UNITED STATES
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FORM
CURRENT REPORT
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| Item 2.02 | Results of Operations and Financial Condition. |
On January 9, 2023, Kura Oncology, Inc. (the “Company”) announced that its preliminary unaudited cash, cash equivalents and short-term investments as of December 31, 2022 were approximately $438 million.
The preliminary unaudited cash position discussed above is subject to the completion of financial closing procedures and other developments that may arise between now and the time the financial results for the fourth quarter of 2022 are finalized, as well as the completion of the audit of the 2022 financial statements. Therefore, actual results may differ materially from these estimates. In addition, the above estimates do not present all information necessary for an understanding of the Company’s financial condition as of December 31, 2022.
The information contained in this Current Report on Form 8-K under Item 2.02 is being furnished and shall not be deemed to be “filed” for the purposes of Section 18 of the Securities and Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section and will not be incorporated by reference into any filing by the Company under the Securities Act of 1933, as amended, or the Exchange Act, unless specifically identified as being incorporated therein by reference.
| Item 8.01 | Other Events. |
On January 9, 2023, the Company updated its corporate presentation materials (the “Presentation”). A copy of the Presentation is attached hereto as Exhibit 99.1 and incorporated herein by reference.
| Item 9.01 | Financial Statements and Exhibits. |
(d) Exhibits.
| Exhibit Number |
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| 99.1 | Presentation Materials of Kura Oncology, Inc. | |
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document) | |
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned thereunto duly authorized.
| KURA ONCOLOGY, INC. | ||||||
| Date: January 9, 2023 | By: | /s/ Teresa Bair | ||||
| Teresa Bair | ||||||
| Chief Legal Officer | ||||||
DEVELOPING PRECISION MEDICINES FOR THE TREATMENT OF CANCER Corporate Presentation – January 2023 Exhibit 99.1
FORWARD-LOOKING STATEMENTS This presentation contains forward-looking statements. Such statements include, but are not limited to, statements regarding our research, preclinical and clinical development activities, plans and projected timelines for ziftomenib, tipifarnib and KO-2806, plans regarding regulatory filings, our expectations regarding the relative benefits of our product candidates versus competitive therapies, and our expectations regarding the therapeutic and commercial potential of our product candidates. The words “believe,” “may,” “should,” “will,” “estimate,” “promise,” “plan”, “continue,” “anticipate,” “intend,” “expect,” “potential” and similar expressions (including the negative thereof), are intended to identify forward-looking statements. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Risks that contribute to the uncertain nature of the forward-looking statements include: our preclinical studies and clinical trials may not be successful; the U.S. Food and Drug Administration (FDA) may not agree with our interpretation of the data from clinical trials of our product candidates; we may decide, or the FDA may require us, to conduct additional clinical trials or to modify our ongoing clinical trials; we may experience delays in the commencement, enrollment, completion or analysis of clinical testing for our product candidates, or significant issues regarding the adequacy of our clinical trial designs or the execution of our clinical trials may arise, which could result in increased costs and delays, or limit our ability to obtain regulatory approval; the commencement, enrollment and completion of clinical trials and the reporting of data therefrom; the COVID-19 pandemic may disrupt our business and that of the third parties on which we depend, including delaying or otherwise disrupting our clinical trials and preclinical studies, manufacturing and supply chain, or impairing employee productivity; our product candidates may not receive regulatory approval or be successfully commercialized; unexpected adverse side effects or inadequate therapeutic efficacy of our product candidates could delay or prevent regulatory approval or commercialization; and we may not be able to obtain additional financing. Additional risks and uncertainties may emerge from time to time, and it is not possible for Kura’s management to predict all risk factors and uncertainties. All forward-looking statements contained in this presentation speak only as of the date on which they were made. Other risks and uncertainties affecting us are described more fully in our filings with the Securities and Exchange Commission. We undertake no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.
