Kura Oncology, Inc. · NASDAQ:KURA
Kura Oncology — Investor Presentation (March 2017)
31 slides from Kura Oncology's investor presentation, Mar 6, 2017
Slide 1: Corporate Overview March 2017
Corporate Overview March 2017 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, KO-947 and KO-539, plans regarding reg
Slide 3: Investment Opportunity: Kura Oncology
Investment Opportunity: Kura Oncology Product candidates focused on indications with significant sales potential to support future commercial build out Lead program, tipifarnib, in multiple Phase 2 trials Multiple data readouts anticipated in 2017 with potential to initiate first pivotal study in 20
Slide 4: Precision Medicines in Cancer Treatment
Precision Medicines in Cancer Treatment Source: www.cancer.gov Discovery and development of targeted therapies that treat cancer based upon the specific molecular or genetic characteristics of the patient’s tumor ADVANTAGES: High translatability from preclinical to clinical studies Leverage clinical
Slide 5: Rapid Progress Since Inception and Multiple Near-term Milestones
Rapid Progress Since Inception and Multiple Near-term Milestones 2015 2016 2017 2018 Initiated P2 HRAS trial for tipifarnib Listed on NASDAQ Initiated P2 PTCL trial Initiated P2 lower-risk MDS trial Reported positive preliminary data from P2 HRAS trial IND accepted for KO-947 KO-539 selected as deve
Slide 6: Pipeline of Selective Drug Candidates For Genetically Defined Cancers
Pipeline of Selective Drug Candidates For Genetically Defined Cancers STAGES OF DEVELOPMENT PROGRAM PRECLINICAL PHASE 1 PHASE 2 ANTICIPATED MILESTONES Tipifarnib (Farnesyl Transferase Inhibitor) Data updates in 1H and 2H 2017 Data in 1H 2017 Data in 2H 2017 Data in 1H 2018 KO-947 (ERK Inhibitor) Pha
Slide 7: Tipifarnib (Farnesyl Transferase Inhibitor)
Tipifarnib (Farnesyl Transferase Inhibitor)
Slide 8: Tipifarnib: A Drug Candidate Developed Ahead of Its Time
Tipifarnib: A Drug Candidate Developed Ahead of Its Time Targeted therapy developed before the advent of personalized medicine approaches Extremely potent and highly selective inhibitor of protein farnesylation In-licensed from Janssen CAPITALIZING ON PREVIOUS CLINICAL EXPERIENCE > 5,000 patients tr
Slide 9: Mechanism of Action of Tipifarnib
Mechanism of Action of Tipifarnib Farnesyl transferase (FT) enzyme attaches farnesyl group to proteins, facilitating localization to the inner membrane of the cell FT targets include members of the Ras superfamily (KRAS/NRAS/HRAS) and other proteins critical for cell signaling Blocking farnesylation
Slide 10: Multiple Shots on Goal Position Tipifarnib Favorably For a First Pivotal Trial
Multiple Shots on Goal Position Tipifarnib Favorably For a First Pivotal Trial 4 ONGOING KURA PHASE 2 TRIALS SUCCESS CRITERA OUTCOME: 1 OR MORE PIVOTAL TRIALS Biomarker validation Evidence of durable, clinical benefit Sufficient ORR Potential for rapid clinical development Opportunity to move into e
Slide 11: Phase 2 Trial in HRAS Mutant Solid Tumors
Phase 2 Trial in HRAS Mutant Solid Tumors RATIONALE: Preclinical data supports role of HRAS as a tumor oncogene Murine models suggested tumor growth inhibition Small Phase 2 trial to evaluate whether HRAS mutant tumors would respond to tipifarnib and nature of response (regression versus disease sta
Slide 12: Preliminary Phase 2 Data Supports HRAS Hypothesis For Tipifarnib
Preliminary Phase 2 Data Supports HRAS Hypothesis For Tipifarnib Squamous cell carcinomas of the head and neck (SCCHN) Salivary gland tumors (SGT) 12/22/2015 (C4 D22) 08/17/2015 (Baseline) Study has proceeded to 2nd stage for cohort 2 and been amended to enroll additional 7 patients with HRAS mutant
Slide 13: HRAS Mutant Squamous Tumors Appear More Sensitive to Tipifarnib than to SOC
HRAS Mutant Squamous Tumors Appear More Sensitive to Tipifarnib than to SOC PRECLINICAL DATA Data source: Kura Oncology CLINICAL DATA* SD C6 Censored Cetuximab Tipifarnib Patient 005-007 (oral cavity SCCNH) PD C2 PR C2 Ongoing in C12 Patient 005-009 (oral cavity SCCNH) Cetuximab/ Paclitaxel Tipifarn
Slide 14: HRAS Mutant SCCHN Represents Significant Unmet Medical Need
HRAS Mutant SCCHN Represents Significant Unmet Medical Need SCCHN comprises different malignant tumors that develop in or around the throat, larynx, nose, sinuses, and mouth. Estimated incidence of SCCHN in the U.S. is 56,000 in 2017 Estimated frequency of HRAS mutations in SCCHN patients ~ 5-6% HRA
Slide 15: Phase 2 Trial in HRAS Mutant Solid Tumors: Evolving SCCHN Treatment Landscape
Phase 2 Trial in HRAS Mutant Solid Tumors EVOLVING SCCHN TREATMENT LANDSCAPE Recruitment of SCCHN patients has become more challenging post-approval of I/O agents I/O agents have become standard-of-care in the U.S. in the overall SCCHN population Post-I/O patients often have very advanced disease KU
