Cognition Therapeutics, Inc. · NASDAQ:CGTX
Cognition Therapeutics — Investor Presentation (October 2024)
38 slides from Cognition Therapeutics's investor presentation, Oct 1, 2024
Slide 1: Targeting Amyloid Beta Oligomers: A Disruptive Approach to the Treatment of CNS Disorders
Targeting Amyloid Beta Oligomers: A Disruptive Approach to the Treatment of CNS Disorders September 2024
Slide 2: Forward-Looking Statements
2 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 curren
Slide 3: Cognition Snapshot
3 Cognition Snapshot Successful Phase 2 AD Trial read out plus signal-finding studies ongoing in other indications Alzheimer’s Disease • Pursuing 2 populations: mild-to-moderate; and early / MCI ✓ Achieved goals of Phase 2 SHINE study in mild-moderate AD - Phase 2 START ongoing in early AD with ACTC
Slide 4: SHINE Study in Mild-to-Moderate Alzheimer's disease
SHINE Study in Mild-to-Moderate Alzheimer’s disease Alzheimer’s Disease
Slide 5: Breaking News – SHINE Phase 2 Alzheimer's Disease Study
5 • Pooled (100 and 300mg arms) CT1812 treatment slowed cognitive decline by 39% on ADAS-Cog 11 vs placebo • All key cognitive and functional outcome measures trending in favor of CT1812 • Efficacious dose with good safety profile • Well-designed and executed study • Supports advancing clinical deve
Slide 6: SHINE Phase 2 Study in Adults with Mild-to-Moderate Alzheimer's Disease
6 SHINE Phase 2 Study in Adults with Mild-to-Moderate Alzheimer’s Disease SHINE COG0201 study (NCT03507790) partially funded by $31M NIA grant R01AG058660 Enrollment Criteria Treatment Period 6 months Assessments Program Objectives ‐ AD diagnosis ‐ PET or CSF biomarker definition of AD ‐ MMSE 18-26
Slide 7: SHINE Patient Population
7 • PET- or biomarker-confirmed Alzheimer’s disease • Majority of participants were female (60%), Caucasian (96%), approximately 72 years of age • Mean MMSE score upon entry: 21.37 • ~60% of patients were carriers of the ApoE4 gene • Characteristics well-balanced between all 3 arms SHINE Patient Pop
Slide 8: SHINE Cognitive Endpoints: ADAS-Cog 11 and MMSE
8 SHINE Cognitive Endpoints: ADAS-Cog 11 and MMSE Magnitude of ADAS-Cog 11 decline at 6 months similar to approved MAbs ADAS-Cog 11 MMSE Pooled vs. pbo: 70% slowing Pooled vs. pbo: 39% slowing Note: n's are at Day 182
Slide 9: SHINE Cognitive Endpoints: ADAS-Cog 13, Cognitive Composite
9 SHINE Cognitive Endpoints: ADAS-Cog 13, Cognitive Composite Consistent results across multiple cognitive endpoints ADAS-Cog 13 Cognitive Composite Pooled vs. pbo: 39% slowing Pooled vs. pbo: 50% slowing Note: n's are at Day 182
Slide 10: Summary of SHINE Safety and Tolerability findings
10 • CT1812 demonstrated a favorable safety and tolerability profile • Most TEAEs were mild or moderate in severity • Similar percentages of adverse events in treated (76.5%) and placebo (78%) groups • No discontinuations due to AEs in the 100mg dose group • Most discontinuations were in 300mg dose
Slide 11: SHINE Response at 6 Months Comparable to Approved MAbs
11 SHINE Response at 6 months Comparable to Approved MAbs Once-daily pill • no ARIA • 39% slowing at 6 months vs Leqembi’s 26% at 18 months 1. van Dyck C et al. Lecanemab in Early Alzheimer’s Disease (2023) NEJM 388:9-21 CLARITY1 : ADAS-Cog 14 response in early AD (MMSE 22-30) Adjusted Mean Change f
Slide 12: SHINE: Summary Exploratory Outcomes - Percent Slowing
12 SHINE: Summary Exploratory Outcomes - Percent Slowing Day 182 Effect as large or larger than approved MAbs ADAS-Cog 11 ADAS-Cog 13 MMSE Cognitive Composite CT1812 Pooled1 39% 39% 70% 50% Lecanemab2 (at 18mo) -- 26% (ADAS-Cog 14) -- 24% (ADCOMS) Donanemab3 (at 18 mo) -- 20% (ADAS-Cog 13) 16% (MMSE
Slide 13: SHINE: Corroborated by Experts
Results of a Commissioned Survey of 51 neurologists SHINE: Corroborated by Experts
Slide 14: CT1812 Market Opportunity: Insights from a Survey of Neurologists
