Kura Oncology, Inc.

Welcome to the Quarter 1, 2021 Cura Oncology, Inc. Earnings Conference Call. My name is Jenny. I'll be your operator for today's call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session. During the question-and-answer session, if you have a question, please press star then 1 on your touch-tone phone. I'm going to turn the call over to Peter Despain. You may begin.

Thank you, Jenny. Good afternoon and welcome to Kerr Oncology's first quarter 2021 conference call. Joining me on the call are Dr. Troy Wilson, our President and Chief Executive Officer, and Dr. Mark Grasso, our Chief Financial Officer and Chief Business Officer. Jim Bosta, our Chief Legal Officer, Dr. Steven Dale, our Chief Medical Officer, Kirsten Flowers, our Chief Commercial Officer, and Kathy Ford, our Chief Operating Officer, are also with us and available to answer questions. Before I turn the call over to Dr. Wilson, I would 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, it 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 Dr. Troy Wilson, President and CEO of Kerr Oncology.

Thank you, Pete, and thank you, everyone, for joining us this afternoon. Over the past quarter, we've continued to make significant progress as a company, and we believe the relative positioning of our menin inhibitor program, KO539, has improved meaningfully. We've also witnessed a number of new developments in the space, including updated clinical data from a competitor program, that further validated menin-MLL as a therapeutic target in AML, as well as the emergence of two additional clinical stage programs. This heightened activity speaks to the mounting excitement surrounding the menin inhibitor space and the significance of driving meaningful clinical activity in genetically defined subsets of AML. It's also served to highlight our leadership position while underscoring the value of an aggressive clinical development strategy and the importance of operational execution. We believe KL539 is well positioned as a potentially best-in-class and first-in-class menin inhibitor. This confidence is supported by a growing body of clinical data, including compelling activity, a favorable safety and tolerability profile, and a wide therapeutic window. As such, we intend to conduct a comprehensive clinical development plan for KL539, both as a monotherapy and in combination, aimed at providing the greatest benefit to patients with acute leukemia. A critical component of our development plan is the determination of an optimal phase 2 dose. In order to better inform a recommended phase 2 dose and beyond, we've amended our COMET-001 trial of KL539 to include two phase 1B expansion cohorts, one at a higher dose and one at a lower dose, each enriched with NPM1 mutant and KMT2A rearranged relapsed and or refractory AML patients. These expansion cohorts should enable us to maximize the benefit risk for KL539 in our target patient populations, similar to what has been done previously with other targeted therapies in AML. We expect to enroll at least 12 patients in each of our two Phase 1B expansion cohorts and assess those patients for safety and tolerability, PK and PD, and efficacy in order to determine the recommended Phase 2 dose. In addition, the amended Phase 1B protocol gives us flexibility to enroll up to an additional 18 patients per cohort as appropriate. Importantly, we believe patients enrolled in the cohort selected as the recommended Phase 2 dose have the potential to be included in the subsequent registration-directed portion of the COMET-001 trial. The amended protocol has been submitted to sites for IRB approval, and we will begin we will shortly begin enrolling patients in the Phase 1B expansion cohorts at both existing and new clinical sites. Meanwhile, we continue to engage with our key opinion leaders and global steering committee to further define a comprehensive clinical development plan for KL539. Additional opportunities include frontline combination studies, additional genetic subtypes, a pediatric development strategy, and other indications such as acute lymphocytic leukemia and myelodysplastic syndrome. We intend to move these efforts forward aggressively pending determination of an optimal dose. We look forward to providing an update including additional phase one data from Comet 001 later in the year. Given the excitement around our Mennon program, it's easy to understand why it's captured Wall Street's attention over the past year. However, we remain just as excited about the opportunity for foreign cell transferase inhibition in oncology, an evolving story best told in three chapters. For those newer to our story, as a prelude, we in-licensed tibifarnib, our first-generation farnesyl transferase inhibitor from Janssen, in December 2014. Previously, it had been studied in more than 5,000 patients and demonstrated compelling and durable anti-cancer activity in certain unselected patients. Using advancements in cancer genetics and tools such as next-generation sequencing, we identified multiple genetically-defined subsets of patients most likely to respond to tibifarnib. The most advanced of these initiatives is focused on patients with head and neck squamous cell carcinoma, or HNSCC, that carry mutations in the HRS gene. We estimate 4% to 8% of HNSCC patients have HRS mutations. This is Chapter 1. Earlier this year, tibifarnib was granted breakthrough therapy designation from FDA for the treatment of patients with recurrent or metastatic HRS mutant HNSCC. The breakthrough therapy designation was based on data from our Phase II RUN-HN trial, which was recently published in the Journal of Clinical Oncology. Development of targeted therapies in HNSCC has lagged behind other cancer indications. Thus, we were very gratified by the FDA's award of breakthrough therapy designation, which acknowledges both the dire unmet need for patients with recurrent or metastatic HRS mutant HNSCC and the promise of tipifarnib to provide clinical benefit to patients. We're motivated by our data and the potential that tipifarnib could represent the first approved small molecule targeted therapy in HNSCC. We remain focused on conducting our AIM-HN registration-directed trial and bringing tipifarnib to market as quickly and as efficiently as possible, providing a beachhead to the development of rational combinations and expansion to larger genetic subtypes. Among these potential combinations, we've prioritized the combination of tipifarnib and a PI3 kinase alpha inhibitor. Our preclinical data suggests that HRAS and PI3 kinase alpha are codependent oncogenes in HNSCC, and that combining tipifarnib with a PI3 kinase alpha inhibitor has potential to provide meaningfully better anti-tumor activity than inhibiting either target alone. We believe this has the potential to increase the total addressable population for tipifarnib to as high as 50% of HNSCC. Building on the promise of tipifarnib as a monotherapy, this combination represents Chapter 2 of our story. We're currently preparing a Phase I-II proof-of-concept study of tipifarnib in combination with a piathre kinase alpha inhibitor in patients who have HRAS overexpressing and or PIK3CA-dependent HNSCC. We expected to initiate this study in the second half of 2021. Meanwhile, through internal efforts and our network of academic collaborations, we've uncovered some compelling opportunities for farnesyl transferase inhibitors in combination with other targeted therapies. This biology is totally novel, and we believe it warrants a greater investment in the therapeutic class. From this investment, we're advancing a discovery stage program to develop a next-generation farnesyl transferase inhibitor designed to target innovative biology and address large oncology indications of high unmet need through rational combinations. This represents Chapter 3 of our story and potentially the largest opportunity. Our goal for this program is to deliver a drug candidate that has comparable potency and selectivity and improved pharmacokinetic and physical chemical properties relative to tipifarnib. We've already identified a number of advanced lead compounds and we anticipate nomination of a development candidate for IND-enabling studies later this year. None of this would have been possible without the pioneering work our team has done over the last five years. While we continue to focus on the opportunity with HRS mutant HNSCC, we view farnesyl transferase inhibition in oncology as a potentially broader and more valuable therapeutic and commercial franchise, and one that has potential to deliver multiple opportunities for additional indications. We look forward to sharing an update with you as the story continues to evolve. With that, I'll now turn the call over to Mark Grasso for a discussion of our financial results for the first quarter 2021.