Lexeo Therapeutics, Inc. · NASDAQ:LXEO
Lexeo Therapeutics — Investor Presentation (August 2026)
35 slides from Lexeo Therapeutics's investor presentation, Aug 12, 2026
Slide 1: Lexeo Therapeutics Corporate Overview August 2026
Lexeo Therapeutics Corporate Overview August 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, the anticipated benefits of its current product c
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: Building a leading cardiac gene therapy platform
Building a leading cardiac gene therapy platform Differentiated AAVrh.10 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 Operating experien
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 Proven clinical experience with 27 patients treated using AAVrh.10 Cardiomyopathies have few disease-
Slide 6: Lexeo's AAVrh.10 is a highly differentiated capsid
Lexeo’s AAVrh.10 is a highly differentiated capsid Lexeo’s AAVrh.10 is a highly differentiated capsid AAVrh.10 has been utilized systemically across LX2006 and LX2020 with no clinically significant complement activation. Both LX2006 and LX2020 have been generally well-tolerated to date Significant e
Slide 7: Optimized Sf9 baculovirus manufacturing platform
Lexeo's optimized Sf9 baculovirus platform combines differentiated manufacturing, attractive economics and demonstrated commercial readiness High yield, strong product quality, and an FDA-endorsed commercial manufacturing process position Lexeo for attractive economics and execution readiness across
Slide 8: Two clinical stage programs address devastating cardiac diseases
Lexeo’s two clinical stage programs address devastating cardiac diseases Leveraging gene therapy to address devastating cardiac diseases with no existing disease-modifying treatments Focus: LX2006 Potential first disease-modifying gene therapy for FA cardiomyopathy Only program with clinical-stage d
Slide 9: Our pipeline
Our pipeline 1 - Friedreich ataxia. 2 - Plakophilin 2 Arrhythmogenic Cardiomyopathy. 3 - Desmoplakin. Programs: Indication: Gene: Phase I/II Phase II/III CARDIOVASCULAR FXN PKP2 GJA1 (encoding for CX43 protein) TNNI3 Lexeo retains global rights across all programs LX2006 LX2020 LX2021 LX2022 Preclin
Slide 10: Friedreich Ataxia Cardiomyopathy (FA-CM) LX2006
Friedreich Ataxia Cardiomyopathy (FA-CM) LX2006
Slide 11: 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 12: Cardiac symptoms may be absent or under-recognized
Cardiac symptoms may be absent or under-recognized even as cardiomyopathy evolves, supporting the need for earlier evaluation and coordinated neurology-cardiology care Typical age of onset between 5-15 Most early signs are movement-related Small subset of children (~5%) present with cardiac symptoms
Slide 13: LX2006 potential to treat the root cause of FA cardiomyopathy
LX2006 has the potential to treat the root cause of FA cardiomyopathy: significant decrease in frataxin in the heart AAV, Adeno-Associated Virus; CAG, Chicken Beta-Actin; cDNA, Copy DNA; FA, Friedreich Ataxia; FXN, Frataxin; Poly-A, Poly Adenosine. AAVrh.10hFXN LX2006 construct: Ubiquitous promoter
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 clinical data show sustained or deepening improvements
LX2006 clinical data show sustained or deepening improvements across cardiac measures of FA; LX2006 generally well tolerated LX2006 generally well tolerated across 17 participants dosed with no Grade 3 treatment-related SAEs to date No clinically significant complement activation Minimal, transient
Slide 16: 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 17: 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 18: Finalized SUNRISE-FA pivotal protocol and SAP for LX2006
Finalized SUNRISE-FA 2 pivotal protocol and SAP for LX2006 Study design: Open-label pivotal study with untreated control arm (no placebo or sham) Dose: 1.2x1012 vg/kg, one-time IV infusion Sample Size: 26 participants, 13 participants treated with LX2006 Key Eligibility Criteria: 16 years and older:
Slide 19: SUNRISE-FA Is Supported by Clinical Evidence and Robust Study Design
SUNRISE-FA 2 Is Supported by Clinical Evidence, Robust Study Design and Execution Readiness Phase I/II data exceeded pivotal-study assumptions, statistical simulations signal potential to meet the primary endpoint, and operational execution is already underway, providing multiple sources of confiden
Slide 20: LX2006 Has Potential to Improve Outcomes Across the Disease Continuum
Patient Impact LX2006 Has Potential to Improve Outcomes Across the Disease Continuum in FA No Cardiomyopathy Mild Cardiomyopathy Moderate Cardiomyopathy Severe Cardiomyopathy Cardiac Disease4 Increasing cardiac dysfunction Increasing mortality risk Loss of ambulation, shortness of breath, arrythmias
Slide 21: Addressable FA patients concentrated within small network of specialty centers
Addressable FA patients are concentrated within a small network of specialty centers, creating a clear and efficient path to patient identification, referral, and treatment for LX2006 if approved Majority of FA patients are managed at a limited number of specialized treatment centers. Most target pa
Slide 22: Strong path forward for LX2006
Strong path forward for LX2006 SUNRISE-FA 2 Initiated with First Patient Enrolled in June 2026 Differentiated AAVrh.10 Capsid and Commercial-Ready CMC Supply Chain Phase I/II Results Exceed the Effect Size in LVMi Used to Power the Pivotal Study Building Internal Commercial Capabilities to Support S
Slide 23: Plakophilin Arrhythmogenic Cardiomyopathy (PKP2-ACM) LX2020
Plakophilin 2 Arrhythmogenic Cardiomyopathy (PKP2-ACM) LX2020
Slide 24: 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 Approximately 23% of individuals with ACM experience SCD as the prese
Slide 25: 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 ACM, arrhythmogenic cardiomyopathy. PKP2 cDNA (full length gene) Rabbit β-globin polyA AAVrh.10hPKP2 LX2020 construct: Cardiac-specific promoter Pro
Slide 26: 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, at >100 bpm, lasting under 30 seconds2; self-terminating Closely associated with increased ris
Slide 27: 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 28: Sustained VT risk predicted by PVC burden and non-sustained VT
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 29: 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 30: HEROIC-PKP2 phase I/II study design
LX2020 is being evaluated in an ongoing phase I/II 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
Slide 31: Interim results demonstrate increased PKP2 expression
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 32: Preclinical Programs
Preclinical Programs
Slide 33: 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 Significant unmet need characterized by extensive fibrosis, high arrh
Slide 34: Clear clinical and regulatory milestones supported by a strong balance sheet
Clear clinical and regulatory milestones supported by a strong balance sheet LX2006 Continued FDA engagement on confirmatory evidence strategy; update expected once finalized Topline data readout expected in second half of 2027 Potential BLA submission under accelerated approval pathway in first hal
Slide 35: Thank You
‘therapeutics Thank You
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