Celcuity Inc.

Good afternoon, ladies and gentlemen, and welcome to the Socuity First Quarter 2025 Financial Results Webcast Conference Call. At this time, all lines are in listen-only mode. Following the presentation, we will conduct a question-and-answer session. If at any time during this call you require immediate assistance, please press star zero for the operator. I would now like to turn the conference over to Apurva Chaluri with ICR Healthcare. Please go ahead.

Thank you, Operator, and good afternoon to everyone. Thank you for joining us to review Salcuity's first quarter 2025 financial results and business update. Earlier today, Salcuity Inc. released financial results for the first quarter ended March 31st, 2025. The press release can be found on the investor section of Salcuity's website. Joining me on the call today are Brian Sullivan, Salcuity's Chief Executive Officer and Co-Founder, Vicki Hahn, Chief Financial Officer, as well as Igor Gorbachevsky, Chief Medical Officer, who will be available during Q&A. Before we begin, I would like to remind listeners that our comments today will include some forward-looking statements. These statements involve a number of risks and uncertainties, which are outlined in today's press release and in our reports and filings with the SEC. Actual events or results may differ materially from those projected in the forward-looking statements. Such forward-looking statements and their implications involve known and unknown risks, uncertainties, and other factors that may cause actual results or performance to differ materially from those projected. On this call, we will also refer to non-GAAP financial measures. These non-GAAP measures are used by management to make strategic decisions, forecast future results, and evaluate the company's current performance. Management believes the presentation of these non-GAAP financial measures is useful for investors' understanding and assessment of the company's ongoing core operations and prospects for the future. You can find the table reconciling the non-GAAP financial measures to GAAP measures in today's press release. And with that, I would now like to turn the call over to Brian Sullivan, CEO of Selcuity. Please go ahead.

