TNYA Tenaya Therapeutics Inc

Exhibit 99.1

Tenaya Therapeutics Reports Promising Early Data from MyPEAK^™-1

Phase 1b/2 Clinical Trial of TN-201 for Treatment of

MYBPC3-Associated Hypertrophic Cardiomyopathy

TN-201 Well Tolerated at 3E13 vg/kg Dose

AAV9 Capsid Demonstrated Robust Delivery of TN-201 Transgene to Heart Muscle Cells

Resulting in Increasing RNA Expression and an Increase in Protein Levels Observed at One Year

Circulating Biomarkers and Other Clinical Measures Mostly Remained Stable or Improved from Baseline

Tenaya Management to Host a Webcast Conference Call Today at 8:00 a.m. ET

SOUTH SAN FRANCISCO, Calif., December 17, 2024 – Tenaya Therapeutics, Inc. (NASDAQ: TNYA), a clinical-stage biotechnology company with a mission to discover, develop and deliver potentially curative therapies that address the underlying causes of heart disease, today reported encouraging early data from the first cohort of patients in the MyPEAK-1 clinical trial of TN-201 gene therapy. TN-201 is being developed for the potential treatment of MYBPC3-associated hypertrophic cardiomyopathy (HCM), a condition caused by insufficient levels of myosin-binding protein C (MyBP-C).

Preliminary data from three patients in the first dose cohort of 3E13 vg/kg (Cohort 1) showed that TN-201 was generally well tolerated, with readily detectable vector DNA in the heart, evidence of transgene RNA expression, and increasing TN-201 mRNA and MyBP-C protein levels over time. Circulating biomarkers of cardiac muscle strain and injury remained largely stable, and other clinical markers of disease showed stability or directional improvement in the first two individuals dosed, though longer-term data are needed to characterize TN-201’s activity. Tenaya will continue to follow these first three patients with additional data readouts from Cohort 1 and the higher dose Cohort 2 anticipated in 2025.

“The initial patients enrolled in the MyPEAK-1 Phase 1b/2 clinical study are like many we see in our clinic: relatively young adults whose HCM is keeping them from having an adequate quality of life, including being able to perform activities of daily living and whose disease is progressing in spite of treatment interventions, putting them at significant risk of dire complications,” said Milind Desai, M.D., M.B.A, Haslam Family Endowed Chair in Cardiovascular Medicine, Vice Chair, Heart Vascular Thoracic Institute, Director of the Hypertrophic Cardiomyopathy Center and at the Cleveland Clinic, and an investigator for the MyPeak-1 Phase 1b/2 clinical trial. “The goal of gene therapy is to halt or even reverse the steady decline in MYBPC3-associated HCM by addressing the underlying genetic cause of disease. Initial data from this first-in-human clinical trial of TN-201 demonstrate tolerability and early evidence of protein expression support additional investigation to build on these findings.”

“TN-201’s emerging safety profile, excellent uptake into cardiomyocytes, and evidence of transgene RNA and protein expression provide important de-risking of the program as we proceed with enrollment of the higher dose cohort,” said Whit Tingley, M.D., Ph.D., Tenaya’s Chief Medical Officer. “In addition, we have observed encouraging early hints of disease stability and improvement among certain clinical measures of disease, offering further reason to believe in TN-201’s promise. Longer-term follow up for all patients in the lower dose cohort and results from the higher dose cohort will further inform our understanding of TN-201 gene therapy’s potential in MYBPC3-associated HCM.”

Interim Phase 1b/2 MyPEAK-1 Results

Data reported today focus on changes over time in the first three patients to receive TN-201 gene therapy. Patients were dosed sequentially with TN-201 via a one-time intravenous infusion of a 3E13 vg/kg dose. Patients enrolled in Cohort 1 were required to be symptomatic adults with MYBPC3-associated nonobstructive HCM at sufficiently high risk of sudden cardiac death to warrant an implantable cardiac defibrillator device (ICD). An assessment of Patient 1 at Week 52, Patient 2 at Week 40 and safety data for Patient 3 at 12 weeks are included in this first readout. All three had objectively severe disease at the time of enrollment with mild-to moderate heart failure symptoms that limited the activities of daily living as measured by New York Heart association (NYHA) classification.

