Kura Oncology, Inc.

Good afternoon, ladies and gentlemen, and welcome to the Q1 2024 Cura Oncology Financial Results 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. This call is being recorded on Thursday, May 2, 2024. I would now like to turn the conference over to Pete Despain, Head of Investor Relations. Please go ahead.

Thanks, Chris. Good afternoon and welcome to Cura Oncology's first quarter 2024 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. Let's jump right in. Last week, we were proud to announce that Ziftomenib is the first investigational treatment to be granted breakthrough therapy designation for the treatment of NPM1 mutant AML. The FDA granted BTD for Ziftomenib based on data from our ongoing COMET001 clinical trial in patients with relapsed refractory NPM1 mutant AML. NPM1 mutant AML is a disease of significant unmet need for which there is no approved targeted therapy. and it represents approximately 30% of new AML cases annually. BTD is awarded for a drug that treats a serious or life-threatening condition and may demonstrate substantial improvement on one or more clinically significant endpoints over available therapies. The designation is intended to expedite development and review of drugs, including an organizational commitment by FDA senior managers and experienced review staff, as well as eligibility for rolling review and priority review. We're highly encouraged by FDA's decision to grant breakthrough therapy designation for Zifdomenib, recognizing its potential as an innovative medicine for patients with NPM1 mutant AML. We look forward to working even more closely with FDA to bring Zifdomenib to patients in urgent need of effective treatments as quickly as possible. Meanwhile, we're on track to complete enrollment of 85 patients in our ongoing COMET-001 registration-directed trial of Zifdomenib in relapsed refractory NPM1 mutant AML by the middle of this year. Ziftamenib is also being evaluated in combination with current standards of care, including venetoclax azacitidine or cytarabine plus donorubicin, commonly known as 7 plus 3, in patients with NPM1 mutant or KMT2A rearranged AML. In January, we reported preliminary clinical data from the first 20 patients in the dose escalation portion of the COMET-007 trial, including five newly diagnosed patients with adverse risk AML and 15 patients with relapsed refractory AML. Ziftomenib demonstrated an encouraging safety and tolerability profile in combination with 7 plus 3 and with venetoclax plus azacitidine, enabling continuous administration of Ziftomenib while effectively mitigating the risk of differentiation syndrome. no differentiation syndrome events of any grade were reported among the first 20 patients. Furthermore, no dose-limiting toxicities, QTC prolongation, drug-drug interactions, or additive myelosuppression were observed. As of the January 11th data cutoff, all five newly diagnosed patients with adverse risk, NPM1 mutant or KMT2A rearranged AML, treated with ziftomenib and 7 plus 3, achieved complete remission with full count recovery for a CR rate of 100%. The overall response rate among the 15 relapsed refractory patients treated with Ziftomedib and Veneza was 53%, including a 40% ORR among the 10 patients who had received prior venetoclax, a setting with very limited effective treatment options. The CRCRH rate among the nine relapsed refractory patients who were MENIN inhibitor naive was 56%. As of the data cutoff, 16 of the first 20 patients remained on trial, including all 11 NPM1 mutant patients. Continuous daily dosing of Zifto-Menev at 200 milligrams QD was well tolerated, and the safety profile was consistent with features of underlying disease and backbone therapies. I'm very pleased to say that our team continues to demonstrate outstanding execution. The 400-milligram dose of Ziftomenib has now been cleared for both the NPM1 mutant and KMT2A-rearranged relapsed refractory venasa cohorts, and enrollment for both of those subsets at the 600-milligram dose is ongoing. We've also cleared the 400-milligram dose of Ziftomenib in the frontline adverse risk NPM1 mutant 7 plus 3 cohorts, and have escalated to the 600 milligram dose. Enrollment of the 400 milligram dose in the frontline KMT2A rearranged 7 plus 3 cohort is ongoing, and we anticipate clearing that dose cohort shortly. At this rate, we expect to identify the recommended phase 2 dose for Ziftomenib in combination with Veneza and in combination with 7 plus 3 by the middle of this year. Concurrently, we plan to initiate a Phase 1b expansion study with a number of combination cohorts, including Venaza in newly diagnosed NPM1 mutant or KMT2A rearranged AML, Venaza in relapsed refractory NPM1 mutant or KMT2A rearranged AML, Venetoclax in relapsed refractory NPM1 mutant AML, and 7 plus 3 in newly diagnosed NPM1 mutant or KMT2A rearranged AML, removing the qualifications for high-risk disease. Each Phase 1b combination cohort is expected to enroll independently, with approximately 20 patients per cohort. In the meantime, we continue dosing patients in our COMET-008 study of Zifto-Manim in combination