Thank you, Apoorva. Good afternoon, everyone, and thank you for joining our first quarter financial results conference call. We have an exciting year ahead of us with multiple upcoming clinical data readouts. We expect to report top-line data from the PIC3CA wild-type patient cohort of our Phase 3 Victoria 1 trial in Q3 2025. and from the PIK3CA mutated patient cohort in Q4 2025. We also anticipate reporting preliminary top line data for the Phase 1B portion of our Phase 1B2 trial in prostate cancer in late second quarter. And finally, we made great progress activating trial sites for our Phase 3 first line Victoria 2 trial over the past few months. In our view, each of our three programs has the potential to generate significant levels of revenue. If these programs ultimately result in regulatory approvals, we estimate that nearly 200,000 late-stage cancer patients globally would be eligible to be treated with getotelicib. Let's turn now to our Victoria 1 trial. Our Phase 3 Victoria 1 trial is designed to evaluate getotelicib in combination with fulvestrin with and without palbociclib in patients with hormone receptor-positive HER2-negative advanced breast cancer whose disease has progressed on or after treatment with a CDK4-6 inhibitor. The VICTORIA-1 trial includes two patient cohorts with independent statistical analysis plans and primary endpoints. The primary endpoints for VICTORIA-1 are progression-free survival, or PFS, as assessed by blinded independent central review. The study is designed to independently evaluate a PIK3CA wild-type cohort and a PIK3CA mutant cohort. For the PIK3CA wild-type cohort, there are two primary endpoints that will be tested hierarchically, whereas the PIK3CA mutant patient cohort has a single primary endpoint. The primary analysis for each patient cohort is triggered upon reaching a predefined number of progression events. And based on the current blinded event rates, we anticipate the primary completion of the PIK3CA wild-type patient cohort will occur in June, which would allow us to announce in a press release top-line data in the third quarter and to present full results from this patient cohort at a medical conference later in 2025. If positive, we expect the data will support our first new drug application, and if approved, our transition to a commercial stage company. If proven effective, gadotelicib in combination with fulvestrin and palbociclib could offer a new standard of care for patients with HR-positive HER2-negative advanced breast cancer whose disease progressed on or after treatment with a CDK4-6 inhibitor. For the PIK3CA mutant patient cohort, we anticipate reporting top-line data in the fourth quarter of 2025. The current second-line treatment paradigm for HR-positive HER2-negative patients with selective estrogen receptor degraders, or SIRDs, like fulvestrin or elacetrin, as single agents, or one of three approved PAM inhibitors combined with endocrine therapy. However, each of the PAM inhibitors only targets a single PAM node, such as PI3K-alpha, AKT, or mTORC1, which is suboptimal because the uninhibited PAM nodes can induce compensatory resistance. In patients who've received prior treatment with a CDK4-6 inhibitor, None of these single-node PAM inhibitors have demonstrated efficacy in patients who have PIK3CA wild-type tumors, while only the PIK3CA-alpha and AKT inhibitor have reported benefit in patients with PIK3CA mutations. And these results are consistent with the non-clinical data that shows these single-node inhibitors are three to four times less potent in breast cancer cells without PIK3CA mutations than in those with them. Of course, we recognize the foundation of Geta Thalyssib's role in this treatment landscape will require that get it to be well-tolerated and report a clinically meaningful result measured in terms of the incremental improvement in both PFS and the hazard ratio relative to standard of care. Breast cancer care wells and regulators generally consider an incremental improvement in PFS of three months relative to its control to be clinically meaningful. Current NPFS, or Median Progression-Free Survival, benchmarks for patients pretreated with a CDK4-6 inhibitor, patient population we're evaluating, are modest. only two non-chemo-related therapies have been evaluated in this patient population and received approval. One reported a 1.9-month incremental median PFS improvement relative to its comparator in patients with ESR1 mutations. The other did not report median progression-free survival improvement relative to current standard of care, but it did report a more favorable safety profile in patients with PIK3CA mutations. Despite the modest or no efficacy improvements on this benchmark, Both of these recently approved drugs has experienced rapid market adoption and penetration. Each drug reached revenue run rates within the first 12 months of launch estimated to be nearly half a billion dollars despite approvals that only addressed 30 to 40% of the eligible second line patient population. We believe this demonstrates the significant interest amongst oncologists for new treatment options for these patients and the relatively low bar required to obtain adoption and market penetration. Potentially more important data point than incremental PFS benefit to consider in advanced breast cancer when assessing the clinical benefit of one therapeutic regimen relative to another is the hazard ratio. And this is because recent randomized studies evaluating therapies for patients with HR-positive HER2-negative advanced breast cancer have enrolled widely heterogeneous patient populations. Since physicians make different treatment decisions for patients depending on on, among other factors, how many lines of therapy, how well they responded to prior therapy, and which type of therapy they may have received, results from these studies can be hard to interpret using absolute median PFS or incremental PFS benefit alone. As a result, top-line MPFS results from these studies don't provide sufficient clarity about the actual benefit a particular patient population may receive. The hazard ratio essentially factors out the differences in study populations, and thus provides physicians with a more objective benchmark. We thus not only hope to report a hazard ratio that is statistically significant, but one that compares favorably to the hazard ratio reported for other therapies available for second-line patients whose disease progressed while receiving a CDK4-6 inhibitor. If gadotilisib ultimately does receive FDA approval for both the PIK3CA wild-type and mutant populations, we estimate the peak revenue potential for this second-line indication could exceed $2 billion with just 40% market penetration. I'd like now to turn to our first-line breast cancer program in our Victoria 2 trial. The Victoria 2 study is a global phase 3 open-label randomized clinical trial evaluating the efficacy and safety of gadotelicib in combination with fulvestrin, plus investigators' choice of either ribociclib or palociclib as a first-line treatment for patients with HR-positive, HER2-negative advanced breast cancer, and these patients are endocrine therapy-resistant. Approximately 638 subjects will be assigned to a cohort based on their PIK3CA mutation status. The primary PFS endpoint for each of the cohorts will be evaluated independently. Prior to initiation of the Phase III portion of the trial, a safety run-in study will be conducted in 12 to 36 participants to assess the safety profile of getatilicib in combination with ribosiclib and fulvestrin. And during the first quarter, we completed our site qualification activities and we're now focused on activating the nearly 200 sites we've qualified across North America, Europe, Latin America, and Asian Pacific. We've also begun screening patients and expect to dose our first patient during the second quarter. Current standard of care first-line treatment for most endocrine therapy-resistant patients includes any of the three approved CDK4-6 inhibitors combined with fulvestrin. Results from a recent trial suggest that the median PFS period for patients receiving one of these three regimens is only seven to eight months. And these results compare poorly to the median PFS of 25 to 27 months reported for patients who are sensitive to endocrine therapy and who receive a similar regimen, highlighting the significant need for more effective therapies for patients with advanced breast cancer that are resistant to endocrine therapy. Now I'd like to turn to our Phase 1b2 trial, That's evaluating the safety and efficacy of getotelicib in combination with darolutamide in patients with metastatic castration-resistant prostate cancer whose disease progressed while receiving a next-generation androgen receptor inhibitor. The Phase 1b2 study evaluates getotelicib in combination with darolutamide, which is an androgen receptor signaling inhibitor, in patients with metastatic castration-resistant prostate cancer. We've completed enrollment of the phase 1B dose escalation portion of the study and anticipate reporting top line data by the end of the second quarter this year. Since we're at an earlier phase in this program, our focus is optimizing the dose and schedule for this tumor type and drug combination. This data set will include approximately 36 patients, half of whom will have received a 120 milligram dose of gadotilicib, the other half a 180 milligram dose. Each are administered on a three week on, one week off schedule. And we're comparing both the landmark PFS at six months and safety profile of these two arms to each other and to historical control data for second-line metastatic castration-resistant prostate cancer patients who were retreated with an androgen receptor inhibitor. And finally, we're excited about the opportunity we announced today to collaborate with the Dana-Farber Cancer Institute and Massachusetts General Hospital to evaluate getotelicib in combination with bemaciclib and letrozole in patients with endometrial cancer. The rationale to initiate this study is based on compelling historical clinical data that indicates women with ER-positive, or type 1, endometrial cancer may benefit from treatment with a PI3K-AKT mTOR inhibitor, like getathalysib, in combination with endocrine therapy. Additionally, results from a prior phase 2 clinical study evaluated getathalysib as a monotherapy in patients with either type 1 or type 2 endometrial cancer, and these results were encouraging. So I'd like now to turn the call over to Vicki to review our finances.