INVESTMENT HIGHLIGHTS * Unaudited, preliminary cash, cash equivalents and short-term investments as of 12/31/22 Targeted Oncology Advancing a pipeline of novel therapies, forging new scientific and clinical paths to give patients a better chance for long-term durable remissions Proprietary Pipeline Menin Inhibitor Program (ziftomenib) Potential to address 35% or more of acute leukemias Encouraging safety, tolerability and clinical activity observed in relapsed/refractory AML patients 30% CR rate among 20 patients with NPM1 mutations at 600 mg RP2D Phase 2 registration-directed trial in NPM1-mutant AML expected to begin in Q1 2023 Combination studies with standards of care expected to begin in 1H 2023 Farnesyl Transferase Inhibitor Programs (tipifarnib & KO-2806) Durable responses as a monotherapy in recurrent/metastatic HRAS-mutant HNSCC patients Proof of mechanism demonstrated in combination with alpelisib in PIK3CA-dependent HNSCC Potential to prevent emergence of resistance to osimertinib in EGFR-mutant NSCLC IND for KO-2806, next-generation FTI, on track for Q1 2023 Strong Financials $438 million in Cash as of December 31, 2022* $25 million equity investment from Bristol Myers Squibb and $125 million term loan facility, if fully drawn, extend cash runway into 2026
KURA LEADERSHIP TEAM AND BOARD OF DIRECTORS Leadership Team Board of Directors Troy Wilson, Ph.D., J.D. President & Chief Executive Officer Teresa Bair, J.D. Chief Legal Officer Troy Wilson, Ph.D., J.D. Chairman Helen Collins, M.D. Steven Stein, M.D. Thomas Malley Diane Parks Carol Schafer Mary Szela Faheem Hasnain Lead Independent Director Stephen Dale, M.D. Chief Medical Officer Kirsten Flowers Chief Commercial & Corporate Strategy Officer Kathy Ford Chief Operating Officer Pete De Spain Senior Vice President, Investor Relations & Corporate Communications Tom Doyle Senior Vice President, Finance & Accounting Mollie Leoni, M.D. Senior Vice President, Clinical Development
DRUG CANDIDATE PIPELINE PROGRAM CLINICAL TRIAL STUDY STARTUP PHASE 1 REGISTRATION DIRECTED ZIFTOMENIB Menin Inhibitor KOMET-001 Monotherapy KOMET-007/008 Combination with standards of care TIPIFARNIB Farnesyl Transferase Inhibitor (FTI) AIM-HN Monotherapy KURRENT-HN Combination with alpelisib KURRENT-LUNG Combination with osimertinib KO-2806 Next-Generation FTI Combination with targeted therapies NPM1-mutant acute myeloid leukemia (AML) HRAS-mutant head and neck squamous cell carcinoma (HNSCC)* PIK3CA-dependent HNSCC Solid Tumors EGFR-mutant NSCLC HRAS-dependent HNSCC NPM1-mutant AML KMT2A-rearranged AML KMT2A-rearranged ALL Non-NPM1-m/KMT2A-r AML * Trial closed to further enrollment
ZIFTOMENIB: MENIN-KMT2A/MLL INHIBITOR IN ACUTE LEUKEMIAS
