Kura Oncology, Inc.

Good day and welcome to the Q2 2024 Cure Oncology conference call. All participants will be in listen-only mode. Should you need assistance, please signal the conference specialist by pressing the star key followed by zero. After today's presentation, there will be an opportunity to ask questions. To ask a question, you may press star then one on your telephone keypad. To withdraw your question, please press star then two. Please note this event is being recorded. I would now like to turn the conference over to Pete Despain, Head of Investor Relations. Please go ahead.

Great. Thank you, Amy. Good afternoon and welcome to Cura Oncology's second quarter 2024 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 Troy, 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 Kuro's filings with the FCC, which are available from the FCC or on the Kuro Oncology website for information concerning risk factors that could affect the company. With that, I'll turn the call over to Troy.

Thank you, Keith, and thank you all for joining us. This task order was highlighted by strong execution across the organization as we continue to generate a robust clinical data package to support broad development of our menin inhibitor program, beginning with Zip2Med. In April, Zip2Med became the first investigational therapy to be granted breakthrough therapy designation for treatment of relapse, refractory, NPM1 mutant acute myeloid leukemia. FDA awarded BTD based on data from our COMET-001 trial, recognizing Zip2Med's potential as an innovative medicine for patients with this devastating disease. In May, we announced completion of enrollment in the registration-directed portion of COMET-001, enrolling more than 85 NPM1 mutant AML patients in fewer than 16 months. We believe this important milestone reinforces Zip2Med's potential best-in-class profile. As a reminder, NPM1 mutant AML represents approximately 30% of new AML cases annually and is a disease of significant unmet need for which there's no approved targeted therapy. With the COMET-001 study now fully enrolled, we look forward to sharing top-line data early next year as we continue to work closely with FDA to expedite development and review of Ziftamentib as a monotherapy. Meanwhile, we continue to evaluate Ziftamentib in combination with current standards of care in patients with both NPM1 mutant and KNT2A rearranged AML. Earlier this year, we reported preliminary clinical data from 20 patients enrolled in the phase one dose escalation portion of our COMET-007 trial. This event demonstrated an encouraging safety and tolerability profile, as well as meaningful evidence of clinical activity when administered in combination with Cytarabine plus Donorubicin, commonly known as 7 plus 3, as well as with Venetoclax plus Azacitabine. Notably, no differentiation syndrome events of any grade were reported, Furthermore, no dose-limiting toxicities, QPC prolongation, drug-drug interactions, or additive myelosuppression were observed. Continuous daily dosing of Ziftamantib at 200 milligrams was well tolerated, and the safety and tolerability profile was consistent with features of underlying disease and back-up therapies. Since that update, our team has continued to demonstrate outstanding execution, and the COMET-007 study has now enrolled more than 100 patients. I'm pleased to report that the safety, tolerability, and clinical activity of Zipdomenib continue to support advancement into both the fit and unfit frontline populations. Two of the four cohorts have cleared the 600 milligram dose and advanced into the Phase 1b expansion study. The two remaining cohorts are expected to clear the 600 milligram dose and advance shortly. The Phase 1b expansion study includes multiple combination cohorts. most notably Ziptomenid plus Vaneza in newly diagnosed NPM1 mutant or KMT2A rearranged AML, as well as Ziptomenid plus 7 plus 3 in newly diagnosed NPM1 mutant or KMT2A rearranged AML, removing the requirement for patients to have high-risk disease. Each combination cohort is enrolling independently, and we expect to enroll approximately 20 patients per cohort. We believe the Phase 1B expansion study will continue to lay the groundwork for helping us to redefine the current standards of care for newly diagnosed patients with both NPM1 mutant and KMT2A rearranged AML in both the fit and unsit populations. We look forward to presenting updated data from the COMET007 combination trial at a medical meeting later this year. It should be a meaningful update. In addition to the progress our team has made with the COMET007 study, we continue to dose patients in our ongoing COMET008 study of Ziptomenid in combination with additional standards of care, including the FLIP3 inhibitor giltaritinib, as well as flagida and low-dose cytarabine. Roughly half of all patients with relapsed or refractory NPM1 mutant AML have co-occurring FLIP3 mutations. and the prognosis for these patients is poor. Preclinical data for Zipdomenib in combination with Flip3 inhibitors has shown strong synergistic effects compared to either single agent alone. When we look across the fit, unfit, and Flip3 mutant AML frontline populations, we believe a best-in-class safety and activity profile and optimal pharmaceutical properties could enable Zipdomenib to become a cornerstone of therapy for patients with acute leukemias. Ultimately, our mission is to develop Zift-O-Menid across the continuum of care for all patients with acute leukemias whose disease is driven by the Menin pathway. Over the past couple of years, we've generated a growing body of preclinical data that supports opportunities for