Inhibikase Therapeutics, Inc. · NASDAQ:IKT

Inhibikase Therapeutics — Investor Presentation (November 2025)

28 slides from Inhibikase Therapeutics's investor presentation, Nov 20, 2025

  1. Slide 1: Corporate Overview November 2025

    Exhibit 99.1 Corporate Overview November 2025

  2. Slide 2: Disclaimer

    Disclaimer This presentation contains information that may constitute “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, as amended. Inhibikase Therapeutics, Inc. (the “Company” or “we”) intends for the forward- looking statements to be covered b

  3. Slide 3: Experienced Leadership with Deep Expertise in PAH

    Experienced Leadership with Deep Expertise in PAH MARK IWICKI CHRIS CABELL, MD MHS FACC DAVID McINTYRE BEC CPA LLB MBA JEFF KAGY Chief Executive Officer Head of R&D, Chief Medical Officer Chief Financial Officer Chief Human Resource Officer JOHN ADAMS, PHD TIM PIGOT CHAD OREVILLO, MPH ALLISON WIDLIT

  4. Slide 4: Inhibikase and IKT-001: Pulmonary Arterial Hypertension (PAH)

    Inhibikase and IKT-001: Pulmonary Arterial Hypertension (PAH) • PAH is a rare, progressive and life-threatening disease with significant unmet need Major unmet need with (1) high mortality, poor • ~30% 5-year mortality , reduced quality of life and high economic burden QoL and high cost • $7.6 Billi

  5. Slide 5: PAH is a Progressive Disease Driven by Uncontrolled Cell Proliferation

    PAH is a Progressive Disease Driven by Uncontrolled Cell Proliferation Proliferation of vascular cells drive vascular remodeling, raising pulmonary artery pressure and leading to progressive right ventricular heart failure and ultimately death 5 PASMCs = Pulmonary artery smooth muscle cells; Vascula

  6. Slide 6: PAH: An Orphan Disease with ~30% 5-Year Mortality Despite Aggressive Treatment

    PAH: An Orphan Disease with ~30% 5-Year Mortality Despite Aggressive Treatment High Unmet Medical Need ~50,000 52 years Progressive and Life Threatening (1) (2) People with PAH in the US Average age at diagnosis (3) • ~30% 5-year mortality despite aggressive treatment with vasodilator therapies • Pr

  7. Slide 7: Illustrative Patient and Treatment Journey in PAH

    Illustrative Patient and Treatment Journey in PAH Progressive pulmonary vasculopathy driving right heart failure (RHF) (1) ESC/ERS 4 Risk Strata (Risk of 1 year Mortality) Low (0-3%) Intermediate Low (2-7%) Intermediate High (9-19%) High (>20%) WHO Class 1 Class 2 Class 3 Class 4 Functional No limit

  8. Slide 8: $7.6B Market Driven by Vasodilators Which Don't Treat Underlying Causes of PAH

    * $7.6B Market Driven by Vasodilators Which Don't Treat Underlying Causes of PAH Novel antiproliferative agents with disease modifying properties expected to revolutionize treatment Vasodilators Anti-proliferative Agents Prostacyclin Pathway ($3.7B) Activin Signaling Pathway ($0.4B) $1.0B $1.0B Epop

  9. Slide 9: Our Solution: An Oral Pro-Drug of Imatinib Optimized for PAH

    Our Solution: An Oral Pro-Drug of Imatinib Optimized for PAH Engineered to realize imatinib’s best-in-class efficacy potential in PAH Gleevec IKT-001 (Imatinib) (Imatinib Pro-Drug) History IKT-001 is an investigational novel pro-drug of imatinib First Approved in 2001; 25 years of real-world experie

  10. Slide 10: IKT-001

    Inhibikase Therapeutics IKT-OO1 ~~.

  11. Slide 11: Imatinib Mechanism of Action in PAH

    Imatinib Mechanism of Action in PAH Targets the Underlying Cause of PAH Overactive kinases implicated in aberrant cell proliferation and migration in the pulmonary vasculature Imatinib inhibits the tyrosine kinase activity of PDGFR and c-kit , blocking cell signaling that drives vascular remodeling

  12. Slide 12: Imatinib Demonstrated Reversal of PAH in Standard Animal Model

    Imatinib Demonstrated Reversal of PAH in Standard Animal Model* Improved Reversal of Reversal of increased right vascular remodeling ventricular pressure survival Day 0 MCT d42 MCT d42/+imatinib Imatinib reverses pulmonary vascular remodeling, right ventricular pressure / remodeling and improves sur

  13. Slide 13: IKT-001 Minimizes GI Imatinib Exposure to Drive Increased Tolerability

    IKT-001 Minimizes* GI Imatinib Exposure to Drive Increased Tolerability 28 Day non-human primate study documents improved GI tolerability blood imatinib IKT-001 >2.5x Improvement in GI Tolerability enzymatic IKT-001 cleavage Dose Associated with GI Toxicity Imatinib: 75 mg per kg per day IKT-001: 20

  14. Slide 14: Single Ascending Dose Study in Healthy Volunteers Establishes Bioequivalence

    Single Ascending Dose Study in Healthy Volunteers Establishes Bioequivalence Patients able to sustain 400mg dose of imatinib showed greater improvements in 6MWD and PVR Bioequivalent IKT-001 Dose Imatinib Dose 300 mg QD 230 mg QD 400 mg QD 306 mg QD 500 mg QD 383 mg QD 14 IKT Data on File

