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September 16, 2025 FARNESYL TRANSFERASE PROGRAM REVIEW Our goal is to develop transformative therapies to extend and improve the lives of patients with cancer
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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, darlifarnib (KO-2806) and tipifarnib, development plans and timelines for our menin inhibitor candidate in diabetes, expectations regarding the relative benefits of our product candidates versus competitive therapies, expectations regarding the therapeutic and commercial potential of our product candidates, anticipated significant near-term milestones, market opportunities and expectations regarding our collaboration with Kyowa Kirin. 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 in the reporting of data from such clinical testing, 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; 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; we may not be able to obtain additional financing; and our collaboration with Kyowa Kirin may not be successful. 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. This presentation may also contain statistical, preclinical and clinical data obtained from and prepared by third parties. The recipient is cautioned not to give undue weight to such disclosures. Neither the Company nor any other person makes any representation as to the acc uracy or completeness of such data or undertakes any obligation to update such data after the date of this presentation. 2
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3 Troy Wilson, Ph.D., J.D. President & Chief Executive Officer Francis Burrows, Ph.D. Chief Scientific Officer Mollie Leoni, M.D. Chief Medical Officer TODAY’S SPEAKERS
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KURA IS ADVANCING A ROBUST PIPELINE OF THERAPEUTIC PRODUCT CANDIDATES 4 Ziftomenib: Potentially Best-in-Class Menin Inhibitor for AML Relapsed/refractory (R/R) and frontline acute myeloid leukemia (AML) U.S. market opportunity could exceed $7B per year NDA in R/R NPM1-m AML under FDA Priority Review with PDUFA target date of 30-Nov-2025; registration-enabling trials in 1L AML on track for 2H 2025 Kyowa Kirin collaboration funds expansive AML development program through 1L U.S. commercialization Target indications include renal cell carcinomas, HNSCC, lung, colorectal, breast, endometrial and NETs Farnesyl Transferase Inhibitors (FTIs) in Large Solid Tumor Indications FTIs may overcome innate and adaptive resistance to PI3K inhibitors, KRAS inhibitors and tyrosine kinase inhibitors (TKIs) in certain indications Presentations of clinical data planned for ESMO Congress in October 2025 Additional Therapeutic Opportunities for Menin Inhibitors Next-generation menin inhibitor candidate nominated for IND- enabling studies for diabetes; development plans and timelines to be shared in future update Ziftomenib + imatinib currently in Phase 1 dose escalation in gastrointestinal stromal tumors (GIST); additional potential $1B opportunity
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5 RATIONALE FOR FTIs: OVERCOMING RESISTANCE TO TARGETED THERAPIES Combination therapy using FTIs has potential to address drug resistance and provide deeper and more durable anti-tumor activity
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6 THERE IS A NEED TO IMPROVE STANDARDS OF CARE FOR PATIENTS TREATED WITH TARGETED THERAPIES Despite impressive progress with small molecule targeted therapies, resistance limits the potential of many agents • Targeted therapies are often effective but insufficient as monotherapies • Combinations (e.g., KRAS/EGFR inhibitors in CRC) have demonstrated enhanced response There is a significant need to identify combination therapeutics, which address mechanisms of innate and adaptive resistance