Thank you, Brian, and good afternoon, everyone. I'll provide a brief overview of our financial results for the first quarter of 2025. Our first quarter net loss was $37 million or $0.86 per share compared to $21.6 million net loss or $0.64 per share for the first quarter of 2024. Our non-GAAP adjusted net loss was $34.7 million or $0.81 per share for the first quarter of 2025 compared to non-GAAP adjusted net loss of $19.9 million or $0.59 per share for the first quarter of 2024. Research and development expenses were $32.2 million for the first quarter of 2025 compared to $20.6 million for the first quarter of 2024. Of the approximately 11.6 million increase in R&D expenses, 5.9 million was related to increased employee and consulting expenses, and 5.7 million primarily related to activities supporting our ongoing clinical trials. General and administrative expenses were 3.9 million for the first quarter of 25, compared to 1.8 million for the first quarter of 2024. Increased employee and consulting related expenses accounted for 1.6 million of the increase. Professional fees, expanding infrastructure, and other administrative expenses accounted for the remaining increase of approximately 0.5 million. Net cash used in operating activities for the first quarter of 2025 was 35.9 million compared to 17.1 million for the first quarter of 2024. We ended the quarter with approximately $205.7 million of cash, cash equivalents, and short-term investments. We expect this cash, cash equivalents, and short-term investments and drawdowns on our debt facility to fund current clinical development program activities through 2026.

