Lexeo Therapeutics, Inc. · NASDAQ:LXEO

Lexeo Therapeutics — Investor Presentation (January 2026)

23 slides from Lexeo Therapeutics's investor presentation, Jan 12, 2026

  1. Slide 1: Lexeo Therapeutics Corporate Overview January 2026

    Lexeo Therapeutics Corporate Overview January 2026 Exhibit 99.3

  2. Slide 2: Forward-looking statements

    Forward-looking statements This presentation contains “forward-looking statements” within the meaning of the federal securities laws, including, but not limited to, Lexeo’s expectations and plans regarding its current product candidates and programs and the timing for receipt and announcement of dat

  3. Slide 3: Dedicated to reshaping heart health through pioneering science

    Dedicated to reshaping heart health by applying pioneering science to fundamentally change how cardiovascular disease is treated Genetic medicine leader with rare cardiac disease focus Proven experience in the clinic Platform designed for safety and scalability Individuals and families impacted by F

  4. Slide 4: Building a leading cardiac gene therapy platform

    Building a leading cardiac gene therapy platform Differentiated AAVrh10 capsid Genetic cardiac disease expertise Innovative AAV manufacturing Operating experience Deep cardiac genetic medicine know-how, anchored by two clinical and two preclinical programs Strong financial position Cash runway into

  5. Slide 5: Advancing cardiac genetic medicines in diseases with high unmet need

    Advancing cardiac genetic medicines in diseases with high unmet need Lexeo cardiac programs and expertise: Clinical: LX2006 Friedreich Ataxia Cardiomyopathy LX2020 PKP2 Arrhythmogenic Cardiomyopathy LX2021 Desmoplakin Cardiomyopathy LX2022 Hypertrophic Cardiomyopathy Cardiomyopathies have few diseas

  6. Slide 6: Lexeo's AAVrh10 is a highly differentiated capsid

    Majority of mortality and severe complement activation in gene therapy at doses ≥1.0E14 vg/kg Lexeo’s AAVrh10 is a highly differentiated capsid Strong expression in the heart AAVrh10 cardiac tropism No history of clinically significant complement activation Cardiac tropism can reduce systemic dose l

  7. Slide 7: Lexeo manufactures AAVrh10 utilizing an optimized Sf9 baculovirus process

    Lexeo manufactures AAVrh10 utilizing an optimized Sf9 baculovirus process Innovative approach High yield, high quality Sf9 baculovirus manufacturing platform compared to conventional manufacturing (e.g. HEK based) Optimal potency Higher yields (1.0E15 vg/L) Greater downstream recovery (>55%) Fewer e

  8. Slide 8: 2025 year in review

    2025 year in review Announced positive data from Phase I/II studies Completed enrollment in HEROIC Phase I/II study Completed two financings totaling $234M of capital; secured runway into 2028 Received FDA Breakthrough Designation Shared interim Phase I/II safety and efficacy data from low dose coho

  9. Slide 9: Our pipeline: focused on diseases with significant unmet need

    Our pipeline: focused on diseases with significant unmet need and clear mechanisms Programs: Indication: Gene: Phase I/II Phase II/III 2026 milestones: CARDIOVASCULAR FXN PKP2 CX43 TNNI3 Lexeo retains global rights across all programs. ~5K US prevalence ~60K US prevalence ~35K US prevalence ~25K US

  10. Slide 10: Friedreich Ataxia Cardiomyopathy (FA-CM) LX2006

    Friedreich Ataxia Cardiomyopathy (FA-CM) LX2006

  11. Slide 11: Cardiac complications are the leading cause of death in Friedreich Ataxia

    Cardiac complications are the leading cause of death in Friedreich Ataxia Ron and his son, Keith, who passed from FA cardiomyopathy at age 24. There are no approved treatments for the cardiomyopathy of FA. Time is of the essence.” - Ron Bartek, Co-founder of FARA Prevalence: Mortality: ~5,000 ~15,00

  12. Slide 12: LX2006 has the potential to treat the root cause of FA cardiomyopathy

    LX2006 has the potential to treat the root cause of FA cardiomyopathy: the significant decrease in frataxin in the heart AAVrh.10hFXN LX2006 construct: LX2006 mechanism: FXN deficiency results in mitochondrial dysfunction and leads to deficient energy production in hypertrophic cardiomyocytes Transf