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7 THERE IS A NEED TO IMPROVE STANDARDS OF CARE FOR PATIENTS TREATED WITH TARGETED THERAPIES Despite impressive progress with small molecule targeted therapies, resistance limits the potential of many agents • Targeted therapies are often effective but insufficient as monotherapies • Combinations (e.g., KRAS/EGFR inhibitors in CRC) have demonstrated enhanced response There is a significant need to identify combination therapeutics, which address mechanisms of innate and adaptive resistance Kura Oncology is pioneering FTIs to enhance the therapeutic potential of targeted therapies • mTOR is a clinically validated target, and FTIs reduce mTOR activation by blocking RHEB farnesylation • RHEB/mTOR inhibition is relevant to anti-VEGF TKIs, KRAS inhibitors and PI3Ka inhibitors Simultaneous inhibition of RHEB/mTOR using FTIs has the potential to address resistance and provide deeper and more durable anti-tumor activity
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OPPORTUNITY IN LARGE SOLID TUMOR MARKETS RAS inhibitors NSCLC CRC VEGFR TKIs RCC NETs RAS/MAPK and PI3K/AKT pathways are central to many precision medicine approaches to solid tumors active inactive PI3K inhibitors Breast Endometrial Ovarian Cervical Urothelial Lung 8> 200K ANNUAL INCIDENT PATIENTS IN THE U.S. ACROSS INDICATIONS
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CLINICAL ACTIVITY HAS POTENTIAL TO READ THROUGH TO ENTIRE CLASS active inactive RAS inhibitors • adagrasib • sotorasib • divarasib • daraxonrasib • elironrasib • KRAS G12X and pan-RAS inhibitors in development VEGFR TKIs and multi kinase inhibitors • cabozantinib • axitinib • lenvatinib • sunitinib • sorafenib • pazopanib • zanzalitinib • combinations with immunotherapies PI3K inhibitors • alpelisib • inavolisib • PI3K inhibitors in development • RLY-2608 • STX-478 9> 200K ANNUAL INCIDENT PATIENTS IN THE U.S. ACROSS INDICATIONS
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10 KO-2806 Class-leading FTI drug candidate aims to address innate and adaptive resistance to various classes of targeted therapies
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Tipifarnib 11 TIPIFARNIB – FIRST-GEN FTI VALIDATES THERAPEUTIC APPROACH OF RHEB/mTORC1 INHIBITION First generation FTI with 5,000 patient safety database Manageable tolerability profile Compelling clinical activity in HRAS-mutant HNSCC Demonstrated combinability (e.g., erlotinib, alpelisib) RP2D: 600 mg BID Twice-daily dosing Extensive first-pass metabolism Limited IP
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12 Darlifarnib DARLIFARNIB (KO-2806) REPRESENTS A CLASS LEADING FTI Next Gen FTI optimized for combination drug development. Preclinical data demonstrates improvements over prior FTIs : Enhanced potency and selectivity Manageable tolerability and combinability (with adagrasib, cabozantinib, and other agents) in long-term in vivo studies Pharmacokinetic and metabolic profiles support projected efficacious dose of << 1200 mg QD Excellent drug-like properties Extended IP protection as an NCE
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13 FTI + TYROSINE KINASE INHIBITOR (TKI) COMBINATIONS IN RENAL CELL CARCINOMA
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14 FTIs ENHANCE ACTIVITY OF VEGF INHIBITORS BY TARGETING THE MTOR NODE Hyperactivated mTORC1 pathway is often observed with advanced RCC and is associated with poor prognosis. Rapalogs, including everolimus and temsirolimus, have been approved in RCC. However, they have had limited uptake in the clinic due to tolerability issues. inactive Blood vessel growth arrest and tumor cell death X X X X Endothelial Cell Deep and durable mTORC1 inhibition
