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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 WIDLITZ, MS, PA
Chief Scientific Officer Chief Commercial Officer EVP, Development Operations VP, Clinical Development 3
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
Billion market with limited treatments that address the underlying etiology Imatinib is an anti-proliferative TKI with potential best-in-class improvements in PVR and Imatinib hit efficacy (2) 6MWD (45 meters*) based on Phase 3 IMPRES and
Phase 2 studies primary endpoints in Phase 3 in PAH Imatinib was not approved due to high discontinuation rate in Phase 3 IMPRES st 2 decades of imatinib clinical experience, together with IKT-001's improved GI tolerability
profile Potential to be the 1 and better-informed study design / study conduct supports potential higher probability of success oral anti-proliferative agent IKT's pro-drug is engineered to realize the potential of imatinib in PAH
& lower discontinuations IKT's Phase 3 is on track to initiate in Q1 of 2026 Strong Leadership Long intellectual property (NCE) runway through 2044 Executing Near Term Proven executive team with extensive PAH / CV
experience Development (1) Hoeper M, et al. Eur Respir J. 2017 (2) Studies conducted by Novartis Pharmaceutical Corporation 4 TKI = tyrosine kinase inhibitor; QoL= Quality of Life; PVR = pulmonary vascular resistance; 6MWD = 6-minute walk distance;
GI= Gastrointestinal; CV = cardiovascular * See Page 19
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; Vascular smooth muscle
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
Progressively worsening symptoms Reduced Quality of Life 15 ~26,000 Chronic breathlessness, and fatigue Approved vasodilators (1) People with PAH in the EU5 Significant limitation on activities of daily living (across the prostacyclin,
nitric oxide, Dizziness, chest pain, anxiety and depression and endothelin pathways) 4 High Economic Burden Average monthly U.S. healthcare costs ~$6,850-$15,650 Acute all cause hospitalization rate of 700 per 1000 1 ~80%
patients per year among Medicare or Medicaid patients Approved anti-proliferative (2) Female Substantial indirect costs due to work loss, caregiver time and disability (1) CVrG Market Strategies report Jun 2025; (2) Badlam et al; CHEST 2021;
(3) Hoeper M, et al. 6 Eur Respir J. 2017; (4) Watzger et al; Pharmacoeconomics 2025
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 limitation of Slight
limitation of Marked limitation in physical Inability to carry out any physical Class physical activity physical activity. activity. Less than ordinary activity activity without symptoms. Signs of Ordinary physical causes undue dyspnea, fatigue,
RHF. Discomfort increased by any activity causes chest pain or near syncope physical activity. Dyspnea and dyspnea, fatigue, chest fatigue present at rest pain, or near syncope 6MWD >440 meters 320 - 440 meters 165 - 319 meters <165
meters -1 -1 -1 -1 NT-ProBNP <300ng.L 300-649ng.L 650-1100ng.L >1100ng.L st 1 Line of Therapy Add On Therapy With Declining Health Status Initiate PDE-5i +ERA Combo Oral/Inhaled Prostacyclin Activin Signaling Inhibitor Infused Prostacyclin
PDE-5i or NO ERA's Pathway Bosentan; Selexipag; Oral Remodulin; Tyvaso, Sotatercept Remodulin IV; Remodulin Sub-Q; Sildenafil; Ambrisentan Tyvaso DPI; Yutrepia Flolan, Veletri Tadalafil; Macitentan Riociguat* CONFIDENTIAL (1) Humbert
et al; ERJ 2023 ERS=European Respiratory Society; ESC=European Society of Cardiology; WHO=World Health Organization; 6MWD= 6 Minute Walk Distance Test; 7 NT-ProBNP= Biomarker of cardiac strain; NO = Nitric Oxide; * Riociguat is a soluble guanylate
cyclase stimulator (sGC)
* $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 Epoprostenol,
Treprostinil, Sotatercept - subcutaneos injection $0.4B Iloprost, Selexipag $0.4B (FDA approval March 2024) Endothelin Pathway ($2.5B) $3.7B $3.7B Ambrisentan, Bosentan, Macitentan $2.5B $2.5B Nitric Oxide Pathway ($1.0B) Sildenafil, Tadalafil,
Riociguat IKT-001 has the potential to be the first oral anti-proliferative agent for the treatment of PAH * 2024 financial year. 2024 annual reports from Janssen, United Therapeutics, Bayer, and Merck. 8 The global PAH market is estimated to grow
at a compound annual growth rate of 3.3% through 2034 (Clarivate, August 2025)
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 experience designed
for better GI tolerability to support optimal Indicated for: Leukemia, Soft Tissue Sarcoma, Myelodysplastic Syndromes, Mastocytosis and GIST efficacy PAH Data Best-in-class improvements in PVR and 6MWD in Phase 2 & 3 Potential to be the first
