Celcuity at Needham Conference: New Frontiers in Cancer Treatment

On Thursday, 10 April 2025, Celcuity (NASDAQ: CELC) presented at the 24th Annual Needham Virtual Healthcare Conference. The company highlighted the potential of its drug, gabatolizumab, in treating breast and prostate cancer. While the company expressed optimism about upcoming data readouts, it also acknowledged the challenges and uncertainties in the competitive oncology landscape.

Key Takeaways

• Celcuity's gabatolizumab is poised to impact breast and prostate cancer treatment, with Phase III VICTORIA-1 study results expected this quarter.
• The company maintains a robust cash position of $235 million, funding operations through 2026, with potential access to an additional $70 million.
• Gabatolizumab aims to establish a new standard for second-line HR-positive breast cancer by inhibiting multiple pathways.
• Celcuity plans to mitigate stomatitis in patients with a preventative mouth rinse, enhancing the drug's safety profile.
• The company is also advancing studies for the PIK3CA mutant population and prostate cancer, with data anticipated later this year.

Financial Results

• Cash Position: Celcuity ended Q4 with $235 million, supporting development through 2026.
• Potential Additional Funding: Access to $70 million is contingent on positive data readouts, including $30 million from a debt facility and $40 million from cash warrants.
• Capital Efficiency: The company is focused on maintaining valuation and capital efficiency in future fundraising.

Operational Updates

• VICTORIA-1 Study: The Phase III study's wild-type cohort data is expected soon, comparing gabatolizumab to fulvestrant.
• PIK3CA Mutant Population Study: Results are anticipated in the second half of the year.
• Frontline Breast Cancer Study (VICTORIA-2): Site selection is underway, with enrollment expected in the second quarter.
• Prostate Cancer Study: Data expected by the end of the quarter, focusing on gabatolizumab with darolutamide.

Future Outlook

• Strategic Goal: Celcuity aims to position gabatolizumab as a benchmark for second-line HR-positive breast cancer treatment.
• Triple Pathway Inhibition: The company hypothesizes that the most effective regimen will target the estrogen receptor, CDK4/6, and the PAM pathway.
• Data-Driven Decisions: Future capital raises will depend on data outcomes and market conditions.

Q&A Highlights

• Tariffs and FDA: No expected impact from tariffs or changes in FDA leadership.
• Gabatolizumab's Uniqueness: Its comprehensive PAM pathway blockade addresses compensatory resistance.
• Dosing Schedule: Aligned with palbociclib to enhance pathway inhibition.
• Route of Administration: The IV formulation is seen as beneficial for reimbursement and patient costs.

In conclusion, Celcuity remains cautiously optimistic about gabatolizumab's potential and invites readers to explore the full conference call transcript for detailed insights.

Full transcript - 24th Annual Needham Virtual Healthcare Conference:

Ita Markowski, Biotech Research Team Member, Needham: Good morning, everyone, and thank you for joining us at and Company's twenty fourth Annual Healthcare Conference. This is the final day and almost made it the whole week without any technical difficulties. So apologize for the delay, but my name is Ita Markowski. I'm a member of the biotech research team here at Needham. It is my pleasure to have Brian Sullivan, chairperson CEO of CellCutie with me today.

As a reminder, any viewers who are watching through our conference portal are able to submit questions to ask ask the question feature below the video feed. So Brian, I will run things, a little quicker today. But before going deeper in the company, I do want to spend just a minute or two on the current market conditions. There's been a lot of changes even within the past week, But can you maybe start by addressing potential impact of tariffs on CellCutti as things stand today at least, as well as the recent leadership change at the FDA? I think the latter is probably more relevant given CellCutti's current stage of development, but I'm curious to hear your thoughts.

Brian Sullivan, Chairperson, CEO, CellCutie: We don't expect the tariffs impact us at all. And as far as the FDA, again, we interact with the agency quite a bit. Just based on breakthrough status, we we have the opportunity to, you know, conduct meetings on a fairly regular basis. And to date, at least, we haven't seen a disruption. We're not seeing any email bounce backs.

So the people that we normally interact with, are still there. And so I I don't know how representative our situation is, but I I can say nothing has changed so far. I obviously can't project that going forward, but, no no cause for concern at this point.

