Kura Oncology, Inc.

Good afternoon, ladies and gentlemen, and welcome to the Q1 2023 Cora Oncology, Inc. Earnings Conference Call. At this time, all lines are in a 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 0 for the operator. This call is being recorded on Wednesday, May 10, 2023. I would now like to turn the conference over to Pete DeSane, Senior Vice President of Investor Relations and Communications. Please go ahead.

Great. Thank you, Julie. Good morning and welcome to Cura Oncology's first quarter 2023 conference call. Joining me on the call are Dr. Troy Wilson, our President and Chief Executive Officer, and Tom Doyle, our Senior Vice President of Finance and Accounting. Before I turn the call over to Dr. Wilson, I'd like to remind you that today's call will include forward-looking statements based on current expectations. Such statements represent management's judgment as of today and may involve risks and uncertainties that could cause actual results to differ materially from expected results. Please refer to Cura's filings with the SEC, which are available from the SEC, or on the Cura Oncology website for information concerning risk factors that could affect the company. With that, I'll now turn the call over to Troy.

Thank you, Pete, and thank you all for joining us. Our strong conviction in Ziptomenib and its potential to be the best-in-class menin inhibitor continues to increase. This confidence is supported by one of the highest complete response rates reported for a targeted therapy in the setting of relapsed refractory leukemia and is reinforced by the rapid pace of enrollment in our registration-directed trial. More on that in just a moment. We're also encouraged by the durable remissions in our Phase I trial driven primarily by single-agent activity of Ziftamentib, and we look forward to sharing an update at the European Hematology Association Congress next month. You got a glimpse of these data in our recently released abstract, which showed that Ziftamentib continues to demonstrate significant clinical activity in patients with heavily pretreated and co-mutated relapsed or refractory NPM1 mutant AML. As of a January 31st data cutoff, Six of the 20 NPM1 patients treated at the recommended phase two dose achieved complete responses with full count recovery. The abstract showed a median duration of response of 8.2 months with a median follow-up of approximately eight months. Four patients were still ongoing at the time of data cutoff. Zifdomenib is well tolerated and the on-target effect of differentiation syndrome is manageable. We are excited by these evolving data and we look forward to reporting updated data as of an early April data cutoff. Now, building on the momentum generated by our positive Phase I data, we announced in February that the first patients were dosed in our Phase II registration-directed trial of Ziftomenib in NPM1 mutant relapsed or refractory AML. Site activation and enrollment in our registration-directed study are outperforming our projections, an indication of the continued enthusiasm surrounding Ziftomenib among investigators and patients. As a reminder, NPM1 mutant AML accounts for approximately 30% of new AML cases annually and represents a disease of significant unmet need for which no approved targeted therapy exists. Once the disease becomes relapsed or refractory, the prognosis for NPM1 mutant AML patients is particularly poor, with an overall survival of approximately six months after initial chemotherapy. NPM1 mutant AML is further compounded with commutations, such as IDH or FLIP3. Notably, in our Phase I trial for ZiptoMedib, two-thirds of NPM1 mutant AML patients who achieved a CR at 600 milligrams had IDH and or FLIP3 commutations, all of whom had failed prior treatment with IDH and or FLIP3 targeted inhibitors. A complete response rate with full count recovery, I'm sorry, a 30% complete response rate with full count recovery after prior failure of these targeted therapies makes the clinical activity of Ziptomenib even more striking. We're also impressed with the potential for Ziptomenib to drive durable remissions as a monotherapy. An additional NPM1 mutant patient who entered the trial with multiple co-mutations, including DNMT3A, following two prior stem cell transplants, achieved a CR with no evidence of minimal residual disease and remains on Zyptomenib for more than 32 cycles as of our January 31st data cutoff. In parallel with our efforts to advance Zyptomenib as a monotherapy, we're preparing to initiate a series of combination studies to significantly broaden the addressable patient population. We believe Zyptomenib is uniquely positioned for these combination strategies. This belief is driven by several key competitive advantages, including no evidence of drug-induced QTC prolongation, no predicted adverse drug-drug interactions, and once-daily oral dosing that should enable convenient administration with current standards of care. Our team is working diligently to initiate the COMET-007 and COMET-008 trials to evaluate Ziftimated in combination with current standards of care in earlier lines of therapy and across multiple patient populations, including both NPM1 mutant and KMT2A-rearranged AML. We've designed these Phase I studies to assess safety, tolerability, and antileukemic activity of ziftomenib in