14 CT1812 Market Opportunity Insights from a Survey of Neurologists Current Options for Alzheimer’s Disease: • Two recently approved monoclonal antibodies: lecanemab and donanemab • Acetylcholinesterase (AChE) inhibitors: donepezil, galantamine, and rivastigmine • NMDA receptor antagonist: memantine
Slide 15: SHINE Data Feedback from Neurologists
15 Academic medical Center Private practice Community hospital VA center Cross Section of Practice Setting General neurology Memory disorder specialist Movement disorder specialist Cross Section of Specialties SHINE Data Feedback from Neurologists Surveyed diverse group of 51 neurologists who treat
Slide 16: Most Appealing Features of CT1812's Product Profile
16 0 2 4 6 8 10 Efficacy Safety Tolerability Dosing Route of Administration Most Appealing Features of CT1812’s Product Profile (10-pt scale) CT1812’s Safety and Oral Delivery Appealed to Neurologists “Ease of dosing as oral medication” “Oral medication without ARIA risks” “Pill form is always welco
Slide 17: Neurologists Enthusiastic About SHINE Results
17 Extremely Positive Positive Neutral Negative Overall Characterization of SHINE Results Neurologists Enthusiastic About SHINE Results Oral, once-daily treatment with cognitive benefit and no increased ARIA risk Appx 84% felt SHINE was positive or extremely positive • The absence of symptomatic ARI
Slide 18: Efficacy Findings Viewed as Significant
18 Efficacy Findings in Particular were Viewed as Significant • Importance on cognitive outcomes echoed in open discussion of the most attractive aspects of the SHINE results - “Consistent improvement in all clinical outcomes” - “Efficacy as good as, or better, than currently promoted anti-amyloid a
Slide 19: Next Steps: Larger Studies with Longer Duration
19 In discussion of next steps for CT1812, neurologists expressed interest in: • Treatment effect in combination with and/or head-to-head against anti amyloid drugs • Treatment effect in combination with and/or head-to-head against AChEi + Namenda • Larger placebo-controlled studies to see longer-te
Slide 20: If Approved, Neurologists Would Consider CT1812
20 58.4% 62.8% • What percentage of your mild patients would you consider candidates for CT1812? • What percent of your moderate patients would you consider candidates for CT1812? If Approved, Neurologists Would Consider CT1812 Monotherapy and combination uses appealed to clinicians 98% of Responden
Slide 21: START Study in early Alzheimer's disease
START Study in early Alzheimer’s disease Alzheimer’s Disease
Slide 22: START - A 540-Person Study in Early AD
22 START - A 540-Person Study in Early AD First study to allow lecanemab as background therapy in combination with CT1812 START COG0203 study (NCT05531656) partially funded by $81M NIA grant R01AG065248 Enrollment Criteria Treatment Period 6 months Assessments Program Objectives ‐ Ages 50-85 ‐ Diagn
Slide 23: CT1812 Also Being Investigated in Two Additional Indications
23 CT1812 is Also Being Investigated in two Additional Indications Alzheimer’s Disease Dementia with Lewy Bodies Dry AMD Geographic Atrophy
Slide 24: Dementia with Lewy Bodies
“The most common dementia you’ve never heard of” Dementia with Lewy Bodies
Slide 25: Lewy Body Dementias are Second only to AD in Prevalence
25 • In the U.S. an estimated 1.4 million people1 have dementia with Lewy bodies (DLB) • It is estimated that 50-80% of patients with DLB have Aβ as well as α-synuclein2 pathology • Core symptoms of DLB include: - Progressive cognitive decline - Fluctuating cognition with variations in attention - I
Slide 26: Evidence Supports CT1812 Potential in DLB
26 Evidence Supports CT1812 Potential in DLB -synuclein oligomers -synuclein oligomers + CT1812 -Synuclein oligomers in red Limegrover CS, et al. J Neurosci Res. 2021. doi: 10.1002/jnr.24782 Neurons rescued from α-synuclein oligomer-induced damage Protection of neurons from α-synuclein oligomers
