Exhibit 99.1 IKT Clinical Development of Therapies Intended to Reverse the Functional Loss in Parkinson’s and Related Disorders 2Q 2021 BUSINESS PRESENTATIONExhibit 99.1 IKT Clinical Development of Therapies Intended to Reverse the Functional Loss in Parkinson’s and Related Disorders 2Q 2021 BUSINESS PRESENTATION

Disclaimer This presentation shall not constitute an offer to sell or a solicitation of an offer to buy any securities, nor shall there be any sale of such securities in any state or jurisdiction in which such offer, solicitation, or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction. This presentation contains information that may constitute “forward-looking statements” within the meaning of Section 27A of the Securities Act, and Section 21E of the Securities Exchange Act of 1934, as amended. Inhibikase Therapeutics, Inc. (the “Company” or “we”) intends for the forward-looking statements to be covered by the safe harbor provisions for forward-looking statements in those sections. Generally, we have identified such forward-looking statements by using the words “believe,” “expect,” “intend,” “estimate,” “anticipate,” “project,” “target,” “forecast,” “aim,” should, “will,” may”, “continue” and similar expressions. Such statements are subject to a number of assumptions, risks and uncertainties which may cause actual results, performance or achievements to be materially different from those anticipated in these forward-looking statements. You should read statements that contain these words carefully because they discuss future expectations and plans which contain projections of future clinical studies, regulatory approvals, product candidate development, results of operations or financial condition or state other forward-looking information. However, the absence of these words or similar expressions does not mean that a statement is not forward-looking. Forward-looking statements are not historical facts, but instead represent only the Company’s beliefs regarding future events, many of which, by their nature, are inherently uncertain and outside of the Company’s control. It is possible that the Company’s actual results and financial condition may differ, possibly materially, from the anticipated results and financial condition indicated in these forward-looking statements. Management believes that these forward-looking statements are reasonable as of the time made. However, caution should be taken not to place undue reliance on any such forward-looking statements because such statements speak only as of the date when made. The Company undertakes no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law. In addition, forward-looking statements are subject to certain risks and uncertainties that could cause actual results to differ materially from the Company's historical experience and our present expectations or projections. Important factors that could cause actual results to differ materially from those in the forward-looking statements are set forth in the Company’s filings with the Securities and Exchange Commission, including its registration statement on Form S-1, as amended (File No. 333-240036), including under the caption Risk Factors. We do not intend our use or display of other entities’ names, trade names, trademarks or service marks to imply a relationship with, or endorsement or sponsorship of us by, any other entity. 22Disclaimer This presentation shall not constitute an offer to sell or a solicitation of an offer to buy any securities, nor shall there be any sale of such securities in any state or jurisdiction in which such offer, solicitation, or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction. This presentation contains information that may constitute “forward-looking statements” within the meaning of Section 27A of the Securities Act, and Section 21E of the Securities Exchange Act of 1934, as amended. Inhibikase Therapeutics, Inc. (the “Company” or “we”) intends for the forward-looking statements to be covered by the safe harbor provisions for forward-looking statements in those sections. Generally, we have identified such forward-looking statements by using the words “believe,” “expect,” “intend,” “estimate,” “anticipate,” “project,” “target,” “forecast,” “aim,” should, “will,” may”, “continue” and similar expressions. Such statements are subject to a number of assumptions, risks and uncertainties which may cause actual results, performance or achievements to be materially different from those anticipated in these forward-looking statements. You should read statements that contain these words carefully because they discuss future expectations and plans which contain projections of future clinical studies, regulatory approvals, product candidate development, results of operations or financial condition or state other forward-looking information. However, the absence of these words or similar expressions does not mean that a statement is not forward-looking. Forward-looking statements are not historical facts, but instead represent only the Company’s beliefs regarding future events, many of which, by their nature, are inherently uncertain and outside of the Company’s control. It is possible that the Company’s actual results and financial condition may differ, possibly materially, from the anticipated results and financial condition indicated in these forward-looking statements. Management believes that these forward-looking statements are reasonable as of the time made. However, caution should be taken not to place undue reliance on any such forward-looking statements because such statements speak only as of the date when made. The Company undertakes no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law. In addition, forward-looking statements are subject to certain risks and uncertainties that could cause actual results to differ materially from the Company's historical experience and our present expectations or projections. Important factors that could cause actual results to differ materially from those in the forward-looking statements are set forth in the Company’s filings with the Securities and Exchange Commission, including its registration statement on Form S-1, as amended (File No. 333-240036), including under the caption Risk Factors. We do not intend our use or display of other entities’ names, trade names, trademarks or service marks to imply a relationship with, or endorsement or sponsorship of us by, any other entity. 22

IKT Company OverviewIKT Company Overview

COMPANY HIGHLIGHTS Driving Functional Reversal of Parkinson’s Disease BY 2025, PARKINSON’S DISEASE § Multi-therapeutic pipeline with emphasis on neurodegeneration inside and out DRUG SALES ARE EXPECTED TO side of the brain § Our lead inhibitor of the Abelson Tyrosine Kinase (c-Abl), IkT-148009, halts and Double Pharma Insights, 2019 reverses functional loss in animal models that recreate progressive human disease SALES ESTIMATES BY § Five clinical programs in neurodegeneration and one clinical program in 2025 ARE EXPECTED TO oncology by close of 2021 CREST § Ongoing Phase 1 trial with IkT-148009 reaches therapeutic drug exposures seen in $6.0 Billion animal 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 § $19 million in investor capital since 2018 § Highly experienced and respected management team, consultants, Board of The U.S. DelveInsight, 2019 Directors and nearly all KOLs in the field on Scientific Advisory Board 4 4COMPANY HIGHLIGHTS Driving Functional Reversal of Parkinson’s Disease BY 2025, PARKINSON’S DISEASE § Multi-therapeutic pipeline with emphasis on neurodegeneration inside and out DRUG SALES ARE EXPECTED TO side of the brain § Our lead inhibitor of the Abelson Tyrosine Kinase (c-Abl), IkT-148009, halts and Double Pharma Insights, 2019 reverses functional loss in animal models that recreate progressive human disease SALES ESTIMATES BY § Five clinical programs in neurodegeneration and one clinical program in 2025 ARE EXPECTED TO oncology by close of 2021 CREST § Ongoing Phase 1 trial with IkT-148009 reaches therapeutic drug exposures seen in $6.0 Billion animal 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 § $19 million in investor capital since 2018 § Highly experienced and respected management team, consultants, Board of The U.S. DelveInsight, 2019 Directors and nearly all KOLs in the field on Scientific Advisory Board 4 4