NPM1-MUTANT AND KMT2A-REARRANGED AML REPRESENT AREAS OF SIGNIFICANT UNMET NEED No FDA-Approved Targeted Therapies Exist Today 1 SEER statistics for AML in the US, accessed April 2020. 2 Döhner et al. Blood. 2017 Jan 26;129(4):424-447. 3 Angenendt L, et al. J Clin Oncol. 2019;37(29):2632-2642. 4. Venugopal S, et al. ASH Abstract 2287, 2021. 5 Issa GC, et al. Blood Cancer J. 2021;11(9):162. 6 Vetro C, et al. Cancer Genet. 2020;240:15-22. ~ 1,000-2,000 new cases annually in U.S.1 Adult patients with KMT2A-rearranged AML have poor prognosis with high rates of resistance and relapse following current standard of care 5, 6 5-year Overall Survival < 20%5 ~ 6,000 new cases annually in the U.S.1 Adult patients with NPM1-mutant AML and select co-mutations and/or relapsed/refractory disease are associated with poor prognosis2 5-year Overall Survival ~ 50%3 NPM1-mutant AML 30% AML Median Overall Survival in patients with R/R NPM1 AML is ~ 6.1 mo.4 KMT2A-rearranged AML 5-10% AML Median Overall Survival in patients with R/R KMT2A-r AML is 6 mo. following 2L treatment and 2.4 mo. following 3L treatment5
ZIFTOMENIB IS A POTENT AND SELECTIVE ORAL INHIBITOR OF THE MENIN-KMT2A/MLL COMPLEX Kühn MW, et al. Cancer Discov. 2016;6(10):1166-1181 Thorsteinsdottir U, et al. Mol Cell Biol. 2001;21(1):224-234 Patel SS, et al. Curr Hematol Malig Rep. 2020;15(4):350-359 Brunetti L, et al. Cancer Cell. 2018;34(3):499-512
KOMET-001 PHASE 1 CLINICAL TRIAL OF ZIFTOMENIB IN PATIENTS WITH RELAPSED OR REFRACTORY (R/R) AML PHASE 1A DOSE ESCALATION PHASE 1B VALIDATION COHORTS PHASE 1B EXPANSION 50 mg ~ ~ 100 mg 1000 mg Cohort 1: 200 mg Cohort 2: 600 mg OBJECTIVES Dose escalation in all-comer patients to establish maximum tolerated dose and/or RP2D Safety and tolerability Pharmacokinetics Early evidence of antitumor activity Enroll 2 genetically enriched cohorts to determine the optimal RP2D in line with FDA’s Project Optimus Safety and tolerability Pharmacokinetics Antitumor efficacy Continue enrollment of Phase 1b validation cohort(s) meeting go/no-go criteria Safety and tolerability Pharmacokinetics Antitumor efficacy Expansion of 600 mg
ZIFTOMENIB DEMONSTRATES ENCOURAGING SAFETY PROFILE AND TOLERABILITY IN PHASE 1B ≥Gr 3 TEAEs Occurring in >10% Participants (Regardless of Causal Assessment) 200 mg 600 mg NPM1-m (N = 4) (N = 20) 0 0 KMT2A-r (N = 13) (N = 16) Differentiation Syndrome 4 (30.8) 4 (25.0) Febrile Neutropenia 0 2 (12.5) Erba et al. ASH 2022 #64 (preliminary data as of October 24, 2022)
CHARACTERIZATION OF DIFFERENTIATION SYNDROME WITH ZIFTOMENIB Erba et al. ASH 2022 #64 (preliminary data as of October 24, 2022) 1 Fianchi et al. Mediterr J Hematol Infect Dis. 2021; 13(1): e2021030; DOI: https://doi.org/10.4084/MJHID.2021.030 Any Grade and ≥ G3 DS in Phase 1a/b population 200 mg N = 17, n (%) 600 mg N = 36, n (%) NPM1-m (all grades) 0/4 (0) 4/20 (20.0) ≥ Gr3 0/4 (0) 1/20 (5.0) KMT2A-r (all grades) 5/13 (38.5) 6/16 (37.5) ≥ Gr3 4/13 (30.8) 4/16 (25.0) Patients with DS event at 600 mg ORR: 3/4 (75%) for NPM1-m; 1/6 (16.7%) for KMT2A-r Extramedullary involvement has a significantly higher frequency in patients with KMT2A(MLL) rearrangements vs. all others, including NPM11
ZIFTOMENIB DEMONSTRATES ENCOURAGING ANTILEUKEMIC ACTIVITY AT 600 MG Erba et al. ASH 2022 #64 (preliminary data as of October 24, 2022) 1 MRD was assessed for 5/7 CRc patients; 3 of those 5 patients (60%) tested were MRD negative CRc includes CR, CRh, CRi, CRp ORR includes CR, CRh, CRi, CRp, MLFS Best Overall Response 200 mg 600 mg NPM1-m Phase 1a + 1b (n=6) (n=20) CR 1 (16.7) 6 (30.0) CR/CRh 1 (16.7) 6 (30.0) CRc 1 (16.7) 7 (35.0) MRD negativity 1 (100.0) 3 (42.9)1 ORR 2 (33.3) 8 (40.0) KMT2A-r Phase 1a + 1b (n=14) (n=18) CR/CRh 0 1 (5.6) CRc 0 2 (11.1) MRD negativity 0 2 (100.0) ORR 0 3 (16.7) Of IDH1/2 co-mutants (7), 57% experienced a CR 2 pts had concurrent IDH1/2 2 pts had both IDH1/2 and FLT3-ITD/TKD
