us to continue developing the drug in the space. What we are not looking for in this first read is any kind of ORR %, and the reason I say that is this is a hodgepodge of different doses and a dose escalation.
Mm-hmm.
It's small N in any given cohort, so I just think it's premature to look for ORRs. The other thing that I think people need to kind of focus on is that every compound in the space, except for us and the Blueprint presentation at ASCO, has largely gotten to treat a naive population. So exon, no prior exon 20 inhibitors or very few patients with a prior exon 20 inhibitor. In the case of Blueprint, 75% of their patients had a prior exon 20 inhibitor. 60% of their patients had brain mets at baseline. We're gonna have very similar demographics for our compound. So in other words, the bar is very high in terms of the kinds of patients that are getting enrolled into-
Mm
... our study. And so all of that is to say it's too early to talk about ORRs. The way that I would think about the sequential de-risking for this program of data sets is, this year, it's about preliminary activity in the CNS-
Mm-hmm
... and the safety tolerability profile. Next year, assuming the drug continues, it'll be about ORR, 'cause at that point, we'll have a large enough data set at 1 or 2 recommended phase two doses that we can start to calculate ORRs.
Mm.
And then again, if it continues beyond next year, the dataset the year after that will be about durability, 'cause then you have a large enough N that's been followed for long enough that you can comment on durability.
Got it. And if we can just touch more specifically on what type of CNS activity we should be looking for. You know, do you need responses just in the brain? Do you need systemic responses?
Yeah, so, any CNS activity-
Yeah
... would be good to see because no one in the space really has shown much-
Mm
... in the way of CNS activity. What I'd say is that the bar here, too, Colleen, is quite high in the sense that go look at what the inclusion/exclusion criteria are for almost every compound in the space. They exclude patients with active brain mets. In other words, if a patient shows up with brain mets, the compounds or the companies will tell you that they have to have been treated with either surgery or radiation before they can even enroll in the study. We don't do that. We say that someone does not need to be treated with radiation or surgery before they can enroll in the study.
So if in a patient like that, we can see stabilization of their brain mets, if we can see disappearance of even, you know, a few of the brain mets, any of that would count as intracranial activity. As probably some of you are aware of, RECIST is really brutal in terms of how it grades responses in the brain. The reason I say that is most of these patients are gonna have non-target lesions. The way RECIST works in terms of grading responses in the brain is you have to get rid of every single target lesion, in other words, have a complete response in the brain, for that to be called a response.
Mm-hmm.
Otherwise, you know, if you get rid of two out of three lesions in the brain, that is what's called non-CR, non-progressive disease. That's the best you can hope for.
Mm.
And then the third category would be progressive disease. So that's why I choose my terms carefully, that we're hoping to show evidence of intracranial activity in at least a couple patients.
Got it. That's helpful. And so moving to ORIC-533, your CD73 inhibitor, you're taking a pretty unique approach with this asset, the only adenosine-targeted therapy in multiple myeloma. So maybe just kind of remind us why you selected multiple myeloma for this asset.
Yeah, I'll take that one. So you're right, most people with adenosine programs are focused on solid tumors and looking at combinations. Being a small biotech, we didn't think it was the best path forward for us. Obviously, we don't own our own PD-1, so we have to think about how to strategically in-source that. So, ironically, when we were a private company, one of our board members, who was and still is one of our top shareholders, who's known Ken Anderson for about 20 years now. Ken Anderson is kind of known as the godfather of multiple myeloma. He's associated with Dana-Farber. He's been doing work with CD73 inhibitors in multiple myeloma. So basically, we got the connection. We entered into a collaboration with Ken.
Basically, Ken has some patient-derived, patient-derived ex vivo models from patients with multiple myeloma. We ran our CD73 in their, this ex vivo model, and we saw a really interesting result. We saw restoration of T-cell activity, we saw multiple myeloma kill. And if you look back at published data with other multiple myeloma drugs in the same models, the data we saw was favorable. So this is what got us really excited about this program, and obviously, kicked off a phase 1b study and started enrolling patients in the first half of last year.
Awesome. So that phase Ib data, you've, you've guided towards initial data 4Q. Maybe walk us through what the, what the expectations are for that readout.
Yeah, this is similar to our other programs. We've been saying this since early this year. This is initial proof of concept data. This is about 30 patients' worth of data, and given it's early data, primarily from a dose escalation portion, this would be about 30 patients. We're looking at safety, we're looking at PK, we're looking at PD, and then any about 50% of these patients, we would estimate to be at clinically relevant doses, and it's in those 15 or so patients that we would want to see, excuse me, we'd want to see some level of preliminary antitumor activity there, and that'll kind of determine, you know, next steps for us.
Got it. And so what, what do you view as the bar for monotherapy activity in late-line multiple myeloma, just given we've seen some recent approvals of BCMA-targeted assets there?
Yeah, that's a great question. The reality is, we, we've seen mixed results with CD73 inhibitors in combination, and there's been actually no single-agent activity that anybody's reported. So I think it's a very low bar, just to properly set expectations there. And you're right, I think with the BCMA-targeted agents, you know, they've seen some really interesting results, you know, 60% response rate. So from a commercial perspective, the bar is really high, from a monotherapy standpoint. So from a commercial perspective and from a mechanistic standpoint, you know, it may make more sense, this program, to move forward in combination, pending some preliminary antitumor activity.
