CELC - NASDAQ

Good afternoon, ladies and gentlemen, and welcome to the Celcuity First Quarter 2025 Financial Results Webcast Conference Call. At this time all lines are in listen-only mode. [Operator Instruction] I would now like to turn the conference over to Apoorva Chaloori with ICR Healthcare. Please go ahead.

Thank you, operator, and good afternoon to everyone. Thank you for joining us to review Celcuity’s first quarter 2025 financial results and business update. Earlier today, Celcuity Inc. released financial results for the first quarter ended March 31, 2025. The press release can be found on the Investors section of Celcuity’s website. Joining me on the call today are Brian Sullivan, Celcuity’s Chief Executive Officer and Co-Founder; Vicky Hahne, Chief Financial Officer as well as Igor Gorbatchevsky, 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 Celcuity. 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 topline data from the PIK3CA wild-type cohort of our Phase 3 VIKTORIA-1 trial in Q3 2025 and from the PIK3CA mutated patient cohort in Q4 2025. We also anticipate reporting preliminary topline data for the Phase 1b portion of our Phase Ib/2 trial in prostate cancer in late second quarter. And finally, we made great progress activating trial sites for our Phase 3 first-line VIKTORIA-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 gedatolisib. Let’s turn now to our VIKTORIA-1 trial. Our Phase 3 VIKTORIA-1 trial is designed to evaluate gedatolisib in combination with fulvestrant with and without palbociclib in patients with hormone receptor positive HER2- advanced breast cancer whose disease has progressed on or after treatment with a CDK4/6 inhibitor. The VIKTORIA-1 trial includes two patient cohorts with independent statistical analysis plans and primary endpoints. The primary endpoints for VIKTORIA-1 are progression free survival or PFS as assessed by blinded independent central review. 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 pre-defined 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 topline 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, gedatolisib in combination with fulvestrant and palbociclib could offer a new standard-of-care for patients with HR+/HER2- advanced breast cancer whose disease progressed on or after treatment with a CDK4/6 inhibitor. For the PIK3CA mutant patient cohort, we anticipate reporting topline data in the fourth quarter of 2025. The current second-line treatment paradigm for HR+/HER2- patients with advanced breast cancer includes selective estrogen receptor degraders or SERD like fulvestrant or elacestrant 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 PI3Kα, 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 gedatolisib’s role in this treatment landscape will require that gedatolisib 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 KOLs and regulators generally consider an incremental improvement in PFS of three months relative to its control to be clinically meaningful. Current mPFS or medium 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 months incremental median PFS improvement relative to its comparator in patients with ESRI 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 $0.5 billion despite approvals that only address 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+/HER2- advanced breast cancer have enrolled widely heterogeneous patient populations. Since physicians make different treatment decisions for patients depending 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, topline mPFS results from these studies don’t provide sufficient clarity about the actual benefit the 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 gedatolisib 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 VIKTORIA-2 trial. The VIKTORIA-2 study is a global Phase 3 open-label randomized clinical trial evaluating the efficacy and safety of gedatolisib in combination with fulvestrant plus investigators choice of either ribociclib or palbociclib, as a first-line treatment for patients with HR+/HER2- 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. Primary PFS endpoint for each of the cohorts will be evaluated independently. Prior to initiation of the Phase 3 portion of the trial, a safety run-in study will be conducted in 12 to 36 participants to assess the safety profile of gedatolisib in combination with ribociclib and fulvestrant. 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 Asia 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 inhibitor combined with fulvestrant. 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 1b/2 trial that’s evaluating the safety and efficacy of gedatolisib 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 1b/2 study evaluates gedatolisib 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 topline data by the end of the second quarter of 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 dataset will include approximately 36 patients, half of whom will have received a 120 milligram dose of gedatolisib, the other half a 180 milligram dose. Each are administered on a three week on, one week off schedule. 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 gedatolisib in combination with abemaciclib 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+ or Type 1 endometrial cancer may benefit from treatment with a PI3K, AKT, mTOR inhibitor like gedatolisib in combination with endocrine therapy. Additionally, results from a prior Phase 2 clinical study evaluated gedatolisib as a monotherapy in patients without a Type 1 or Type 2 endometrial cancer and these results were encouraging. So, I’d like now to turn the call over to Vicky 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 trial. General and administrative expenses were $3.9 million for the first quarter of 2025 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 draw downs 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. [Operator Instructions] 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, VIKTORIA-1, you’re using, the Blinded Independent Central Review analysis, which can take longer, 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?

So, the primary completion date essentially is referencing the data cut-off date when you stop collecting data and that’s typically done, and 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 if we achieve, we are very confident about achieving with completing, the achieving the primary completion date, we think that Q3 is 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.

Okay. Got it. Okay. And then, understanding that overall survival might not be full mature at the topline, 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 in the queue. Thanks for taking my questions.

Okay. Thanks.

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

Hi, good afternoon. This is Ethan on for Andy. Thanks for taking our question. Wanted to get your thoughts on the potential impact of SERENA-6 on the second-line setting for HR+ patients. Just curious what could broad adoption from this mean for geda in the wild-type population? And, also kind of a similar question, what could the potential impact be to geda in 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 fulvestrant 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 are patients who received CDK4/6 and eventually progressed. And so if our data is favorable, we would expect physicians to then seek to continue treatment with the CDK4/6 inhibitor with one that includes gedatolisib. 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 SERD combinations get used.

Your next question comes from the line of Tara Bancroft from TD Cowen. 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 datasets and indication like SERENA-6 that was just mentioned and other marketed products? And what do KOL want to see in order to use it? Thanks so much.

No, I appreciate the question. At this time, with the data fairly imminent, we’re not going to comment specificity about those types of projections. We’ve commented, because the analysis is easier to do that 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.

[Operator Instructions]. Your next question comes from the line of Gil Blum from Needham and Company. Your line is now open. Please go ahead.

Good afternoon and thanks for taking my questions. 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 PIK3CA timeline? And as a follow-on, what’s an 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 how those results are distributed within the three, the aggregate total of events for all three arms. And we’re now at a point where the potential for variability is de-minimus and so that’s why we have confidence about being able to establish a data cutoff in June. And as far as Q4 for the PIK3CA mutant, we’re confident about that. It’s 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.

Next question comes from the line of Oliver McCammon from LifeSci 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 VIKTORIA-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 PI3Kα, AKT, or mTORC1 pathway in prostate cancer and more specifically what you think the potential is for multi-node inhibition versus single-node inhibitors like capivasertib? And then, I’m also curious if you plan to share [PSC] (ph) data at the time of the update late in the second quarter? Thanks again for the question.

Sure. And so, the data that’s been reported with either in particular AKT inhibitors, those have been the inhibitors from this general class of drugs that have been evaluated in patients with metastatic castration resistant prostate cancer. Capivasertib reported positive data with patients who have hormone sensitive prostate cancer that was favorable in patients who have PTEN mutations and so a subgroup of the total population. The non-clinical data that we’ve reported and published indicates the geda is equally active independent of the status of PTEN, which is the primary mutation in prostate cancer. And capivasertib hasn’t demonstrated activity or it’s significantly less active in tumor cells, prostate tumor cells that lack PTEN mutations. And so, we think that data is encouraging because it demonstrates the role of the pathway plays and similar to breast cancer, gedatolisib in non-clinical models has shown to be significantly more potent and cytotoxic than let’s say an AKT inhibitor like capivasertib or the other drugs that have been approved that address the PAM pathway. And so, that was a major part of the rationale for evaluating geda 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 geda, 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 Celcuity, 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.