Lexeo Therapeutics, Inc. · NASDAQ:LXEO
Lexeo Therapeutics — Investor Presentation (March 2026)
32 slides from Lexeo Therapeutics's investor presentation, Mar 30, 2026
Slide 1: Lexeo Therapeutics Corporate Overview March 2026
Lexeo Therapeutics Corporate Overview March 2026 Exhibit 99.2
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
Slide 3: Reshaping heart health with 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
Slide 4: Advancing cardiac genetic medicines in diseases with high unmet need
Lexeo: advancing cardiac genetic medicines in diseases with high unmet need Leveraging gene therapy to address devastating cardiac diseases with no existing disease-modifying treatments Focus: LX2006 Only program with clinical-stage data in FA cardiomyopathy, which accounts for death in up to 80% of
Slide 5: Cardiac complications are the leading cause of death in Friedreich Ataxia
Cardiac complications are the leading cause of death in Friedreich Ataxia 1 - Payne R.M. JACC Basic Transl Sci, 2022;13;7(12):1267-1283. - Friedreich’s Ataxia Research Alliance, 2024. - Norrish G., et al. Arch Dis Child, 2022;107(5), 450–455. - Reetz, K., et al. Lancet Neurol, 2025;24(7):614-624. FA
Slide 6: Building a leading cardiac gene therapy platform
Building a leading cardiac gene therapy platform Differentiated AAVrh10 capsid Proven cardiac tropism allows for lower doses and improved therapeutic index Innovative AAV manufacturing Optimized Sf9 baculovirus manufacturing platform designed to support future commercial scale-up Genetic cardiac dis
Slide 7: 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 Proven clinical experience with 27 patients treated using AAVrh10 Cardiomyopathies have few disease-m
Slide 8: Compelling cardiac tropism of AAVrh10 capsid
Yucatan Minipig Biodistribution(1) NHP Biodistribution(2) I-124 Vector Levels (% total body) Compelling Cardiac Tropism Greater Trends of Functional Improvement Versus AAV9 in PKP2-ACM Model(1) Greater Increase in EF Greater Reduction in EDV Greater Reduction in ESV +61% +32% -28% -18% -37% -23% Not
Slide 9: Lexeo manufactures AAVrh10 using optimized Sf9 baculovirus process
Lexeo manufactures AAVrh10 utilizing an optimized Sf9 baculovirus process Optimal potency Higher yields (1.0E15 vg/L) Greater downstream recovery (>55%) Fewer empty AAV capsids (<25%) Improved genomic purity owing to lack of plasmid transfections Scalable manufacturing Sustainable and defined starti
Slide 10: Our pipeline: focused on diseases with significant unmet need
Our pipeline: focused on diseases with significant unmet need and clear mechanisms 1 - Friedreich ataxia. 2 - Plakophilin 2 Arrhythmogenic Cardiomyopathy. 3 - Desmoplakin. Programs: Indication: Gene: Phase I/II Phase II/III 2026 milestones: CARDIOVASCULAR FXN PKP2 CX43 TNNI3 Lexeo retains global rig
Slide 11: Friedreich Ataxia Cardiomyopathy (FA-CM) LX2006
Friedreich Ataxia Cardiomyopathy (FA-CM) LX2006
Slide 12: Cardiac complications are the leading cause of death in Friedreich Ataxia
Cardiac complications are the leading cause of death in Friedreich Ataxia 1 - Payne R.M. JACC Basic Transl Sci, 2022;13;7(12):1267-1283. - Friedreich’s Ataxia Research Alliance, 2024. - Norrish G., et al. Arch Dis Child, 2022;107(5), 450–455. - Reetz, K., et al. Lancet Neurol, 2025;24(7):614-624. FA
Slide 13: Timely, multidisciplinary care is critical to manage FA cardiomyopathy
Timely, multidisciplinary care is critical to diagnose and manage FA cardiomyopathy There are no approved treatments for the cardiomyopathy of FA. Time is of the essence. Ron Bartek, Co-founder of FARA Ron Bartek and his son, Keith, who passed from FA cardiomyopathy at age 24 - Regner S, et al. Amer
Slide 14: Elevated LVMI predicts mortality in FA
Elevated LVMI predicts mortality in FA and is not expected to decrease significantly without intervention HR - Hazard Ratio; CI - Confidence Internal; LVMI - Left Ventricular Mass Index. Note: 10g/m2 represents approximately 10% change in LVMI based on echocardiography measurements of upper bound of
