SEQUEL (COG0202) Topline Results A Pilot Electroencephalography (EEG) Study to Evaluate the Effect of CT1812 Treatment on Synaptic Activity in Subjects with Mild to Moderate Alzheimer’s Disease

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3 • Aβ oligomers impair synaptic and neuronal activity • Will displacement of Aβ oligomers from synapses after treatment with CT1812 lead to a detectable change in EEG patterns? SEQUEL Hypothesis • Izzo NJ, et al. Preclinical and clinical biomarker studies of CT1812: A novel approach to Alzheimer’s disease modification. Alzheimer’s Dement. 2021;1–18 • Izzo NJ, et al. Alzheimer’s therapeutics targeting amyloid beta 1-42 oligomers II: Sigma-2/PGRMC1 receptors mediate Abeta 42 oligomer binding and synaptotoxicity PLoS One. 2014 Nov 12; 9(11):e111899 • Izzo NJ, et al. Alzheimer’s therapeutics targeting amyloid beta 1-42 oligomers I: Abeta 42 oligomer binding to specific neuronal receptors is displaced by drug candidates that improve cognitive deficits PLoS One. 2014 Nov 12; 9(11):e111898 • Limegrover, CS, et al. Alzheimer’s Protection Effect of A673T Mutation May Be Driven by Lower Aβ Oligomer Binding Affinity. J Neurochem. 2020; 00: 1– 15. doi:10.1111/jnc.15212 CT1812 Small Molecule TMEM97 PGRMC1 LilrB2 NoGo PrPc

4 Confidential SEQUEL (COG0202): Single-site qEEG Study in 16 Adults with Mild-to-moderate Alzheimer’s Disease Two-group cross-over design Inclusion Criteria Period One (4 weeks) Period Two (4 weeks) Assessments ‐ CSF positive for Aβ ‐ MRI consistent with Alzheimer's disease diagnosis ‐ MMSE 18-26 ‐ No add’l CNS disorders ‐ Safety and PK ‐ Measurement of synaptic function via qEEG by relative theta power ‐ CSF and plasma biomarkers ‐ Cognition (ADAS-Cog-14, ADCS-CGIC, A-IADL-Q, NTB)* 1:1 Oral QD Administration Placebo (n=8) CT1812 (n=8), 300mg CT1812, 300mg Placebo https://clinicaltrials.gov/ct2/show/NCT04735536

5 Design: Two-group cross-over study in 16 adults with mild-to-moderate AD Single site: VUmc Alzheimer’s Center, Amsterdam Primary objectives: • Assess safety, tolerability, PK of CT1812 following repeated dosing for 28 days • Evaluate efficacy of CT1812 in restoring synaptic function through quantitative EEG as measured by: - Global relative theta power (primary endpoint) - Global alpha AECC, global relative alpha power, global relative beta power – key pre-specified exploratory endpoints - Additional pre-specified EEG exploratory endpoints Exploratory objectives: • Cognitive measures: impact of CT1812 on cognitive and global functioning, as measured by the following: - ADAS-Cog-14, ADCS-CGIC, A-IADL-Q - Neuropsychological test battery (NTB), Controlled Word Association Test (COWAT), Trail Making Test (TMT) Parts A & B, and Wechsler Memory Digit Span (VMDS) - Exploratory – biomarkers – pending Study Design

Topline Data Overview • Disposition and demographics • Safety and tolerability • Topline EEG findings

7 • 34 subjects screened; 16 randomized • 15 completed the study - No subjects discontinued due to AEs - One patient discontinued after treatment period 1 due to withdrawal of consent (death in the family) • n=14 for placebo period (one participant missed visit 7); n=16 for CT1812 period • Mean Age: 66.4 years • 50% Female • 100% White, non-Hispanic • Baseline cognitive measures: - Mean MMSE: 21.1 - ADAS-Cog14: 30.2 - Amsterdam IADL: 52.6 • ApoE genotypes: - 31.3% ApoE e3/e3 - 37.5% ApoE e3/e4 - 31.3% ApoE e4/e4 • Time since diagnosis: 1.14 years COG0202 Disposition and Demographics Disposition Demographics

8 • CT1812 was well-tolerated - All AEs were mild and moderate - No Severe AEs, No SAEs, No AEs leading to death or discontinuation • TEAEs: - Occurred in 11 participants in the CT1812 period and 6 participants in the placebo period - 6 TEAEs were categorized as related to study drug (3 in CT1812 period and 3 in placebo period) • Most common AEs by MedDRA system organ class: - GI: nausea, diarrhea - Injury & procedural complications: procedural headache • Consistent with previous studies – 1 participant with mild (2X ULN) elevated liver enzymes Safety and tolerability profile consistent with previous studies COG0202 SEQUEL: Safety and Tolerability

9 • Amyloid burden can be measured by PET • Canonical biomarkers assessed via serum and blood • Anatomic changes can be measured by vMRI • Cognition and executive function can be measured with ADAS-Cog and other scales • Neurophysiology / quantitative EEG: - Global and regional brain activity - Regional connectivity Introducing quantitative EEG Biomarkers of Disease