with additional standards of care, including the FLT3 inhibitor giltaritinib, FlagIDA, or low-dose ARAS-C for treatment of relapsed refractory NPM1 mutant or KMT2A rearranged AML. Roughly half of all patients with relapsed refractory NPM1 mutant AML have co-occurring FLT3 mutations, and the prognosis for these patients is poor. Preclinical data for Zifdomenib in combination with FLT3 inhibitors demonstrate strong synergistic effects compared to either single agent alone. We believe a best-in-class safety and efficacy profile as well as optimal pharmaceutical properties, will enable ZiftoMedib to become a cornerstone of therapy for patients with acute leukemias. This belief is backed by increasing investigator enthusiasm, as evidenced by rapid enrollment across all of our ongoing ZiftoMedib studies, and further bolstered by breakthrough therapy designation by FDA. Ultimately, our mission is to develop ZiftoMedib across the continuum of care for all patients with acute leukemias whose disease is driven by the MENIN pathway. We also have a growing body of preclinical data that supports attractive opportunities for MENIN inhibitors beyond acute leukemias. Based on internal preclinical data, we believe there may be a role for ZiftoMedib in the treatment of certain solid tumors, and we're working towards submission of an investigational new drug application for the first of these solid tumor indications in the second half of this year. We look forward to sharing some of the preclinical data that support this opportunity at a scientific or medical meeting later this year. Meanwhile, we continue to make progress toward a next-generation menin inhibitor, which we intend to direct toward an additional, soon-to-be-disclosed indication. And we remain in a strong financial position, enabling us to invest in research, development, and precommercial activities to maximize the value of ZyptoMeneb and support our other pipeline assets. Now let's turn our attention to our farnesyl transferase inhibitor programs. We continue to build upon the impressive clinical benefit we've demonstrated with tififarnib as a monotherapy in patients with recurrent and metastatic head and neck cancer. We have been evaluating the combination of tififarnib with the targeted therapy alpelosib in PIK3CA-dependent head and neck squamous cell carcinoma in a Phase I dose escalation study that we call Current HA. We remain pleased by the manageable safety and tolerability profile of tififarnib in combination with alpelosib, and we are encouraged by the clinical activity observed at multiple dose levels. We expect a complete enrollment of two dose expansion cohorts to help inform selection of the optimum biologically active dose for the combination by the end of 2024, and we look forward to presenting preliminary clinical data from the current HN trial of tififarnib and alpelicib at a medical meeting in the first half of 2025. We believe the manageable safety and tolerability we've observed with the combination of tipifarnib and alpelicib also significantly de-risks development of our next generation farnesyl transferase inhibitor, KO2806, as we begin to evaluate it in combination with other targeted therapies. Despite the success of targeted therapies such as tyrosine kinase inhibitors and KRAS inhibitors, a considerable need remains to drive enhanced antitumor activity while addressing mechanisms of innate and adaptive resistance. We are developing our next-generation farnesyl transferase inhibitor, KO2806, to address this need. KO2806 was designed to improve upon the potency, pharmacokinetic, and physical chemical properties of tippy farning. Last year, we presented compelling preclinical data supporting the rationale for combining KO2806 with distinct classes of targeted therapies, including tyrosine kinase inhibitors and KRATS inhibitors. In October, we began dosing patients with KO2806 as a monotherapy in a phase one dose escalation trial that we call FIT001. That trial uses an innovative design that enables us to begin dose escalation of KO2806 in combination cohorts very early on in the study, while continuing to dose escalate concurrently as a monotherapy. In fact, we dosed the first patient with KO2806 in combination with cabozantinib in clear-cell renal cell carcinoma in February, just four months after KO2806 entered the clinic. And we are on track to dose the first patient in combination with Atagraciv in KRAS G12C-mutated non-small-cell lung cancer by the middle of this year. As a reminder, the study of KO2806 and Atagraciv is supported by a clinical collaboration and supply agreement with Mirati now part of Bristol-Myers Squibb. While our focus with KO2806 remains on renal cell carcinoma and KRAS-driven tumors, its rapid development progress provides us with further flexibility as we consider potential development paths forward in head and neck squamous cell carcinoma. If successful, we believe KO2806 could become the ideal combination partner for multiple targeted therapies in large solid tumor indications. With that, I'll now turn the call over to Tom for a discussion of our financial results.