Slide 15: LX2006 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 Frataxin deficiency results in mitochondrial dysfunction and leads to deficient energy production in hypertrophic cardiomyocytes Transfer of FXN gene to cardiomyocytes is intended
Slide 16: LX2006 evaluated in SUNRISE-FA and Weill Cornell trials
LX2006 is being evaluated in parallel Lexeo-sponsored SUNRISE-FA and Weill Cornell investigator-initiated trials SUNRISE-FA and Weill Cornell trials share a similar study design, enabling data from the two studies to be evaluated together 2 Key Inclusion Criteria 3 Key Measurements 1 Study Design &
Slide 17: LX2006 clinical data show improvements across cardiac and neurologic measures
LX2006 clinical data show sustained or deepening improvements across both cardiac and neurologic measures of FA LX2006 generally well tolerated across 17 participants dosed with no Grade 3 treatment-related SAEs to date No clinically significant complement activation Minimal, transient LFT elevation
Slide 18: Cardiac function improvement in individual with later stage cardiomyopathy
Cardiac function improvement observed in individual with later stage cardiomyopathy Effect of LX2006 on Cardiac Function Majority of Participants (16/17) Baseline LVEF: Normal Post therapy: No change One Participant (#13) with later stage cardiomyopathy Baseline LVEF: Low (35%) Post Therapy: Signifi
Slide 19: Change in mFARS: Open Label Cohort vs. UNIFAI Matched Control
Mean Change from Baseline (95% CI) Change in mFARS: Open Label Cohort (n=16) vs. UNIFAI Matched Control (n=45) mFARS validated clinical scale measures FA neurological progression; higher scores represent disease worsening Majority of LX2006-treated participants demonstrate mFARS improvement or stabi
Slide 20: Plakophilin Arrhythmogenic Cardiomyopathy (PKP2-ACM) LX2020
Plakophilin 2 Arrhythmogenic Cardiomyopathy (PKP2-ACM) LX2020
Slide 21: 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,
Slide 22: LX2020 delivers 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 ACM, arrhythmogenic cardiomyopathy. PKP2 cDNA (full length gene) Rabbit β-globin polyA AAVrh.10hPKP2 LX2020 construct: Cardiac-specific promoter Pro
Slide 23: 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
Slide 24: PVCs may trigger ventricular tachycardia
Premature ventricular contractions (PVCs) may trigger ventricular tachycardia (VT); measures are related but driven by potentially different mechanisms (1) Cerrone et al. Nature Comm, 2017. (2) Kim et al. Circulation, 2019. (3) Sato P. et al. Circulation Research, 2009. (4) Oxford E.M et al. Circula
Slide 25: Sustained VT risk predicted by PVC burden and NSVT events
In people with ACM, sustained VT risk is predicted by increased PVC burden and by non-sustained VT events PVC burden in ACM decreases initially after diagnosis but persists long term1 Initial drop driven by lifestyle change (exercise modification) and medication PVCs remain elevated (>500/24h) and v
Slide 26: 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
Slide 27: LX2020 ongoing phase 1/2 study (HEROIC-PKP2)
LX2020 is being evaluated in an ongoing phase 1/2 study (HEROIC-PKP2); enrollment completed in Q4 2025 2 Key Inclusion Criteria 3 Key Measurements 1 Study Design & Objective Design: 52-week open-label study with a 4-year long term follow up Objective: To assess the safety and efficacy of LX2020 in i
Slide 28: Interim results show 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 change in PKP2 expression from baseline (western blot) Mean PVC change PVCs reduced or stabilized in majority of participants with >6
Slide 29: Preclinical Programs
Preclinical Programs
Slide 30: Lexeo advancing two preclinical cardiac gene therapy programs
Lexeo is also advancing two preclinical cardiac gene therapy programs +2026 research collaboration with Johnson & Johnson exploring novel routes of administration for cardiac AAV gene therapy to maximize safety and efficacy LX2021 High unmet need characterized by extensive fibrosis, high arrhythmic
Slide 31: 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
Slide 32: Thank You
therapeutics Thank You
Lexeo Therapeutics — Investor Presentation (March 2026) on 6ix