COMPANY HIGHLIGHTS: MULTI-THERAPEUTIC PIPELINE Multi-Indication Pipeline in Neurodegeneration, Oncology and Infectious Disease 5COMPANY HIGHLIGHTS: MULTI-THERAPEUTIC PIPELINE Multi-Indication Pipeline in Neurodegeneration, Oncology and Infectious Disease 5

COMPANY HIGHLIGHTS Selected Financial and Stock Data § $20.4M non-dilutive grant revenue pre-IPO (NIH, DoD, States) § $19M equity sales since 2018, $18M from Initial Public Offering with ThinkEquity § 10,133,345 issued and outstanding common shares as of 5/14/2021 § 3,574,658 Options (WAEP $2.43) § 721,913 Warrants (WAEP $5.83) § 53% held by insiders, 16.5% held by institutions March 31, Balance Sheet 2021 Current assets: Cash $ 9,609,631 Grants Receivable 332,674 Prepaid research and development 712,674 Prepaid expenses and other current assets 1,218,956 Total Current Assets $ 11,874,035 Total Current Liabilities 3,837,464 Working Capital 8,036,5717 Active grant funding available in accounts held by U.S. Treasury 772,420 Total Working Capital $ 8,808,991 6 6 6COMPANY HIGHLIGHTS Selected Financial and Stock Data § $20.4M non-dilutive grant revenue pre-IPO (NIH, DoD, States) § $19M equity sales since 2018, $18M from Initial Public Offering with ThinkEquity § 10,133,345 issued and outstanding common shares as of 5/14/2021 § 3,574,658 Options (WAEP $2.43) § 721,913 Warrants (WAEP $5.83) § 53% held by insiders, 16.5% held by institutions March 31, Balance Sheet 2021 Current assets: Cash $ 9,609,631 Grants Receivable 332,674 Prepaid research and development 712,674 Prepaid expenses and other current assets 1,218,956 Total Current Assets $ 11,874,035 Total Current Liabilities 3,837,464 Working Capital 8,036,5717 Active grant funding available in accounts held by U.S. Treasury 772,420 Total Working Capital $ 8,808,991 6 6 6

ONGOING TRIALS IN SAFETY AND DOSING Accelerated Clinical Development Timeline Pre-IPO plan, Dec. 2020 Sequential Single Ascending Dose (SAD) in 8 cohorts, followed by Multiple Ascending Dose (MAD) in 4 cohorts PD patients in late 4Q21 or 1Q22 Phase 1b (Overlapping, Up to 6 Months) Phase 1 SAD / MAD (12-14 Months) 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 u MONTHS Phase 1b (Overlapping, Up to 6 Months) Phase 1 SAD / MAD (6-7 Months) Accelerated plan, Mar. 2021 Interleaving SAD and MAD cohorts, reducing Phase 1 duration by 6+ months MAD cohorts of PD patients added to protocol and under FDA regulatory review. Anticipated enrollments in early 3Q21 7ONGOING TRIALS IN SAFETY AND DOSING Accelerated Clinical Development Timeline Pre-IPO plan, Dec. 2020 Sequential Single Ascending Dose (SAD) in 8 cohorts, followed by Multiple Ascending Dose (MAD) in 4 cohorts PD patients in late 4Q21 or 1Q22 Phase 1b (Overlapping, Up to 6 Months) Phase 1 SAD / MAD (12-14 Months) 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 u MONTHS Phase 1b (Overlapping, Up to 6 Months) Phase 1 SAD / MAD (6-7 Months) Accelerated plan, Mar. 2021 Interleaving SAD and MAD cohorts, reducing Phase 1 duration by 6+ months MAD cohorts of PD patients added to protocol and under FDA regulatory review. Anticipated enrollments in early 3Q21 7

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 disease 36% 35% 30% 47% ARTHRITIS HEART / CIRCULATORY PSYCHOSIS DEMENTIA 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. 9THE 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 disease 36% 35% 30% 47% ARTHRITIS HEART / CIRCULATORY PSYCHOSIS DEMENTIA 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. 9

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 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 of dysfunctional synuclein in the gut leads to progressive disease that mirrors the human disease course in the brain 10HOW 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 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 of dysfunctional synuclein in the gut leads to progressive disease that mirrors the human disease course in the brain 10

IKT Causation of Parkinson’s and How Inhibikase Proposes to Modify DiseaseIKT Causation of Parkinson’s and How Inhibikase Proposes to Modify Disease

