Cognition Therapeutics : CGTX Corporate Deck

Targeting Amyloid Beta Oligomers:

A Disruptive Approach to the Treatment of Alzheimer's Disease

June 2024

Forward-looking Statements

FORWARD-LOOKING STATEMENTS

This presentation contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. All statements contained in this presentation, other than statements of historical facts or statements that relate to present facts or current conditions, including but not limited to, statements regarding our cash, financial resources and product candidates, including CT1812, and any expected or implied benefits or results, including that initial clinical results observed with respect to CT1812 will be replicated in later trials, and our clinical development plans, including statements regarding our clinical studies of CT1812 in animal models and any analyses of the results therefrom, are forward-looking statements. These statements, including statements related to the timing and expected results of our clinical trials, involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance, or achievements to be materially different from any future results, performance, or achievements expressed or implied by the forward-looking statements. In some cases, you can identify forward-looking statements by terms such as "may," "might," "will," "should," "expect," "plan," "aim," "seek," "anticipate," "could," "intend," "target," "project," "contemplate," "believe," "estimate," "predict," "forecast," "potential" or "continue" or the negative of these terms or other similar expressions. We have based these forward-looking statements largely on our current expectations and projections about future events and financial trends that we believe may affect our business, financial condition, and results of operations. These forward-looking statements speak only as of the date of this presentation and are subject to a number of risks, uncertainties and assumptions, some of which cannot be predicted or quantified and some of which are beyond our control. Factors that may cause actual results to differ materially from current expectations include, but are not limited to: competition, our ability to secure new (and retain existing) grant funding, our ability to grow and manage growth, maintain relationships with suppliers and retain our management and key employees; our ability to successfully advance our current and future product candidates through development activities, preclinical studies and clinical trials and costs related thereto; uncertainties inherent in the results of preliminary data, preclinical studies and earlier-stage clinical trials being predictive of the results of early or later-stage clinical trials; the timing, scope and likelihood of regulatory filings and approvals, including regulatory approval of our product candidates; changes in applicable laws or regulations; the possibility that the we may be adversely affected by other economic, business or competitive factors, including ongoing economic uncertainty; our estimates of expenses and profitability; the evolution of the markets in which we compete; our ability to implement our strategic initiatives and continue to innovate our existing products; our ability to defend our intellectual property; impacts of ongoing global and regional conflicts; the impact of the COVID-19 pandemic on our business, supply chain and labor force; and the risks and uncertainties described more fully in the "Risk Factors" section of our annual and quarterly reports filed with the Securities & Exchange Commission that are available on www.sec.gov. These risks are not exhaustive, and we face both known and unknown risks. You should not rely on these forward-looking statements as predictions of future events. The events and circumstances reflected in our forward-looking statements may not be achieved or occur, and actual results could differ materially from those projected in the forward-looking statements. Moreover, we operate in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties that we may face. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise.

TRADEMARKS

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MARKET & INDUSTRY DATA

Projections, estimates, industry data and information contained in this presentation, including the size of and growth in key end markets, are based on information from third-party sources and management estimates. Although we believe that these third party-sources are reliable, we cannot guarantee the accuracy or completeness of these sources. Our management's estimates are derived from third-party sources, publicly available information, our knowledge of our industry and assumptions based on such information and knowledge. Our management's estimates have not been verified by any independent source. All of the projections, estimates, market data and industry information used in this presentation involve a number of assumptions and limitations, and you are cautioned not to give undue weight to such information. In addition, projections, estimates and assumptions relating to us and our industry's future performance are necessarily subject to a high degree of uncertainty and risk due to a variety of factors, including, but not limited to, those described above, that could cause future performance to differ materially from our expressed projections, estimates and assumptions or those provided by third parties.

