Celcuity Inc.

Greetings and welcome to Cellcuity's full year 2022 financial results conference call. At this time, all participants are in a listen-only mode. A brief question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. It is now my pleasure to introduce your host, Robert Ewell with ICR Westwick. Thank you, Robert. You may begin.

Thank you, operator, and good afternoon to everyone on the call. Thank you for joining us to review Salcuity's fourth quarter and full year 2022 financial results and business update. Earlier today, Salcuity released financial results for the fourth quarter and full year ending December 31, 2022. The press release can be found on the investor section of the website. Joining me on the call today are Brian Sullivan, CellQt'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 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, Robert, and good afternoon, everyone. We had an eventful and productive 2022. Our primary goal for the year was to begin enrollment of our Phase III Victoria I clinical trial for our lead candidate, Getatilisib. This trial is enrolling patients with advanced HR-positive HER2-negative breast cancer whose disease progressed after treatment with a CDK4-6 inhibitor. We began 22 working with the US FDA and the European Medicines Agency to finalize feedback on our clinical trial protocol. Once we received this feedback, we finalized our protocol and then completed selection of over 200 clinical trial sites across five continents to participate in the study. These sites include some of the world's leading breast cancer institutions. After formally activating the study in the third quarter, we were very pleased to dose our first patient this past December. The dosing of the first patient in the Victoria 1 clinical trial triggered the closing of a $100 million private placement and drawdown of a $20 million term loan tranche in December. Proceeds from the private placement, combined with the debt facility and the company's current cash, cash equivalents, and marketable securities, are expected to be sufficient to fund Salcuity's current operating plan through 2025. So far, we are very encouraged by the activity at our Victoria 1 trial sites. We remain on track with our prior guidance and continue to expect data for the PIK3CA non-mutated patient subgroup to be available in the second half of 24 and data for the PIK3CA mutated patient subgroup to be available in the first half of 25. The scientific rationale for launching the VICTORIA-1 study was predicated on two key factors. First, there was a significant unmet need for better second-line therapeutic options for HR-positive HER2-negative breast cancer patients who received prior CDK4-6 inhibitors. Current therapeutic options offer only modest progression-free survival benefits. And second, we reported very promising results from our Phase 1b study that evaluated getotilizib plus palociclib combined with either letrozole or fluvescine. For patients lacking PIK3CA mutations, Published data for approved second-line therapies indicate they only offer median PFS of two to four months. For patients who have PIK3CA mutations, the published data for median PFS of approved therapies is approximately seven months. The clinical efficacy data we initially reported in 2021 from our Phase 1b study compares very favorably to these published results. We've since updated our data to reflect 13 months of additional follow-up, and we presented this data in a spotlight poster presentation at the 2022 San Antonio Breast Cancer Symposium in December. Updates included efficacy results broken out for patient subgroups according to PIK3CA mutation status in each of the four expansion arms. For the patients in Arm D of the Phase 1D study, those who received the Phase 3 dosing schedule of getotilicin, the ORR, or objective response rate, was 60% in PIK3CA wild-type patients, and the percentage of patients who were progression-free at 12 months was 49%. These results compare very favorably to published data for Fulvestrin, the control drug for PIK3CA wild-type patients in our Victoria 1 study. In a recent randomized study, Fulvestrin reported an objective response rate of 6% and a 12-month PFS rate of 12% for Fulvestrin. For the RMD patients who had PIK3CA mutations, the objective response rate was 73%, and a 12-month PFS rate was 60%. Again, these results compare very favorably to published results for the alpalypsib and fulvestrin regimen, the control for PIK3CA-mutated patients in the Victoria 1 study. In two clinical trials, the objective response rate for alpalypsib plus fulvestrin averaged 20%, and the 12-month PFS rate averaged 25%. The comparable objective response rates... and 12-month PFS rate in the PIK3CA wild-type and mutated patient subgroups is driven by, we believe, two key factors. First, the PIK3 mTOR pathway is a driver in HR-positive breast cancer regardless of whether the patient's tumor has an activating PIK3CA mutation or not. And second, inhibiting the four class I PIK3CA mutations or isoforms and the two mTOR complexes is required to most efficaciously address PI3K mTOR pathway activity. This is the optimal approach biologically because it avoids the cross-activation of uninhibited subunits and resulting drug resistance that can occur with PI3K isoform-specific or mTOR-specific inhibitors. Completely blockading the pathway also enhances the potential to induce synergistic inhibition with other targeted therapies, such as CDK4-6 inhibitors. Getotelicib's differentiated mechanism of action as an equipotent PAN-PI3K mTOR inhibitor thus uniquely suits, we believe, to address the need for more effective second-line breast cancer therapies. We believe this data and the unmet need we are seeking to address played a key role in the FDA's decision to grant breakthrough therapy designation in July last year to Getotelicib in combination with Pabliciclib and Fulvestrin. for the treatment of HR-positive HER2-negative advanced breast cancer. We were also very encouraged by the updated efficacy results for the 41 patients in our Phase 1b study who had not received prior treatment for advanced disease. These patients received getotelicib combined with palvocyclib and letrozole as first-line treatment. In the combined group of treatment-naive patients from escalation arm A and expansion arm A, median PFS was 42.3 months, and the objective response rate was 79%. These results compare very favorably to the median PFS of 24.5 months and 55% objective response rate reported in the Paloma 3 study for palocyclib plus letrozole. Of note is that the median PFS in expansion RMA patients alone was not reached as of the June 22 