Kura Oncology : Corporate Presentation - May 2024

DEVELOPING PRECISION MEDICINES FOR THE TREATMENT OF CANCER

Corporate Presentation - May 2024

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 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; 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.

This presentation also contains statistical 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 accuracy or completeness of such data or undertakes any obligation to update such data after the date of this presentation.

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Investment Highlights

Targeted	Advancing a pipeline of novel investigational therapies, forging new scientific and clinical paths to give
Oncology	patients a better chance for long-term, durable remissions
	Menin Inhibitor Program (Ziftomenib)
	• Potential to address up to 50% of acute leukemias through monotherapy and combinations
	• 35% CR rate among 20 patients with NPM1-mutant AML treated at recommended Phase 2 dose
	• Positive preliminary combination data in NPM1-m and KMT2A-r AML, including 100% CR rate with 7+3 in 1L,
	56% CR/CRh rate with ven/aza in R/R menin inhibitor naïve patients and mitigation of differentiation syndrome
Proprietary	• Breakthrough Therapy Designation granted by FDA for the treatment of patients with R/R NPM1-mutant AML
• Completion of enrollment in Phase 2 registration-directed trial in NPM1-mutant AML expected by mid-2024
Pipeline
Farnesyl Transferase Inhibitor Programs (Tipifarnib & KO-2806)
	• Durable responses observed with tipifarnib as a monotherapy in R/M HRAS-mutant HNSCC patients
	• Compelling safety profile and activity observed with tipifarnib plus alpelisib in PIK3CA-dependent HNSCC
	• Preclinical data support clinical combinations of next-gen FTI KO-2806 with adagrasib and cabozantinib
	• Clinical collaboration with BMS to evaluate KO-2806 and adagrasib in KRASG12C-mutated NSCLC
	• Now dosing patients in dose-escalation trial of KO-2806 as monotherapy and in combination with
	cabozantinib in ccRCC; combo with adagrasib expected to start by mid-2024
Strong	• $25 million strategic equity investment from Bristol Myers Squibb
Financials	• $527 million in cash as of March 31, 2024* provides runway into 2027

* Cash, cash equivalents and short-term investments

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Experienced Leadership Team and Board of Directors

Leadership Team

Troy Wilson, Ph.D., J.D.	Teresa Bair, J.D.	Stephen Dale, M.D.	Kathy Ford
President &	Chief Legal Officer	Chief Medical Officer	Chief Operating Officer
Chief Executive Officer

	Pete De Spain		Mollie Leoni, M.D.	Francis Burrows, Ph.D.		Tom Doyle
	Executive Vice President,	Executive Vice President,	Senior Vice President,	Senior Vice President,
Investor Relations & Corporate		Clinical Development	Translational Research	Finance & Accounting
	Communications
	Board of Directors
	Troy Wilson, Ph.D., J.D.		Faheem Hasnain		Helen Collins, M.D.		Thomas Malley
	Chairman		Lead Independent Director
	Carol Schafer		Diane Parks		Mary Szela

Brian Powl

Chief Commercial Officer

Roger Bakale, Ph.D.

Senior Vice President,

Manufacturing and

Supply Chain

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Drug Candidate Pipeline

PROGRAM	CLINICAL TRIAL	STUDY STARTUP	DOSE-ESCALATION	DOSE-VALIDATION	REGISTRATION DIRECTED	ANTICIPATED MILESTONE
		NPM1-mutant acute myeloid leukemia (AML)			Complete enrollment of 85
				patients by mid-2024
	KOMET-001
	KMT2A-rearranged acute
				Now dosing patients
	Monotherapy
	lymphoblastic leukemia
	(Relapsed/refractory)
	Non-NPM1-mutant / Non-
					Now dosing patients
		KMT2A-rearranged AML
	KOMET-007	NPM1-mutant AML				Identify RP2D by mid-2024
	Combination with
ZIFTOMENIB					/ Advance to frontline
venetoclax + azacitidine
KMT2A-rearranged AML				AML in 2H2024
Menin Inhibitor	(Relapsed/refractory)
	KOMET-007	NPM1-mutant AML
	Combination with					Identify RP2D by mid-2024
	cytarabine + daunorubicin
	KMT2A-rearranged AML
	(Frontline)
	KOMET-008	NPM1-mutant AML
	Combinations with					Now dosing patients
	gilteritinib, FLAG-IDA, LDAC
	KMT2A-rearranged AML
	(Relapsed/refractory)
TIPIFARNIB	KURRENT-HN					Identify optimal
Farnesyl Transferase	PIK3CA-dependent head and neck squamous cell carcinoma (HNSCC)		biologically active dose
Combination with alpelisib		by end of 2024 / Present
Inhibitor (FTI)						preliminary data in 1H2025
		Solid tumors				Now in dose escalation as
	FIT-001				monotherapy
KO-2806
Clear cell renal cell				Now dosing patients in
Monotherapy, combinations
			combo with cabozantinib
Next-Generation FTI	with cabozantinib and	carcinoma (ccRCC)
	adagrasib	KRASG12C-mutantnon-small				Dose first patients in
		cell lung cancer (NSCLC)				combo with adagrasib by
					mid-2024