Menin inhibitors beyond acute leukemias, including the potential for Zift-O-Menid in certain solid tumors. Earlier today, we announced FDA clearance of our investigational new drug application for Ziftimenib in combination with Imatinib for treatment of advanced gastrointestinal stromal tumors. GIST is the most common form of sarcoma, characterized as KIT-dependent solid tumors. KIT inhibitors are associated with favorable outcomes for patients with GIST, and Imatinib is the frontline standard of care in this patient population. For patients who progress on imatinib, subsequent treatment options consist of other KIT inhibitors. However, these options are limited by moderate efficacy and challenging tolerability. The Menin-MLL complex regulates KIT expression in GIST cells, and Menin inhibitors display additive therapeutic activity in combination with imatinib in imatinib-sensitive GIST models. Our preclinical data suggests ZyptoMentib has potential to resensitize patients to Imatinib and induce deep, durable responses. Building upon an initial report from the Armstrong lab, we've generated a substantial amount of preclinical data that further support the opportunity for ZyptoMentib and GIST. We look forward to presenting these data for the ZyptoMentib and Imatinib combination at an upcoming scientific meeting. And following the IMD clearance announced this morning, We plan to initiate a proof-of-concept study evaluating Zipdomenib in combination with Imatinib in patients with advanced GIST after failure of Imatinib early next year. If successful, the potential opportunity in GIST appears to be mutationally agnostic, enabled by Zipdomenib's favorable pharmaceutical properties with an addressable market as significant as our frontline opportunities in AML. In June, we reported preclinical data supporting the potential therapeutic utility of menin inhibitors in the treatment of diabetes. The new findings were presented at the American Diabetes Association Scientific Sessions in Orlando. Type 2 diabetes is marked by an inadequate number of functional pancreatic beta cells, which results in insufficient insulin production, leading to hyperglycemia. Ziftamentib demonstrated meaningful levels of glycemic control in the preclinical in vivo model, including reduced fasting blood glucose levels and percent HbA1c within 27 days, as well as consistent improvement in both insulin sensitivity and insulin production. The preclinical data showed that the effects of Ziftamentib were fully maintained following dose discontinuation. suggesting restoration of beta cell mass. A decline in pancreatic beta cell function and or mass has been defined as a key contributing factor to disease progression in type 2 diabetes. Notably, in human islet microtissues originating from donor samples, zistaminib induced beta cell proliferation, while non-beta cell proliferation was not detectable, demonstrating menin is a viable therapeutic target for beta cell mass-specific expansion. We're advancing multiple next-generation menin inhibitor drug candidates targeting type 2 diabetes and potentially type 1 diabetes, and we expect to nominate the first of these next-generation development candidates in early 2025. Now let's turn our attention briefly to our farnesyl transferase inhibitor programs. Despite success of targeted therapies, a considerable need remains to drive enhanced antitumor activity while addressing mechanisms of innate and adaptive resistance. We're developing our next-generation farnesyl transferase inhibitor, KO-2806, to address these needs. 2806 is designed to improve upon the potency, pharmacokinetic, and physical-chemical properties of earlier FDI drug candidates. Last year, we presented compelling preclinical data supporting the potential for KO-2806 to address mechanisms of innate and adaptive resistance in distinct classes of targeted therapies, including tyrosine kinase inhibitors and KRAS inhibitors. Late last year, 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 enabled us to begin dose escalation of 2806 in combination cohorts very early on in the study while continuing to dose escalate concurrently as a single agent. In February, we dosed the first patient with KO2806 in combination with cabizantinib in clear cell renal cell carcinoma just four months after KO2806 entered the clinic. And I'm pleased to report we recently dosed the first patient in a combination study with Atagracid in KRAS T12C mutated non-small cell lung cancer. As a reminder, the study of KO-2806 and Adagracib is supported by a clinical collaboration and supply agreement with Mirati, now a Bristol-Myers Squibb company. If successful, we believe KO-2806 could drive enhanced anti-tumor activity and become an ideal combination partner to multiple targeted therapies in large solid tumor indications. Meanwhile, we continue to evaluate the combination of tipifarnib with the targeted therapy alpelicin in PIK3CA-dependent head and neck squamous cell carcinoma in a phase one dose escalation study that we call CurrentHN. We remain pleased by the manageable safety and tolerability profile of tipifarnib in combination with alpelicin, and we're encouraged by the clinical activity observed at multiple dose levels. We remain on track to complete enrollment of the two expansion cohorts, to help inform selection of the optimal biologically active dose for the combination by the end of this year. And we look forward to presenting preliminary clinical data from the current HN trial of Tipi Farnam and Alkalisib at a medical meeting in the first half of 2025. With that, I'll turn the call over to Tom for a discussion of our financial results.