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TM © 2026 Caspian Therapeutics, Inc., and Kura Oncology, Inc. All Rights Reserved. CASPIAN THERAPEUTICS Corporate and Clinical Update October 13, 2026
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TM This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. The words “believe,” “may,” “should,” “will,” “estimate,” “plan,” “continue,” “anticipate,” “intend,” “expect,” “potential,” “vision” and similar expressions (including the negative thereof) are intended to identify forward-looking statements. Such statements include, but are not limited to, statements regarding, among other things, the potential future value of Caspian Therapeutics, Inc. (“Caspian”) and ability of the stockholders of Kura Oncology, Inc. (“Kura”) to benefit from the same; the potential benefits of Caspian’s operating model; the expectation for Caspian’s financing to fund the advancement of KO-7246 through IND-enabling development and initial clinical proof-of-concept in diabetes and support the advancement of a second menin inhibitor development candidate; the strength of the preclinical findings related to KO-7246; the potential of KO-7246 to combine with current and emerging standards of care, including GLP-1s; the potential of KO-7246 to be a best-in-class menin inhibitor and a disease-modifying therapy for diabetes; Caspian’s plans to submit an IND for KO-7246; and the expectation for the initial clinical program to evaluate KO-7246 for safety, tolerability, pharmacokinetics, pharmacodynamics and measures of β-cell function and endogenous insulin production in patients with diabetes. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Factors that contribute to the uncertain nature of the forward-looking statements include risks associated with the conduct of preclinical studies and clinical trials; the risk of the FDA not permitting Kura’s or Caspian’s planned trials to proceed; the risk that Kura’s or Caspian’s product candidates may not receive regulatory approval; the potential for Kura’s or Caspian’s product candidates to have unexpected adverse side effects; the risk that Kura or Caspian may not be able to obtain additional financing; the risks associated with reliance on outside financing to meet capital requirements; the risk that compounds that appeared promising in early research or clinical trials do not demonstrate safety and/or efficacy in later preclinical studies or clinical trials; risks associated with reliance on third parties to successfully conduct clinical trials; and other risks associated with the process of discovering, developing and commercializing drugs 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 are described more fully in Kura’s filings with the Securities and Exchange Commission. Kura undertakes 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 Kura 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. KURA ONCOLOGY FORWARD-LOOKING STATEMENTS 2
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TM Troy Wilson, Ph.D., J.D. President & Chief Executive Officer, Kura Oncology Founder and Executive Chairman of the Board, Caspian Therapeutics Francis Burrows, Ph.D. Chief Scientific Officer, Kura Oncology Robert Spencer, Ph.D. President & Chief Operating Officer, Caspian Therapeutics PARTICIPANTS 3
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TM MORE THAN A DECADE OF MENIN RESEARCH AT KURA 4 Scientific Foundation Dedicated Development • Pioneering research in the biology of menin inhibition • Chemistry effort over 10 years has produced an extensive portfolio of proprietary menin inhibitors • Kura contributed KO- 7246, related IP, and know-how to Caspian • Diabetes requires specialized capabilities and a strategy tailored to metabolic disease • Caspian provides dedicated leadership and financing • Shared services enable Caspian to focus on preclinical and clinical development • Caspian is led and advised by diabetes experts Novel Mechanism of Action • Following fundamental biology • Selective stimulation of beta islet cell proliferation • Potential to combine with current and emerging standards of care, including GLP-1s
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TM • $50 million financing led by BVF Partners • Investors include T1D Fund, Invus, Montanova, Eli Lilly and Company, Kura, and others • Kura retains approximately half ownership of Caspian, giving Kura’s stockholders participation in Caspian’s potential future value • Proceeds are expected to fund KO-7246 IND-enabling development and initial clinical proof-of-concept, plus advancement of a second menin inhibitor candidate for diabetes and cardiometabolic diseases FINANCING 5 Capital aligned to initial clinical proof-of-concept