NEURODEGENERATION Investigating Causation in Parkinson’s Reveals c- Abl as a Primary Culprit § Parkinson’s Disease (PD) is a neurodegenerative disease which limits function of nerve cells throughout the brain and gut. § PD conditions include: Tremors Slowed Movement Impaired Balance Permanent Constipation Speech Loss Cognitive Decline Memory Loss and Reflux Disease α-Synuclein Is normally in a helix- 1 turn-helix configuration § α-Synuclein, an abundant and non-essential protein, has long been thought to be linked to the cause of Parkinson’s Disease Ø Normally, α-Synuclein plays a role in neurotransmission by dopamine. Ø In the disease state, α-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 α- synuclein cannot cause disease on their own. Ø Plaques are internalized and activate c-Abl. In the disease state, α-Synuclein reorganizes to form fibrous aggregates Ø c-Abl is actually driving the disease. 2 (“Plaques”) 1 Biochim Biophys Acta. 1818:1013-8 (2012) 2 Pathogens 7:50 (2018) 12NEURODEGENERATION Investigating Causation in Parkinson’s Reveals c- Abl as a Primary Culprit § Parkinson’s Disease (PD) is a neurodegenerative disease which limits function of nerve cells throughout the brain and gut. § PD conditions include: Tremors Slowed Movement Impaired Balance Permanent Constipation Speech Loss Cognitive Decline Memory Loss and Reflux Disease α-Synuclein Is normally in a helix- 1 turn-helix configuration § α-Synuclein, an abundant and non-essential protein, has long been thought to be linked to the cause of Parkinson’s Disease Ø Normally, α-Synuclein plays a role in neurotransmission by dopamine. Ø In the disease state, α-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 α- synuclein cannot cause disease on their own. Ø Plaques are internalized and activate c-Abl. In the disease state, α-Synuclein reorganizes to form fibrous aggregates Ø c-Abl is actually driving the disease. 2 (“Plaques”) 1 Biochim Biophys Acta. 1818:1013-8 (2012) 2 Pathogens 7:50 (2018) 12

CE L L E N T R Y THE PATH TO NEURODEGENERATION Stressors Trigger the Production of α-Synuclein Plaques Which Activates c-Abl to Drive Neurodegeneration 1 The Effects and Stressors Trigger α-Synuclein Forms C-Abl is a Sentinel which Patrols for NEURODEGENERATION Results of Activated Abnormalities the Production of Fibrous Aggregates we call c-Abl Kinase Inside a Gut or Brain Neuron α-Synuclein Plaques Sensing α-synuclein c-Abl’s sensor GI Conditions Oxidative / Plaques of misfolded α- plaques, activated c-Abl identifies nitrosative stress synuclein are abnormal, Chemically Modifies α- but benign α-synuclein plaques Parkinson’s 39 Point mutation in one or synuclein at Tyr (pY39), as a threat and Disease more proteins causing converting it into its toxic, activates in response hyperaggregation pathologic form (Mutant α-syn, LRRK2, Treatment at this stage 3 GBA1) is ineffective C-Abl further chemically modifies Parkin, disrupting α-synuclein mitochondrial integrity and duplication / triplication survival pathways that could clear α-synuclein toxicity 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 13 http://media.biogen.com/node/22876/htmlCE L L E N T R Y THE PATH TO NEURODEGENERATION Stressors Trigger the Production of α-Synuclein Plaques Which Activates c-Abl to Drive Neurodegeneration 1 The Effects and Stressors Trigger α-Synuclein Forms C-Abl is a Sentinel which Patrols for NEURODEGENERATION Results of Activated Abnormalities the Production of Fibrous Aggregates we call c-Abl Kinase Inside a Gut or Brain Neuron α-Synuclein Plaques Sensing α-synuclein c-Abl’s sensor GI Conditions Oxidative / Plaques of misfolded α- plaques, activated c-Abl identifies nitrosative stress synuclein are abnormal, Chemically Modifies α- but benign α-synuclein plaques Parkinson’s 39 Point mutation in one or synuclein at Tyr (pY39), as a threat and Disease more proteins causing converting it into its toxic, activates in response hyperaggregation pathologic form (Mutant α-syn, LRRK2, Treatment at this stage 3 GBA1) is ineffective C-Abl further chemically modifies Parkin, disrupting α-synuclein mitochondrial integrity and duplication / triplication survival pathways that could clear α-synuclein toxicity 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 13 http://media.biogen.com/node/22876/html

INHIBIKASE’S PROOF ACTIVATED C-ABL IS THE GATEWAY IN THE DISEASE PATH α-Synuclein Plaques Do Not Cause Disease Without c-Abl 1 Modification in Humanized Preclinical Models α-Synuclein plaque in the ABSENCE OF c-Abl CAUSES NO NEURODEGENERATION AFTER 6 MONTHS No c-Abl = No neurodegeneration Injection (Inj) of an expression vector for the A53T form of synuclein doesn’t degrade neurons until the expression of A53T is turned on Once turned on, A53T induces 50% neurodegeneration in 6 months. Control NOTE loss is visible in the dark patches of stained neurons on the right half. The left half was an Synuclein aggregate internal control and is unaffected. Synuclein aggregate with c- When the expression of A53T is turned on, Abl deleted but c-Abl is genetically deleted from the mouse brain, you don’t get any neurodegeneration. Thus, even though the clumps ofa-syn are present in the right region of the brain, they don’t cause disease until c-Abl **: p < 0.0001, p = 0.0154, p = 0.0001, p acts on them = 0.0225, left-to-right 1 Brain 142:2380ff (2019) 14INHIBIKASE’S PROOF ACTIVATED C-ABL IS THE GATEWAY IN THE DISEASE PATH α-Synuclein Plaques Do Not Cause Disease Without c-Abl 1 Modification in Humanized Preclinical Models α-Synuclein plaque in the ABSENCE OF c-Abl CAUSES NO NEURODEGENERATION AFTER 6 MONTHS No c-Abl = No neurodegeneration Injection (Inj) of an expression vector for the A53T form of synuclein doesn’t degrade neurons until the expression of A53T is turned on Once turned on, A53T induces 50% neurodegeneration in 6 months. Control NOTE loss is visible in the dark patches of stained neurons on the right half. The left half was an Synuclein aggregate internal control and is unaffected. Synuclein aggregate with c- When the expression of A53T is turned on, Abl deleted but c-Abl is genetically deleted from the mouse brain, you don’t get any neurodegeneration. Thus, even though the clumps ofa-syn are present in the right region of the brain, they don’t cause disease until c-Abl **: p < 0.0001, p = 0.0154, p = 0.0001, p acts on them = 0.0225, left-to-right 1 Brain 142:2380ff (2019) 14

