Kura Oncology, Inc. · NASDAQ:KURA
Kura Oncology — Investor Presentation (June 2016)
32 slides from Kura Oncology's investor presentation, Jun 16, 2016
Slide 1: Kura Oncology Corporate Presentation
Troy Wilson, Ph.D., J.D. President and CEO June 16, 2016 Exhibit 99.1
Slide 2: Forward-looking statements
Forward-looking statements This presentation contains forward-looking statements. Such statements include, but are not limited to, statements regarding our research, pre-clinical and clinical development activities, plans and projected timelines for tipifarnib, and our other programs, plans regardin
Slide 3: Corporate Overview
Corporate Overview Advance pipeline of targeted therapeutics for solid tumors and blood cancers Utilize precision medicine approaches to identify patients most likely to benefit from treatments; fast-to market strategy Development Strategy Experienced Team Pipeline Solid Financials Key roles in onco
Slide 4: Diverse Development Pipeline
Diverse Development Pipeline PROGRAM LEAD OPTIMIZATION PRECLINICAL PHASE 1 PHASE 2 HRAS Mutant Solid Tumors Peripheral T Cell Lymphoma MAPK Pathway Tumors Acute Leukemias Lower Risk Myelodysplastic Syndromes Multiple Opportunities to Position Tipifarnib for Registration-Enabling Phase 3 Program in 2
Slide 5: Tipifarnib – Lead Product Candidate
Tipifarnib – LEAD Product CANDIDATE Licensed worldwide rights in oncology from Janssen Broad development program, which preceded precision medicine approach Studied in > 5,000 patients Generally well-tolerated Objective responses observed in multiple unselected patient populations Evidence of durabl
Slide 6: Mechanism of action of Tipifarnib
Mechanism of action of Tipifarnib Geranylgeranyl transferase Alternative prenylation of KRAS and NRAS Tipifarnib Targets of FT include members of the RAS superfamily of small GTP-binding proteins critical to cell cycle progression Farnesyl transferase KRAS NRAS HRAS Cell membrane Tumors with KRAS an
Slide 7: Tipifarnib MOA supports development in HRAS mutant solid tumors
Tipifarnib MOA supports development In HRAS mutant solid Tumors Growth and survival of normal cells is driven by growth factor interaction with cell receptors and intracellular signaling Mutation of HRAS protein can switch signaling into a permanently “on” state, driving tumor growth and proliferati
Slide 8: Overview – HRAS mutant solid tumors
Overview – HRAS mutant solid tumors What are HRAS Mutant Tumors? HRAS mutant solid tumors include salivary gland, urinary tract, cervical, upper aerodigestive tract and other cancers Estimated annual incidence of approximately 8,000 patients in U.S. Prognosis varies with certain histologies having v
Slide 9: Rationale and design of Phase 2 trials in HRAS mutant tumors
Rationale and design of phase 2 trials in hras mutant tumors Rationale: HRAS has potential to be driver oncogene (Costello Syndrome, urothelial cancer) Tipifarnib is active in PDX models of HRAS mutant tumors Design of Current Phase 2 Clinical Trials: Primary Objective: ORR 18 patient Phase 2 study
Slide 10: Development of Tipifarnib in hematology/oncology disorders
Development of Tipifarnib in hematology / oncology Disorders Previous clinical activity observed across multiple hematologic malignancies, including: Lymphomas Leukemias Myeloproliferative disorders Myelodysplastic diseases Multiple farnesylated proteins / pathways implicated in heme/onc disorders E
Slide 11: Overview – peripheral T-cell lymphoma
Overview – peripheral t-cell lymphoma What is PTCL? Peripheral T-cell lymphomas (PTCLs) are a diverse group of usually aggressive non-Hodgkin lymphomas Characterized by the presence of malignant T-cells or natural killer (NK) cells Estimated annual U.S. incidence of approximately 5,000 patients Over
Slide 12: Rationale and design of trials in PTCL
Rationale and design of trials in PTCL Rationale: Previous Phase 2 study in patients with relapsed/ refractory PTCL showed encouraging activity* Durable responses - median DOR: ~11 months Potential biomarkers that may predict activity of tipifarnib Design of Current Phase 2 Clinical Trial: Primary O
Slide 13: Farnesylation of key signaling proteins in T cells supports development approach
Farnesylation of key signaling proteins in t cells supports development approach T cell lymphoma cells are constantly activated due to TCR complex mutations, dysregulation or mutations of signal transduction components. Normal T cells are activated by interaction of their T cell receptors (TCR) and
Slide 14: Farnesylation of key signaling proteins in T cells supports development approach
Farnesylation of key signaling proteins in t cells supports development approach A subset of T cell lymphomas is characterized by Th1 cytokine production. Both Th1 cytokine production and tumor cell survival are regulated by farnesylated HRAS. Upon treatment of PTCL with tipifarnib, we expect to inh
Slide 15: Overview – Lower risk myelodysplastic syndromes
Overview – Lower risk Myelodysplastic syndromes What is MDS? Myelodysplastic syndromes (MDS) are a group of blood and bone marrow disorders with both proliferative and dysplastic phenotypes Characterized by ineffective hematopoiesis leading to cytopenias Autoimmunity known to play a role in the onse
Slide 16: Previous Phase 2 data supports development in lower risk MDS
Previous phase 2 data supports development in Lower risk MDS Rationale: Previous Phase 2 study sponsored by J&J demonstrates tipifarnib is active in MDS* Identification of potential biomarkers Design of Current Phase 2 Clinical Trial: Primary Objective: RBC transfusion independence Initially, 44 eli
Slide 17: KIR2DS2 as a potential biomarker in MDS
KIR2DS2 as a potential biomarker IN MDS 0 200 400 600 800 1000 0 20 40 60 80 100 Time (days) Survival probability (%) Time (days) Tipifarnib Treated Patients (n=34) NCI CTEP-20 Study P = 0.0074 High KIR2DS2 Median OS: 564 days Low KIR2DS2 Median OS: 153 days 0 200 400 600 800 1000 1200 0 20 40 60 80
Slide 18: Signaling pathways in MDS have potential to yield predictive biomarkers
Signaling pathways in mds have potential to yield predictive biomarkers During aging, loss of CD28 and gain of KIR2DS2 result in overproduction of Th1 cytokines and may induce autoimmunity against the bone marrow. Aging
Slide 19: Signaling pathways in MDS have potential to yield predictive biomarkers
Signaling pathways in mds have potential to yield predictive biomarkers By monitoring KIR2DS2 and other markers, we may be able to identify those patients with bone marrow dysplasia who could benefit from tipifarnib.