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15 FTIs ENHANCE ACTIVITY OF VEGF INHIBITORS BY TARGETING THE MTOR NODE Farnesyl transferase inhibitors (FTIs) inhibit mTORC1 signaling by blocking the farnesylation of RHEB, which can no longer properly localize to activate mTORC1.1,2,3 FTI (tipifarnib) markedly reduces the localization of RHEB to lysosomes, which underlies its loss of activity upon defarnesylation 1Smith, AE. et al. Cancer Res 2023. 83(19):3252-63. 2Patel, HV. Smith, AE. et al. bioRxiv 2024.12.20.629824. 3Gasendo, JG. et al. Cancer Res 2025. 85(8_Supplement_1):6370 inactive Blood vessel growth arrest and tumor cell death X X X X Endothelial Cell Deep and durable mTORC1 inhibition
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16 • Cabozantinib partially inhibits mTOR signaling in its target cell type – tumor endothelial cells • Addition of KO-2806 fully inhibits mTOR signaling, leading to enhanced anti-angiogenic activity • Similar observations when KO-2806 is combined with axitinib or lenvatinib KO-2806 ENHANCES ANTI-ANGIOGENIC ACTIVITY OF CABOZANTINIB KI-12-0073 RCC PDX, Day 14
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17 KO-2806 CONSISTENTLY IMPROVES RESPONSES TO TKIs IN RCC XENOGRAFTS Caki1 RCC Axitinib Lenvatinib Cabozantinib KO-2806 -100 -50 0 50 300 600 900 Caki1 CDX % Change in tumor volume KO-2806 TKI TKI + KO-2806 *VHL WT KO-2806 consistently improves responses to TKIs (axitinib, lenvatinib, cabozantinib) in an RCC CDX model KO-2806 consistently improves responses to cabozantinib in various TKI naïve RCC CDX and PDX models RCC models *VHL mutant and WT models tested
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18 RCC XENOGRAFTS PROGRESSING ON ANTI-VEGFR TKIs RESPOND TO KO-2806 / CABOZANTINIB COMBINATION 0 10 20 30 40 50 0 500 1000 1500 2000 Treatment Days Tumor volume (mm3) Axitinib 0 10 20 30 40 50 0 500 1000 1500 2000 Treatment Days Tumor volume (mm3) Lenvatinib Caki1 (RCC)
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19 RCC XENOGRAFTS PROGRESSING ON ANTI-VEGFR TKIs RESPOND TO KO-2806 / CABOZANTINIB COMBINATION Lenvatinib pre-treated 0 10 20 30 40 50 0 500 1000 1500 2000 Treatment Days Tumor volume (mm3) switch Lenvatinib → Cabozantinib Lenvatinib 0 10 20 30 40 50 0 500 1000 1500 2000 Treatment Days Tumor volume (mm3) Axitinib → Cabozantinib Axitinib switchAxitinib pre-treated Caki1 (RCC)
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20 RCC XENOGRAFTS PROGRESSING ON ANTI-VEGFR TKIs RESPOND TO KO-2806 / CABOZANTINIB COMBINATION 0 10 20 30 40 50 0 500 1000 1500 2000 Treatment Days Tumor volume (mm3) Lenvatinib → Cabo + KO-2806switch Lenvatinib → Cabozantinib Lenvatinib 0 10 20 30 40 50 0 500 1000 1500 2000 Treatment Days Tumor volume (mm3) Axitinib → Cabozantinib Axitinib → Cabo + KO-2806 Axitinib switch Caki1 (RCC) • The combination of cabozantinib and KO-2806 reverses progression on first-line TKI therapy • Switching to cabo slows tumor growth, but the FTI combo drives consistent tumor regression Lenvatinib pre-treatedAxitinib pre-treated
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21 RCC XENOGRAFTS PROGRESSING ON ANTI-VEGFR TKIs RESPOND TO KO-2806 / CABOZANTINIB COMBINATION • KO-2806 enhances activity of cabo and other TKIs across their full activity range in ccRCC models • Enhancement of antiangiogenic TKI activity by FTI-mediated RHEB/mTOR inhibition is effective in tumors progressing on first- or second-line TKI monotherapy KO-2806 combination therapy induces regressions in tumors previously exposed to cabozantinib
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22 FTI COMBINATIONS IN PIK3CA-DRIVEN TUMORS