Ita Markowski, Biotech Research Team Member, Needham: Great. Great. And now now we can, with that out of the way, move more into CellCutity. I think most people are familiar with the company in general, but maybe just if you could touch on a little bit about yearly program, get it to list it.

There have been previous attempts to target p I three k. So what makes your product unique in that sense?

Brian Sullivan, Chairperson, CEO, CellCutie: Sure. Well, one of the most important, considerations, to take into account when evaluating, you know, our drug, gabatolizumab, is is that it's addressing a pathway that's very different from most oncogenic pathways. And and that's because this pathway, we refer to as the PAM pathway, PI3K, AKT, mTOR, has multiple components or nodes that need to be targeted because they interact with each other. And essentially, inhibiting one of these nodes in the absence of the other can drive compensatory resistance, which essentially negatively impacts efficacy. And so when this pathway's role was first discovered, pretty much every major pharma developed a pan PI3K mTOR inhibitor to address what was understood to be the biological imperative in addressing disease involving this pathway, which was comprehensively blockaded.

It was only because that was challenging to equipotently hit all these targets and doing so without inducing a lot of toxicity that you saw a migration towards what we refer to as single node inhibition, hitting alpha or mTORC1 or AKT. But that wasn't necessarily the optimal approach to address efficacy. Get up essentially solves the riddle. At least in our view, it solves the riddle. We're able to, with very low nanomolar concentration, inhibit this path comprehensively.

And to date, safety data we've generated suggests that patients can tolerate the drug and stay on it. Discontinuation rate associated with our drug has been very low, less than ten percent, nine percent in breast cancer. And their most recent study, four percent with our phase three dose. So that suggests that we are able to get the benefit of comprehensive blockade without the drawbacks that I think other inhibitors of this pathway have encountered from a safety standpoint.

Ita Markowski, Biotech Research Team Member, Needham: Right. I think that's a good overview of maybe some of the differentiating features. I do wanna spend majority of today's conversation on the upcoming pivotal readout. But before we do, can you maybe just take a minute to recap the Phase I data you saw while also touching on there are some differences in activity between arms T and D of this study?

Brian Sullivan, Chairperson, CEO, CellCutie: Sure. So the study, evaluated one hundred and thirty eight patients in various arms that enrolled specific populations, treatment naive, prior CDK, or prior endocrine only, in different schedules. And so all patients received Galatilica with Palvo and either Letrozole or Filvestrant, depending on their treatment status. Each of the arms met the OOR endpoint. In the treatment naive patients, frontline patients, the objective response rate was seventy nine percent, and the median PFS was over forty eight months.

So compares very favorably to what's been reported, let's say, with palbolaetrazole, where twenty five months meeting PFS was the outcome for those patients. In RMD of the study, we think is the most relevant second line portion of that study because these patients were treated with our phase three dosing schedule. The objective response rate was sixty three percent, and the median PFS was twelve point nine months. And, again, those compare to historical benchmarks for patients in this setting where, for instance, fulvestrant, which is a control in our phase three study, has reported in a number of studies in the population we're evaluating in our VICTOREA-one of around two to three months median PFS. So we think know, we we have shown at least with our preliminary data, you know, good distance from what we think is likely to occur with our control therapy.

As far as RMC and RMD, you know, RMC was and RMD both were evaluating patients with treatment with prior CDK. There are two primary factors that need to be taken into account to explain the differences in outcomes. So RMC had a thirty six percent objective response rate, median of five months. So not as favorable as RMC. So the difference in outcomes we think reflects, first, the fact that they enrolled different patient populations.

You know, RMC enrolled more heavily pretreated patients. Two thirds of the patients were third line or worse. Fifty percent had prior chemo, whereas RMD had only twenty percent prior chemo and only and two thirds were second line patients. The other variable that's important to understand is that in arm c, patients were only on their prior therapy for about five months, whereas in arm d, they were on their prior therapy for about thirteen months. And that's that's typically a pretty good prognostic factor of what outcomes to be in their subsequent treatment.

