Kura Oncology, Inc. · NASDAQ:KURA
Kura Oncology — AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics 2019
10 slides from Kura Oncology's conference presentation, 2019
Slide 1: Preliminary results from a phase 2 trial of tipifarnib in HNSCC with HRAS mutations
Preliminary results from a phase 2 trial of tipifarnib in Head and Neck Squamous Cell Carcinomas (HNSCCs) with HRAS mutations. Alan Ho1, Irene Brana2, Robert Haddad3, Jessica Bauman4, Keith Bible5, Laurence Faugeras6, Sjoukje Oosting7, Deborah J. Wong8, Myung-Ju Ahn9, Valentina Boni10, Caroline Even
Slide 2: Disclosure Information: Alan Ho, MD, PhD
Disclosure Information: Alan Ho, MD, PhD AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics • I have the following financial relationships to disclose: • Consultant for: Kura Oncology (travel/lodging/conference fees only), AstraZeneca, TRM Oncology, Sun Pharmaceutic
Slide 3: Mutant HRAS Oncogene Activity is Uniquely Dependent on Farnesylation
Mutant HRAS Oncogene Activity is Uniquely Dependent on Farnesylation • HRAS activity requires covalent addition of a Antitumor activity in HNSCC PDX models (N=36) farnesyl hydrophobic group to its C-terminal tail 200 HRAS wild type for membrane localization and downstream HRAS-mutant signaling. 150
Slide 4: Study Design
Study Design1 Original Protocol • Key Eligibility: No curative therapy available, HRAS mutation, measurable disease HNSCC Extension Cohort (N=30) (RECIST v1.1), ECOG PS 0 – 1 • 2 cohorts: Cohort 1: Thyroid. Cohort 2: Any other solid tumor; amended to HNSCC • HRAS variant allele frequency (VAF) ≥20%
Slide 5: Patient Demographics: HRAS mutant HNSCC
Patient Demographics: HRAS mutant HNSCC1 Total Total Patients Treated1, n (%) 21 (100) Total Evaluable for Efficacy2, n (%) 18 (85.7) Age, yrs, median (min, max) 64 (20, 89) Male, n (%) 14 (66.7) Site of Primary Tumor, n (%) Oral Cavity 11 (52.4) Pharynx 6 (28.6) Larynx 3 (14.3) Other 1 (4.8) Number
Slide 6: Tipifarnib treatment results in 56% ORR with durable responses in HRAS mutant HNSCC
Tipifarnib treatment results in 56% ORR with durable responses in HNSCC HRAS mutant ≥20% VAF1 Maximum Change in Tumor Burden2 Time on Treatment ORR 56% (95% CI 0.31, 0.78) N= 18 evaluable patients Treatment Cycles PR SD Not yet efficacy evaluable Not efficacy evaluable * unconfirmed PR (uPR) 600 mg
Slide 7: PFS in HNSCC HRAS mutant ≥20% VAF
PFS in HNSCC HRAS mutant ≥20% VAF1 Tipifarnib appears better than SOC for the treatment of HNSCC with HRAS mutations at ≥20% VAF 10 PRs, 8 SDs 0 PRs, 6 SDs, 11 PDs 2 Preliminary data as of 17 Oct 2019 1 Efficacy evaluable subjects with HRAS VAF ≥20% and serum albumin ≥ 3.5 g/dL or HRAS VAF ≥35% enro
Slide 8: Safety and tolerability of tipifarnib in HRAS mutant HNSCC
Safety and tolerability of tipifarnib in HRAS mutant HNSCC1 • All HNSCC patients meeting HRAS VAF criteria (N = 20)1 had at least 1 treatment-emergent adverse event (TEAE). No study drug related deaths reported. • TEAEs were consistent with the known safety profile of tipifarnib. Most frequently obs
Slide 9: Conclusions
Conclusions • Tipifarnib demonstrated compelling antitumor activity in a heavily pretreated cohort of recurrent/metastatic HNSCC carrying HRAS mutations. • Per protocol ORR = 56% (95% CI 0.31, 0.78), 48% ORR by ITT • Responses were rapid and durable with 8.3 mos median PFS for patients with PR and 4
Slide 10: Acknowledgements
Acknowledgements • Patients, their families and caregivers • Study Investigators and their study teams • Kura Oncology AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, Abstract 384 10