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FTIs ENHANCE PRECLINICAL ACTIVITY OF PI3K INHIBITORS ACROSS TUMOR TYPES BY INHIBITING THE mTORC1 NODE 0 10 20 30 40 50 NSCLC Esophageal Glioma Ovarian HNSCC Bladder CRC Cervical Breast Endometrial 43.1 34.0 26.5 18.3 17.7 14.9 9.2 8.4 7.7 5.0 PIK3CA alteration frequency (%) AACR GENIE v17.0 • PIK3CA is one of the most commonly mutated genes in solid cancers • Feedback reactivation of PI3K–mTOR signaling limits benefit of PI3K inhibitors, necessitating development of rational combination strategies • FTIs blunt mTORC1 effects by blocking farnesylation of RHEB, leading to more effective reduction of mTOR signaling, while sparing mTORC2 23 inactive X X X X
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24 TIPIFARNIB ENHANCES THE ACTIVITY OF ALPELISIB IN PRECLINICAL MODELS OF PIK3CA-MUTANT HNSCC Tipifarnib inhibits mTOR signaling rebound observed with alpelisib alone Combination of tipifarnib and alpelisib results in deep regression in a PIK3CA- mutant HNSCC CDX model 0 6 12 18 24 0 25 50 75 100 CAL33 phospho-S6 (S235/236) Time post dose (hours) Signal intensity (% of DMSO) Alpelisib Combination HNSCC -100 -50 0 50 100 % Change in tumor volume (relative to day 0) Tipifarnib CombinationVehicle Alpelisib CAL33 HNSCC xenograft tumors
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25 Addition of KO-2806 consistently enhances the activity of both mutant-selective PI3K inhibitors in preclinical models Ovarian CRC CRC Cervical Ovarian TNBC Endometrial Cervical HR+ breast Bladder HR+ breast-100 0 100 200 300 400 500 600 Change in tumor volume (% of baseline) SD PR RLY-2608 STX-478 KO-2806+PI3Ki 0 10 20 30 0 500 1000 HR+ breast MCF7 Days of treatment Tumor volume (mm3) Vehicle KO-2806 (5 mg/kg BID) STX-478 (100 mg/kg QD) Combination 0 5 10 15 20 25 0 200 400 600 800 1000 Cervical CaSki Days of treatment Tumor volume (mm3) Vehicle KO-2806 (5 mg/kg BID) STX-478 (100 mg/kg QD) Combination 0 5 10 15 20 25 0 200 400 600 Bladder HT1197 Days of treatment Tumor volume (mm3) Vehicle KO-2806 (5 mg/kg BID) RLY-2608 (100 mg/kg BID) Combination KO-2806 ENHANCES ANTI-TUMOR ACTIVITY OF PI3K INHIBITORS ACROSS DIFFERENT INDICATIONS
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26 FTI COMBINATIONS IN KRAS-DRIVEN TUMORS
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FTIs ENHANCE ACTIVITY OF RAS INHIBITORS BY TARGETING THE mTORC1 NODE • Partial inhibition and/or rebound of mTOR signaling limits single agent efficacy of (K)RAS inhibitors • KO-2806 inhibits RHEB farnesylation leading to a sustained blockade of mTORC1 signaling and enhancing the anti-tumor activity of RAS inhibitors across the class 0 12 24 36 48 0 25 50 75 100 NCI-H2122 phospho-p70 S6K (T389) Time post dose (hours) Signal intensity (% of DMSO) Adagrasib Combination 0 12 24 36 48 0 25 50 75 100 GP2D phospho-p70 S6K (T389) Time post dose (hours) Signal intensity (% of DMSO) Daraxonrasib Combination NSCLC CRC mTORC1 activity Time post-dose (hours) Time post-dose (hours) mTORC1 activity 27 inactive X X X X
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KO-2806 ENHANCES ANTI-TUMOR ACTIVITY OF RAS INHIBITORS IN NSCLC AND CRC PRECLINICAL MODELS KO-2806 enhances activity of all classes of RAS inhibitors across their full activity range in both NSCLC and CRC CDX and PDX models Patel, HV. Smith, AE. et al. Biorxiv 2024.12.20.629824. NSCLC CRC CRC 28
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29 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN NSCLC MODEL 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) Adagrasib 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) Sotorasib 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) Adagrasib 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) RMC-6236 NCI-H2122 (KRASG12C NSCLC)
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0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) switch Sotorasib Sotorasib → Adagrasib 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) switch Adagrasib Adagrasib → RMC-6236 30 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN NSCLC MODEL 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) RMC-6236 NCI-H2122 (KRASG12C NSCLC) 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) Adagrasib
