Kura Oncology, Inc.

Please stand by. Good day and welcome to the Cura Oncology second quarter 2022 conference call. Today's conference is being recorded. At this time, I would like to turn the conference over to Pete DeSpain, Senior Vice President of Investor Relations. Please go ahead, sir.

Thank you, Sarah. Good afternoon and welcome to Cura Oncology's second quarter 2022 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 will now turn the call over to Troy.

Thank you, Pete, and thank you all for joining us this afternoon. Last year, as we continued in dose escalation with our menin inhibitor, Ziftamenib, in an all-comer population of patients with relapsed or refractory acute myeloid leukemia, we sought FDA feedback regarding the design of our registration-directed trial. In the context of those discussions, FDA advised we spend more time in our Phase I study to identify an optimal dose. Guidance we now know was part of a broader FDA initiative in oncology drug development aptly named Project Optimus. In agreement with FDA, we enrolled a Phase Ib study with two dose expansion cohorts, 200 milligrams and 600 milligrams, each comprised of 12 patients with NPN1 mutant or KMT2A rearranged relapsed refractory AML. I'm pleased to report we've nearly completed our assessment of these patients in the expansion cohorts for efficacy, safety, and tolerability, as well as pharmacokinetics and exposure, and we believe we've identified a recommended phase two dose for Zyft-Amendib. We're working diligently to gather the data package for submission to FDA and look forward to sharing the recommended phase two dose for Zyft-Amendib later this year pending the agency's review, along with top line data from the Phase 1B study, with a more complete data set reserved for presentation at a medical meeting in the fourth quarter. In the meantime, enrollment in COMET-001 has continued, and we're pleased to announce that we've enrolled an additional 18 patients in the Phase 1B study in less than three months at what we believe to be the recommended Phase 2 dose, an indication of the continued enthusiasm surrounding zift amenib among investigators and patients. We continue to believe data from all patients treated at the recommended phase two dose will have potential to contribute to the registrational patient population. In parallel with our efforts to advance zift amenib as a monotherapy, we've been working to operationalize a series of combination studies in the relapsed and frontline settings. We've designed these studies to assess the safety, tolerability, and therapeutic activity of Ziftimenib in combination with current standards of care in AML, including venetoclax and azacitidine, FLT3 inhibitors, and standard induction, cytarabine, donorubicin chemotherapy, commonly referred to as 7 plus 3. We remain enthusiastic about the potential for Ziftimenib in the treatment of acute leukemias as we prepare to transition into the Phase II registration-directed portion of COMET001 and initiate our combination studies pending determination of our recommended Phase II dose. Although our MENIN program continues to capture much of the attention, we remain just as motivated by opportunities for farnesyl transferase inhibition in oncology. One of the first therapeutic applications of an FTI as a targeted therapy was via direct inhibition of an oncogenic protein, namely HRAS. We've demonstrated the potential for tififarnib to drive durable responses in recurrent and metastatic HRS mutant head and neck squamous cell carcinoma, or HNSCC, and our ongoing AMHN registration-directed trial continues in that indication. More recently, we've begun efforts to build upon the initial monotherapy activity of tififarnib with a focus on overcoming drug resistance. Late last year, we initiated the current HN study designed to evaluate the combination of tipifarnib and dalpelicib, an inhibitor of PI3 kinase alpha, in selected HNSCC patient cohorts. We believe that HRAS and PI3 kinase alpha are codependent oncogenes in HNSCC, and the combination of the two inhibitors has potential to provide improved antitumor activity relative to the inhibition of either target alone. The combination also has potential to increase the total addressable population for tippy-farnib to as much as 50% of patients with recurrent and metastatic HNSCC. The initial cohort of the current HN study includes patients with PIK3CA-dependent HNSCC, and I'm pleased to report that we recently dosed the first patient in a second cohort comprised of patients with HRAS overexpression. Our goal with the current HN trial is to identify a recommended Phase II dose and schedule for the combination in each patient cohort. We're encouraged by the preliminary safety and tolerability of the combination, as well as early evidence of clinical activity, and we believe we may be in a position to share preliminary proof-of-mechanism data from patients in the PIC3CA-dependent HNSCC cohort later this year. Beyond HNSCC, we continue to elucidate the role of FDIs in preventing or delaying the emergence of resistance for certain classes of targeted therapy with potential to drive deeper and more durable responses in large solid tumor indications. One of these emerging combination opportunities was unveiled earlier this year at the American Association for Cancer Research annual meeting. The preclinical data generated through a collaboration within CIRM support potential for tipifarnib to prevent emergence of resistance to osimertinib and other potent EGFR inhibitors in EGFR mutant non-small cell lung cancer. We're preparing to initiate a phase one study of tipifarnib in combination with osimertinib in EGFR mutated non-small cell lung cancer, which we call current lung, later this quarter. We intend to perform initial clinical evaluation of tipifarnib and osimertinib to gather valuable experience and data, while in parallel advancing KO2806, the lead development candidate in our next generation FTI program through IND-enabling studies. KO2806 represents a next-generation farnesyl transferase inhibitor with improved PK, exposure, and bioavailability relative to tibifarnib. In addition to combining FTIs with EGFR inhibitors, we continue to investigate combinations with other potent targeted therapies in preclinical studies that may represent additional opportunities. We intend to evaluate KO2806 in combination with these targeted therapies, and we remain on track to submit an IND application for KO2806 in the fourth quarter. With that, I'll now turn the call over to Tom for a discussion of our financial results.