Kura Oncology, Inc.

Good afternoon, ladies and gentlemen, and welcome to the Q4 2023 Cora Oncology Incorporated 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 Tuesday, February 27, 2024. I would now like to turn the conference over to Pete Despain, Head of Investor Relations. Please go ahead.

Great. Thank you, Eric. Good afternoon and welcome to Cura Oncology's fourth quarter and full year 2023 conference call. Joining me on the call are Dr. Troy Wilson, our President and CEO, 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 CURRAS filings with the SEC, which are available from the SEC or on the CURRAS 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 month, we reported preliminary clinical data from the first 20 patients in COMET007, the phase one dose escalation trial of our MENIN inhibitor, Zifdomenib, in combination with standards of care in patients with NPM1 mutant and KMT2A rearranged acute myeloid leukemia. The first 20 patients were enrolled in fewer than four months, from July to November of last year, including five newly diagnosed patients with adverse risk AML and 15 patients with relapsed refractory AML. Ziptomenib demonstrated a highly encouraging safety and tolerability profile in combination with Cytarabine plus Donorubicin, or 7 plus 3, as well as with Venetoclax plus Azacitidine, enabling continuous administration of Ziptomenib while effectively mitigating the risk of differentiation syndrome. In fact, 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 data cutoff on January 11th, all five newly diagnosed patients with adverse risk NPM1 mutant or KMT2A rearranged AML treated with ziftometabin 7 plus 3 achieved a complete remission with full count recovery, for a CR rate of 100%. The overall response rate among the 15 relapsed refractory patients treated with Ziptomenib 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. Notably, the CR-CRH rate among the nine relapsed refractory patients who were Mennon 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 Ziptomenib at 200 milligrams QD was well tolerated and the safety profile was consistent with features of underlying disease and backbone therapies. As we reported on January 30th, the 200 milligram dose of Ziptomenib has been cleared in both relapsed refractory venasa cohorts and enrollment at the 400-milligram dose continues. In the meantime, I'm pleased to report we've also escalated to the 400-milligram dose of ziptomenib in the frontline adverse risk NPM1 mutant 7 plus 3 cohort, and we anticipate clearing the 200-milligram dose in the frontline KMT2A rearranged 7 plus 3 cohort shortly. At this rate, we expect to determine the recommended phase 2 dose for ziptomenib in combination with Veneza, and in combination with 7 plus 3 by the middle of this year. After determination of the recommended phase 2 dose, we plan to initiate a phase 1B dose validation expansion with Ziftomenib in Veneza in newly diagnosed patients with NPM1 mutant and KMT2A rearranged AML. In the meantime, we're now dosing patients in our COMET008 study of ziptomenib in combination with additional standards of care, including the FLIP3 inhibitor giltaritinib, flagida, or LDAC, all for the treatment of relapsed refractory NPM1 mutant or KMT2A rearranged AML. Roughly half of patients with relapsed or refractory NPM1 mutant AML have co-occurring FLIP3 mutations, and the prognosis for these patients is particularly poor. Preclinical data for ZiftoMedib in combination with FLIP3 inhibitors demonstrate strong synergistic effects compared to either single agent alone. We believe a best-in-class safety and activity profile and optimum pharmaceutical properties will enable ZiftoMedib to become a cornerstone of therapy for patients with acute leukemias. This belief is supported by growing investigator enthusiasm as evidenced by rapid enrollment across all of our ongoing Zipdomenib studies. We continue to be encouraged by the rate of enrollment in COMET-001, our Phase II registration-directed trial of Zipdomenib in patients with relapse, refractory, NPM1 mutant AML, and we remain on pace to complete enrollment of all 85 patients in the trial by the middle of this year. Our mission is to develop Zipdomenib across the continuum of care for all patients with acute leukemias whose disease is driven by the Menin pathway, including pediatrics, where poor outcomes unfortunately remain. In December, we announced Ziptomenib was selected for the Leukemia and Lymphoma Society's Pediatric Acute Leukemia Master Clinical Trial, commonly known as PEDL. As part of the study, Ziptomenib will be evaluated in combination with chemotherapy in pediatric patients with relapsed refractory KMT2A rearranged, NUP98 rearranged, or NPM1 mutant acute leukemia. In addition, we recently began dosing patients with KMT2A rearranged acute lymphoblastic leukemia, a relatively small group of patients but with a very large unmet medical need, as well as a cohort of patients who have neither NPM1 mutant nor KMT2A rearranged AML. We also have a growing body of preclinical data that supports attractive opportunities for menin inhibitors beyond acute leukemias. We're now preparing to initiate a proof-of-concept study in an undisclosed solid tumor indication later this year. Meanwhile, we continue to make progress toward a next-generation menin inhibitor, which we intend to direct to an additional, soon-to-be-disclosed indication. And with our recent financing, we remain in a strong financial position, which enables us to invest aggressively in research, development, and pre-commercial activities to maximize the value of ziftamenib and support our other pipeline assets. Now let's turn our attention to our farnesyl transferase inhibitor programs, beginning with KO2806. Despite success of targeted cancer drugs, such as tyrosine kinase inhibitors and KRAS inhibitors, a considerable need remains to drive enhanced anti-tumor activity while addressing mechanisms of innate and adaptive resistance. We are developing our next generation farnesyl transferase inhibitor, KO-2806, to address this need. 2806 was designed to improve upon the potency, pharmacokinetic, and physicochemical properties of earlier FTI drug candidates. Last year, we presented compelling preclinical data supporting the rationale for combining KO2806 with distinct classes of targeted therapies, including tyrosine kinase inhibitors and KRAS inhibitors. In October, we began dosing patients with KO2806 as a monotherapy in a phase one dose escalation trial that we call FIT001. FIT001 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. We're now preparing to dose the first patients with KO2806 in combination with cabozantinib in clear cell renal cell carcinoma and in combination with adagracib in KRAS G12C mutated non-small cell lung cancer by the middle of this year. Recall in November we announced a clinical collaboration and supply agreement with Mirati Therapeutics, now Bristol Myers Squibb, to support that latter study. We're encouraged that the strong operational execution seen in the Zift-O-Menib trials has carried over to the FIT-001 study and look forward to realizing the promise of the combinations. If successful, we believe KO-2806 could become an ideal combination partner for multiple targeted therapies in large solid tumor indications. Meanwhile, we continue to evaluate our first-generation FTI, Tipifarnib, in combination with the targeted therapy alpelicib, building on impressive clinical benefit we observed with tipifarnib alone in head and neck cancer. We continue to evaluate patients in the dose escalation study of tipifarnib and alpelicib, which we call current HN. Given encouraging clinical activity observed at multiple dose levels, we're adding additional patients to help inform selection of the optimal biologically active dose for the combination. Once we determine the OBAD later this year, we'll determine the next steps for the program. Importantly, we are encouraged that tipifarnib continues to demonstrate a favorable safety and tolerability profile at its full dose in combination with alpelosib. We believe this significantly de-risks development of our next generation FTI, KO2806, as we begin to evaluate it in combination with other targeted therapies. With that, I'll now turn the call over to Tom Doyle for a discussion of our financial results.