So net net, the patients in RMC had less favorable prognostic factors. You know, they're basically more heavily pretreated, so you wouldn't expect them to do as well. But we think the other factor that's very important to consider is the different dosing schedule. You know, RMC patients were treated on a weekly basis, once a week, whereas patients in RMD were treated three weeks on, one week off. And the rationale for that approach was that it synchronizes the dose schedule with the palbociclib dose schedule.

And because in this disease, you have three pathways interact that essentially are driving the disease and interacting with each other, our hypothesis is that it's important to inhibit these pathways simultaneously, or if you're not inhibiting them, inhibiting them to do that simultaneously as well. And so we saw a wide difference when we did some regression work, analysis of other factors that could explain the big difference in, objective response rates and PFS between the arms. And and what was clear from that analysis was that the dosing schedule was the most important factor. And so that's why we took that fact that, schedule forward, into phase three.

Ita Markowski, Biotech Research Team Member, Needham: And I think that's a good opportunity to just remind everyone a little bit more about the study design of the ongoing phase three, as well as maybe how the eligibility criteria are different than the phase one. And maybe one additional question just because it's come up. So when you're speaking about the study design, did you also mention how there's measures to essentially prevent outperformance of the fulvestrant arm. I know, you know, typically, it's two to three months, but some recent studies like post Monarch, showed a little higher, but I think there's some caveats with that data.

Brian Sullivan, Chairperson, CEO, CellCutie: Okay. Well, as far as the design, so we we are evaluating all comers, and then, we're assessing their PIK3CA status and assigning, patients who lack a mutation, to a wild type cohort, and then those with mutation to a mutated cohort. The statistical analysis plans for each of those cohorts is separate. And we're reporting out we expect to report out the data for the wild type cohort of patients this quarter. In that study, you know, with three arms, so we're evaluating the triplet of GATA, PALOVO, fulvestrant, and then comparing as the primary analysis, primary endpoint, that to fulvestrant.

We also have and that's arm a versus arm c. And then in arm b, we have a doublet, get a fulvestrant. And we're also comparing that to arm c fulvestrant. And that's a co primary endpoint. And we're testing those endpoints hierarchically.

So, essentially, we have to you know, it it allows us to spare alpha analysis that makes it efficient. But test a versus c, you know, the triplet versus fulvestrant first, if favorable, then test b versus c. And a similar approach in the wild in the mutant cohorts where we're comparing the triplet, in this case, to a control of alpolypsin fulvestrant. And then we have a separate arm that's is more of an export for to provide exploratory data with the doublet of geta fulvestrant. As as far as, you know, the differences in the population for the phase three versus the phase one, we think there are two key criteria that are different and actually kind of result in what we think would be considered a more favorable prognosis for the phase three population and the phase phase 1b.

In the phase three trial, we're not enrolling patients. They're not eligible if they've received prior chemo in the advanced setting, whereas the early phase study did. And that's relevant because patients who have received prior chemo in the advanced setting tend to receive less benefit from a targeted therapy. And so, again, probably to the good. The other difference is that the the phase one b study only enrolled patients who had visceral disease.

Eighty percent had liver lung mets, which was disproportionately high amount. None of the patients had bone only mets. And whereas in the phase three study, we are allowing patients who have bone only mets as long as they have a measurable soft tissue component, lytic or lytic plastic lesion. And that's relevant because patients who have bone only disease tend to respond more favorably, have a more durable progression free survival period than patients who have, you know, visceral mets. And and so by including a portion of those patients, which we think it's likely to be in the fifteen percent range.

Again, it it's a more favorable prognostic factor. The other way to look at it is is that in R and D, the median duration of of of the patient's prior therapy was around thirteen months. The typical treatment period for women who are receiving a CDK foursix and endocrine therapy, who are endocrine sensitive, is about twenty months, plus or minus. And so we would expect the patients who are enrolling in this study to have had duration of treatment that's closer to that twenty month period than the thirteen month period. We can't project exactly what we think.

But we think most of the patients that we enroll primarily be second line. Patients who've had two endocrine therapies are eligible. But we think just because of the treatment paradigm, it's most likely that we will have a population that's primarily receiving their second line of therapy.

Ita Markowski, Biotech Research Team Member, Needham: Great. Great. And, you know, there's a lot of attention, the wild type readout or the wild type portion of the study is expected to read out in the coming months. Can you just guide us on what you're looking for in terms of activity, and particularly in terms of medium PFS? But I know you also, have been talking about hazard ratio as well.

