Inhibikase Therapeutics, Inc. · NASDAQ:IKT
Inhibikase Therapeutics — Investor Presentation (August 2025)
24 slides from Inhibikase Therapeutics's investor presentation, Aug 14, 2025
Slide 1: Corporate Overview August 2025
Corporate Overview August 2025 Exhibit 99.2
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 by
Slide 3: Experienced Leadership with Deep Expertise in PAH
CHRIS CABELL, MD MHS FACC Head of R&D, Chief Medical Officer MARK IWICKI Chief Executive Officer JOHN ADAMS, PHD Chief Scientific Officer DAVID McINTYRE BEC CPA LLB MBA Chief Financial Officer CHAD OREVILLO, MPH EVP, Development Operations ALLISON WIDLITZ, MS, PA VP, Clinical Development JEFF KAGY C
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 ~30% 5-year mortality(1), reduced quality of life and high economic burden $7.6 Billion market with limited treatments that address the underlying etiolog
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 PASMCs = Pulmonary artery smooth muscle cells; Vascular
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 ~50,000 People with PAH in the US(1) ~26,000 People with PAH in the EU5(1) ~80% Female(2) 52 years Average age at diagnosis(2) (1) CVrG Market Strategies report Jun 2025; (2) Badlam et al; CHEST 2021; (3) Hoeper M, et al.
Slide 7: PAH: Patient and Treatment Journey
PAH: Patient and Treatment Journey CONFIDENTIAL Initiate PDE-5i +ERA Combo Oral/Inhaled Prostacyclin Activin Signaling Inhibitor Infused Prostacyclin PDE-5i or •NO Pathway Sildenafil; Tadalafil; Riociguat* ERA’s Bosentan; AmbrisentanMacitentan Selexipag; Oral Remodulin; Tyvaso, Tyvaso DPI; Yutrepia
Slide 8: $7.6B Market Driven by Vasodilators Which Don't Treat Underlying Causes of PAH
Nitric Oxide Pathway ($1.0B) $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 2024 annual reports from Janssen, United Therapeutics, Bayer, and Merck Sildenafil, Tadalaf
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 (Imatinib) IKT-001 (Imatinib Pro-Drug) History First Approved in 2001; 25 years of real-world experience Indicated for: Leukemia, Soft Tissue Sarcoma, Myelody
Slide 10: Development and Regulatory Timeline
2024 2025 2026 2027 2028 H1 H2 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 Q1 Q2 Clinical Development Regulatory Development and Regulatory Timeline Pre-IND Meeting with FDA KOL Feedback: Refining Ph 2b Protocol Phase 2b (n=150) IKT-001 v Placebo Interim Safety Analysis Topline data FDA File Ph 2b Protocol
Slide 11: Scientific and Clinical Rationale
Scientific and Clinical Rationale
Slide 12: Imatinib Mechanism of Action in PAH Targets the Underlying Cause of PAH
Imatinib Mechanism of Action in PAH Targets the Underlying Cause of PAH CONFIDENTIAL Modified from Savage and Antman, 2005 and Barst, R J Clin Invest 2005 Overactive kinases implicated in aberrant cell proliferation and migration in the pulmonary vasculature Imatinib inhibits the tyrosine kinase act
Slide 13: Imatinib Demonstrated Reversal of PAH in Standard Animal Model
Imatinib Demonstrated Reversal of PAH in Standard Animal Model Day 0 MCT d42 MCT d42/+imatinib Schermuly et al., JCI 2005 Reversal of right ventricular pressure Improved survival Reversal of vascular remodeling STI571 = imatinib; MCT = monocrotaline *P < 0.05 versus control; †P < 0.05 versus MCT at
Slide 14: 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) Primary Endpoint Change in 6MWD at 24 weeks Secondary Endpoints Changes in hemodynamics (PVR, CO, mPAP, RAP) at 24 weeks Time to cli
Slide 15: Phase 3 IMPRES: Statistically Significant Improvement in Function & Hemodynamics
Phase 3 IMPRES: Statistically Significant Improvement in Function & Hemodynamics 32-meter improvement in 6WMD and 32% reduction in PVR at week 24 Hoeper et al; Circulation 2013 Phase 3 IMPRES study hit its primary endpoint along with key clinically relevant secondary endpoints Change in 6MWD Change
Slide 16: Phase 3 IMPRES: Top AEs were GI Related
Phase 3 IMPRES: 3 of the Top 5 AEs were GI Related Majority of patients were unable to maintain 400 mg target dose of imatinib Hoeper et al; Circulation 2013 AE = Adverse event; GI = Gastrointestinal Phase 3 IMPRES hit its primary endpoint DESPITE only 48/103 participants maintaining 400mg dose for
Slide 17: IMPRES: Efficacy Impacted by Tolerability of 400mg Per Day
IMPRES: Efficacy Impacted by Tolerability of 400mg Per Day Patients able to sustain 400mg dose showed greater improvements in 6MWD and PVR Changes in PVR at Week 24 Changes in 6MWD at Week 24 N=40 N=24 N=79 N=44 N=23 N=78 Hoeper et al; Circulation 2013 Suppl. Appendix Meters Dynes/sec/cm-5 (Baseline
Slide 18: Contemporary Study of Imatinib Supports 400mg Dose for Best Efficacy
Contemporary Study of Imatinib Supports 400mg Dose for Best Efficacy Higher Exposure associated with larger treatment effect Higher Exposure = Larger Improvement More than 50% of subjects who completed the study were on 200mg per day or less One-third of patients who started the study at either 300m
Slide 19: Rapid and Sustained Hemodynamic Effect & Disease Modification of Imatinib in PAH
Rapid and Sustained Hemodynamic Effect & Disease Modification of Imatinib in PAH Early & Continued Improvement 24% reduction in Total Pulmonary Resistance (TPR); Patients at 200mg or less leaves “efficacy on the table” 24% Reduction in TPR Early Improvement in TPR Slow return to BL * Rothman et al.,
Slide 20: Inhibikase Therapeutics IKT-001
Inhibikase Therapeutics IKT-OO1
Slide 21: >2.5x Improvement in GI Tolerability
>2.5x Improvement in GI Tolerability Dose Associated with GI Toxicity Imatinib: 75 mg per kg per day IKT-001: 200 mg per kg per day IKT-001 Minimizes GI Imatinib Exposure to Drive Increased Tolerability 28 Day non-human primate study documents improved GI tolerability imatinib enzymatic cleavage blo
Slide 22: IKT-001-201: A Phase 2b Study of IKT-001 in PAH
IKT-001-201: A Phase 2b Study of IKT-001 in PAH Randomized double-blind, placebo-controlled study to evaluate efficacy and safety of once daily IKT-001 Primary Endpoints: PVR at week 26, change from baseline Safety and tolerability Secondary Endpoints: 6MWD WHO Functional Class Pharmacokinetics Incl
Slide 23: Key Investment Highlights
Inhibikase and IKT-001: Pulmonary Arterial Hypertension (PAH) Anthos: Key Investment Highlights PAH is a rare, progressive and life-threatening disease with significant unmet need ~30% 5-year mortality(1), reduced quality of life and high economic burden $7.6 Billion market with limited treatments t
Slide 24: Thank You
Inhibikase Therapeutics Thank You
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