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TM • Caspian leads development • Robert Spencer, President and Chief Operating Officer, leads program development • Program responsibility • Seasoned Board of Directors provides oversight • Kura capabilities • Caspian has access to Kura’s research, development, and corporate capabilities through an Intercompany Services Agreement • Development focus • Established expertise and infrastructure allow Caspian to direct resources toward development OPERATING MODEL 6 Dedicated leadership with access to established Kura capabilities
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TM © 2026 Caspian Therapeutics, Inc., and Kura Oncology, Inc. All Rights Reserved. Asako McCloskey, Yahu Liu, and Francis Burrows Kura Oncology, Inc. Next-Generation Menin Inhibitor KO-7246 Regenerates β Cell Mass in Diabetic Rodent and Human Islet Models 62nd European Association for the Study of Diabetes (EASD) Annual Meeting Milan, Italy September 29, 2026
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TM • Mammalian physiology: Pregnancy demonstrates that lowering menin signaling is associated with adaptive β-cell expansion.1 • Human Genetics: MEN1 loss establishes that reduced menin activity can profoundly increase pancreatic - cell proliferation.2 • Pharmacologic Validation: Several chemically distinct menin inhibitors now provide a way to control this pathway reversibly. • Implication: These observations support pharmacologic menin inhibition as a strategy to restore functional β-cell capacity in both T1D and T2D. 8 1Karnik S.K. et al. Science 2007, 318(5851): 806-809. 2Agarwal S. et al. Ann N Y Acad Sci. 2004, 1014:189-98. KMT2Amenin Brake genes of -cell proliferation KMT2A menin p18 p27 Brake genes of -cell proliferation p18 p27 i) Under normal physiological conditions ii) During pregnancy Pancreatic -cells do not proliferate -cells proliferate and -mass expands Insulin “up” to prevent gestational diabetes Menin as an epigenetic molecular brake of -cell proliferation MULTIPLE LINES OF EVIDENCE SUPPORT DISEASE-MODIFYING POTENTIAL FOR MENIN INHIBITORS IN THE TREATMENT OF DIABETES
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TM KO-7246 PROVIDES DURABLE GLYCEMIC CONTROL AND COMPLEMENTS GLP-1 THERAPY IN DB/DB MOUSE MODEL OF TYPE 2 DIABETES 9 • Semaglutide reduced blood glucose levels rapidly but transiently • KO-7246 significantly reduced FBG and elevated insulin levels over a 7-week period • First-generation menin inhibitor ziftomenib produced similar results1 • No hypoglycemia observed in any KO-7246-treated animals *, p<0.05; ****, p<0.001 1McCloskey A. et al., Poster 845-P, Presented at the 84th American Diabetes Association Scientific Sessions, June 21-24, 2024.
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TM KO-7246 EXPANDS PANCREATIC Β-CELL MASS IN DB/DB PRECLINICAL MODELS 10 vehicle ziftomenib KO-7246 semaglutide Insulin IHC (β-cell signals in brown) 20x 20x 20x 20x 10 mice/group, 49d treatment period; each point represents the average of three slices/mouse * *** *, p<0.05; ***, p<0.005 Expansion provides direct evidence supporting proposed regenerative mechanism
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TM KO-7246 DEMONSTRATED ROBUST, DURABLE GLUCOSE REDUCTION ACTIVITY IN STZ RAT MODEL OF TYPE 1 DIABETES 11 Full restoration of glycemic control achieved in model of insulin insufficiency • KO-7246 robustly and durably reduced FBG and enhanced HOMA-, comparing favorably to BMF-219 • Kinetics and post-dose stability of activity support -cell mass regeneration MOA of KO-7246 0 10 20 30 40 50 60 70 80 0 200 400 600 800 1000 HOMA-β Treatment Days HOMA-B * washout (1 month) 0 10 20 30 40 50 60 70 80 0 10 20 30 40 4h fasting glucose Treatment Days 4h FBG (mmol/L) Vehicle Insulin KO-7246 BMF-219 7 washout (1 month) ** ns ns ns; not significant; *, p<0.05; **; p<0.01
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TM 12 0 10 20 30 40 50 60 70 80 0 10 20 30 40 50 Insulin treatment days 4h FBG (mM) 7 washout 8/8 0 10 20 30 40 50 60 70 80 0 10 20 30 40 50 BMF-219 200/170 mpk treatment days 4h FBG (mM) 7 washout Responders Non-responders 0 10 20 30 40 50 60 70 80 0 10 20 30 40 50 Vehicle treatment days 4h FBG (mM) 7 washout 1/8 Vehicle 0 10 20 30 40 50 60 70 80 0 10 20 30 40 50 KO-7246 200 mpk treatment days 4h FBG (mM) 7 washout Responders Non-responders 5/8 KO-7246 BMF-219 Insulin Vehicle KO-7246 BMF-219 Healthy Control 0 20 40 60 80 100 120140160 % -cell mass compared to healthy control % healthy median (Healthy median = 100%) Responders Non-responders* ns vehicle healthy Representative islet images (insulin IHC, 20x) KO-7246 BMF-219 • Responders all achieved and maintained complete glycemic control • Islets regenerated to 40-90% of healthy controls by Day 56 • BMF-219 did not reduce FBG or increase -cell mass ns; not significant; *, p<0.05 KO-7246 BUT NOT BMF-219 FULLY RESTORED ISLET FUNCTION IN STZ T1D RAT MODEL Response appeared dependent on residual β-cell capacity, consistent with regenerative mechanism