So what are your expectations going into

Brian Sullivan, Chairperson, CEO, CellCutie: it? Sure. So we expect to stay in this quarter. If if you look at, I think there have been four randomized studies that have a useful fulvestrant's control enrolling a population similar to ours. And the key factors to take into account are, you know, do they have measurable disease or not?

Are they have they had prior CDK? You know? And and those are the two most important characteristics to to consider when looking at that data. Those results, you know, three of those studies reported two months median PFS for fulvestrant, you know, 1.9, one point nine, two point one. The other study about 2.8, two point nine.

And so we think it's most likely I mean, just if if we just use that data and say you know, develop a probability, we'd say it's most probable that it would be in that two and a half, three months range. And as far as, you know, what we need to see, you know, we again, there's two two components to that. One is what do you need to see to be clinically relevant? You know, what what is a clinically meaningful outcome? And, you know, the input we received from KOLs in this area as well as regulators is that you need to show an incremental benefit of roughly three months relative to control.

Now we would certainly hope to be better than that. You know, we're not indicating that's, you know, where where we'd be % satisfied, but but certainly that gets you in the game. And there's a good example of a drug that was recently launched in breast cancer that had a benefit of about that much called capivacitor, which is only approved to treat patients with a PIK three c m mutation. But nonetheless, you know, in that study area, Bovastin was two months, and their BNPFS was five point five months in patients who had prior CDK. Well, that drug in less than in in twelve months, you know, their run rate revenue run rate was 600,000,000, which tells me two things.

One, there's a very, very strong interest in any drug for this patient population that can provide an incremental benefit. And in the case of capivacitor, it didn't demonstrate superiority relative to what had been the standard of care for these patients, which is a drug called alpulipsid, you know, p a three alpha inhibitor. You know, the the alpulipsid reported about seven months in a separate study. So it would suggest that CAPI at best is maybe comparable efficacy, but has a much better safety profile. And so with only a better safety profile, dramatic shift away from apalipsa, dramatic increase in overall penetration of of this drug for this population.

And so it just, I think, provides some validation of the relevance of of, you know, incremental three month benefit, being important. The other characteristic that matters, and you alluded to this, is the hazard ratio. Because what's what's occurring now is that there are several studies that will be reporting or have reported recently that are enrolling a pretty heterogeneous population, which means they're enrolling first second line patients, patients who've had prior CDK or not. And as a result, when you report that data, it's very hard to interpret. And certainly, if you're an oncologist, you need to know, well, how well can I expect this drug to work in a patient who's already had CDK four six?

And so the data that that's been provided then, the absolute numbers are hard to just assign much weight to. So the hazard ratio helps net that out, and it allows you, you know, to do a cross trial comparison that factors out some of the differences in the control arm, for instance, because it allows you to, you know, in effect, isolate the proportional effect on the drug. And and so, you know, we we we think that will help give a tool to investigators. And and and we've we've heard from them that, you know, improvement in the hazard hazard ratio ultimately when the data has, you know, different hard to interpret data sets, you know, ultimately becomes what they have to rely on. And so we think that'll that'll be very relevant.

And so we'll we'll make sure we we help put, you know, that type of data in in the proper context because that's really what we're talking about is how to assess data properly. You know, nine months if your control was five months is different than nine months if your control was two months. So the absolute number is the most relevant. It's it's the comparative result to your control and the proportion of benefit that provides.

Ita Markowski, Biotech Research Team Member, Needham: Right. Right. And maybe just on the topic, it's like you said, it is coming up very soon. In terms of what we can expect from a disclosure perspective for the top line results, do you think it's mostly gonna be focused around, medium TFS hazard ratio and then saving some of the other analyses for a medical meeting per se?

Brian Sullivan, Chairperson, CEO, CellCutie: Yes. No. That's exactly, what we expect to do.

Ita Markowski, Biotech Research Team Member, Needham: Okay. And I do wanna spend some time just because they've garnered a lot of attention recently on next gen SERDs and CDK inhibitors in development. What are your thoughts on the potential impact of these agents on the space?