combination with key regimens such as venetoclax and azacitidine, the FLT3 inhibitor giltaritinib, and the chemotherapy regimen of 7 plus 3. Our approach to combinations is to establish ziftomenib as a foundational therapy that can be combined safely with various commonly used regimens, and then prioritize those combinations that represent the largest unmet medical need and the greatest potential commercial value, namely venetoclax and FLT3 inhibitor-containing regimens. Notably, up to half of NPM1 mutant AML patients also exhibit commutations in the FLT3 gene. the safety profile of Zifdomenib, we believe it may be the ideal menin inhibitor to combine with FLT3 inhibitors to address this population, a difficult to treat group that represents approximately 15% of AML. We also believe that rational combination approaches will help to mitigate differentiation syndrome in the KMT2A rearranged population. as has previously been demonstrated in the development of IDH inhibitors in combination with azacitidine. We're very excited about the potential for our combination studies to further unlock the value of Zifdomedib for patients with acute leukemias. We've begun site activation in the first of these studies, COMET007, and we're on track to dose first patients this quarter. We're very proud of our team's execution and grateful for the continued support of our studies investigators. Their enthusiasm, coupled with a growing body of clinical data and multiple emerging lines of evidence, reinforce our confidence in ZiptoMenev as the best-in-class menin inhibitor. We look forward to sharing more at our upcoming presentation at EHA. Now let's turn our attention to our farnesyl transferase inhibitor programs. Over the past several years, we've pioneered the development of FTIs as combination agents to prevent or delay emergence of resistance to certain classes of targeted therapy in large solid tumor indications. Although targeted therapies have demonstrated meaningful clinical activity across a range of solid tumors, adaptive resistance almost invariably emerges over time, which limits the ability of targeted therapies to drive sustained clinical benefit. We have generated a growing body of preclinical and clinical data that support the combination of FTIs with multiple classes of targeted therapies, including EGFR inhibitors as well as PI3 kinase inhibitors. In April, we presented encouraging preclinical data at the American Association for Cancer Research annual meeting, which supports the potential use of FTIs in combination with two additional distinct classes of targeted therapy. The first of two posters revealed robust synergy between tipifarnib and the standard of care antiangiogenic TKI, Exitinib, in cell and patient-derived xenograft models of clear cell renal cell carcinoma. The second poster reported regression of multiple models of KRAS inhibitor-resistant non-small cell lung cancer through the addition of tipifarnib either to adagracib or satoracib therapy. These promising preclinical data illustrate the potential for FTIs to drive enhanced anti-tumor activity, as well as address mechanisms of both innate and adaptive resistance to targeted therapies. In addition, we believe these data strongly support our rationale to combine our next generation FTI, KO2806, with TKIs in clear cell renal cell carcinoma, as well as KRAS G12C mutant inhibitors in non-small cell lung cancer. In January, we were pleased to announce FDA clearance of our investigational new drug application for KO2806 for the treatment of advanced solid tumors, an important next step for this program. Now we intend to evaluate safety, tolerability, and preliminary anti-tumor activity of KO2806 in a phase one dose escalation study, which we're calling FIT001. We're now in study startup, and we look forward to dosing the first patients in FIT001 later this year. Concurrent with the dose escalation as monotherapy, we also plan to evaluate KO2806 in dose escalation combination cohorts in advanced solid tumors. Meanwhile, we continue to evaluate tipifarnib in combination with the PI3 kinase alpha inhibitor alpelosive, a combination that has potential to address up to half of all patients with recurrent and metastatic HNSCC. We're encouraged by the preliminary activity observed in our ongoing current HN trial, including a durable partial response in a patient with PIK3CA-mutated squamous cell carcinoma of the tonsil. We're also very pleased by our ability to combine tipifarnib with another targeted therapy, in this case alpelizib, with no dose-limiting toxicities reported to date. We remain on track to determine the optimal biologically active dose in mid-2023. We continue to unlock the potential therapeutic and commercial value of farnesyl transferase inhibition, the challenging but we believe increasingly substantial opportunity that has potential to address large solid tumor indications such as renal cell carcinoma as well as cancers of the lung and colorectal system. As with our menin inhibitor program, we believe FTII programs have potential to create significant value for patients, healthcare providers, and our shareholders. We're confident we have the leadership, experience, and operational and financial resources to realize that value. With that, I'll now turn the call over to Tom Doyle for a discussion of our financial results.