DECREASING BONE MARROW BLAST COUNTS CONSISTENTLY REPORTED Erba et al. ASH 2022 #64 (preliminary data as of October 24, 2022)
CLINICAL ACTIVITY OF ZIFTOMENIB OPTIMAL AT 600 MG ORAL, DAILY DOSING Preliminary data as of October 24, 2022
ZIFTOMENIB INDUCES RAPID AND EXTENSIVE DIFFERENTIATION OF NPM1-MUTANT LEUKEMIA Baseline Bone Marrow Cellular BM (40%) with 75% blasts consistent with relapsed AML Cycle 1 Day 28 ziftomenib Hypercellular BM (>95%) with striking granulocytic hyperplasia and <1% blasts 61 yo male with NPM1-m, FLT3-ITD, and IDH2 AML Baseline bone marrow blasts: 75% Prior therapies 7+3, Midostaurin, HiDAC, gilteritinib Initiated ziftomenib at 600 mg DS during C1 Bone pain, ↓BP WBC ↑58K Response MLFS after Cycle 1 CR after Cycle 3 Erba et al. ASH 2022 #64 (preliminary data as of October 24, 2022)
EVIDENCE OF CLINICAL BENEFIT IN PATIENTS WITH NPM1-MUTANT AML Preliminary data as of October 24, 2022 22 yo male with NPM1-m AML Baseline bone marrow blasts: 90% Prior therapies Cytarabine + idarubicin (7+3) Initiated ziftomenib at 600 mg DS during Cycle 1 (Gr2; non-serious) Non-cardiac chest and bone pain; ↓ fibrinogen (89 from 456 at baseline) Response CRmrd- after Cycle 1 Transplant scheduled 44 yo female with NPM1-m, DNMT3A and IKZF1 AML Baseline bone marrow blasts: 14% Prior therapies Cytarabine + anthracycline NOS; mitoxantrone, etoposide + cytarabine; HiDAC+ fludarabine + melphalan; 1st SCT + cyclophosphamide; lenalidomide + bortezomib; decitabine + venetoclax + gilteritinib; ASP1235; busulfan + fludarabine; 2nd SCT + methotrexate Initiated ziftomenib at 200 mg No DS Experienced TRAEs of Gr4 lipase increased and Gr3 pancreatitis at C2D28; Gr3 pulmonary embolus during C17 Response CRmrd- after Cycle 1 CRmrd- maintained and currently at Cycle 31
EVIDENCE OF CLINICAL BENEFIT: EXAMPLE OF A KMT2A-REARRANGED NON-RESPONDING PATIENT 47 yo female with KMT2A-r, TERT and BRAF AML Baseline bone marrow blasts: 52% Prior therapies ddAC + paclitaxel, CPX-35, SCT, Aza, FLAG Ida-ven, DLI, RT - gums Initiated ziftomenib at 200 mg DS during C1 Muscle and EMD pain, ↑temp, ↓BP, WBC ↑ 5.2 Response Bone marrow blasts 2% end of Cycle 2 Best overall response for the patient of SD due to residual extramedullary disease After 2 cycles Baseline Erba et al. ASH 2022 #64 (preliminary data as of October 24, 2022)