Brian Sullivan, Chairperson, CEO, CellCutie: Well, I think the data has been pretty clear. I mean, I think there's been four or five now that have reported data. Several haven't shown any activity in either ESR1 mutant or wild type. The ones that have shown activity have only shown activity in patients that have an ESR1 mutation. And the first one that was approved, elacitrant, reported an incremental benefit relative to fulvestrant in the assert one mutant patients of around one point nine months.

Hazard ratio was 0.55. Amlunestrant, for instance, in that same population only reported a hazard ratio of point seven two. Veritas didn't didn't provide specific guidance, so I can't speculate there. But but they enrolled kind of a similar population. They excluded patients who are endocrine resistant, so you'll you'll need to focus on the hazard ratio there.

But I think bottom line is those drugs most likely will will primarily, become, what's used in the third line. If if if our data is the way we hope it is, we would expect to establish hopefully a new benchmark for second line patients. And then these these surds for patients who have an ESR one mutation would likely be used there. They're getting combined with other drugs. You know, some of the of the data that's been presented today is is hard to interpret, so it's unclear yet exactly what would get approved with those drugs.

So I I don't wanna speculate on that. But I I think and, our underlying hypothesis in in this setting is that to the standard of care regimen will be the regimen that addresses the biology underlying biological drivers of the the disease most effectively. And in HR positive breast cancer, we have three cooperative pathways, the estrogen receptor pathway, CDK four six, cyclin d one, and and the PAM pathway. And we think ultimately the regimen that will establish standard of care will be the one that can effectively inhibit all three of those pathways. And so then I think that suggests that a doublet or a monotherapy will will have a difficult time offering comparable efficacy because there'll be an untreated disease mechanism, the PAM pathway, that will will potentially limit its efficacy.

And as a result, those those doublets or those monotherapies would most likely then be used as a subsequent line of therapy, third line. We'll see. I mean, obviously, all hinges on our data. But but, you know, that's that's our hypothesis and kind of how we we see things shaking out if if our hypothesis is proven correct.

Ita Markowski, Biotech Research Team Member, Needham: Sure. Sure. And and you did mention that, you know, this was a surge that there's been mainly activity restricted to ESR1 mutations. I know it's different mechanisms of action, but is there any plans or is there a sub analysis for ESR1, status in the VICTORIA-one study? And have you had any data from the phase one to suggest whether there's different activity levels?

Brian Sullivan, Chairperson, CEO, CellCutie: Right. We had some limited data in the early phase. It was small sample size. We haven't reported it. But I can say there was nothing about it that suggested any differences in that.

And and for instance, if you look at fulvestrant, just one data point, no difference in outcomes in patients who have or don't have ESR1 mutations. So, you know, I think it's unlikely we would like, you know, we we don't we wouldn't expect to see different results. Most importantly, because to the extent that you maybe are not inhibiting the estrogen receptor pathway, effectively, if patients have an ASILI mutation, most likely what's happening is this tumor cells are becoming more reliant on these other pathways, CDK foursix or PAM. So if you're essentially shutting off those escape routes, you may limit the negative effect that a suboptimized ER inhibition would create because you're essentially maybe addressing the resistance mechanism that, let's say, fulvestrant doesn't address as effectively as an oral SERD. But but that, you know, that's a TBD.

Ita Markowski, Biotech Research Team Member, Needham: Okay. Yeah. And I think I think that makes sense. And, yeah, one, I guess, unique feature of ketotelisib is is an IV formulation, versus a lot of the other FIC three inhibitors are oral. Based on your market research so far, do you think physicians will have a preference of IV versus oral?

What does your data suggest so far?

Brian Sullivan, Chairperson, CEO, CellCutie: Sure. Well, I I think, again, it's always important to put the route of administration in its proper context. You know, you know, oncologists who are, you know, selecting therapies for their patients are focused on three criteria, and one of which is by far the most important, which is efficacy. They're treating patients who have fatal illness. They're trying to prolong their lives and delay the progression of their disease as long as possible.

And so guidelines as well as just treatments paradigms are really focused around giving patients the most efficacious therapy that they can tolerate. And so that's the second criteria. How well can these patients tolerate a drug? So all things being equal, if you've got two drugs with similar efficacy, the one that's more tolerable will win. And that's what we're seeing in the mutant space with CAPI versus opalipsin.