I will now hand the call back to Brian. We're now ready to turn the call over for questions.

Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press the star followed by the number one on your touchtone phone. You will hear a prompt that your hand has been raised. Should you wish to decline from the polling process, please press the star followed by the number two. If you are using a speakerphone, please lift the headset before pressing any keys. One moment, please, for your first question. Your first question comes from the line of Maury Raycroft from Jefferies. Your line is now open. Please go ahead.

Hi. Congrats on the progress, and thanks for taking my questions. I was going to ask one on Victoria 1. You're using the Blind Independent Central Review Analysis, which can take a longer amount of time to analyze versus investigator-assessed. And so just wondering if you can provide more perspective on how long you think it will take to lock the data set sometime in June and then to get to the actual results in 3Q. Just wondering if you can give more perspective on the amount of time there. Sure.

Sure. The primary completion date essentially is referencing the data cutoff date when you stop collecting data. And that's typically done, in our case, will be done when you've achieved the prescribed event threshold. And so from there, you are engaged in the data cleaning process. And ultimately, at that point, you lock the database. So we expect that in Q3. And we're If we achieve what we're very confident about achieving with completing the primary completion date, we think that Q3 is an absolutely certain time when we would have the data available. And we're not going to get into more specificity in terms of month, but again, I think there's no further risk of delay at this point in the trial of being able to report these results.

Understood. But I guess for that amount of time from locking the database to reporting the data, any general estimate on how long that could take?

I mean, typically you would see no more than three months and typically less than that.

Got it. Okay. And then understanding that overall survival might not be fully mature at the top lines. Do you think you would be able to provide some sort of an update on just the directionality of survival trend that you're seeing between the three arms at the data readout?

The data readout that we expect to make in a press release will only include the median PFS and the hazard ratios for the two primary analyses. The subsequent data will be analyzed, or rather presented, at the medical conference later in the year.

Got it. Okay.

I'll stop there and hop back into the queue.

Thanks for taking my questions. Okay. Thanks.

Your next question comes from the line of Andrew Behrens from Learing. Your line is now open. Please go ahead.

Hi, good afternoon. This is Eason. I'm for Andy. Thanks for taking our question. I wanted to get your thoughts on the potential impact of Serena 6 on the second line setting for HR-positive patients. Just curious, you know, what, you know, could broad adoption from this mean for get a in the wild-type population, and also kind of a similar question, you know, what could the potential impact be to get in the, you know, the mutant patient population as well? Thank you.

Sure. Well, we don't think that would affect us at all. These are still essentially first-line CDK4-6 patients. It's actually current practice amongst many doctors, depending on the profile of their patients, to transition them off letrozole to fulvestrin, depending on how they believe their patients are progressing. So this trial essentially identified a more precise way of determining the timing and what appears to be a very effective way of doing that. But the patients in our trial are essentially consistent with the patients that this trial evaluated, which were patients who received CDK4-6 and eventually progressed. And so if our data is favorable, we'd expect physicians to then seek to continue treatment with the CDK4-6 inhibitor with one that includes get a telicid. And I don't think the practice will vary between those patients who lack PIK3CA mutations versus those who do have PIK3CA mutations. I think the primary effect may be on how other CDK4-6 plus oral SIRT combinations get used.

Operator?

Yes, your next question comes from the line of Tara Bancroft from TD Cowan. Your line is now open. Please go ahead.

So I was wondering if you could provide any updated thoughts on what minimum HR you would consider to be good data in the wild type update, not just for hitting stats, but in relation to other data sets and indication like Serena 6 that was just mentioned and other marketed products. What do KOLs want to see in order to use it? Thanks so much.