data cutoff. We will present updated efficacy data for expansion RMA as well as for the combined data for the two arms with treatment-naive patients at the ESMO breast cancer meeting in May. These results provide another demonstration of the intrinsic role the PI3K mTOR pathway plays as a disease driver in advanced HR-positive HER2-negative breast cancer. The data also highlight the potential opportunity to develop getotelicib as a first-line treatment option. While a randomized first-line study evaluating getotelicib combined with pabliciclib plus letrozole is not practical for us to pursue at this time, this promising data certainly warrants evaluation in the future. Another important goal for us in 2022 was to begin evaluating and prioritizing new potential indications for getafilicib. This evaluation includes assessment of previous trials for other PI3K and mTOR inhibitors, review of other pathways linked to the PI3K mTOR pathway, and conduct of non-clinical studies to characterize the activity of getafilicib and other PI3K, AKT, mTOR inhibitors in different tumor types. A significant body of literature has characterized the crosstalk and reciprocal feedback loops between hormonal pathway signaling and the PI3K-AK-MTOR signaling cascade in multiple tumor types. This interaction plays an essential role in disease recurrence and progression in prostate and gynecological cancers, in addition to breast cancer. As has been demonstrated in breast cancer, co-targeting the hormonal and PI3K-AKT-MTOR pathways is a promising treatment strategy But the approach is confounded by the feedback and feedforward loops between PS3K isoforms, AKT, and mTOR that cross-activate uninhibited subunits. This literature review, as well as considerations of the unmet needs in various tumor types, led us to focus our initial non-clinical research studies on prostate and gynecological cancers. We presented the results, first results from our studies, which focused on prostate cancer in February 23, at the American Society of Clinical Oncology Genitourinary Cancer Symposium. We've previously discussed how most PI3K mTOR inhibitors selectively spare or weakly inhibit one or more key PI3K mTOR pathway components and how this can enable drug resistance depending on the mutation status of a patient's tumor. In prostate cancer, the P10 gene is linked to PI3K and it is frequently mutated. Inhibitors that only target a single PI3K mTOR component or AAKT, have demonstrated limited clinical efficacy in P10-deficient prostate cancer and no efficacy in P10 wild-type tumors. As has been found with breast cancer, this suggests that more comprehensive inhibition of the PS3K mTOR pathway may be required. We thus posited getofelicib as a pan-PS3K mTOR inhibitor would be effective in both P10 wild-type and P10-deficient prostate cancer models. To assess this hypothesis, We evaluated a panel of prostate cancer cell lines with different PTEN status for their sensitivity to getotelicib and six other inhibitors that target at least one component of the PI3K-AKT mTOR pathway. The results from these studies were very encouraging and supportive of our hypotheses. Our assessments confirmed that getotelicib was the only inhibitor that was as potent and efficacious in PTEN wild type as PTEN mutated prostate cancer cells. In addition, in every assessment, which included cytotoxicity, potency, cell death, DNA replication, and signaling, Geta-Telicib exhibited superior activity relative to all of the other PI3K, AKT, or mTOR inhibitors evaluated. Of particular note was the contrast between Geta-Telicib and the AKT inhibitor, Capivaciturb. Capivaciturb has been evaluated in prostate cancer clinical trials, but it has only reported modest efficacy to date, in PTEN-mutated tumors, and no efficacy in PTEN-wild-type tumors. The results from our non-clinical studies with capovaciturib are consistent with these clinical results. We found that capovaciturib was tenfold less potent in PTEN-wild-type than PTEN-mutated cancer cells, and generally inferior to the pan-PSRK drugs, and much less active than gadotilicib. We believe these results, in the contrast with getathalysib, provide further demonstration of the importance of comprehensively, rather than selectively, blockading the PI3K mTOR pathway. To assess getathalysib's in vivo activity in prostate cancer, we evaluated getathalysib in three different prostate cancer mouse xenograft models. We first evaluated getathalysib as a single agent in PTEN wild-type and PTEN loss xenograft models that were insensitive to the androgen receptor inhibitor enzalotamide. In both models, gadotilisib induced more than 80% tumor growth inhibition, whereas enzalotamide had no activity. We also evaluated a prostate cancer xenograft model that was sensitive to enzalotamide. In this model, gadotilisib induced 80% tumor growth inhibition as a single agent and 116% inhibition when it was combined with enzalotamide. We will present results for our next set of clinical studies at the American Association for Cancer Research annual meeting which is being held in Orlando, Florida from April 14th through the 19th. These studies evaluated a panel of gynecological cell line models with getafilicib and several other PI3K-AKT mTOR inhibitors. An abstract summarizing this data was published last week. Consistent with our findings in prostate cancer, getafilicib exhibited superior activity relative to all of the other PI3K-AKT mTOR inhibitors evaluated. Based on the results from these internal non-clinical studies and on Geta-Tylisib's highly differentiated mechanism of action and PKDPD profile, we think there is a significant opportunity for us to develop Geta-Tylisib in these tumor types. We will provide an update on our clinical development priorities later this year. Now I would like to shift our discussion to the diagnostic side of our business that centers on Celsignia, CellQID's third generation diagnostics platform. As you may recall, the enrollment in the FACT-1 and FACT-2 trials that are evaluating early-stage breast cancer patients selected using our Celsignia HER2 signaling diagnostic were impacted by COVID-19-related delays up through early 2022. These trials are now enrolling patients with early-stage breast cancer whose HER2 pathway is hyperactive, as detected with our Celsignia test. Our goal is to provide our Celsignia test as a companion diagnostic so that pharmaceutical companies can expand the number of patients eligible to receive their targeted therapy. We expect to announce interim results from these studies in the second half of 2023. With that, I'll now turn our call over to Vicki Hahn, our CFO, to review our financial results.