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0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) +KO-2806 RMC-6236 RMC-6236 + KO-2806 (add-in) 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) switch Adagrasib Adagrasib → RMC-6236 Adagrasib → RMC-6236 + KO-2806 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) switch Sotorasib Sotorasib → Adagrasib Sotorasib → Adagrasib + KO-2806 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) +KO-2806 Adagrasib Adagrasib + KO-2806 (add-in) 31 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN NSCLC MODEL NCI-H2122 (KRASG12C NSCLC)
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0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) +KO-2806 RMC-6236 RMC-6236 + KO-2806 (add-in) RMC-6236 + KO-2806 (upfront) 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) +KO-2806 Adagrasib Adagrasib + KO-2806 (upfront) Adagrasib + KO-2806 (add-in) 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) switch Adagrasib Adagrasib → RMC-6236 Adagrasib → RMC-6236 + KO-2806 0 10 20 30 40 50 0 200 400 600 800 1000 Treatment Days Tumor volume (mm3) switch Sotorasib Sotorasib → Adagrasib Sotorasib → Adagrasib + KO-2806 32 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN NSCLC MODEL NCI-H2122 (KRASG12C NSCLC)
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0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) MRTX1133 33 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN CRC MODEL 0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) MRTX1133 GP2D (KRASG12D CRC) 0 20 40 60 80 0 100 200 300 400 500 1000 2000 Treatment Days Tumor volume (mm3) RMC-6236
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0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) switch MRTX1133 MRTX1133 → RMC-6236 34 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN CRC MODEL 0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) MRTX1133 GP2D (KRASG12D CRC) 0 20 40 60 80 0 100 200 300 400 500 1000 2000 Treatment Days Tumor volume (mm3) RMC-6236
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35 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN CRC MODEL GP2D (KRASG12D CRC) 0 20 40 60 80 0 100 200 300 400 500 1000 2000 Treatment Days Tumor volume (mm3) +KO-2806 RMC-6236 RMC-6236 + KO-2806 add-in 0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) switch MRTX1133 MRTX1133 → RMC-6236 MRTX1133 → RMC-6236 + KO-2806 0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) +KO-2806 MRTX1133 MRTX1133 + KO-2806 add-in
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36 KO-2806 RE-SENSITIZES RELAPSING TUMORS TO MUTANT SELECTIVE OR PAN-RAS INHIBITION IN CRC MODEL 0 20 40 60 80 0 100 200 300 400 500 1000 2000 Treatment Days Tumor volume (mm3) +KO-2806 RMC-6236 RMC-6236 + KO-2806 add-in upfront 0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) +KO-2806 MRTX1133 MRTX1133 + KO-2806 add-in upfront 0 20 40 60 80 0 100 200 300 400 500 1000 2000 3000 Treatment Days Tumor volume (mm3) switch MRTX1133 MRTX1133 → RMC-6236 MRTX1133 → RMC-6236 + KO-2806 GP2D (KRASG12D CRC) • KO-2806 enhances activity of all classes of RAS inhibitors across their full activity range in both NSCLC and CRC models • KRAS inhibitor/KO-2806 combination therapy induces regressions in NSCLC and CRC tumors previously exposed to mutant-selective or pan-RAS inhibitor monotherapy