Well, again, if you go further down that list, if you've got two drugs, comparable efficacy, comparable tolerability, route of administration, which one's more convenient? You know, can become the tiebreaker. Absent that, we just don't think the route of administration is going be a big factor for most patients or physicians because of what I just said. Unless the patient has some logistical challenges in being able to come to the office. But we think that'll be, a, addressable with different techniques for getting drug to patients.

But b, you know, for the most part, you know, the the these patients are close enough to a facility to get administered. But there's some other factors that are relevant as well. You know, for instance, the largest drugs, the most important drugs in breast cancer are all infused drugs, you know, Herceptin, Perjeta, you know, new drug that's been launched recently, and HER two, as well as pembro. And secondly so there's an infrastructure. These doctors are used to prescribing.

Isn't obviously chemo is used in later line settings that's IV administered. But IV therapies are a medical benefit. And so the reimbursement process for them is much more streamlined. Oral therapies fall into the pharmacy benefit and can have a lot of pre approvals that just make access to the drug more difficult and more problematic. Secondly, again, oncologists can recover costs, treating patients with infused therapies that they can't recover with oral therapies.

You know, treating them, you know, infusing is is a expense they can recover. And general care management process is easier. Another factor that doctors are very sensitive to is exposing their patients to significant out of pocket costs. You know, most patients, you know, they're average Americans. They they they can't afford big out of pocket.

Medical benefit really has much, much more limited out of pocket exposure than pharmacy benefits. So so the short story is we actually think it will be an advantage for us net net because of the factors I just mentioned. And, ultimately, what's gonna really make the difference or really make drive the decision will be efficacy, and we hope we have a significant advantage there.

Ita Markowski, Biotech Research Team Member, Needham: Right. And do wanna make sure we spend a few minutes, on the PIK3CA mutant population because there is, a readout expected second half of this year. What do you think a win looks like in that population?

Brian Sullivan, Chairperson, CEO, CellCutie: Well, again, it's similar to in the wild type. If we can show an incremental benefit, relative to our control of, three months or more, that that'll be a big win. You know, again, Capavacitor a showed a three month benefit relative to fulvestrant, but but, really, that wasn't the standard of care in that setting. It was alpulipsum. And they didn't demonstrate.

I mean, it was just untested, but you can compare the trials and say, well, clearly, it doesn't seem that it was any better. But, again, had a better safety profile. In our case, we we think showing an incremental benefit is is not unreasonable for us to expect. But, also, you know, our our data suggests we we will be well, you know, well tolerated. And and, you know, the general level of discontinuation rate that we've reported so far is is less than has been reported for a drug like captivasitur or certainly elpulipsin.

And so we think we have a couple potential levers that will be in our favor. But baseline three months will get us over the hump, and then we have the benefit as well of favorable safety profile being better.

Ita Markowski, Biotech Research Team Member, Needham: Yeah. Yeah. And speaking of the safety profile, I know that as rates of hyperglycemia and discontinuation are favorable. There was some stomatitis, I believe, seen in the phase one study. Can you just mention how you are mitigating that?

Brian Sullivan, Chairperson, CEO, CellCutie: Sure. So two things. In the phase one b, what was, I guess, we thought reassuring was that when patients were treated for stomatitis with dexamethasone mouth rinse, for most patients stomatitis reversed, which is why we were able to have such good, we interpreted as very good, low discontinuation rates. So that's one factor that even with the rates of stomatitis we had in phase 1B, it didn't impact patient's ability to stay on the treatment. But nonetheless, a study had found with everolimus, which induces stomatitis, a more severe stomatitis that isn't as responsive to post manifestation treatment.

They did a study, though, because it was impacting their ability to get tape used, where they provided dexamethasone as a prophylaxis. Patients would use it prior to using the drug and and use it for the first two months of treatment. And that significantly reduced the incidence of stomatitis and severity of cases that were reported. And so we're we're using we're we're mandating that patients for the first two months of treatment to first two cycles use a dexamethasone mouth rinse. And and so as a result, based on at least the data that was reported for everolimus in their study, it's called the SWISS study, we would expect to see lower rates, potentially substantially lower rates of stomatitis than were reported in the phase one b study.