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ZIFTOMENIB: MENIN-KMT2A/MLL INHIBITOR IN ACUTE LEUKEMIAS

Ziftomenib Demonstrates Potential to Become a

Cornerstone of AML Therapy

Targets foundational mutations at the core of up to 50% of AML cases

• Compelling clinical data support frontline opportunity
• • Good tolerability profile, enabling continuous administration in combination with SOC
  • Combinations appear to mitigate the risk of differentiation syndrome
  • No observed or predicted drug-drug interactions
  • Encouraging preliminary evidence of clinical activity
• Strong investigator enthusiasm as evidenced by rapid enrollment across studies
• • First 20 patients enrolled in KOMET-007 combination trial in less than four months
  • Now dosing patients in KOMET-008 combination trial with SOCs, including FLT3 inhibitor
  • KOMET-001monotherapy registrational trial expected to complete enrollment by mid-2024

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Ziftomenib Targets the Menin-KMT2A Pathway, a Foundational Target in AML

• NPM1-m and KMT2A-r drive overexpression of HOXA9/MEIS1 genes, critical for transformation to AML
• KMT2A(MLL) sits upstream from major AML targets (i.e., FLT3, IDH1/2, DNMT3A)
• KMT2A(MLL)-dependentgenes contribute to therapeutic resistance and relapse to current therapies
• Menin inhibition downregulates HOXA9/MEIS1, leading to differentiation of leukemic blasts

Proliferation

genes

'Stemness'

genes

Myeloid lineage differentiation genes

1. Lu et al. Cancer Cell 2016;30(1):92-107; 2. Ferreira et al. Oncogene 2016;35(23):3079-82; 3. Jeong et al. Nat. Genet 2014;46(1):17-23; 4. Wang et al. Blood 2005;106(1):254-64; 5. Chowdhury et al. EMBO Rep 2011;12(5):463-9; 6. Schmidt et al. Leukemia 2019;33(7):1608-19; 7. Xu et al. Cancer Cell

2016;30(6):863-78; 8. Collins & Hess. Curr Opin Hematol 2016;23(4):354-61; 9. Brunetti et al. Cancer Cell 2018; 34(3):499-512.	8

KOMET-001 Phase 1/2 Study of Ziftomenib in Relapsed / Refractory AML

Phase 1a

Dose Escalation

Completed

50 mg	100 mg	~	1000 mg
QD	QD		QD

NPM1-m,KMT2A-r, Other

Phase 1b	Phase 1b
Validation Cohorts	Expansion
Completed	Completed
Cohort 1: 200 mg QD	Expansion of 600 mg QD
Cohort 2: 600 mg QD
NPM1-mor KMT2A-r	NPM1-m

OBJECTIVES

Phase 2

Registration-Enabling

(Ongoing)Ongoing

600 mg

QD

NPM1-m

• Safety and tolerability
• Pharmacokinetics
• Early evidence of antitumor activity

• Safety and tolerability
• Pharmacokinetics
• Clinical activity

Continue enrollment of Phase 1b validation cohort(s) consistent with FDA's Project Optimus

• Safety and tolerability
• Pharmacokinetics
• Clinical activity

• Primary endpoint:
• • CR/CRh
• Secondary endpoints:
• • Duration of CR/CRh
  • Transfusion independence
  • CR/CRh MRD negativity
  • Adverse events

CR, complete remission; CRh, complete remission with partial hematological recovery; FDA, United States Food and Drug Administration;	9
MRD, measurable residual disease; R/R, relapsed/refractory; RP2D, recommended phase 2 dose.

Ziftomenib Demonstrates Optimal Pharmaceutical Properties

Clinical data from KOMET-001 demonstrate:

• Ziftomenib demonstrates a dose-dependent increase in exposure up to RP2D at 600 mg
• Ziftomenib is not a clinically meaningful CYP3A4 substrate
• • No dose adjustment of ziftomenib needed when administered with a CYP3A4 inhibitor (e.g., azoles)
• Ziftomenib is not a clinically meaningful CYP3A4 inhibitor
• • No dose adjustment needed for CYP3A4 substrates (e.g., venetoclax)
• No drug-induced QTc prolongation observed at any dose

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