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37 FTIs have been successfully combined in preclinical models with multiple drug classes, including PI3Kα inhibitors, KRAS inhibitors and antiangiogenic tyrosine kinase inhibitors KO-2806 (darlifarnib) is a next-generation FTI, optimized for combination approaches with improved pharmaceutical properties Preclinical data support combination therapy using darlifarnib to address resistance and provide more durable activity CONCLUSIONS FROM PRECLINICAL EXPERIENCE WITH FARNESYL TRANSFERASE INHIBITORS The targeting of innate and adaptive resistance via FTIs in combination with targeted therapies has demonstrated the potential to drive deep responses in preclinical models FTIs address a resistance pathway common to many targeted therapies across a range of large indications
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38 CLINICAL DEVELOPMENT OF KO-2806
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Monotherapy Safety, tolerability, clinically active dose and therapeutic window Tipifarnib is very well understood and an excellent “tool compound” KO-2806 is an improved FTI with potential broad application 39 CLINICAL DEVELOPMENT OF KO-2806 – AREAS OF FOCUS Combinations Safety, tolerability and ability to combine with approved standards of care Evidence of ability to drive deeper and more durable responses Evidence of ability to resensitize patients to standards of care Later stage development Clinical data to support later stage development in combinations with additional PI3K inhibitor, KRAS inhibitor and TKI drug candidates across multiple solid tumors
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40 PHASE 1 STUDY OF KO-2806 AS MONOTHERAPY IN ADVANCED SOLID TUMORS A phase 1 study of the next-generation farnesyltransferase inhibitor (FTI) KO-2806 as monotherapy in advanced solid tumors G. Hanna, Dana-Farber Cancer Institute Sunday, October 19, 2025; 12:00 PM CEST Publication Number 981P = TRIAL OBJECTIVES1 ❑ Evaluate the safety and tolerability of KO-2806 ❑ Characterize the PK of KO-2806 when administered as monotherapy ❑ Inform the selection of RP2D of KO-2806 ❑ Evaluate the antitumor activity of KO-2806 = KEY POINTS ❑ Conducted in patients with HRAS-, KRAS- and NRAS-mutant tumors ❑ Clinical activity expected in HRAS-mutant patients only ❑ Efficient means to determine MTD and RP2D 1. Ongoing study – Clinicaltrials.gov identifier NCT06026410 https://clinicaltrials.gov/study/NCT06026410 PK – pharmacokinetics; RP2D – recommended Phase 2 dose; MTD – maximum tolerated dose
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41 PHASE 1 STUDY OF KO-2806 IN COMBINATION WITH CABOZANTINIB IN RENAL CELL CARCINOMAS Farnesyltransferase inhibitor (FTI) KO- 2806 in combination with cabozantinib (cabo) in renal cell carcinoma (RCC): Preliminary results from FIT-001 phase 1 trial A. Ayanambakkam, University of Oklahoma Health Sciences Center Saturday, October 18, 2025; 12:00 PM CEST Publication Number 2604P = TRIAL OBJECTIVES1 ❑ Characterize PK of the combination agents when administered in combination therapy ❑ Inform the selection of RP2D of the combination ❑ Evaluate the antitumor activity of the combination = KEY POINTS ❑ Conducted in 2L+ RCC patients ❑ Preliminary clinical activity in combination 1. Ongoing study – Clinicaltrials.gov identifier NCT06026410 https://clinicaltrials.gov/study/NCT06026410 PK – pharmacokinetics; RP2D – recommended Phase 2 dose
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42 PHASE 1 STUDY OF TIPIFARNIB AND ALPELISIB IN R/M PIK3CA-M HNSCC Tipifarnib (TIP) and alpelisib (ALP) in recurrent/metastatic head and neck squamous cell carcinoma (R/M HNSCC): Phase 1 results from KURRENT-HN G. Hanna, Dana-Farber Cancer Institute Monday, October 20, 2025; 12:00 PM CEST Publication Number 1349P = TRIAL OBJECTIVES1 ❑ Evaluate safety and tolerability of tipifarnib in combination with alpelisib ❑ Characterize PK of tipifarnib and alpelisib when administered in combination therapy ❑ Determine the MTD and OBAD of the combination ❑ Evaluate the antitumor activity of tipifarnib in combination with alpelisib = KEY POINTS ❑ Conducted in patients with R/M PIK3CA-m HNSCC ❑ Neither agent alone expected to demonstrate meaningful clinical responses in this population 1. Ongoing study – Clinicaltrials.gov identifier NCT04997902 https://clinicaltrials.gov/study/NCT04997902 R/M HNSCC – recurrent / metastatic head and neck squamous cell carcinoma; PK – pharmacokinetics; MTD – maximum tolerated dose; OBAD – optimal biologically active dose