and only once-daily oral anti-proliferative but not approved due to high discontinuations. Contemporary tyrosine kinase inhibitor (TKI) for PAH imatinib study* reinforces imatinib efficacy potential and supports improved discontinuation profile *
Rothman et al., AJRCCM 2025. PVR = Pulmonary Vascular Resistance; 6MWD= 6 Minute Walk Distance test; 9 GI = Gastrointestinal; GIST = Gastrointestinal Stromal Tumor
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 Pulmonary vasculature
with Normal pulmonary aberrant cell proliferation vasculature 11 Modified from Savage and Antman, 2005 and Barst, R J Clin Invest 2005
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 survival STI571
= imatinib; MCT = monocrotaline *P < 0.05 versus control; P < 0.05 versus MCT at day 28 or hypoxia at day 21; P < 0.05 versus MCT at day 42 or hypoxia at day 35. * Schermuly et al., JCI 2005 12
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: 200 mg per kg per
day Pro-drug linker gut gut wall GI = gastrointestinal 13 * In preclinical studies
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
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 12 16
20 24 Primary Endpoint Key Inclusion Criteria Change in 6MWD at 24 weeks Functional Class II-IV 2 or more background PAH therapies Secondary Endpoints -5 PVR 800 dynes.s.cm Changes in hemodynamics
(PVR, CO, mPAP, RAP) at 24 weeks 6MWD 150 meters and 450meters Time to clinical worsening 16 PVR = pulmonary vascular resistance; CO = cardiac output; mPAP = mean pulmonary arterial pressure; RAP = right arterial
pressure; 6MWD = 6-minute walk distance
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 endpoints 17 PVR
= Pulmonary Vascular Resistance; 6MWD= 6 Minute Walk Distance test Hoeper et al; Circulation 2013
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 Majority of
patients at highest dose of 0.7 mg/kg Majority of patients at lowest dose of 200 mg Note: Head-to-head trials were not conducted with Sotatercept and Imatinib and these trials had different trial designs, patient enrollment criteria and treatment
regimens. In addition, 1 Hoeper et al; NEJM 2023; 18 the applicable measurements for the referenced trials were observed over different time periods and using different assays. As a result, the safety data from these trials may not be 2 Hoeper et
al; Circulation 2013 directly comparable
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 -50 50 45
meter placebo adjusted -100 improvement in 6MWD 40 -150 -200 30 -250 22 -300 20 -350 -400 -371 10 5 -450 -437 0 -500 400mg for > 50% of 400mg for < 50% of Placebo treatment treatment N=40 N=24 N=79 N=44 N=23 N=78 -5 (Baseline*: 355 meters
imatinib; 366 meters placebo) (Baseline*: 1202 dynes/sec/cm imatininb; -5 1181 dynes/sec/cm placebo) * Baseline data is not available for the sub-population of patients on 400mg of imatinib for > 50% of treatment so baseline data above reflects
19 Hoeper et al; Circulation 2013 Suppl. Appendix entire study population. PVR= Pulmonary vascular resistance; 6MWD = 6-minute walk distance Meters -5 Dynes/sec/cm
* 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 Comparable
patient characteristics and baseline PVR scores to modern PAH trials Average lower dose than IMPRES nevertheless delivered significant reduction in TPR and improvement in 6MWD Dose adjustments to address tolerability allowed most Higher exposure
associated patients to remain in the study with larger treatment effect Percentage change in total pulmonary resistance from baseline at 60 days in relation to plasma level (area under curve in g*h/L) of imatinib at steady state (red-100md QD,
orange-200mgQD, cyan-300mg QD, blue- 400mg QD) * Rothman et al., AJRCCM 2025. 17 patient open-label study. Patients were implanted with the CardioMEMS HF System which is a small, wireless sensor 20 implanted in the pulmonary artery to monitor
pulmonary artery pressure. Patients remained in the study for up to 24 weeks.
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., AJRCCM
2025. 17 patient open-label study. Patients were implanted with the CardioMEMS HF System which is a small, wireless sensor 21 implanted in the pulmonary artery to monitor pulmonary artery pressure. Patients remained in the study for up to 24
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 profile of
imatinib in other indications Peripheral edema 45 (44) 20 (20) IKT-001 is designed to have an improved AE profile which Diarrhea 36 (35) 19 (19) will allow for higher doses Vomiting 31 (30) 10 (10) Periorbital edema 30 (29) 7 (7) IKT-001 is