Kura Oncology, Inc. · NASDAQ:KURA
Kura Oncology — Investor Presentation (June 2017)
39 slides from Kura Oncology's investor presentation, Jun 14, 2017
Slide 1: Corporate Overview June 2017
Corporate Overview June 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 disease indications with significant commercial potential Lead program, tipifarnib, in multiple Phase 2 trials Encouraging clinical data in ongoing Phase 2 studies of HRAS mutant squamous cell carcinomas of the head and neck (SCCHN)
Slide 4: Precision Medicines in Cancer Treatment
Precision Medicines in Cancer Treatment 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 and pathology trends t
Slide 5: Kura's Development Programs Seek to Address Areas of Significant Unmet Need
Kura’s Development Programs Seek to Address Areas of Significant Unmet Need Head and Neck Tipifarnib KO-947 Lung Tipifarnib KO-947 Leukemias Tipifarnib KO-539 Lymphomas Tipifarnib Lower-Risk MDS Tipifarnib Product Candidate Tumor Type Estimated U.S. Incidence Tipifarnib (Phase 2) HRASmut SCCHN 2,800
Slide 6: 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 7: 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 Tipifarnib (Farnesyl Transferase Inhibitor) KO-947 (ERK Inhibitor) KO-539 (Menin-MLL Inhibitor) HRAS Mutant Solid Tumors Peripheral T-cell Lymphomas Lower-risk Myelodysplas
Slide 8: Tipifarnib (Farnesyl Transferase Inhibitor)
Tipifarnib (Farnesyl Transferase Inhibitor)
Slide 9: Tipifarnib: A Drug Candidate Whose Time Has Come
Tipifarnib: A Drug Candidate Whose Time Has Come Extremely potent and selective inhibitor of protein farnesylation In-licensed from Janssen Developed before advent of personalized medicine approaches CAPITALIZING ON PREVIOUS CLINICAL EXPERIENCE Well characterized and manageable safety profile (> 5,0
Slide 10: Mechanism of Action of Tipifarnib
Mechanism of Action of Tipifarnib Farnesyl transferase (FT) enzyme attaches farnesyl group to proteins, facilitating localization to the inner cell membrane FT targets include members of the Ras superfamily (KRAS / NRAS / HRAS) and other proteins critical for cell signaling Blocking farnesylation pr
Slide 11: 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 12: 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 13: 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) Study has proceeded to 2nd stage for cohort 2 and been amended to enroll additional 7 patients with HRAS mutant SCCHN Cohort 1 in HRAS mutant thyroid ca
Slide 14: 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 Tip
Slide 15: 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% HRAS-
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: Progress Towards Success Criteria for First Phase 2 Trial
Progress Towards Success Criteria for 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 lines of thera
Slide 18: Tipifarnib as a Potential Treatment for Peripheral T-cell Lymphoma
Tipifarnib as a Potential Treatment for Peripheral T-cell Lymphoma BACKGROUND: Diverse group of aggressive non-Hodgkin lymphomas characterized by presence of malignant T-cells or natural killer (NK) cells Patients have a poor overall survival of about 40%. Effective options for relapsed patients are
Slide 19: Preliminary Phase 2 Data Identify CXCL12 as a Potential Biomarker in PTCL
Preliminary Phase 2 Data Identify CXCL12 as a Potential Biomarker in PTCL* Preliminary data as of May 1, 2017 * Witzig et al., Preliminary Results from a Phase II Study of Tipifarnib in Relapsed or Refractory T-Cell Lymphoma., 2017 International Conference on Malignant Lymphoma, Lugano, Switzerland.