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Overview

THE CHALLENGE

Despite 35 years of research based on the Amyloid Cascade Hypothesis, there is only ONE approved therapy and major unmet needs persist for the rapidly growing population of people with Alzheimer's Disease

THE OPPORTUNITY

Strong scientific evidence supports the Amyloid Oligomer Hypothesis, ie, that oligomers-notplaques-are the MOST NEUROTOXIC form of amyloid beta that underlie cognitive decline

OUR SOLUTION

Lead asset is CT1812: An oral small molecule that potently antagonizes amyloid oligomers via a unique mechanism of action

• Currently in two PHASE 2 AD trials: early-mild (currently enrolling) and mild-moderate (results expected mid-2024)
• In clinical trials for two additional CNS/retina indications based on its MOA
• Clinical studies, including completion of Phase 1, show promising EFFICACIOUS effects with good tolerability
• Completely REVERSES cognitive dysfunction in preclinical models of AD

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CGTX Overview

First-in-Class Science

Late-Stage Pipeline

Multi-billion Dollar Opportunities

Financially Disciplined

Experienced Leadership Team

Scientific leaders advance understanding of oligomer toxicity in Alzheimer's disease

Advancing mid-to-late-stage clinical trials in multiple indications in mild-to- moderate Alzheimer's disease and DLB

Targeting multi-billion-dollar diseases; under-served markets; potential first- to-market in mild-to-moderate dementia with Lewy bodies

Major trials supported by $171 million non-dilutive grants from NIH and others. Cash runway through 2Q 2025

Executive team with big pharma leadership experience; R&D staff with depth of neuroscience drug development expertise

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The Science of Oligomers

What are Amyloid Beta Oligomers?

Small, globular protein aggregates that form early in the process of amyloid growth and exhibits characteristics that are distinct from amyloid monomers, fibrils, and plaques

Aβ Monomers

Aβ Oligomers

Dimer

Trimer

Quadramer

Pentamer

Hexamer

Dodecamer

• Bredo L, et al. FEBS Letters. 2015;589:2640-2648

The Amyloid Cascade has Driven Alzheimer's Disease Research for the Past 35 Years

APP	Aß	Aß	Aß	Aß
	monomers	oligomers	protofibrils	fibrils

Amyloid

plaque

• Chen G, et al. Acta Pharmacologica Sinica. 2017:1205-1235

Two Decades of Research has Shown: Amyloid Oligomers are the Primary Driver of Cognitive Decline in Alzheimer's Disease

APPAß monomers

Aß

oligomers

Aß	Aß
protofibrils	fibrils

• Chen G, et al. Acta Pharmacologica Sinica. 2017:1205-1235

Aβ Oligomers Instigate Multiple Facets of AD Neuropathology

Neural death

Plasticity

dysfunction

Synapse

deterioration

Aβ

Oligomers

Oxidative	Microglia
stress	activation

Tau

phosphorylation

• Cline EN, et al. J Alzheimer's Dis. 2018;64:S567-S610

Genetic and Preclinical Evidence Supports this Consensus

Genetic evidence points to Aβ-mediatedneuro-toxicity as primary driver of Alzheimer's disease

• Osaka mutation
• • High Aβ oligomer levels  much higher risk of AD4
  • Consistent with real-world evidence correlating high Aβ oligomer brain level with AD symptom severity5
• APOE4/4 mutation
• • 3X higher Aβ oligomers in homozygotes  10-12Xhigher risk of aggressive AD6-8
• Icelandic mutation
• • Low Aβ oligomer levels & low binding affinity  much lower risk of AD9
• Arctic mutation
• • Reduced Aβ clearance and increased Aβ protofibril formation
     risk of early-onset aggressive AD10

Preclinical data supports role of Aβ-mediated neurotoxicity in cognitive deficit

• Aβ oligomers  neuro- and synapto- toxicity11-15
• Aβ oligomers injected into rodent hippocampus  memory loss16,17
• Aβ oligomer accumulation in transgenic models  memory loss18,19

11 See Reference Slide