STUDY Pathologic, c-Abl-Modified α-Synuclein (pY39) is Present in 1 Parkinson’s Patient Brain Toxic pY39-a-Synuclein Toxic pY39-a-Synuclein Abundant Prominent in Lewy Bodies In Substantia Nigra (SN) of Patients 1 J Clin Invest. 126, 2970-88 (2016) 15STUDY Pathologic, c-Abl-Modified α-Synuclein (pY39) is Present in 1 Parkinson’s Patient Brain Toxic pY39-a-Synuclein Toxic pY39-a-Synuclein Abundant Prominent in Lewy Bodies In Substantia Nigra (SN) of Patients 1 J Clin Invest. 126, 2970-88 (2016) 15

ONGOING TRIALS IN SAFETY AND DOSING\ Low Toxicity, Brain Penetrant c-Abl Inhibitor in Clinical Development 1 14-Day Toxicology in Rat/Monkey NOVEL ABL KINASE RELATIVE INHIBITOR POTENCY Human equivalent dose of 600 mg Cardiovascular None § No observed toxicity from off target 148019 8 Renal None kinase inhibition Liver None 148003 12 § No CNS toxicity Bone marrow None 148027 17 § No toxicity observed even on 210+ Sternum None day dosing in mice at >150 Blood None 148032 23 mg/kg/day PBMCs Slight increase in neutrophils within § Nearly complete neuroprotection in 148009 18* normal limits a-synuclein progressive disease Cytotoxicity None in primary or models 01427 36 mature cells Sustainable brain > 1 micromolar § Multi-kilogram clinical batch Imatinib 1 concentration production completed, 6 step 1 Ongoing chronic toxicology studies in rat and synthesis monkey have completed 13 weeks Imatinib is a template for design * Compositions of matter patent protection through 2036 16ONGOING TRIALS IN SAFETY AND DOSING\ Low Toxicity, Brain Penetrant c-Abl Inhibitor in Clinical Development 1 14-Day Toxicology in Rat/Monkey NOVEL ABL KINASE RELATIVE INHIBITOR POTENCY Human equivalent dose of 600 mg Cardiovascular None § No observed toxicity from off target 148019 8 Renal None kinase inhibition Liver None 148003 12 § No CNS toxicity Bone marrow None 148027 17 § No toxicity observed even on 210+ Sternum None day dosing in mice at >150 Blood None 148032 23 mg/kg/day PBMCs Slight increase in neutrophils within § Nearly complete neuroprotection in 148009 18* normal limits a-synuclein progressive disease Cytotoxicity None in primary or models 01427 36 mature cells Sustainable brain > 1 micromolar § Multi-kilogram clinical batch Imatinib 1 concentration production completed, 6 step 1 Ongoing chronic toxicology studies in rat and synthesis monkey have completed 13 weeks Imatinib is a template for design * Compositions of matter patent protection through 2036 16

ONGOING TRIALS IN SAFETY AND DOSING Dose Proportional Clinical Pharmacokinetics and Favorable Adverse Event Profile Clinical Pharmacokinetics of IkT-148009-SAD Cmax AUC Linear (Cmax) Linear (AUC) 5000 70000 4500 R² = 0.9925 60000 4000 50000 3500 3000 40000 2500 R² = 0.9995 30000 2000 1500 20000 1000 10000 500 0 0 0 10 20 30 40 50 60 70 80 Human safety to date Oral Dose (mg) Ø No clinically significant adverse events have been observed across 5 dosing cohorts Significance of clinical pharmacokinetics 1 Ø 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 17 Mean Cmax (ng) Mean AUC 0-∞ (ng-h/mLONGOING TRIALS IN SAFETY AND DOSING Dose Proportional Clinical Pharmacokinetics and Favorable Adverse Event Profile Clinical Pharmacokinetics of IkT-148009-SAD Cmax AUC Linear (Cmax) Linear (AUC) 5000 70000 4500 R² = 0.9925 60000 4000 50000 3500 3000 40000 2500 R² = 0.9995 30000 2000 1500 20000 1000 10000 500 0 0 0 10 20 30 40 50 60 70 80 Human safety to date Oral Dose (mg) Ø No clinically significant adverse events have been observed across 5 dosing cohorts Significance of clinical pharmacokinetics 1 Ø 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 17 Mean Cmax (ng) Mean AUC 0-∞ (ng-h/mL

ONGOING TRIALS IN SAFETY AND DOSING Low Oral Dose in Humans Reaches The 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 Ø Laboratory efficacy studies in mice have an AUC equivalent to clinical exposure at 25 mg/day oral dose. Ø Long half-life at low oral dose suggests long-term exposure to drug on a daily basis 18ONGOING TRIALS IN SAFETY AND DOSING Low Oral Dose in Humans Reaches The 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 Ø Laboratory efficacy studies in mice have an AUC equivalent to clinical exposure at 25 mg/day oral dose. Ø Long half-life at low oral dose suggests long-term exposure to drug on a daily basis 18

