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the Functional Loss in Parkinson's and Related Disorders 3Q 2021 BUSINESSPRESENTATIONExhibit 99.1 IKT Clinical Development of Therapies Intended to Reverse the Functional Loss in Parkinson's and Related Disorders 3Q 2021
BUSINESSPRESENTATION
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COMPANY HIGHLIGHTS Driving Functional Reversal of Parkinson's
Disease BY 2025, PARKINSON'S Five clinical programs in neurodegeneration and one clinical program in DISEASE DRUG SALES oncology planned by close of 2021 ARE EXPECTED TO Multi-therapeutic pipeline with emphasis on
neurodegeneration inside and out Double Pharma Insights, 2019 side of the brain Our lead inhibitor of the Abelson Tyrosine Kinase (c-Abl), IkT-148009, halts and SALES ESTIMATES reverses functional loss in animal models that recreate
progressive human BY 2025 ARE EXPECTED TO disease CREST Phase 1 trial with IkT-148009 reached therapeutic drug exposures seen in animal $6.0 Billion models at just 25 mg oral dose 1x/day in humans Pharma Insights, 2019 Multiple patent
families for lead compound with expiration of 2036 and beyond $20.4 million in grants and contracts from NIH, DoD, the Michael J. Fox Foundation and the Georgia Research Alliance, all peer-reviewed THE COUNTRY WITH THE HIGHEST DIAGNOSED
PREVALENCE IS $63 million gross proceeds in investor capital in 2021 The U.S. Highly experienced and respected management team, consultants, Board of DelveInsight, 2019 Directors and nearly all KOLs in the field on Scientific Advisory
Board 3 3COMPANY HIGHLIGHTS Driving Functional Reversal of Parkinson's Disease BY 2025, PARKINSON'S Five clinical programs in neurodegeneration and one clinical program in DISEASE DRUG SALES oncology planned by close of 2021 ARE
EXPECTED TO Multi-therapeutic pipeline with emphasis on neurodegeneration inside and out Double Pharma Insights, 2019 side of the brain Our lead inhibitor of the Abelson Tyrosine Kinase (c-Abl), IkT-148009, halts and SALES ESTIMATES
reverses functional loss in animal models that recreate progressive human BY 2025 ARE EXPECTED TO disease CREST Phase 1 trial with IkT-148009 reached therapeutic drug exposures seen in animal $6.0 Billion models at just 25 mg oral dose 1x/day
in humans Pharma Insights, 2019 Multiple patent families for lead compound with expiration of 2036 and beyond $20.4 million in grants and contracts from NIH, DoD, the Michael J. Fox Foundation and the Georgia Research Alliance, all
peer-reviewed THE COUNTRY WITH THE HIGHEST DIAGNOSED PREVALENCE IS $63 million gross proceeds in investor capital in 2021 The U.S. Highly experienced and respected management team, consultants, Board of DelveInsight, 2019 Directors and
nearly all KOLs in the field on Scientific Advisory Board 3 3
COMPANY HIGHLIGHTS: MULTI-THERAPEUTIC PIPELINE Multi-Indication Pipeline
in Neurodegeneration, Oncology and Infectious Disease 4COMPANY HIGHLIGHTS: MULTI-THERAPEUTIC PIPELINE Multi-Indication Pipeline in Neurodegeneration, Oncology and Infectious Disease 4
IKT Parkinson's Disease Market & Strategy IKT
Parkinson's Disease Market & Strategy
THE MARKET 1 Parkinson's Disease in the U.S. Large Market,
Opportunity For Disease Modification Chronic Disease for a Long Time 700,000 - 1,000,000 1/3 of a Patient's Lifespan = 25 years U.S. Patients 60,000 38,000 60 DEATHS / YEAR NEW CASES / YR AVERAGE AGE OF ONSET Other illnesses complicate
development Men twice as likely as women to contract 36% 35% 30% 47% disease ARTHRITIS HEART / CIRCULATORY PSYCHOSIS DEMENTIA 1 Parkinson's Disease Foundation Decisions Resources 2016, ParkinsonismRelatDisord . 2012;18:1073-1078, ,
Neuroepidemiology 2010;34:143-151 , J Neurol Neurosurg Psychiatry. 1997 Jan;62(1):10-5. 2 6THE MARKET 1 Parkinson's Disease in the U.S. Large Market, Opportunity For Disease Modification Chronic Disease for a Long Time 700,000 -