Slide 16: Defined Patient Populations Are Actionable with Targeted Therapies
Defined Patient Populations Are Actionable with Targeted Therapies ONCOGENE INDICATION U.S. INCIDENCE APPROVED DRUGS 2016 REVENUES1 Bcr-Abl CML ~ 9,000 Imatinib, Nilotnib, Dasatinib, Bosutinib, Ponatinib > $4,000 M ALK NSCLC ~ 9,000 Crizotinib, Ceritinib, Alectinib ~ $800M BRAF Malignant melanoma ~
Slide 17: Kura is On Track to Achieve Success Criteria for the First Phase 2 Trial
Kura is On Track to Achieve Success Criteria for the First Phase 2 Trial 4 ONGOING KURA PHASE 2 TRIALS SUCCESS CRITERA OUTCOME: 1 OR MORE PIVOTAL TRIALS Biomarker validation Evidence of durable, clinical benefit Sufficient ORR Potential for rapid clinical development Opportunity to move into earlier
Slide 18: Three Additional Tipifarnib Phase 2 Trials Ongoing with Data Readouts
Three Additional Tipifarnib Phase 2 Trials Ongoing with 2 Data Readouts Anticipated in 2017 PTCL LOWER RISK MDS CMML Subjects n=18 (Potential for expansion to n=30) n = up to 58 n ~ 20 Primary Endpoints ORR (IWC) RBC transfusion independence ORR using MDS/MPN IWG criteria Rationale Prior Phase 2 exp
Slide 19: KO-947 (ERK Inhibitor)
KO-947 (ERK Inhibitor)
Slide 20: KO-947: Potent Inhibitor of Extracellular Signal-regulated Kinase (ERK)
KO-947: Potent Inhibitor of Extracellular Signal-regulated Kinase (ERK) Aberrant signaling caused by mutations or dysregulation of the MAPK pathway associated with numerous tumor types Inhibitors of RAF and MEK have validated the MAPK pathway in cancer Competitors have demonstrated clinical activity
Slide 21: KO-947 Demonstrates Prolonged MAPK Pathway Modulation In Vivo
KO-947 Demonstrates Prolonged MAPK Pathway Modulation In Vivo Pharmacodynamic Modulation After a Single Oral Dose KRAS H2122 Model 0h 6h 24h 32h 48h 72h 50 mg/kg pRSK 100 mg/kg 200 mg/kg 300 mg/kg 200 mg/kg pRSK pRSK pRSK pRSK GAPDH GAPDH GAPDH GAPDH GAPDH KO-947 GDC-0994 Extended pharmacology of KO
Slide 22: KO-947: Translational Research Identified Potential Lead Clinical Indications
KO-947: Translational Research Identified Potential Lead Clinical Indications MAPK PATHWAY MUTATIONS MAPK PATHWAY DYSREGULATION Tumor volume (mm3) Pancreatic Lung Colorectal KO-947 Q2d KO-947 2Qw KO-947 Q2d 5-FU KO-947 Q2d GEM Tumor A Tumor B Tumor C Treatment time (days) Tumor volume (mm3) Robust a
Slide 23: Kura is Pursuing a Precision Medicine-Based Approach Toward Development of KO-947
KURA is Pursuing a Precision Medicine-Based Approach Toward Development of KO-947 GOAL Indications with potential for single agent activity, enabling accelerated development ADVANTAGES OF A PRECISION MEDICINE-BASED APPROACH High potential for translatability from preclinical to clinical studies Leve
Slide 24: KO-539 (Menin-MLL Inhibitor)
KO-539 (Menin-MLL Inhibitor)
Slide 25: KO-539: Potential First-in-class Inhibitor of the Menin-MLL Interaction
KO-539: Potential First-in-class Inhibitor of the Menin-MLL Interaction Chromosomal translocations of the MLL gene play a causative role in the onset, development and progression of a subset of acute leukemias MLL-r fusion proteins and a similar mutation, MLL partial tandem duplication, drive overex
Slide 26: KO-539 Displays Prolonged Efficacy in Xenograft Model
KO-539 Displays Prolonged Efficacy in Xenograft Model KO-539 is a potent and selective inhibitor of the menin-MLL interaction KO-539 demonstrated robust efficacy in in vivo models of MLL-r AML Tumor regressions sustained at 30 days following end of dosing period Dosing Period In Vitro Potency KO-539
Slide 27: Anticipated Milestones
Anticipated Milestones PROGRAM UPDATE ESTIMATED TIMEFRAME Tipifarnib (Farnesyl Transferase Inhibitor) Additional data from Phase 2 study in HRAS mutant SCCHN 1H and 2H 2017 Data from Phase 2 study in PTCL 1H 2017 Data from Phase 2 clinical trial in lower risk MDS 2H 2017 Data from Phase 2 clinical t
Slide 28: 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 Pharmaceutical Sciences Pingda Ren, Ph.D. Chief Medical Officer Antonio Gualberto, M.D., Ph.D. Chief Financial Officer Heidi Henson, CPA SVP and General Counsel Anne
Slide 29: Board and Advisors
Board and Advisors BOARD OF DIRECTORS Faheem Hasnain Former President and CEO, Receptos, Inc. Robert Hoffman EVP and CFO, Innovus Pharmaceuticals, Inc. Thomas Malley Mossrock Capital Steven Stein, M.D. Chief Medical Officer, Incyte Corporation Troy Wilson, Ph.D., J.D. CEO and President, Kura Oncolog
Slide 30: Why Invest in Kura Oncology?
Why Invest in Kura Oncology? Precision Medicine Strategy in Oncology Advancing Therapeutic Pipeline Lead product candidate in multiple Phase 2 trials Encouraging clinical data in ongoing Phase 2 study of HRAS mutant squamous cell carcinomas of the head and neck (SCCHN) Potential to select indication
Slide 31: Kura: Developing Precision Medicines to Treat Cancer
eQKURA KURA DEVELOPING PRECISION MEDICINES TO TREAT CANCER