ONGOING TRIALS IN SAFETY AND DOSING Updated Phases and Development Intervals for 2021 Single Ascending Dose (SAD) § 8 dosing cohorts (25 – 400 mg, 1x/day) § 8 patients/cohort, 2:1 randomized § Sentinel dosing § Primary objectives safety, tolerability , pharmacokinetics (PK), urine and plasma concentrations Phase 1b Phase 1 Multiple Ascending Dose (MAD) Multiple Ascending Dose (MAD) § 4 dosing cohorts, doses determined from SAD PK § Enroll cohort of Parkinson’s patients with GI evaluations at middle of MAD period and safety § Timing coordinated with 3 month toxicology readout § 8 patients/dose, 3:1 randomized, 7 day dosing 1x/day § Primary objectives safety, tolerability, pharmacokinetics § Primary objectives safety, tolerability, pharmacokinetics § Secondary objectives functional assessment of motor and cognitive function in brain, motor (PK), urine, plasma spinal fluid concentrations, trough function in GI concentration and Maximum Tolerated Dose Phase 1 SAD / MAD (6-7 Months) Phase 1b (Overlapping, Up to 6 Months) 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 MONTHS u Phase 1 Chronic Toxicology Studies (11 Months) Comparative Toxicology to Imatinib at Toxic Dose RAT: 3 and 6-month dosing • 3-month readout (July, 2021) extends patient dosing period covered by pivotal toxicology for Phase 1b MONKEY: 3 and 9-month dosing • 3-month readout (July, 2021) extends patient dosing period covered by pivotal toxicology for Phase 1b 19ONGOING TRIALS IN SAFETY AND DOSING Updated Phases and Development Intervals for 2021 Single Ascending Dose (SAD) § 8 dosing cohorts (25 – 400 mg, 1x/day) § 8 patients/cohort, 2:1 randomized § Sentinel dosing § Primary objectives safety, tolerability , pharmacokinetics (PK), urine and plasma concentrations Phase 1b Phase 1 Multiple Ascending Dose (MAD) Multiple Ascending Dose (MAD) § 4 dosing cohorts, doses determined from SAD PK § Enroll cohort of Parkinson’s patients with GI evaluations at middle of MAD period and safety § Timing coordinated with 3 month toxicology readout § 8 patients/dose, 3:1 randomized, 7 day dosing 1x/day § Primary objectives safety, tolerability, pharmacokinetics § Primary objectives safety, tolerability, pharmacokinetics § Secondary objectives functional assessment of motor and cognitive function in brain, motor (PK), urine, plasma spinal fluid concentrations, trough function in GI concentration and Maximum Tolerated Dose Phase 1 SAD / MAD (6-7 Months) Phase 1b (Overlapping, Up to 6 Months) 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 MONTHS u Phase 1 Chronic Toxicology Studies (11 Months) Comparative Toxicology to Imatinib at Toxic Dose RAT: 3 and 6-month dosing • 3-month readout (July, 2021) extends patient dosing period covered by pivotal toxicology for Phase 1b MONKEY: 3 and 9-month dosing • 3-month readout (July, 2021) extends patient dosing period covered by pivotal toxicology for Phase 1b 19

IKT Proof of Functional Reversal in the Brain and Gut in Animal Models of DiseaseIKT Proof of Functional Reversal in the Brain and Gut in Animal Models of Disease

ANIMAL STUDY BASIS OF IkT-148009 THERAPY Oral IkT-148009 in Mice Humanized for Parkinson’s Disease in Brain Reverses Functional Loss Baseline Neuromuscular Toxic Levels of Synuclein Are Treatment Started 6 Weeks After Onset of Near Normal Behavior Returned Following Introduced Into One Side of the Coordination Conditions Treatment Behavioral Marker Mouse Brain Defect in one hemisphere makes mice run in circles Toxicity renders the mice trembling and only able to run Mice completed 30 turns/10 min in circles when treated a dose of 100 mg/kg dose Healthy Mice Run In Circles at the Average Rate of 25 Turns : 10 Min NEARLY COMPLETE RESCUE 21ANIMAL STUDY BASIS OF IkT-148009 THERAPY Oral IkT-148009 in Mice Humanized for Parkinson’s Disease in Brain Reverses Functional Loss Baseline Neuromuscular Toxic Levels of Synuclein Are Treatment Started 6 Weeks After Onset of Near Normal Behavior Returned Following Introduced Into One Side of the Coordination Conditions Treatment Behavioral Marker Mouse Brain Defect in one hemisphere makes mice run in circles Toxicity renders the mice trembling and only able to run Mice completed 30 turns/10 min in circles when treated a dose of 100 mg/kg dose Healthy Mice Run In Circles at the Average Rate of 25 Turns : 10 Min NEARLY COMPLETE RESCUE 21

ANIMAL STUDY BASIS OF 148009 THERAPY Oral IkT-148009 Suppresses c-Abl Activation in the Brain that Correlates with Functional Recovery IkT-148009 engages the c-Abl target in the brain Activated c-Abl in disease Baseline Inhibition of c-Abl below baseline by IkT-148009 22 Normal Mice Normal Mice +148009 Parkinson’s Mice Parkinson’s Mice +148009 Parkinson’s Mice +148009 and elacridarANIMAL STUDY BASIS OF 148009 THERAPY Oral IkT-148009 Suppresses c-Abl Activation in the Brain that Correlates with Functional Recovery IkT-148009 engages the c-Abl target in the brain Activated c-Abl in disease Baseline Inhibition of c-Abl below baseline by IkT-148009 22 Normal Mice Normal Mice +148009 Parkinson’s Mice Parkinson’s Mice +148009 Parkinson’s Mice +148009 and elacridar

ANIMAL STUDY BASIS OF 148009 THERAPY Oral IkT-148009 Preserves Neural Anatomy in the Brain IkT-148009 stopped loss of neurons, accounting for functional recovery Placebo IkT-148009 only, no disease A53T induced disease A53T-induced disease + IkT-148009 Normal # neurons Rescued # neurons (≥ 80%) Disease # neurons (< 50%) 23ANIMAL STUDY BASIS OF 148009 THERAPY Oral IkT-148009 Preserves Neural Anatomy in the Brain IkT-148009 stopped loss of neurons, accounting for functional recovery Placebo IkT-148009 only, no disease A53T induced disease A53T-induced disease + IkT-148009 Normal # neurons Rescued # neurons (≥ 80%) Disease # neurons (< 50%) 23