1,000,000 1/3 of a Patient's Lifespan = 25 years U.S. Patients 60,000 38,000 60 DEATHS / YEAR NEW CASES / YR AVERAGE AGE OF ONSET Other illnesses complicate development Men twice as likely as women to contract 36% 35% 30% 47% disease ARTHRITIS
HEART / CIRCULATORY PSYCHOSIS DEMENTIA 1 Parkinson's Disease Foundation Decisions Resources 2016, ParkinsonismRelatDisord . 2012;18:1073-1078, , Neuroepidemiology 2010;34:143-151 , J Neurol Neurosurg Psychiatry. 1997 Jan;62(1):10-5. 2
COMMON FEATURES OF MISFOLDED PROTEIN DISEASES Causation in
Parkinson's and Alzheimer's is closely 1 related What role does the misfolded protein play? 1 Nat. Neurosci. 21: 1332-1340 (2018) 7COMMON FEATURES OF MISFOLDED PROTEIN DISEASES Causation in Parkinson's and Alzheimer's is
closely 1 related What role does the misfolded protein play? 1 Nat. Neurosci. 21: 1332-1340 (2018) 7
CAUSE OF NEURODEGENERATION Evaluation of the Misfolded Protein
Seed' in Parkinson's Reveals c-Abl as the Primary Culprit, NOT the Misfolded Protein Parkinson's Disease (PD) is a neurodegenerative disease which limits function of nerve cells throughout the brain and gut following
misfolding of non-essential a-Synuclein. -Synuclein, an abundant and non-essential protein -Synuclein Is normally in a 1 helix-turn-helix configuration Normally, -Synuclein plays a role in neurotransmission by
dopamine. In the disease state, -Synuclein is remodeled into protein aggregates we call plaques, which have been thought to be the cause of disease. The Company and it's collaborators have demonstrated that plaques of
-synuclein cannot cause disease on their own. Plaques are internalized and activate c-Abl. c-Abl is actually driving the disease. In the disease state, -Synuclein reorganizes to form fibrous 2 aggregates
("Plaques") 1 Biochim Biophys Acta. 1818:1013-8 (2012) 2 Pathogens 7:50 (2018) 8CAUSE OF NEURODEGENERATION Evaluation of the Misfolded Protein Seed' in Parkinson's Reveals c-Abl as the Primary Culprit, NOT the
Misfolded Protein Parkinson's Disease (PD) is a neurodegenerative disease which limits function of nerve cells throughout the brain and gut following misfolding of non-essential a-Synuclein. -Synuclein, an abundant and
non-essential protein -Synuclein Is normally in a 1 helix-turn-helix configuration Normally, -Synuclein plays a role in neurotransmission by dopamine. In the disease state, -Synuclein is remodeled into protein
aggregates we call plaques, which have been thought to be the cause of disease. The Company and it's collaborators have demonstrated that plaques of -synuclein cannot cause disease on their own. Plaques are internalized and
activate c-Abl. c-Abl is actually driving the disease. In the disease state, -Synuclein reorganizes to form fibrous 2 aggregates ("Plaques") 1 Biochim Biophys Acta. 1818:1013-8 (2012) 2 Pathogens 7:50 (2018) 8
THE PATH TO NEURODEGENERATION Stressors Trigger the Production of
Misfolded -Synuclein 2 Which Activates c-Abl to Drive Neurodegeneration 1 Nat Rev Neurosci. 2, 492-501 (2001) 2 Werner and Olanow (2021), under review 3
https://ir.prothena.com/news-releases/news-release-details/update-phase-2-pasadena-study-prasinezumab-prx002rg7935 9 http://media.biogen.com/node/22876/htmlTHE PATH TO NEURODEGENERATION Stressors Trigger the Production of Misfolded -Synuclein
2 Which Activates c-Abl to Drive Neurodegeneration 1 Nat Rev Neurosci. 2, 492-501 (2001) 2 Werner and Olanow (2021), under review 3
THE PATH TO DISEASE MODIFICATION Biochemistry of Parkinson's
Disease Initiation and 1 Progression Disease process Treatment effect 1 Werner and Olanow (2021), under review, J Clin Invest. 2016; 126: 2970-2988 , Brain 2019; 142:2380-2401 , Cell 2011; 144: 689-702 , Nat Neurosci. 2013; 16: 1392-1400 , 10 Adv
Neurobiol. 2017; 15:403-425 THE PATH TO DISEASE MODIFICATION Biochemistry of Parkinson's Disease Initiation and 1 Progression Disease process Treatment effect 1 Werner and Olanow (2021), under review, J Clin Invest. 2016; 126: 2970-2988 ,