Slide 20: Overview – chronic myelomonocytic leukemia
Overview – chronic myelomonocytic leukemia What is CMML? Chronic myelomonocytic leukemia (CMML) is a clonal disorder of bone marrow stem cells that shares characteristics of both myoproliferative and myelodysplastic diseases Increased monocytes and blasts in the peripheral blood and bone marrow, as
Slide 21: Previous clinical data supports development in CMML
Previous Clinical data supports development in CMML Rationale: Observed clinical activity in previous studies including CMML patients* Opportunity to use response as primary endpoint Potential to treat 1st line patients Data from previous Phase 1 AML study supports higher dose in alternate week dosi
Slide 22: Excluding RAS mutants may enhance efficacy in CMML
Excluding ras mutants may enhance efficacy in CMML NCI CTEP-20 Phase 2 trial in 34 previously untreated elderly or unfit AML patients* NRAS gene status determined for 32 patients Higher response rate in AML patients with WT NRAS treated with tipifarnib may translate to CMML population Analysis of pa
Slide 23: Multiple paths to registration-enabling Phase 3 studies
multiple Paths to registration-enabling phase 3 studies HRAS Solid Tumors PTCL Lower Risk MDS CMML* Subjects Thyroid n=18 Solid n=18 Urothelial n=18 n=18 (Potential for expansion to n=30) n = 54 n = 20 1° Endpoint ORR (RECIST v1.1) ORR (IWC) RBC transfusion independence ORR using MDS/MPN IWG criteri
Slide 24: KO-947 – Strong activity in MAPK pathway models with flexible dosing
ko-947 – STRONG ACTIVITY IN MAPK Pathway MODELS with flexible dosing ATP competitive inhibitor of the extracellular receptor kinase (ERK) Aberrant signaling caused by mutations or dysregulation of the MAPK pathway associated with numerous tumor types KO-947 induced tumor regression in multiple tumor
Slide 25: KO-947: Translational research identified potential lead clinical indications
KO-947: Translational Research identified potential lead clinical indications Treatment time (days) Tumor volume (mm3) MAPK Pathway Mutations MAPK Pathway Dysregulation Pancreatic Lung Colorectal Tumor A Tumor B Tumor C Treatment time (days) Tumor volume (mm3) Robust anti-tumor activity demonstrated
Slide 26: KO-947: Rationale for further study
KO-947: RATIONALE FOR FURTHER STUDY IND-enabling studies and preparation ongoing Translational research identified potential lead indications Potential biomarkers identified IV route of administration selected for initial clinical study Opportunity to advance oral program to broaden indication set D
Slide 27: Menin-MLL inhibitor program
Menin-mll inhibitor program Chromosomal translocations of the MLL gene play a causative role in the onset, development and progression of a subset of acute leukemias Potential first-in-class program targeting menin-MLL interaction for treatment of MLL-rearranged and MLL-PTD AML and ALL Estimated U.S
Slide 28: Near-term milestones
near-term milestones PROGRAM EVENT ANTICIPATED TIMING Tipifarnib Phase 2 clinical trial in HRAS mutant solid tumors Ongoing Tipifarnib Phase 2 clinical trial in PTCL Ongoing Tipifarnib Phase 2 IST in HRAS mutant urothelial cancer Ongoing Tipifarnib Phase 2 clinical trial in lower risk MDS Ongoing KO
Slide 29: Experienced management team
Experienced management team Chief Executive Officer Troy Wilson, Ph.D., J.D. Chief Scientific Officer Yi Liu, Ph.D. SVP, Chemistry and Pharm. Sciences Pingda Ren, Ph.D. Chief Medical Officer Antonio Gualberto, M.D., Ph.D. Chief Financial Officer Heidi Henson, CPA SVP and General Counsel Annette Nort
Slide 30: Board and advisors
Board and advisors Former President and CEO, Receptos, Inc. Faheem Hasnain SVP Finance and CFO, AnaptysBio, Inc. Robert Hoffman CEO and President, Kura Oncology, Inc. Troy Wilson, Ph.D., J.D. Professor and Chairman, Dept. Cellular & Molecular Pharmacology, UCSF Kevan Shokat, Ph.D. Director Emeritus
Slide 31: Corporate Overview
Corporate Overview Advance pipeline of targeted therapeutics for solid tumors and blood cancers Utilize precision medicine approaches to identify patients most likely to benefit from treatments; fast-to market strategy Development Strategy Experienced Team Pipeline Solid Financials Key roles in onco
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