No, I appreciate the question. At this time, you know, with the data, you know, fairly imminent, you know, we're not going to comment specificity about, you know, those types of projections. We've commented because the analysis is easier to do that, you know, an incremental three months would be considered clinically meaningful. Certainly, any statistically significant hazard ratio that's consistent with three months would also be considered clinically meaningful. how the regimen and the results specifically stack up against other regimens will just be a function of how those two sets of data compare.

Okay, great. Thanks.

As a reminder, if you wish to ask a question, please press star 1. Your next question comes from the line of Gail Blum from Lee Dam and Company. Your line is now open. Please go ahead.

Good afternoon, and thanks for taking our question. So just to fully clarify this, what exactly drove the slight change in timing for the wild type readout, and should we expect to see no change in the PIC3CA timeline? And as a follow-on, What investment, if any, would you need to do to support the endometrial cancer collaboration?

Thank you. Sure. As far as what drove it, again, I think we've indicated on prior calls that because this is a three-arm trial and the primary analysis is driven by reaching an event threshold in each of two different analyses, it's imprecise for us to estimate the timing. I think there's this variance in um, uh, in, uh, how those, uh, results are distributed within the, the three, uh, the, the aggregate total, uh, of events for all three arms. And we're, we're now at a point where, you know, the, the potential for variability is, is de minimis. And so that's why we have confidence about, uh, being able to, uh, establish a data cutoff in June. Um, and, uh, As far as Q4 for the PIK3CM mutant, we're confident about that. It's a less complicated tracking of event threshold because even though the three arms, the third arm comprises only about 15% of the total. So the primary analysis event threshold is much more closely aligned to the aggregate of the three arms. And as far as the endometrial study that we announced, We are supplying drug product and providing clinical support to that study, so we don't think we'll have any incremental financial effect on the company.

Operator?

Next question comes from the line of Oliver McCammon from Whiteside Capital. Your line is now open. Please go ahead.

Hi, thanks for the update and taking my question. Maybe we'll take a break from Victoria 1 for a moment. I'm curious if you can just remind us on some of the prior proof-of-concept data for targeting the PI3K-AKT mTOR pathway in prostate cancer, and more specifically, what you think the potential is for multi-node inhibition versus single-node inhibitors like capivacidib. And then I'm also curious if you plan to share PSA data at the time of the update late in the second quarter. Thanks again for the question.

Sure. And so, you know, the data that's been reported with either, in particular, AKT inhibitors, those that have been the inhibitors from this general class of drugs that have been evaluated in patients with metastatic castration-resistant prostate cancer. Now, Capivacitur reported positive data with patients who have hormone-sensitive patients prostate cancer that was favorable in patients who have P10 mutations, and so a subgroup of the total population. You know, the non-clinical data that we've reported and published indicates that GET is equally active independent of the status of P10, which is the primary mutation in prostate cancer. And, you know, capivacitib hasn't demonstrated activity, or it's significantly less active in tumor cells, prostate tumor cells that lack P10. P10 mutations. And so we think that data is encouraging because it demonstrates the role that the pathway plays. And similar to breast cancer, gadotilisib in non-clinical models has shown to be significantly more potent and cytotoxic than, let's say, an AKT inhibitor like capivacetib or the other drugs that have been approved that address the PAM pathway. And so, yeah, it was a major part of the rationale for evaluating GETA in this setting, that A, the pathway has been demonstrated to be approved, and B, the drugs that have demonstrated activity are, at least non-clinically, less active than GETA, which we think creates a very strong rationale for the trial. As far as the update, the update will really just focus on the primary analysis and safety data, and then the rest of the data we would expect to report at a medical meeting in 2025.

Super helpful. Thank you again. You're welcome.

There are no further questions at this time. Please continue, Mr. Brian Sullivan.

Well, thank you. We appreciate your interest in Cellcuity, and we'll be attending and presenting at several investor conferences over the next few weeks, so I look forward to seeing some of you there. Goodbye.

Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.