EVIDENCE OF FUNCTIONAL RECOVERY IN THE GUT Oral IkT-148009 in Mice Humanized for Parkinson’s Disease in Gut Reverses Functional Loss METHOD OF MEASUREMENT POST TREATMENT RESULTS α-Synuclein Aggregates Introduced Into At 3 months defecation slows to 500 min (3x normal); At 6 months Gut Slows Gut Transit Time defecation slows to 800 min (5x normal); Normal = 165 min Carmine dye NOTES 1.If it weren’t for 6 outliers in 96 measures, average would be 170 min, essentially 100% Neuron count read recovery. out by Whole Gut Transit Time - The 2.We find the time it takes for a neuroanatomy is mouse to defecate nearly completely restored by measuring the number and distribution of neural ganglia in the tissue. Vehicle (Control) IkT – 148009 Vehicle (Control) IkT – 148009 Measure defecation rate A53T Human α-Synuclein A53T Human α-Synuclein 24EVIDENCE OF FUNCTIONAL RECOVERY IN THE GUT Oral IkT-148009 in Mice Humanized for Parkinson’s Disease in Gut Reverses Functional Loss METHOD OF MEASUREMENT POST TREATMENT RESULTS α-Synuclein Aggregates Introduced Into At 3 months defecation slows to 500 min (3x normal); At 6 months Gut Slows Gut Transit Time defecation slows to 800 min (5x normal); Normal = 165 min Carmine dye NOTES 1.If it weren’t for 6 outliers in 96 measures, average would be 170 min, essentially 100% Neuron count read recovery. out by Whole Gut Transit Time - The 2.We find the time it takes for a neuroanatomy is mouse to defecate nearly completely restored by measuring the number and distribution of neural ganglia in the tissue. Vehicle (Control) IkT – 148009 Vehicle (Control) IkT – 148009 Measure defecation rate A53T Human α-Synuclein A53T Human α-Synuclein 24

IKT Proof of Toxicity Clearance in the Brain and Gut in Animal Models of DiseaseIKT Proof of Toxicity Clearance in the Brain and Gut in Animal Models of Disease

EFFECT ON CAUSE OF DISEASE Oral IkT-148009 Treatment Clears Toxic a-Synuclein in the brain and gut Clearance of toxicity in the gut Clearance of toxicity in the brain Green: Pathological a-synuclein Red: Neural ganglia in gut Aggregates Cleared during treatment with IkT- 148009 IkT-148009 drives clearance of pathological α-synuclein (green dots have been cleared) 26EFFECT ON CAUSE OF DISEASE Oral IkT-148009 Treatment Clears Toxic a-Synuclein in the brain and gut Clearance of toxicity in the gut Clearance of toxicity in the brain Green: Pathological a-synuclein Red: Neural ganglia in gut Aggregates Cleared during treatment with IkT- 148009 IkT-148009 drives clearance of pathological α-synuclein (green dots have been cleared) 26

RESEARCH ADVANCES ARE TRANSFORMATIONAL Advances in pre-clinical models and clinical dosing § IKT-148009 drives functional recovery inside and outside of the brain § IKT-148009 drives clearance of the toxic form of a- synuclein § Low oral doses in humans achieve therapeutic exposure levels observed in animal efficacy studies § Early clinical outcomes with IkT-148009 have accelerated development and provide a path for early entry into Parkinson’s patients Targeting c-Abl we believe is transformational to treatment of neurodegeneration 27RESEARCH ADVANCES ARE TRANSFORMATIONAL Advances in pre-clinical models and clinical dosing § IKT-148009 drives functional recovery inside and outside of the brain § IKT-148009 drives clearance of the toxic form of a- synuclein § Low oral doses in humans achieve therapeutic exposure levels observed in animal efficacy studies § Early clinical outcomes with IkT-148009 have accelerated development and provide a path for early entry into Parkinson’s patients Targeting c-Abl we believe is transformational to treatment of neurodegeneration 27

COMPANY HIGHLIGHTS Upcoming Milestones IkT-148009 Five clinical programs by close of 2021 Completion of Phase 1 Healthy Volunteer Study SAD/MAD 3Q21 Anticipated dosing of Parkinson’s patients by early 3Q21 Completion of chronic toxicology studies 4Q21 IkT-001Pro IND filing 3Q221 Bioequivalence study 3Q21 Superiority evaluation relative to Standard-of-Care in CML patients anticipated to commence 1Q22 Team Build-out, Medicinal Chemistry, Pre-clinical Research, General and Administrative build out 28 28COMPANY HIGHLIGHTS Upcoming Milestones IkT-148009 Five clinical programs by close of 2021 Completion of Phase 1 Healthy Volunteer Study SAD/MAD 3Q21 Anticipated dosing of Parkinson’s patients by early 3Q21 Completion of chronic toxicology studies 4Q21 IkT-001Pro IND filing 3Q221 Bioequivalence study 3Q21 Superiority evaluation relative to Standard-of-Care in CML patients anticipated to commence 1Q22 Team Build-out, Medicinal Chemistry, Pre-clinical Research, General and Administrative build out 28 28