SUMMARY: KOMET-001 PHASE 1 CLINICAL TRIAL OF ZIFTOMENIB Ziftomenib demonstrates an encouraging safety profile and tolerability Reported events most often consistent with features and manifestations of underlying disease No evidence of drug-induced QTc prolongation Differentiation syndrome, an on-target effect, manageable with mitigation strategy Clinical activity of ziftomenib monotherapy is optimal at the 600 mg daily dose Positive NPM1-m benefit/risk balance with pronounced activity and 30% CR rate (n=20) High levels of ziftomenib tissue penetration likely drive clearance of extramedullary disease Monotherapy data supportive of combination strategies No predicted adverse drug-drug interactions Optimization of KMT2A-r benefit/risk planned via rational combination strategies, to maximize patients’ time on treatment Oral, QD dosing allows for convenient administration and combination with standards of care Erba et al. ASH 2022 #64 (preliminary data as of October 24, 2022)
DEVELOPMENT APPROACH STUDY STARTUP PHASE 1 REGISTRATION DIRECTED TRIAL MONOTHERAPY (Relapsed/refractory) COMBINATION WITH VENETOCLAX + AZACYTIDINE (Relapsed/refractory, frontline) COMBINATION WITH CYTARABINE + DAUNORUBICIN (7+3) (Frontline) COMBINATION WITH GILTERITINIB (Relapsed/refractory) COMBINATION WITH FLAG-IDA (Relapsed/refractory) COMBINATION WITH IDAC/LDAC (Relapsed/refractory) POST-TRANSPLANT MAINTENANCE COMBINATION WITH FLA (Relapsed/refractory) COMBINATION WITH BV-DAM (Frontline) NPM1-mutant acute myeloid leukemia (AML) NPM1-mutant AML KMT2A-rearranged AML KMT2A-rearranged AML NPM1-mutant AML NPM1-mutant AML NPM1-mutant AML KMT2A-rearranged AML KMT2A-rearranged ALL Non-NPM1-m/KMT2A-r AML Investigator-sponsored studies KMT2A-rearranged AML NPM1-mutant AML NPM1-mutant AML KMT2A-rearranged AML Pediatric AML & ALL Pediatric ALL ZIFTOMENIB CLINICAL DEVELOPMENT PATH
FARNESYL TRANSFERASE INHIBITOR PROGRAMS
Direct Inhibition of Oncogenic Proteins Overcoming Drug Resistance Preventing Emergence of Resistance Monotherapy activity in mutant tumors Overcome drug resistance to PI3Ka inhibitor in HNSCC Prevent emergence of resistance to EGFR inhibitor in NSCLC EVOLUTION IN THE THERAPEUTIC APPLICATIONS OF FARNESYL TRANSFERASE INHIBITORS
ORR 55% N=20 evaluable patients Red, PR; blue, SD; green, not evaluable for efficacy; diamond, patient initiated treatment at 600 mg twice a day; cross, patient withdrew consent; arrow in bar, start of response; arrow, active treatment. Numbers at the end of the bars represent VAF for each patient. Median OS (months) 95% CI Lower Upper HNSCC with high VAF, including additional patient (N=18) 15.4 7.0 46.4 Ho, et al. J Clin Oncol. 2021 June 10;39(17):1856-1864. doi: 10.1200/JCO.20.02903. Ho et al. ASCO 2020 #6504 (preliminary exploratory data as of 9/30/19) Efficacy-evaluable patients with HRAS mutant variant allele frequency (VAF) ≥ 20% and serum albumin ≥ 3.5 g/dL, or HRAS VAF ≥ 35% One patient treated off-protocol through compassionate use TIPIFARNIB DEMONSTRATES DURABLE ANTI-TUMOR ACTIVITY IN PATIENTS WITH RECURRENT OR METASTATIC HRAS-MUTANT HNSCC
Tipifarnib granted Breakthrough Therapy Designation for the treatment of patients with HRAS-mutant HNSCC based on data from RUN-HN study AIM-HN is a global, multi-center, registration-directed trial in patients with recurrent or metastatic HNSCC after one prior line of platinum therapy Evidence of meaningful clinical activity observed in AIM-HN; however, trial closed to further enrollment due to significant feasibility challenges Currently evaluating clinical data from RUN-HN and AIM-HN to inform future development of the program Given significant overlap between patients with HRAS overexpression and mutation, HRAS-mutant HNSCC patients in the U.S. may be eligible to enroll in ongoing KURRENT-HN study AIM-HN: REGISTRATION-DIRECTED TRIAL OF TIPIFARNIB