But regardless, we think because of the way how well patients respond to dexamethasone even after it's manifested, we think it's one of those adverse reactions that is very well managed and has has ultimately minimal impact on on patients' ability to to stay on the drug.

Ita Markowski, Biotech Research Team Member, Needham: And you're also evaluating get a frontline setting breast cancer. Can you just talk about where that study is currently?

Brian Sullivan, Chairperson, CEO, CellCutie: Sure. So, you know, we've selected our sites. We've begun activating those, and we expect to enroll the first patient in this quarter, second quarter. You know, this is a study that's that's focused on patients who are are considered to be endocrine therapy resistant. And they have much worse prognosis.

These are patients who had early breast cancer. And while they were on their adjuvant endocrine therapy, typically, letrozole or tamoxifen, the disease progressed either while they're on that therapy or or shortly thereafter within twelve months. So it's not a good prognosis for those patients. They don't respond that well to the current standard of care, about seven months based on some data that was reported recently. And so we we think big unmet need.

There's there's evidence because the drug, an alpha inhibitor, was approved to treat this patient population. We view that as as as kind of a very, very validating to our hypothesis. We We we think we'll have a number of advantages relative to that drug. But, nonetheless, we think we're solving we have the opportunity to solve a big unmet need.

So we've got roughly 200 sites identified, selected that'll be global similar to Victoria one. All of the Victoria one sites that we wanted to participate in Victoria two are are participating. So, you know, that's gratifying to us that these these patient these these sites worked with GETTA, and based on that experience, you know, wanted to continue to help us develop it. We are doing safety plan. I guess we're running out of time, but just one other fact.

In that study, we're allowing investigator choice of CDK. So we'll actually be allowing investigators to use either ribo ribociclib or palbociclib, which will, you know, we think we we it has been viewed favorably by investigators.

Ita Markowski, Biotech Research Team Member, Needham: Great. And like you mentioned, we are getting close to time. Hopefully, you could just run a couple minutes over, since you had a late start. But you do also have a prostate cancer study ongoing with data coming soon. What are you hoping to see from this initial readout?

Brian Sullivan, Chairperson, CEO, CellCutie: So the the primary endpoint. So we're testing, geta, combined with darolutamide, which is an AR inhibitor, and single arm study was testing two doses. So we're at the dose finding stage of this, in this, program. So we have two doses, hundred and twenty milligram, and then hundred and eighty milligram, dosed, three weeks on one week off. Where our primary endpoint is landmark PFS at six months, and we're comparing that to historical control, where in this setting, patients are getting a switch of androgen receptor therapy from what they received in the frontline setting.

They get, you know, roughly five, five and a half months. And so we'll be comparing six month rates for for that patient populate for for those for those studies to what we see and, you know, do a do a statistical analysis to see whether we see a a meaningful difference. And that would be the data that we'd like to report top line, sometime this towards the end of this quarter.

Ita Markowski, Biotech Research Team Member, Needham: Okay. And then maybe one final one for me. Just especially important in the current market conditions. Can you remind everyone company's financial position runway and then anything that wasn't covered this conversation? I think we So so

Brian Sullivan, Chairperson, CEO, CellCutie: we so we had 235,000,000 at the end of q four, and we expect that to allow us to fund our development programs through '26. If our data is positive, you know, we would gain access to an incremental 30,000,000 from our debt facility. We have some warrants that'll expire after our data comes out that we there are cash warrants that we would expect to be exercised that would bring in, if they're exercised, an incremental 40,000,000. So immediately after, we have not immediately after, but very soon after we have data, we would expect to have access to an incremental 70,000,000, which which is good in this capital environment. You know, we, you know, we we're mindful of valuation, and we wanna, you know, be capital efficient in, how we raise subsequent, capital.

If data's favorable, it wouldn't it's it's not unusual for companies to raise money in conjunction with that data, and, you know, we certainly will be considering that as well.

Ita Markowski, Biotech Research Team Member, Needham: Great. Well, thank you for the time today, Brian, and it's gonna be exciting next few months for Celcuity.

Brian Sullivan, Chairperson, CEO, CellCutie: Yes. Well right. Well, thank you for having me.

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