TN-201 was generally well tolerated with a manageable safety profile.

TN-201 achieved robust transduction into cardiomyocytes and measurable transgene RNA expression. TN-201 RNA expression and levels of MyBP-C protein increased over time.

Cardiac biopsy samples were collected for analysis at Week 8 for Patients 1 and 2 and Week 52 for Patient 1 to confirm and characterize transduction of TN-201 DNA in the heart, the presence of TN-201 transgene mRNA, and changes in MyBP-C protein. Baseline biopsies have been added to the MyPEAK-1 protocol, beginning with Patient 3 to provide further insights into the changes in MyBP-C protein levels over time.

Clinical measures of HCM mostly remained stable or improved from baseline

“Taken together, the TN-201 data reported today are in line with our overall expectations at this early juncture in the study. The high levels of cardiac transduction and early evidence of increasing transgene expression support our confidence in TN-201’s potential at this early stage. We look forward to building on these results over time,” said Faraz Ali, Tenaya’s Chief Executive Officer. “We deeply appreciate the support we are receiving from the larger community of HCM clinicians and affected families, and we are especially grateful to our study investigators and to the first three patients in Cohort 1 without whom the promise and potential of TN-201 could not be explored.”

Investor and Analyst Conference Call and Live Webcast

Tenaya management will host a conference call and webcast today beginning at 8:00 am. ET/5:00 AM PT to discuss the initial MyPEAK-1 results. Investors and analysts may access the call here. A live webcast of the conference call, including an accompanying slide presentation, will be available on the Investors section of Tenaya’s website. A replay of the webcast, and accompanying slides, will be available on the Tenaya website for approximately 90 days following the call.

About the MyPEAK-1 Phase 1b/2 Clinical Trial

The MyPEAK-1 Phase 1b/2 clinical trial (Clinicaltrials.gov ID: NCT05836259) is an ongoing, multi-center, open-label, dose-escalating study designed to assess the safety, tolerability and clinical efficacy of a one-time intravenous infusion of TN-201 gene replacement therapy. The trial is enrolling symptomatic (New York Heart Association Class II or III) adults who have been diagnosed with MYBPC3-associated HCM. MyPEAK-1 is testing doses of 3E13 vg/kg and 6E13 vg/kg in two cohorts of three patients each. MyPEAK-1 may enroll up to 24 MYBPC3-associated HCM adults with either nonobstructive or obstructive forms of HCM in planned dose expansion cohorts.

To learn more about gene therapy for HCM and participation in the MyPEAK-1 study, please visit HCMStudies.com.

About MYBPC3-Associated Hypertrophic Cardiomyopathy Variants in the Myosin Binding Protein C3 (MYBPC3) gene are the most common genetic cause of hypertrophic cardiomyopathy (HCM), accounting for approximately 20% of the overall HCM population, or 120,000 patients, in the United States alone.⁽¹⁾ MYBPC3-associated HCM is a severe and progressive condition affecting adults, teens, children and infants. Mutations of the MYBPC3 gene result in insufficient expression of a protein, called MyBP-C, needed to regulate heart contraction. The heart becomes hypercontractile and the left ventricle thickens, resulting in symptoms such as chest pain, shortness of breath, palpitations and fainting. Patients whose disease is caused by MYBPC3 mutations are more likely than those with non-genetic forms of HCM to experience earlier disease onset and have high rates of serious outcomes, including heart failure symptoms, arrhythmias, stroke and sudden cardiac arrest or death.⁽²⁾ There are currently no approved therapeutics that address the underlying genetic cause of HCM.

About TN-201

TN-201 is an adeno-associated virus serotype 9 (AAV9)-based gene therapy designed to deliver a working MYBPC3 gene to heart muscle cells via a single intravenous infusion, increasing MyBP-C protein levels to address the underlying cause of MYBPC3-associated HCM with the aim of halting or even reversing disease after a single dose. The U.S. Food and Drug Administration has granted TN-201 Fast Track, Orphan Drug and Rare Pediatric Drug Designations. TN-201 has also received orphan medicinal product designation from the European Commission.