Brain 2019; 142:2380-2401 , Cell 2011; 144: 689-702 , Nat Neurosci. 2013; 16: 1392-1400 , 10 Adv Neurobiol. 2017; 15:403-425
IKT How Inhibikase Will Modify Disease
IS A SMALL MOLECULE c-ABL INHIBITOR IkT-148009: Low Toxicity,
Selective, Brain Penetrant c- Abl Inhibitor in Clinical Development Selective Inhibitor of c-Abl and Abl2/Arg No organ toxicity bypasses toxicity of cancer drugs High brain penetrance 1 Table 1: IC of Commercial c-Abl inhibitors for inhibition of
wildtype Abl-family kinases vs. IkT-148009 50 Inhibitor c-Abl/Abl1 Abl2/Arg c-Kit PDGFRa PDGFRb 1 Toxicology in Rat/Monkey (nM) (nM) (nM) (nM) (nM) Human equivalent dose of 600 mg Cardiovascular None Imatinib 828 1000 31 100 100 Renal None Dasatinib
0.6 * 79 * * Liver None Nilotinib 48 41 279 * * Bone marrow None Ponatinib 0.37 * * 1.1 * Sternum None Blood None IkT-148009 33 14 2975 1009 881 PBMCs Slight increase in * = not determined neutrophils within normal limits Cytotoxicity None in
primary or mature cells Sustained brain > 1 micromolar concentration 1 Ongoing chronic toxicology studies in rat and monkey have completed 13 weeks 1 See SelleckChem.com 12IS A SMALL MOLECULE c-ABL INHIBITOR IkT-148009: Low Toxicity, Selective,
Brain Penetrant c- Abl Inhibitor in Clinical Development Selective Inhibitor of c-Abl and Abl2/Arg No organ toxicity bypasses toxicity of cancer drugs High brain penetrance 1 Table 1: IC of Commercial c-Abl inhibitors for inhibition of wildtype
Abl-family kinases vs. IkT-148009 50 Inhibitor c-Abl/Abl1 Abl2/Arg c-Kit PDGFRa PDGFRb 1 Toxicology in Rat/Monkey (nM) (nM) (nM) (nM) (nM) Human equivalent dose of 600 mg Cardiovascular None Imatinib 828 1000 31 100 100 Renal None Dasatinib 0.6 * 79
* * Liver None Nilotinib 48 41 279 * * Bone marrow None Ponatinib 0.37 * * 1.1 * Sternum None Blood None IkT-148009 33 14 2975 1009 881 PBMCs Slight increase in * = not determined neutrophils within normal limits Cytotoxicity None in primary or
mature cells Sustained brain > 1 micromolar concentration 1 Ongoing chronic toxicology studies in rat and monkey have completed 13 weeks 1 See SelleckChem.com 12
MODIFIES DISEASE c-Abl inhibition by IkT-148009 blocks the four pillars
of Parkinson's Disease in Validated Animal Models a-Synuclein Toxicity Neurodegeneration Motor Dysfunction Neuroinflammation IkT-148009 clears to IkT-148009 preserves IkT-148009 restores IkT-148009 suppresses baseline in the as much as 85% as
much as 90% to near baseline organs of disease of brain neurons of lost function in the organs of disease 13MODIFIES DISEASE c-Abl inhibition by IkT-148009 blocks the four pillars of Parkinson's Disease in Validated Animal Models a-Synuclein
Toxicity Neurodegeneration Motor Dysfunction Neuroinflammation IkT-148009 clears to IkT-148009 preserves IkT-148009 restores IkT-148009 suppresses baseline in the as much as 85% as much as 90% to near baseline organs of disease of brain neurons of
lost function in the organs of disease 13
IKT Clinical DevelopmentIKT Clinical Development
PHASE 1 TRIAL IN SAFETY AND DOSING Phase 1:Dose Proportional Clinical
Pharmacokinetics and No Clinically Significant Adverse Events Category Demographic Value (% of Total N=42) Gender Female 12 (28.6) Male 30 (71.4) Age Average (SD) 56.2 (6.33) Median 56.5 Range 45, 68 Ethnicity Hispanic or Latino 6 (14.3) Not
Hispanic or Latino 36 (85.7) Black or African Race 28 (66.7) American White 13 (31.0) Other - mixed 1 (2.4) Adverse events 1 (2.4), Grade 1, two weeks post-dose 15PHASE 1 TRIAL IN SAFETY AND DOSING Phase 1:Dose Proportional Clinical Pharmacokinetics
and No Clinically Significant Adverse Events Category Demographic Value (% of Total N=42) Gender Female 12 (28.6) Male 30 (71.4) Age Average (SD) 56.2 (6.33) Median 56.5 Range 45, 68 Ethnicity Hispanic or Latino 6 (14.3) Not Hispanic or Latino 36