10 • An EEG reading compares electrical activity between electrodes on the scalp • Fast waves in the alpha and beta frequencies dominate healthy EEG patterns • Alzheimer's disease is associated with slower waves – a theta or delta pattern • The dominance of one wave pattern over another is referred to as "relative power" Brain Waves – a Brief Primer

11 Assess safety, tolerability, PK of CT1812 following repeated dosing for 28 days • Evaluate efficacy of CT1812 in restoring synaptic function through quantitative EEG as measured in rank order: - Global relative theta power (primary endpoint) - Global alpha AECC, global relative alpha power, global relative beta power – key pre-specified exploratory endpoints - Additional pre-specified EEG exploratory endpoints SEQUEL: Topline EEG Data

12 SEQUEL Topline Results Positive trends in first three ranked outcomes measures -0.0400 -0.0300 -0.0200 -0.0100 0.0000 0.0100 0.0200 0.0300 Global Relative Theta Power CT1812 Placebo normalizing p=0.123 * Nominally significant -0.02 -0.015 -0.01 -0.005 0 0.005 0.01 0.015 Global Alpha AECc (Connectivity) CT1812 Placebo normalizing * p=0.034 -0.0300 -0.0200 -0.0100 0.0000 0.0100 0.0200 0.0300 Global Relative Alpha Power CT1812 Placebo p=0.149 normalizing

13 • CT1812 treatment was associated with a reduction in global relative theta power Positive trends in brain activity - reduced global & regional theta power - following 4 wks of treatment SEQUEL Topline Results -0.0300 -0.0200 -0.0100 0.0000 0.0100 0.0200 0.0300 Global Relative Theta Power CT1812 Placebo p=0.123

14 • Decreases in relative ​theta power were also observed in specific brain regions: ​frontal, temporal, posterior (parietal ​and occipital), and central - Statistical significance was only achieved in the central region (p<0.006) Positive trends in brain activity - reduced regional theta power - following 4 wks of treatment SEQUEL Topline Results -0.04 -0.03 -0.02 -0.01 0 0.01 0.02 0.03 Regional Relative Theta Power CT1812 Placebo Frontal Temporal Posterior Central p=0.168 p=0.253 p=0.300 p=0.006

15 • In addition, an analysis of the qEEG results showed that CT1812 treatment was associated with greater connectivity between brain regions - This suggests that the brain’s ability to communicate and exchange information between regions can be rescued by CT1812 Positive trends in brain activity - increased connectivity - observed following 4 wks of treatment SEQUEL Topline Results -0.015 -0.01 -0.005 0 0.005 0.01 0.015 0.02 Global Alpha AECc (Connectivity) CT1812 Placebo * p=0.034 * Nominally significant

16 • Increases in relative ​power in the alpha band were observed globally - Fast alpha waves are considered to be part of the normal background rhythm of a healthy brain - ​In Alzheimer’s, alpha waves lose their dominance and are gradually replaced by slower-oscillating, lower-amplitude theta and delta waves ​ Positive trends in brain activity - increased alpha power - observed following 4 wks of treatment SEQUEL Topline Results -0.0300 -0.0200 -0.0100 0.0000 0.0100 0.0200 0.0300 Global Relative Alpha Power CT1812 Placebo p=0.149

17 • CT1812 was well tolerated in this 28-day study - All AEs were mild to moderate - There were no serious or severe AEs - No AEs led to study discontinuation or death​ • Strong trends on pre-specified qEEG measures - Consistent trend across all qEEG measures - Nominally significant treatment differences including global alpha AECc and central relative theta power​ • In conclusion, CT1812 has demonstrated an impact on brain activity in mild-to-moderate Alzheimer’s patients Conclusions

18 • Studies to date provide evidence of: - Target engagement (SNAP) - Anatomical effect (SPARC) - Preliminary cognitive improvement (SHINE cohort A) - Neurophysiology (SEQUEL) • Supportive biomarker evidence of biological effect • Fully funded proof-of-concept studies ongoing: - Early Alzheimer’s disease - Mild-to-moderate Alzheimer’s disease - Dementia with Lewy bodies Evidence of CT1812 Impact on Alzheimer’s Disease

19 Alzheimer's Development DLB Development GA / Dry AMD Development 2019 2020 2021 2022 2023 2024 2025 Ph2 SHINE (COG0201) Mild-Mod AD Ph2 START (COG0203) Early AD Ph2 SEQUEL (COG0202) qEEG Ph2 SHIMMER (COG1201) DLB Ph2 MAGNIFY (COG2201) GA Topline SHINE Topline End-of-Phase 2 meeting SHIMMER Topline End-of-Phase 2 meeting IND clearance Protocol clearance LPI FPI LPI LPI LPI SHINE/SPARC biomarker data Interim analysis (n=24) Multiple Near-term Catalysts Expected

Thank You Tony Caggiano, MD, PhD CMO and Head of R&D 914-221-6730 acaggiano@cogrx.com Lisa Ricciardi President & CEO 917-658-5789 lricciardi@cogrx.com John Doyle Chief Financial Officer 603-860-1078 jdoyle@cogrx.com