About Tenaya Therapeutics

Tenaya Therapeutics is a clinical-stage biotechnology company committed to a bold mission: to discover, develop and deliver potentially curative therapies that address the underlying drivers of heart disease. Tenaya employs a suite of integrated internal capabilities, including modality agnostic target validation, capsid engineering and manufacturing, to generate a portfolio of genetic medicines aimed at the treatment of both rare genetic disorders and more prevalent heart conditions. Tenaya’s pipeline includes TN-201, a gene therapy for MYBPC3-associated hypertrophic cardiomyopathy (HCM), TN-401, a gene therapy for PKP2-associated arrhythmogenic right ventricular cardiomyopathy (ARVC), TN-301, a small molecule HDAC6 inhibitor intended for heart failure with preserved ejection fraction (HFpEF), and multiple early-stage programs in preclinical development. For more information, visit www.tenayatherapeutics.com.

Forward Looking Statements

This press release contains forward-looking statements as that term is defined in Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Statements in this press release that are not purely historical are forward-looking statements. Words such as “will,” “anticipated,” “believe,” “look forward,” “potential,” and similar expressions are intended to identify forward-looking statements. Such forward-looking statements include, among other things, the planned timing to report additional data from MyPEAK-1; the clinical, therapeutic and commercial potential of, and expectations regarding TN-201; the value of additional MyPEAK-1 data to inform the potential of TN-201; the inferences regarding MyBP-C protein and mRNA expression; statements regarding the continued development TN-201 and TN-201 clinical outcomes, which may materially change as patient enrollment continues or more patient data become available; and statements made by Tenaya’s Chief Medical Officer and Chief Executive Officer and investigator for MyPEAK-1. The forward-looking statements contained herein are based upon Tenaya’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. These forward-looking statements are neither promises nor guarantees and are subject to a variety of risks and uncertainties, including but not limited to: availability of MyPEAK-1 data at the referenced time; the timing and progress of MyPEAK-1; the potential failure of TN-201 to demonstrate safety and/or efficacy in clinical testing; the potential for any MyPEAK-1 clinical trial results to differ from preclinical, interim, preliminary or expected results; Tenaya’s ability to enroll and maintain patients in clinical trials, including MyPEAK-1; risks associated with the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics and operating as an early stage company; Tenaya’s continuing compliance with applicable legal and regulatory requirements; Tenaya’s ability to raise any additional funding it will need to continue to pursue its product development plans; Tenaya’s reliance on third parties; Tenaya’s manufacturing, commercialization and marketing capabilities and strategy; the loss of key scientific or management personnel; competition in the industry in which Tenaya operates; Tenaya’s ability to obtain and maintain intellectual property protection for its product candidates; general economic and market conditions; and other risks. Information regarding the foregoing and additional risks may be found in the section titled “Risk Factors” in Tenaya’s Quarterly Report on Form 10-Q for the fiscal quarter ended September 30, 2024 and other documents that Tenaya files from time to time with the Securities and Exchange Commission. These forward-looking statements are made as of the date of this press release, and Tenaya assumes no obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law.

Contact

Michelle Corral

VP, Corporate Communications and Investor Relations

IR@tenayathera.com

Investors

Anne-Marie Fields

Precision AQ (formerly Stern Investor Relations)

annemarie.fields@precisionaq.com

Media

Wendy Ryan

Ten Bridge Communications

wendy@tenbridgecommunications.com

Exhibit 99.2

TN-201 MyPEAK-1 Phase 1b Study Initial Cohort 1 Data December 17, 2024 

Today’s speakers Milind Desai, M.D., Director at the Cleveland Clinical Faraz Ali, MBA HCM Center; Vice Chair of Heart Chief Executive Officer Vascular Thoracic Institute and MyPEAK-1 investigator Michelle Corral Whit Tingley, M.D., PhD Vice President, Corporate Chief Medical Officer Communications and Investor Relations 2