Slide 20: HRAS Inhibition Blocks Signaling Downstream from CXCL12/CXCR4 in Tumor T-cells
HRAS Inhibition Blocks Signaling Downstream from CXCL12/CXCR4 in Tumor T-cells T-cell tumors secrete growth factors for stromal cells, and stromal cells produce growth factors for T-cells, including the chemokine CXCL12 (SDF-1).1-4 CXCL12 is necessary for the maintenance of T-cell tumors (e.g. T-LL)
Slide 21: Phase 2 Trial for PTCL – Implications and Current Status
Phase 2 Trial for PTCL – Implications and Current Status Preliminary data suggest tipifarnib has antitumor activity in PTCL, particularly in patients with AITL histology and PTCL-NOS histology with high levels of CXCL12 gene expression and absence of single nucleotide gene variations in the 3'-untra
Slide 22: CXCL12/CXCR4 is a Critical Pathway in Malignant Cells
CXCL12/CXCR4 is a Critical Pathway in Malignant Cells – Potential Applications Beyond PTCL Hematopoietic stem cells (HSCs) migrate from the BM endosteal niche to the vascular niche to initiate hematopoiesis. Hematopoietic precursors are retained in the vascular niche by CXCL12/CXCR4 while undergoing
Slide 23: Analysis of Clinical Data from Previous Tipifarnib Trials
Analysis of Clinical Data from Previous Tipifarnib Trials Suggests Potential for CXCL12/CXCR4 as a Biomarker in Indications Beyond PTCL J&J previously studied tipifarnib without genetic selection in newly diagnosed AML in elderly patients with poor-risk AML (CTEP-20) and in relapsed and refractory A
Slide 24: Two Additional Tipifarnib Phase 2 Trials Ongoing with Data Readouts Anticipated in 1H 2018
Two Additional Tipifarnib Phase 2 Trials Ongoing with 2 Data Readouts Anticipated in 1H 2018 SUCCESS CRITERA Biomarker validation Evidence of durable, clinical benefit Sufficient ORR Potential for rapid clinical development Opportunity to move into earlier lines of therapy Attractive U.S. oncology c
Slide 25: KO-947 (ERK Inhibitor)
KO-947 (ERK Inhibitor)
Slide 26: 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 MAPK pathway associated with numerous tumor types Inhibitors of RAF and MEK have validated MAPK pathway in cancer Competitors have demonstrated limited clinical activity
Slide 27: 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 28: KO-947 Translational Research Identified Potential Lead Clinical Indications
KO-947 Translational Research Identified Potential Lead Clinical Indications EXTENSIVE PRECLINICAL EVALUATION OF KO-947 ANTI-TUMOR ACTIVITY IN MAPK DYSREGULATED TUMORS KO-947 evaluated in ~200 PDX models across 20 potential indications Identified broad tumor classes sensitive to ERK inhibition (> 50
Slide 29: KO-947 is Active in Preclinical Models of KRAS- and BRAF-Mutant Adenocarcinomas
KO-947 is Active in Preclinical Models of KRAS- and BRAF-Mutant Adenocarcinomas BRAF-V600E Colorectal PDX KRAS-G12V Pancreatic PDX KO-947 Q2D Gemcitabine 2QW KO-947 Q2D, 2QW KO-947 Q2D 5-FU 2QW KRAS-G12D Colorectal PDX KO-947 Q2D, 2QW KRAS-G12C NSCLC PDX Vehicle 120mg/kg Q2D 210mg/kg 2QW Tumor volum
Slide 30: KO-947 is Highly Active in Preclinical Models in Biomarker Subsets of SCCHN
KO-947 is Highly Active in Preclinical Models in Biomarker Subsets of SCCHN Final dose 3/3 CRs on QW dosing Tumor volume (mm3) Treatment time (days) Final dose Restart dosing Vehicle 120mg/kg Q2D 300mg/kg QW 2/3 CRs on Q2D or QW dosing Tumor volume (mm3) Treatment time (days) Complete Responses in S
Slide 31: Precision Medicine-Based Approach Toward Development of KO-947
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 Leverage clinical and p
Slide 32: KO-539 (Menin-MLL Inhibitor)
KO-539 (Menin-MLL Inhibitor)
Slide 33: 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 34: 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 35: Anticipated Milestones
Anticipated Milestones PROGRAM MILESTONES ESTIMATED TIMEFRAME Tipifarnib (Farnesyl Transferase Inhibitor) Initiate Phase 2 clinical trial in CMML ü Additional data from Phase 2 clinical trial in HRAS mutant SCCHN ü Data from Phase 2 clinical trial in PTCL ü Additional data from Phase 2 clinical tria
Slide 36: 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 37: 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 38: 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 studies of HRAS mutant SCCHN and PTCL Potential to initiate first pivotal study in 2018 Two additional Ph
Slide 39: Kura Oncology – Developing Precision Medicines to Treat Cancer
eQKURA KURA DEVELOPING PRECISION MEDICINES TO TREAT CANCER