TIPIFARNIB HAS POTENTIAL TO OVERCOME RESISTANCE TO TREATMENT WITH PI3Kα INHIBITORS IN HNSCC The PI3K pathway is the most frequently activated pathway in HNSCC ~30% of tumors harbor PIK3CA mutation or amplification Feedback reactivation of PI3K –mTOR signaling drives innate resistance to PI3K inhibitors Necessitates development of rational combination strategies Tipifarnib blocks hyperactivated growth factor signaling via multiple farnesylation-dependent proteins, including HRAS and RHEB
COMBINATIONS OF TIPIFARNIB AND PI3Kα INHIBITOR DEMONSTRATE ROBUST ACTIVITY IN HNSCC PDX MODELS Malik et al. EORTC-NCI-AACR 2020 #159 Tipifarnib used at reduced dose to simulate potential lower doses in combination (80à60mg/kg BID) BYL-719 used at reduced dose to simulate potential lower doses in combination (60à40mg/kg QD) Mean Tumor Volume ± SEM Days of treatment HRAS-mutant PIK3CA-mutant Wild-Type E545K
HRAS-MAPK and PI3K-mTOR are complementary pathways in HNSCC Overexpression of WT HRAS reported to induce resistance to PI3Kα inhibition HRAS is reported to preferentially activate PI3K (vs. KRAS; vs. MAPK) HRAS mutation/overexpression and PIK3CA mutations/amplifications account for up to 45% of HNSCC1 PIK3CA mutations/amplification: 30-40% (25% estimated overlap with HRAS-overexpressing tumors) HRAS overexpression: 20-30% HRAS mutations: 4-8% (83% overexpress HRAS) Preclinical data is supportive of the combination; enhanced activity observed in both HRAS-mutant/overexpressed and PIK3CA-mutant/amplified populations of HNSCC Preliminary clinical data demonstrate that tipifarnib plus alpelisib can induce a durable clinical response in PIK3CA-dependent HNSCC1 1 Soifer H et al, ENA 2022 PB041 References: Yan J et al (1998) J Bio Chem 273:24052 ; Gupta S et al (2007) Cell 129:957 ; Zhao L et al (2008) Proc Natl Acad Sci 105:2652 COMBINATION OF TIPIFARNIB AND PI3Kα INHIBITOR HAS SIGNIFICANT THERAPEUTIC POTENTIAL IN HNSCC
Clinical collaboration to evaluate tipifarnib in combination with alpelisib for the treatment of patients with HNSCC whose tumors have HRAS overexpression and/or PIK3CA mutation and/or amplification Under the collaboration, Kura sponsors the trial and supplies tipifarnib and Novartis supplies alpelisib Enrolling patients in PIK3CA-dependent and HRAS-overexpression cohorts KURRENT-HN: PHASE 1/2 COMBINATION TRIAL OF TIPIFARNIB AND ALPELISIB IN PATIENTS WITH HNSCC Phase 1 clinical trial of tipifarnib and alpelisib in patients with recurrent/metastatic HRAS-overexpressed and/or PIK3CA-amplified and/or PIK3CA-mutated HNSCC