ABOUT US Management Team with Deep Experience in Drug Development and Commercialization Executive MiltonWerner,PhDPresident&CEO Previously, Dr. Werner served as Director of Research at Celtaxsys. From September 1996 until June 2007, Dr. Werner was a Head of the Laboratory of Molecular Biophysics at The Rockefeller University in New York City. Throughout his scientific career, Dr. Werner has been an innovator integrating chemistry, physics, and biology into a comprehensive approach to solving problems in medicine. Dr. Werner is the author or co-author of more than 70 research articles, reviews, and book chaptersand has given lectureson his research workthroughoutthe world. JosephFrattaroli,CPAChiefFinancialOfficer Mr. Frattaroli is a certified public accountant with more than 15 years of experience in public company filings and compliance for Nasdaq and OTC Markets companies. Previously, he provided chief financial officer and consulting services for several emerging biopharmaceutical and medical device companies, with responsibilities that included capital formation, deal structuring, and assisting private companies in their transition to becoming publicly traded SEC registrants. C. WarrenOlanow,MD,InterimChiefMedicalOfficerandChiefExecutiveOfficerofCLINTREX. Dr. Olanow is the former Henry P. and Georgette Goldschmidt Professor and Chairman of the Department of Neurology at the Mount Sinai School of Medicine Prior to joining Mount Sinai, he served on the faculties of McGill University, Duke University, and the University of South Florida. He is the former President of the Movement Disorder Society, past President of the International Society of Motor Disturbances, and former Treasurer of the American Neurological Association. He has served on the executive committee of the Michael J. Fox Foundation Scientific Advisory Board, and he is the former Chairman of the Scientific Advisory Board of the Bachmann-Strauss Parkinson Foundation and of the Dystonia Foundation. Dr. Olanow is the former Co-Editor-in-Chief of the journal Movement Disorders. Dr. Olanow received his medical degree from the University of Toronto, performed his neurology training at the New York Neurological Institute at Columbia Presbyterian Medical Center at Columbia University, and undertook postgraduate studies in neuroanatomyat Columbia Universityand authoredmore than 600 articles in the field ofneurodegeneration. 29ABOUT US Management Team with Deep Experience in Drug Development and Commercialization Executive MiltonWerner,PhDPresident&CEO Previously, Dr. Werner served as Director of Research at Celtaxsys. From September 1996 until June 2007, Dr. Werner was a Head of the Laboratory of Molecular Biophysics at The Rockefeller University in New York City. Throughout his scientific career, Dr. Werner has been an innovator integrating chemistry, physics, and biology into a comprehensive approach to solving problems in medicine. Dr. Werner is the author or co-author of more than 70 research articles, reviews, and book chaptersand has given lectureson his research workthroughoutthe world. JosephFrattaroli,CPAChiefFinancialOfficer Mr. Frattaroli is a certified public accountant with more than 15 years of experience in public company filings and compliance for Nasdaq and OTC Markets companies. Previously, he provided chief financial officer and consulting services for several emerging biopharmaceutical and medical device companies, with responsibilities that included capital formation, deal structuring, and assisting private companies in their transition to becoming publicly traded SEC registrants. C. WarrenOlanow,MD,InterimChiefMedicalOfficerandChiefExecutiveOfficerofCLINTREX. Dr. Olanow is the former Henry P. and Georgette Goldschmidt Professor and Chairman of the Department of Neurology at the Mount Sinai School of Medicine Prior to joining Mount Sinai, he served on the faculties of McGill University, Duke University, and the University of South Florida. He is the former President of the Movement Disorder Society, past President of the International Society of Motor Disturbances, and former Treasurer of the American Neurological Association. He has served on the executive committee of the Michael J. Fox Foundation Scientific Advisory Board, and he is the former Chairman of the Scientific Advisory Board of the Bachmann-Strauss Parkinson Foundation and of the Dystonia Foundation. Dr. Olanow is the former Co-Editor-in-Chief of the journal Movement Disorders. Dr. Olanow received his medical degree from the University of Toronto, performed his neurology training at the New York Neurological Institute at Columbia Presbyterian Medical Center at Columbia University, and undertook postgraduate studies in neuroanatomyat Columbia Universityand authoredmore than 600 articles in the field ofneurodegeneration. 29