(85.7) Black or African Race 28 (66.7) American White 13 (31.0) Other - mixed 1 (2.4) Adverse events 1 (2.4), Grade 1, two weeks post-dose 15
PHASE 1 TRIAL IN SAFETY AND DOSING Phase 1:Dose Proportional Clinical
Pharmacokinetics and No Clinically Significant Adverse Events Clinical Pharmacokinetics of IkT-148009-SAD Cmax AUC Linear (Cmax) Linear (AUC) 5000 70000 4500 R = 0.9925 60000 4000 50000 3500 3000 40000 2500 R = 0.9995 30000 2000 1500
20000 1000 10000 500 0 0 0 10 20 30 40 50 60 70 80 Oral Dose (mg) Human safety to date No clinically significant adverse events have been observed across 5 dosing cohorts Significance of clinical pharmacokinetics 1 High exposures at
low oral dose, linearly dose proportional. Exposures at 75 mg IkT-148009 comparable to 500 mg imatinib 1 FDA summary data for approval 21-335 16 Mean Cmax (ng) Mean AUC 0- (ng-h/mLPHASE 1 TRIAL IN SAFETY AND DOSING Phase 1:Dose Proportional
Clinical Pharmacokinetics and No Clinically Significant Adverse Events Clinical Pharmacokinetics of IkT-148009-SAD Cmax AUC Linear (Cmax) Linear (AUC) 5000 70000 4500 R = 0.9925 60000 4000 50000 3500 3000 40000 2500 R = 0.9995 30000 2000
1500 20000 1000 10000 500 0 0 0 10 20 30 40 50 60 70 80 Oral Dose (mg) Human safety to date No clinically significant adverse events have been observed across 5 dosing cohorts Significance of clinical pharmacokinetics 1 High exposures
at low oral dose, linearly dose proportional. Exposures at 75 mg IkT-148009 comparable to 500 mg imatinib 1 FDA summary data for approval 21-335 16 Mean Cmax (ng) Mean AUC 0- (ng-h/mL
PHASE 1 TRIAL IN SAFETY AND DOSING Phase 1: Low Oral Dose in Humans
Reaches Therapeutic Exposures of Animal Models Clinical Pharmacokinetics IkT-148009 compared to therapeutic dose in animal models of progressive disease t t C AUC 1/2 max max 0- mg/day (h) (h) (ng/mL) (h*ng/mL) 1 IkT-148009 Mean 25 25.2 6
945 23200 Clinical N=6 1 IkT-148009 Mean 1.25 12.7 2.2 2562 19650 Efficacy, mouse model N=5 1 25 mg/day in humans equivalent to 0.128 mg/day in mouse assuming a 25 g mouse Oral doses analyzed between 12.5 mg 1x/day to 75 mg 1x/day across 4 cohorts
analyzed. 8 patients/cohort, 32 patients total 3:1 randomized against placebo. Therapeutic exposures defined Laboratory efficacy studies in mice have an AUC equivalent to clinical exposure at 25 mg/day oral dose. Long half-life at low
oral dose suggests long-term exposure to drug on a daily basis 17PHASE 1 TRIAL IN SAFETY AND DOSING Phase 1: Low Oral Dose in Humans Reaches Therapeutic Exposures of Animal Models Clinical Pharmacokinetics IkT-148009 compared to therapeutic dose in
animal models of progressive disease t t C AUC 1/2 max max 0- mg/day (h) (h) (ng/mL) (h*ng/mL) 1 IkT-148009 Mean 25 25.2 6 945 23200 Clinical N=6 1 IkT-148009 Mean 1.25 12.7 2.2 2562 19650 Efficacy, mouse model N=5 1 25 mg/day in humans
equivalent to 0.128 mg/day in mouse assuming a 25 g mouse Oral doses analyzed between 12.5 mg 1x/day to 75 mg 1x/day across 4 cohorts analyzed. 8 patients/cohort, 32 patients total 3:1 randomized against placebo. Therapeutic exposures defined
Laboratory efficacy studies in mice have an AUC equivalent to clinical exposure at 25 mg/day oral dose. Long half-life at low oral dose suggests long-term exposure to drug on a daily basis 17
HOW THE GI TRACT ILLUMINATES A NOVEL WAY TO TREAT PATIENTS Model
studies suggest the gut could be where Parkinson's disease originates in the body and is a critical organ for 1 analysis The Gut-Brain Connection Enables Innovation in Trial Design Parkinson's May Begin in the Gut Easy access Can
demonstrate disease benefit with quantitative endpoints Biopsy and Biomarkers Large effect size GI disorders resulting from kinase a modification of -synuclein: Dysphagia Unresolvable constipation Gastroesophageal reflux Gastroparesis Introduction