35yo, male, nonsmoker, HPV16 positive SCC of tonsil Stage III cT4N2M0; PD-L1 CPS = 60 Prior Treatments CDDP/rad for 1 mo (Nov-Dec2019), BOR UNK Cemiplimab/ISA101b (Jun-Nov2021), BOR PD PIK3Cα R88Q mutation (44%) and HRAS OE (3+ staining in 100% of tumor cells) by IHC from May 2021 biopsy DL1 tipifarnib, DL2 alpelisib; completed 6 cycles G1/2 TRAE, G3 lipase elevation; presented clinical benefit and improvement in respiratory symptoms 81% reduction in target lesions after 1 cycle of treatment 84% reduction in target lesions after 3 cycles (BOR) Continued on-study for >27 weeks maintaining QoL Soifer H et al, ENA 2022 PB041; Data cut as of 14Sep2022; Preliminary raw data DURABLE CLINICAL RESPONSE OBSERVED IN PATIENT WITH PIK3Cα -DEPENDENT HNSCC
Drug-tolerant cells (DTCs) arise within days of osimertinib exposure DTCs are characterized by Rho pathway activation RhoB, RhoE and LaminB are farnesylation-dependent proteins that are selectively upregulated in DTCs Genetic or pharmacologic inhibition of these targets kills DTCs and prevents the emergence of osimertinib-resistant mutant cells Combination of tipifarnib and osimertinib delays relapse in vivo TIPIFARNIB PREVENTS EMERGENCE OF RESISTANCE TO OSIMERTINIB IN VIVO
Preclinical data generated through a collaboration with INSERM (the French National Institute of Health and Medical Research), suggest the potential to prevent emergence of resistance to EGFR inhibitor, osimertinib Figarol et al. AACR 2022 #7934 TIPIFARNIB PREVENTS EMERGENCE OF RESISTANCE TO OSIMERTINIB IN VIVO
TIPIFARNIB PREVENTS EMERGENCE OF RESISTANCE TO OSIMERTINIB IN VIVO Phase 1 clinical trial of tipifarnib and osimertinib in patients with treatment-naïve, locally advanced, or metastatic EGFR-Mutant NSCLC ORR = overall response rate; DOR – duration of response; PFS = progression-free survival
NEXT-GENERATION FARNESYL TRANSFERASE INHIBITOR (FTI) KO-2806 nominated as development candidate for IND-enabling studies FTIs represent an attractive therapeutic target and commercial franchise in oncology with compelling opportunities in combination with other targeted therapies Goal is to develop a next-generation FTI with improved potency, pharmacokinetic and physicochemical properties IND-enabling studies ongoing; on track for IND application acceptance for KO-2806 in Q1 2023 Potency: Good Selectivity: Excellent Dose: 600 mg Frequency: BID Tipifarnib Improved potency, pharmacokinetic and physicochemical properties KO-2806
FORECASTED MILESTONES & FINANCIAL HIGHLIGHTS *Optimal biologically active dose **Unaudited, preliminary cash, cash equivalents and short-term investments as of 12/31/2022 PROGRAM MILESTONE ESTIMATED TIME OF ACHIEVEMENT ZIFTOMENIB (KO-539) Menin Inhibitor Dose first patient in Phase 2 registration-directed portion of KOMET-001 Q1 2023 Dose first patient in KOMET-007 (venetoclax+azacitidine, 7+3) 1H 2023 Dose first patient in KOMET-008 (gilteritinib, FLAG-IDA, IDAC/LDAC) 2H 2023 TIPIFARNIB Farnesyl Transferase Inhibitor (FTI) Dose first patient in KURRENT-LUNG study (osimertinib) 1H 2023 Determine OBAD* for PIK3CA cohort in KURRENT-HN study (alpelisib) Mid-2023 KO-2806 Next-Generation FTI Acceptance of Investigational New Drug application Q1 2023 Financial Highlights* Nasdaq: KURA $438M in Cash as of December 31, 2022** Shares outstanding: 68.3M basic; 9.3M options, RSU’s & warrants
DEVELOPING PRECISION MEDICINES FOR THE TREATMENT OF CANCER Corporate Presentation – January 2023