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TM TRANSIENT PHARMACOLOGIC MENIN INHIBITION IS FUNDAMENTALLY DIFFERENT FROM LIFELONG MEN1 LOSS Enhanced endogenous insulin production persists after -cell proliferation • MEN1 Syndrome patients develop proliferative insulinomas after years/decades of biallelic MEN1 loss • > 500 AML patients have been dosed daily with menin inhibitors for multiple years without MEN1 Syndrome symptoms • Animals dosed to Day 56 and observed to Day 86 • C-peptide significantly elevated after one month washout (indicating greater β-cell mass) • Negligible levels of residual cell proliferation in all groups (indicating limited active cell division) Vehicle Insulin KO-7246 Healthy Control 0.0 0.2 0.4 0.6 0.8 % insulin+ Ki67+ cells in islet, after 1-mo washout % insulin+ Ki67+ cells /total cells in islet ns ns ns Vehicle Insulin KO-7246 BMF-219 0 5 10 15 Day 86, stimulated c-peptide (After 1 month washout) c-peptide (ng/mL) * Responders Non-responders ns; not significant; *, p<0.05 13
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TM 14 KO-7246 induced -cell proliferation in multiple donor samples Solvent KO-7246, low KO-7246, high Harmine Solvent KO-7246, low KO-7246, high 0.0 0.1 0.2 0.3 0.4 0.4 0.6 0.8 1.0 Proliferating Beta Cell Fraction EdU+NKX6.1+/NKX6.1+ % *** * 5.5 mM STD 8 mM High • KO-7246 dose-dependently induced -cell proliferation under glucotoxic conditions • DYRK1A inhibitor harmine was unselective Solvent KO-7246, low KO-7246, high Harmine Solvent KO-7246, low KO-7246, high 0 10 20 30 Proliferating Non-Beta Cell Fraction EdU+NKX6.1-/NKX6.1- % 5.5 mM STD 8 mM High • Harmine also induced proliferation of non--cells • KO-7246 had no effect on non-- cell proliferation ns; not significant; *, p<0.05; **; p<0.01, ***, p<0.005; ****, p<0.001 Solvent KO-7246, low KO-7246, high Harmine Solvent KO-7246, low KO-7246, high 0 10 20 25 30 35 40 45 Total Beta Cell Fraction NKX6.1+/DAPI+ % ** *** *** 5.5 mM STD 8 mM High • KO-7246 dose-dependently increased the -cell fraction under glucotox conditions • Harmine had a net negative effect on the -cell fraction KO-7246 INDUCED PROLIFERATION OF HUMAN -CELLS
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TM KO-7246 balomenib Icovamenib (BMF-219) menin-MLL FP IC50 (nM) 7.7 23.1 >10,000 MV4-11 CTG IC50 (nM) 7.9 28.1 218 mouse MV4-11 CDX model robust efficacy efficacy at 4x daily dose no efficacy even at 8x daily dose CDK9 %inhibition at 1.0 µM 0 not tested >80 (IC50 =19.1 nM) Menin-Dependent AML Model Kinase Family Tree KO-7246 BMF-219 KO-7246 AND BALOMENIB ARE DIFFERENTIATED FROM BMF-219 • KO-7246 and balomenib are validated menin inhibitors, but KO-7246 is more active in vitro and in vivo • BMF-219/Icovamenib inhibits several kinases, including CDK9, but has no discernable activity towards menin vehicle BMF-219, 8x ziftomenib, 2x balomenib, 4x KO-7246, 1x 15
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TM • Menin inhibition has the potential to restore endogenous β-cell capacity in patients with Type 1 and Type 2 diabetes • KO-7246 combines a validated menin-based mechanism of action with robust, disease-modifying pharmacology across a range of diabetes models • Potent menin inhibition demonstrated in multiple in vitro and in vivo menin-dependent models • Produced durable glycemic control through β-cell regeneration in multiple preclinical diabetes models • IND-enabling development of this potential best-in-class menin inhibitor underway with initial clinical evaluation planned thereafter KO-7246 HAS POTENTIAL TO BE A DISEASE-MODIFYING THERAPY FOR PATIENTS WITH TYPE 1 OR TYPE 2 DIABETES 16
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TM Clinical entry IND-enabling studies to establish the nonclinical safety and exposure profile in parallel with manufacturing and drug supply readiness to support clinical entry. Chronic administration Characterize safety, tolerability, pharmacokinetics and pharmacodynamics to inform repeated dosing. KO-7246 CLINICAL DEVELOPMENT 17 Initial objective: safety, exposure and endogenous insulin production Patient selection Consider residual beta cell capacity and baseline endogenous insulin production. Both Type 1 and Type 2 diabetes are relevant to the broader opportunity. Initial proof of concept Acceptable safety and exposure with interpretable improvement in endogenous insulin production, assessed using stimulated C-peptide.
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TM © 2026 Caspian Therapeutics, Inc., and Kura Oncology, Inc. All Rights Reserved. Q&A