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43 OPPORTUNITY Large Market and Multiple Anticipated Catalysts
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44 VEGFR TKI Opportunities • Potential to combine with cabozantinib and other TKIs in RCC and potentially in NET • Potential to combine with TKI and I/O in 1L RCC KRAS and PI3K Opportunities • Potential to combine with multiple agents in KRAS- and PI3K-driven cancers across major solid tumors • Potential for synergistic efficacy, lifecycle management and multi-drug revenues 19 22 43 57 44 41 TKI combo PI3Kai combo RASi combo Annual US Incidence, 2025 thousands of patients RCC Neuroendocrine Breast Cancer Others CRC NSCLC ~40 ~100 ~85 LARGE POTENTIAL OPPORTUNITY IN KO-2806 WITH > 200K ANNUAL INCIDENT PATIENTS IN THE U.S.
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45 Ziftomenib ANTICIPATED MILESTONES: STEADY CADENCE OF DATA READ-OUTS ACROSS MULTIPLE PROGRAMS EXPECTED Present full data from KOMET-001 Phase 2 registration-directed trial in R/R NPM1-m AML ✓ Present preliminary clinical data from KOMET-007 Phase 1b trial in 1L intensive AML ✓ PDUFA target action date of Nov 30, 2025 for ziftomenib NDA in R/R NPM1-m AML 4Q 2025 Initiate KOMET-017 Phase 3 registration-enabling trials in 1L NPM1-m and KMT2A-r intensive and non-intensive AML 2H 2025 Commercial launch of ziftomenib in R/R NPM1-m AML 2H 2025 Present preliminary clinical data from Phase 1b expansion of KOMET-007 in 1L non-intensive AML 2H 2025 KO-2806 / tipifarnib Initiate one or more expansion cohorts in combination with cabozantinib in RCC 1H 2026 Present preliminary clinical data from FIT-001 trial for KO-2806 as monotherapy and combo with cabozantinib in RCC1 4Q 2025 Present clinical data from the KURRENT-HN trial of tipifarnib in combo with alpelisib in PIK3CA-dependent HNSCC1 4Q 2025 Next-gen Menin Nominate a development candidate for next-generation menin inhibitor program for diabetes ✓ 1Abstracts accepted for presentation at 2025 European Society for Medical Oncology (ESMO) Congress in October 2025. Posters #2604P, #981P, #1349P.
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46 FINANCIAL HIGHLIGHTS (NASDAQ: KURA) Cash, Cash Equivalents and Marketable Securities Anticipated Significant Near-Term Milestones Shares Outstanding in cash, cash equivalents and short-term investments as of June 30, 2025 Kura anticipates collaboration plus cash balance as of June 30, 2025 to fund ziftomenib AML program to potential commercialization in frontline combinations in potential near-term milestones, including launch of ziftomenib in the monotherapy R/R setting 19.1M options, RSUs, PSUs, warrants & pre- funded warrants as of June 30, 2025 $630.7M $375M 86.8M COMMON STOCK
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47 Up Next: FTI Clinical Update from ESMO 2025 Please join us for a virtual investor event to discuss the preliminary clinical data presented at the ESMO Congress 2025 and KO -2806 development plans Saturday, October 18, 2025 10:30 a.m. PT / 1:30 p.m. ET A live webcast and archived replay of each event will be available on the Events page in the Investors section of Kura’s website.
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QUESTIONS & ANSWERS
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THANK YOU Our goal is to develop transformative therapies to extend and improve the lives of patients with cancer