  13. Slide 13: Lexeo's role in advancing FA cardiomyopathy research

    Lexeo’s role in advancing FA cardiomyopathy research Objective: Assess the safety and efficacy of LX2006 in individuals with cardiomyopathy associated with FA Dose: 1.8E11 vg/kg (Cohort 1), 5.6E11 vg/kg (Cohort 2), 1.2E12 vg/kg (Cohort 3) Key Endpoints: frataxin expression, LVMI, lateral wall thickn

  14. Slide 14: LX2006 clinical data show sustained or deepening improvements

    LX2006 clinical data show sustained or deepening improvements in the majority of participants across both cardiac and neurologic measures of FA LX2006 generally well tolerated across 17 participants dosed with no Grade 3+ SAEs to date No clinically significant complement activation Minimal, transien

  15. Slide 15: Plakophilin-2 Arrhythmogenic Cardiomyopathy (PKP2-ACM) LX2020

    Plakophilin-2 Arrhythmogenic Cardiomyopathy (PKP2-ACM) LX2020

  16. Slide 16: Arrhythmogenic cardiomyopathy caused by mutations in the PKP2 gene

    Arrhythmogenic cardiomyopathy caused by mutations in the PKP2 gene: devastating genetic heart disease with clearly defined mechanism PKP2-ACM is a rare, genetic cardiac disease caused by loss of function mutations in the PKP2 gene Progressive replacement of cardiac muscle with fatty fibrotic tissue,

  17. Slide 17: LX2020 delivers a full-length PKP2 gene to cardiomyocytes

    Mutations in the PKP2 gene are the most common genetic cause of ACM; LX2020 delivers a full-length PKP2 gene to cardiomyocytes, restoring the desmosome PKP2 cDNA (full length gene) Rabbit β-globin polyA AAVrh.10hPKP2 LX2020 construct: PKP2-ACM: LX2020 mechanism: Cardiac-specific promoter Absence of

  18. Slide 18: Individuals with ACM experience high arrhythmia burden

    Individuals with ACM experience high arrhythmia burden with a spectrum of severity Early indicator of electrical instability that can trigger more severe/sustained arrhythmia >3 ventricular beats in a row, lasting under 30 seconds; self-terminating Closely associated with increased risk of sustained

  19. Slide 19: Lexeo's role in advancing PKP2-ACM research

    Phase I/II Trial Lexeo’s role in advancing PKP2-ACM research Retrospective EMR Review and Prospective Observational Natural History Study Objective: Assess the safety and efficacy of LX2020 in individuals with PKP2-ACM Dose: 2.0E13 vg/kg (Cohort 1), 6.0E13 vg/kg (Cohorts 2, 3) Key Endpoints: PKP2 ex

  20. Slide 20: Interim results demonstrate increased PKP2 expression and reduced arrhythmia burden

    Interim results demonstrate increased PKP2 expression and potential for LX2020 to reduce severe arrhythmia burden n=3 n=8 n=5 n=5 n=2 n=3 n=3 n=8 n=5 n=5 n=2 n=3 Mean PKP2 change from baseline (western blot, GAPDH normalized) Mean PVC change PVCs reduced or stabilized in majority of participants wit

  21. Slide 21: Lexeo is also advancing two preclinical cardiac gene therapy programs

    Lexeo is also advancing two preclinical cardiac gene therapy programs LX2021 +2026 research collaboration with Johnson & Johnson exploring novel routes of administration for cardiac AAV gene therapy to maximize safety and efficacy LX2021 Desmoplakin Cardiomyopathy LX2022 Hypertrophic Cardiomyopathy

  22. Slide 22: Lexeo – a leader in cardiac gene therapy

    Lexeo – a leader in cardiac gene therapy Leader in cardiac genetic medicine addressing high unmet need and clear market opportunity Catalyst rich 2026 with multiple key milestones expected across two clinical stage programs Differentiated AAVrh10 capsid and innovative Sf9 baculovirus manufacturing p

  23. Slide 23: Thank You

    therapeutics Thank You

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