Slide 27: SHIMMER Study Brings Together Experts and New Tools
27 • Until recently, DLB could only be confirmed upon autopsy, making clinical research difficult • SHIMMER was designed to have the best chance available to detect signals of improvement - Cognition partnered with experts at U Miami Miller School of Medicine and LBDA - Using validated clinical1 and
Slide 28: SHIMMER Study in Dementia with Lewy Bodies
28 SHIMMER Study in Dementia with Lewy Bodies Conducted in collaboration with experts at LBDA and University of Miami SHIMMER COG1201 study (NCT05225415) partially funded by $30M NIA grant R01AG071643 Enrollment Criteria Treatment Period 6 months Assessments Program Objectives ‐ Age 50-85 ‐ DLB diag
Slide 29: Geographic Atrophy
Damage to the macula resulting from advanced dry age-related macular degeneration (dry AMD) Geographic Atrophy
Slide 30: Rationale for CT1812 in Dry AMD/Geographic Atrophy
30 Rationale for CT1812 in Dry AMD/Geographic Atrophy Opportunity: crosses blood-retinal barrier to reach retina without an injection What is dAMD/GA Geographic atrophy (GA), the most advanced form of dry AMD, effects ~5M people WW and is associated with significant vision loss Unmet Need Complement
Slide 31: Dry AMD and Geographic Atrophy
31 20 million people in North America have AMD3 • AMD is leading cause of blindness over 50 yr1 • Dry AMD is a progressive condition accounting ~90% of all AMD cases - Advanced dry AMD, or GA, affects approximately two million people in the U.S. • Only two drugs are approved for dry AMD2 - Until 202
Slide 32: CT1812 Protects RPE Cells and the Photoreceptors they Support
32 • Photoreceptors – specialized neurons necessary for sight – require support from retinal pigment epithelial (RPE) cells that are damaged in dry AMD • CT1812 has been shown to rescue RPE cells in vitro • CT1812’s potential to preserve vision through this mechanism is being tested in Phase 2 CT181
Slide 33: Cellular and Molecular Pathogenesis of Dry AMD
33 Cellular and Molecular Pathogenesis of Dry AMD (dAMD) Receptor-bound POS Lysosome (LAMP 1/2) Autophagy Body (LC3b) Early Compartment (Rab 5) Rab 7 In dry AMD, RPE cells are unable to successfully recycle photoreceptor outer segments ( ) through the autophagy process CT1812 restores trafficking an
Slide 34: MAGNIFY Trial in dAMD/GA
34 MAGNIFY Trial in dAMD/GA Potential first oral drug for geographic atrophy Enrollment Criteria Treatment Period 6 months Assessments Program Objectives ‐ Age: ≥ 50 ‐ Diagnosis of dry AMD ‐ BCVA ≥ 24 letters (ETDRS) ‐ GA lesion ≥ 2.5 and ≤17.5mm2 ‐ Change in GA lesion area (FAF) ‐ Ellipsoid zone ar
Slide 35: Completed Studies Support Potential; Ongoing Trials Expand CT1812
35 Completed Studies Support Potential in Mild-to-Moderate AD SPARC2 • 23 participants • Preservation of brain atrophy via volumetric MRI • No change in SV2A treated or pbo SNAP3 • 3 participants • Rapid displacement of Aβ oligomers via CSF • Replication of preclinical findings via MEI SEQUEL1 • 16
Slide 36: The Promise of CT1812
36 The Promise of CT1812 • First-in-class Aβ oligomer antagonism via sigma-2 receptor • Consistent efficacy in Alzheimer’s disease studies - ARIA unlikely to occur based on MoA • Potential first-to-market for DLB • Potential first oral for dAMD/GA • Well tolerated safety profile anticipated • Oral a
Slide 37: Current Financial Position
37 Current Financial Position Cash and cash equivalents $28.5 M Expected cash runway into 2Q 2025 Grant funding for CT1812 studies Preclinical through Phase 2 ~$171 M Approximate funding used ($113.7 M) Remaining grant funding $57.3M As of June 30, 2024
Slide 38: Thank You
Tony Caggiano, MD, PhD CMO and Head of R&D acaggiano@cogrx.com Lisa Ricciardi President & CEO lricciardi@cogrx.com John Doyle Chief Financial Officer jdoyle@cogrx.com Thank You
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