  15. Slide 15: Clinical Rationale

    Inhibikase Therapeutics Clinical Rationale

  16. Slide 16: IMPRES – Imatinib Phase 3 Study

    IMPRES – Imatinib Phase 3 Study Randomized, double blind, placebo-controlled study to assess the efficacy, safety and tolerability of 400mg imatinib once daily (n=202) Imatinib 200mg 400mg with ability to down titrate to 200mg if unable to tolerate 400mg (n=103) Placebo (n=99) Titration Weeks 0 4 8

  17. Slide 17: Phase 3 IMPRES: Statistically Significant Improvement in Function & Hemodynamics

    Phase 3 IMPRES: Statistically Significant Improvement in Function & Hemodynamics Placebo-adjusted 32-meter improvement in 6WMD and 32% reduction in PVR at week 24 Change in Pulmonary Change in Change in 6MWD Vascular Resistance Cardiac Output IMPRES hit its primary endpoint along with key secondary

  18. Slide 18: Imatinib Showed Comparable Efficacy to Sotatercept

    Imatinib Showed Comparable Efficacy to Sotatercept Majority of sotatercept subjects at highest dose while majority of imatinib subjects at lowest dose 1 2 Imatinib P3 IMPRES Sotatercept P3 STELLAR 0 0 1 Endpoint: Median Treatment Difference = 33.4m 1 Endpoint: Mean Treatment Difference = 32m Majorit

  19. Slide 19: IMPRES: Patients able to sustain 400mg dose showed greater improvements

    IMPRES: Patients able to sustain 400mg dose showed greater improvements Placebo-adjusted 6MWD Improvement of 45m at Week 24 in Patients at 400 mg for >50% of Treatment Changes in 6MWD at Week 24 Changes in PVR at Week 24 400mg for > 50% of 400mg for < 50% of treatment treatment Placebo 60 0 50 -10 -

  20. Slide 20: Contemporary Study of Imatinib Supports Findings from IMPRES

    * Contemporary Study of Imatinib Supports Findings from IMPRES Doses between 200mg – 400mg delivered meaningful efficacy response Dose Dependent Improvement in Primary Endpoint 2025 Publication Using Imatinib in PAH PAH patients (13/17) with implanted devices to assess continuous cardiac function Co

  21. Slide 21: Rapid and Sustained Hemodynamic Effect & Disease Modification of Imatinib in PAH

    Rapid and Sustained Hemodynamic Effect & Disease Modification of Imatinib in PAH 24% reduction in Total Pulmonary Resistance (TPR) Early & Continued Improvement Slow return to BL 1 Early Improvement 3 in TPR Slow return to baseline 2 suggests disease 24% Reduction modification in TPR * Rothman et al

  22. Slide 22: Imatinib Phase 3 IMPRES Study: Top AEs were GI Related

    Imatinib Phase 3 IMPRES Study: 3 of the Top 5 AEs were GI Related Majority of patients were unable to maintain 400 mg target dose of imatinib Imatinib Placebo n=103 (%) n=98 (%) Adverse Events 100 (97) 94 (96) • The AE profile in IMPRES was similar to the established Nausea 57 (55) 23 (24) AE profil

  23. Slide 23: A Modern PAH Trial with IKT-001 may have Greater Potential for Success

    A Modern PAH Trial with IKT-001 may have Greater Potential for Success What’s changed … deeper clinical experience with imatinib enabling better study conduct, modern study design and anticipated improved GI tolerability with IKT-001 Ph 3 IMPRES Hit 6MWD & PVR But … High (2009-2011) Primary Endpoint

  24. Slide 24: Inhibikase Therapeutics

    Inhibikase Therapeutics

  25. Slide 25: Anticipated Phase 3 Study of IKT-001 in PAH

    Anticipated Phase 3 Study of IKT-001 in PAH Interim Analysis @ Wk 24 (PVR Change from BL (n=140)); Primary Endpoint 6MWD Change From BL (n=346 @ Wk24) Enrollment Continues Phase 3 – Part A Phase 3 – Part B Uninterrupted Double Blind Treatment (n=346) Double Blind Treatment (n=140) ^ ^ n=173 300 400

  26. Slide 26: Development Progress and Projected Timelines

    Development Progress and Projected Timelines Progress Towards Initiation of IKT’s Phase 3 Study in PAH Projected Events st Expected 1 Site Activation in Phase 3 IMPROVE-PAH Study (IKT- ✓ 1H 2024 FDA Pre-IND for IKT-001 in PAH Q4 2025 / Q1 001 for Measuring Pulmonary Vascular Resistance and Outcome 2

  27. Slide 27: Inhibikase and IKT-001: Pulmonary Arterial Hypertension (PAH)

    Inhibikase and IKT-001: Pulmonary Arterial Hypertension (PAH) • PAH is a rare, progressive and life-threatening disease with significant unmet need Major unmet need with (1) high mortality, poor • ~30% 5-year mortality , reduced quality of life and high economic burden QoL and high cost • $7.6 Billi

  28. Slide 28: Thank You

    Inhibikase Therapeutics Thank You ~~.

Inhibikase Therapeutics — Investor Presentation (November 2025) on 6ix