Board Industry-Leading of Directors Advisors Mr. Dennis Berman has been a co-founder, board member, Dr. Roy Freeman, MD is Professor of Neurology at the Robert Hauser, MD and/or seed investor in many private biotechnology and Professor of Neurology, University of South Florida Harvard Medical School and Director of the Center for technology companies, five of which have gone public. He College of Medicine - Director USF Parkinson’s Disease Autonomic and Peripheral Nerve Disorders in the Department currently serves as the President of Molino Ventures, LLC a and Movement Disorders Center of Neurology at Beth Israel Deaconess Medical Center in board advisory and venture capital firm and was co-founder Boston, Massachusetts. Dr. Freeman is former chairman of Jeffrey Kordower, PhD and Executive Vice President of Corporate Development of the World Federation of Neurology research group on the Alla V and Solomon Jesmer Professor of Aging & Tocagen. Other public companies for which Mr. Berman has autonomic nervous system, former President of the American Neurological Sciences Rush University Medical Center served as a seed investor, co-founder, and/or board member Autonomic Society, and former chairman of the Autonomic include Intervu (one of the first software-as-a-service Section of the American Academy of Neurology. Dr. Freeman Dr. Ken Marek companies), which was acquired by Akamai; Kintera, Inc. (an President and Senior Scientist, Institute of is Editor-in-Chief of Autonomic Neuroscience: Basic and online fundraising pioneer), which was acquired by Neurodegenerative Disorders Clinical and on the editorial boards of The Clinical Journal of Blackbaud; Gensia (focused on purine/pyrimidine metabolism Pain, Pain: Clinical Updates, and Clinical Autonomic Dr. Ted Dawson, MD, PhD compounds), which was acquired by Teva; and Viagene (the Research. He is a founder of several companies in pain and Neurodegeneration and Stem Cell Programs, Institute for first U.S. gene therapy company that utilized a non- neurodegenerative disease and is on the scientific advisory Cell Engineering, Departments of Neurology, Physiology, replicating retrovirus), which was acquired by boards of many large and small pharmaceutical and Pharmacology, and Molecular Sciences - The Johns Chiron/Novartis. Mr. Berman also was a seed investor in biotechnology companies. Hopkins University School of Medicine Calabrian (a water treatment company), which was acquired Dr. Valina Dawson, PhD by SK Capital. Neurodegeneration and Stem Cell Programs, Institute for Cell Engineering, Departments of Neurology and Dr. Paul Grint, MD has more than two decades of experience Ms. Elizabeth O’Farrell recently retired from a 25-year career Physiology in biologics and small-molecule research and development, with Eli Lilly and Company, lastly serving as Chief The Johns Hopkins University School of Medicine including the successful approval and commercialization of Procurement Officer and Leader, Global Head of Shared products in the infectious diseases, immunology, and Dr. Warren Olanow, MD, FRCPC Services from 2012 to 2017. Prior to that, she advanced oncology therapeutic areas. He on the Board of Amplyx Henry P. and Georgette Goldschmidt Professor and through a number of executive management positions Chairman Emeritus, Mount Sinai School of Medicine Pharmaceuticals and Synedgen. Has served on the Board of including Senior Vice President, Policy and Finance; Senior Clintrex, Inc. Cardea Bio, on the Board of Amplyx Pharmaceuticals, on the Vice President, Finance; Chief Financial Officer, Lilly USA; Board of Synedgen and was CEO and member of the Board Chief Financial Officer, Lilly Canada; and General Auditor. Dr. Karl Kieburtz, MD, MPH of Directors of AmpliPhi Biosciences. Dr. Grint has also Before joining Eli Lilly, Ms. O’Farrell currently serves on the Robert J. Joynt Professor in Neurology, Senior Associate served in senior management roles at Cerexa, Forest board of PDL BioPharma, Geron Corporation where she is a Dean for Clinical Research, Director of the Clinical Laboratories, Kalypsys, Pfizer, IDEC Pharmaceuticals, and member of the Audit Committee and. member of the board of &Translational Science Institute, Founder Center for Schering-Plough Corporation. He is a Fellow of the Royal directors of Lensar and serves as member and chair of their Audit Human Experimental Therapeutics (CHET)- University of College of Pathologists, and holds a bachelor’s degree from Committee. Ms. O’Farrell holds a BS in accounting with honors Rochester Medical Center Clintrex, Inc. St. Mary’s Hospital College, University of London and a and an MBA in management information systems, both from Dr. Jay Pasricha, MBBS, MD medical degree from St. Bartholomew’s Hospital College, Indiana University. Director, Johns Hopkins Center for Neurogastroenterology University of London. Professor of Medicine 30Board Industry-Leading of Directors Advisors Mr. Dennis Berman has been a co-founder, board member, Dr. Roy Freeman, MD is Professor of Neurology at the Robert Hauser, MD and/or seed investor in many private biotechnology and Professor of Neurology, University of South Florida Harvard Medical School and Director of the Center for technology companies, five of which have gone public. He College of Medicine - Director USF Parkinson’s Disease Autonomic and Peripheral Nerve Disorders in the Department currently serves as the President of Molino Ventures, LLC a and Movement Disorders Center of Neurology at Beth Israel Deaconess Medical Center in board advisory and venture capital firm and was co-founder Boston, Massachusetts. Dr. Freeman is former chairman of Jeffrey Kordower, PhD and Executive Vice President of Corporate Development of the World Federation of Neurology research group on the Alla V and Solomon Jesmer Professor of Aging & Tocagen. Other public companies for which Mr. Berman has autonomic nervous system, former President of the American Neurological Sciences Rush University Medical Center served as a seed investor, co-founder, and/or board member Autonomic Society, and former chairman of the Autonomic include Intervu (one of the first software-as-a-service Section of the American Academy of Neurology. Dr. Freeman Dr. Ken Marek companies), which was acquired by Akamai; Kintera, Inc. (an President and Senior Scientist, Institute of is Editor-in-Chief of Autonomic Neuroscience: Basic and online fundraising pioneer), which was acquired by Neurodegenerative Disorders Clinical and on the editorial boards of The Clinical Journal of Blackbaud; Gensia (focused on purine/pyrimidine metabolism Pain, Pain: Clinical Updates, and Clinical Autonomic Dr. Ted Dawson, MD, PhD compounds), which was acquired by Teva; and Viagene (the Research. He is a founder of several companies in pain and Neurodegeneration and Stem Cell Programs, Institute for first U.S. gene therapy company that utilized a non- neurodegenerative disease and is on the scientific advisory Cell Engineering, Departments of Neurology, Physiology, replicating retrovirus), which was acquired by boards of many large and small pharmaceutical and Pharmacology, and Molecular Sciences - The Johns Chiron/Novartis. Mr. Berman also was a seed investor in biotechnology companies. Hopkins University School of Medicine Calabrian (a water treatment company), which was acquired Dr. Valina Dawson, PhD by SK Capital. Neurodegeneration and Stem Cell Programs, Institute for Cell Engineering, Departments of Neurology and Dr. Paul Grint, MD has more than two decades of experience Ms. Elizabeth O’Farrell recently retired from a 25-year career Physiology in biologics and small-molecule research and development, with Eli Lilly and Company, lastly serving as Chief The Johns Hopkins University School of Medicine including the successful approval and commercialization of Procurement Officer and Leader, Global Head of Shared products in the infectious diseases, immunology, and Dr. Warren Olanow, MD, FRCPC Services from 2012 to 2017. Prior to that, she advanced oncology therapeutic areas. He on the Board of Amplyx Henry P. and Georgette Goldschmidt Professor and through a number of executive management positions Chairman Emeritus, Mount Sinai School of Medicine Pharmaceuticals and Synedgen. Has served on the Board of including Senior Vice President, Policy and Finance; Senior Clintrex, Inc. Cardea Bio, on the Board of Amplyx Pharmaceuticals, on the Vice President, Finance; Chief Financial Officer, Lilly USA; Board of Synedgen and was CEO and member of the Board Chief Financial Officer, Lilly Canada; and General Auditor. Dr. Karl Kieburtz, MD, MPH of Directors of AmpliPhi Biosciences. Dr. Grint has also Before joining Eli Lilly, Ms. O’Farrell currently serves on the Robert J. Joynt Professor in Neurology, Senior Associate served in senior management roles at Cerexa, Forest board of PDL BioPharma, Geron Corporation where she is a Dean for Clinical Research, Director of the Clinical Laboratories, Kalypsys, Pfizer, IDEC Pharmaceuticals, and member of the Audit Committee and. member of the board of &Translational Science Institute, Founder Center for Schering-Plough Corporation. He is a Fellow of the Royal directors of Lensar and serves as member and chair of their Audit Human Experimental Therapeutics (CHET)- University of College of Pathologists, and holds a bachelor’s degree from Committee. Ms. O’Farrell holds a BS in accounting with honors Rochester Medical Center Clintrex, Inc. St. Mary’s Hospital College, University of London and a and an MBA in management information systems, both from Dr. Jay Pasricha, MBBS, MD medical degree from St. Bartholomew’s Hospital College, Indiana University. Director, Johns Hopkins Center for Neurogastroenterology University of London. Professor of Medicine 30