Awesome. And so on that topic, you already have a collaboration with Pfizer that you signed late last year, potentially looking at their BCMA CD3 bispecific antibody. So maybe what would go into that decision, whether to start that study, and how quickly could you move forward into the combination setting?
Yeah, we love that deal. Obviously, late last year, we did announce kind of two deals with Pfizer. It was a $25 million equity investment, which they invested in our stock, and it was a 60% premium. And more importantly, we entered into a collaboration agreement for a potential phase 2 study. In this phase 2 study, we would be combining our CD73 inhibitor with their BCMA-targeted agent, which just got approval. And the beauty of it is we have not given up any economics or control. It's totally our discretion on when we wanna move forward, if we wanna move forward with Pfizer. So I think it's just a function of looking at the phase 1 data in totality and see if it makes sense to move forward or not.
Again, that'll be our decision based on the data.
Great. And let's touch briefly on your preclinical asset. PLK4 is the target there, so maybe remind us where that is in development.
... Yeah, so this is a internally developed program. This is a synthetic lethality approach. About 20% of patients in breast cancer express TRIM37 amplification, and TRIM37 amplification requires PLK4 for growth and survival. So basically, we're getting at it indirectly by hitting PLK4. We declared our drug candidate late last year, and, well, you know, it's currently in preclinical talks. So assuming all goes well, that could be an IND candidate for us in 2024.
Great. And so pretty recently, you signed an $85 million PIPE transaction. So maybe talk to us about the rationale, provide some color on that decision.
Yeah. So, I'd say over the last 12-18 months, we've had a number of investors that have expressed interest in getting into the story. Given the limited liquidity in our stock, it's difficult to do that in the open market. You know, and then we've had one investor who led the deal, Nextech, who we've known for a number of years, and we've known the other investors for equally as long. So we just thought it made sense to kind of top off the balance sheet late last year. They all went under CDA, they all signed long-term lockup agreements, and we're actually able to get a premium on the PIPE, about 15% to the 30-day VWAP, which really is unforeseen, you know, not seen very often, I should say.
Mm-hmm.
So basically, what that gives us is more flexibility. Obviously, it takes off some of a financing risk. Obviously, nobody knows what the market's gonna look like later this year, or going into the new year, and it also extended our cash runway from the first half of 2025 into late 2025, and that assumes all three of our programs move forward successfully.
Great. So maybe just as we're wrapping up here, you know, ORIC has been kind of flying under the radar, I feel like, the last year and a half. But now we're on the cusp of 3 first-in-human readouts in the next 6 months. So maybe just in summary, you know, kind of wrap up for investors why they should be, you know, paying attention to ORIC over the next 6-12 months.
There's a lot to dig into.
Yeah
... in the pipeline, I would say. I think that for most companies of our stage and size, my guess is there's one program they can talk about, maybe two. In our case, we have three bona fide shots on goal for truly differentiated, potentially best-in-class programs. And I think, hopefully we've made clear today, we take it very seriously. People often use this phrase of potentially best-in-class and sort of throw it around as a cliché catchphrase.
Mm-hmm.
We really take that seriously. So when we do the diligence on these programs, whether it's internally discovered programs or when we're doing diligence on an in-licensed program, there must be at least one, if not more, hooks of how this is going to differentiate itself, either preclinically or in the clinic, or through the clinical development plan. And I think you have hopefully seen that in the case of 114, it's about brain penetrance. In the case of 533, it's a small molecule, oral inhibitor of CD73. There's one other one out there, everything else is an antibody. And while everyone else is developing in combo with PD-1 and pick your favorite tumor type, we found a certain angle in multiple myeloma.
And then in the case of PRC2, while that field has been riddled with poor drug properties, we've got a compound that we found that looks like, at least based on the preclinical profiling, has better drug properties. And so in all those ways, I think we've created multiple high probability shots on goal. When we discontinued ORIC-101, which, which was the lead program that we IPO'd on in April 2020, we discontinued that early last year. We, and, you know, also at the same time with the rest of small cap biotech, was sort of getting kicked in the teeth a little bit.
Mm-hmm.
I think now as we've continued to advance the rest of the pipeline, as we get closer to data readouts, there's been a lot more interest in the pipeline. The PIPE that Dominic mentioned, you know, that was catalyzed by this reversal in interest from investors. There was, like Dominic said, 12 investors that were interested in, at some point going in to be participating in a PIPE, and we went to 5, and not the rest.
Yeah.
And all five converted, and we didn't take all the money that was on offer.
Mm-hmm
... from those five either. So we wanted to do a prudent top-up of the balance sheet ahead of the upcoming data readouts. And I think that there's a lot for folks to dig into. I mean, one of the most common questions that we get when investors come into a meeting with us is, "Where are other investors focused? Where are they spending their time?
Mm-hmm.
We literally tell them: It's a third, a third, a third on each of the programs. It just... In the aggregate, investor interest is fairly equally distributed across the three clinical programs. So I love having three bona fide shots on goal. For anyone who can spend the time to diligence even one of those programs, I think you'll find that the, the valuation is quite attractive where we stand, and if you can actually spend the time to diligence more than one program, then I think there's a lot going on in our pipeline.
Yeah. Absolutely. Well, that was, I think, a fantastic summary and a very exciting time indeed for you guys. So thanks for being with us today.
Thank you, Paula.