Forward-looking statement This presentation contains forward-looking statements within the meaning of Section 27A of the Securities Act and Section 21E of the Securities Exchange Act of 1934, as amended, that are based on our management’s beliefs and assumptions and on information currently available to our management. Forward-looking statements are inherently subject to risks and uncertainties, some of which cannot be predicted or quantified. All statements other than statements of historical facts contained in this presentation, including statements regarding the planned timing to report additional data from MyPEAK-1; the ongoing enrollment of patients in Cohort 2 of MyPEAK-1; the clinical, therapeutic and commercial potential of, and expectations regarding TN-201; the value of additional MyPEAK-1 data to inform the potential of TN-201; the inferences regarding MyBP-C protein and mRNA expression; and statements regarding the continued development TN-201 and TN-201 clinical outcomes, which may materially change as patient enrollment continues or more patient data become available, are forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as “anticipated” “purpose,” “focus,” “believe,” “expected,” “look forward,” “plan,” “potential,” “may,” “future,” “will,” 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 trends that we believe may affect our financial condition, results of operations, business strategy and financial needs. These forward-looking statements are subject to a number of risks, uncertainties and assumptions described in our filings with the SEC, including, but not limited to the section titled “Risk Factors” in our Quarterly Report on Form 10-Q for the fiscal quarter ended September 30, 2024, and other documents we have, or will file with the SEC. These filings, filed, are available on the SEC website at www.sec.gov. Such risks include, among other things: the availability of MyPEAK-1 data at the referenced times; the timing and progress of MyPEAK-1; the potential failure of TN-201 to demonstrate safety and/or efficacy in clinical testing; the potential for any MyPEAK-1 clinical trial results to differ from preclinical, interim, preliminary or expected results; our ability to enroll and maintain patients in clinical trials, including MyPEAK-1; risks associated with the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics and operating as an early stage company; our continuing compliance with applicable legal and regulatory requirements; our estimates of the number of patients who suffer from the diseases we are targeting and the number of patients that may enroll in our clinical trials; our ability to raise any additional funding it will need to continue to pursue its product development plans; our reliance on third parties; our manufacturing, commercialization and marketing capabilities and strategy; the loss of key scientific or management personnel; competition in the industry in which we operate; our ability to obtain and maintain intellectual property protection for its product candidates; general economic and market conditions; and other risks . These risks are not exhaustive. New risk factors emerge from time to time and it is not possible for our management to predict all risk factors, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in, or implied by, any forward-looking statements. You should not rely upon forward-looking statements as predictions of future events. Although we believe that the expectations reflected in the forward-looking statements are reasonable, we cannot guarantee future results, levels of activity, performance or achievements. In light of the significant uncertainties in these forward-looking statements, you should not regard these statements as a representation or warranty by us or any other person that we will achieve our objectives and plans in any specified time frame or at all. The forward-looking statements made in this presentation relate only to events as of the date on which such statements are made. Except as required by law, we undertake no obligation to update publicly any forward-looking statements for any reason after the date of this presentation. This presentation also contains estimates and other statistical data made by independent parties and by us relating to market size and growth and other data about our industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such estimates. In addition, projections, assumptions, and estimates of our future performance and the future performance of the markets in which we operate are necessarily subject to a high degree of uncertainty and risk. This presentation contains trademarks, service marks, trade names and copyrights of Tenaya Therapeutics, Inc. and other companies which are the property of their respective owners. This is showing as marked but we retained this from the original draft since the deck has patient population numbers. This is not included in the PR or 8-K. 3

Introductory comments Faraz Ali, Chief Executive Officer

Initial MyPEAK-1 Cohort 1 data derisks safety; reaffirms AAV9 as capsid of choice 1 Safety: TN-201 well tolerated; safety profile is consistent with other gene therapies • No cardiotoxicities • Liver enzyme elevations manageable and reversible • DSMB endorsed dose escalation 2 Biopsy: TN-201 reaches heart cells and achieves expression • Robust cardiac transduction that exceeds expectations • Durable and increasing mRNA expression over time • Protein levels modestly higher from 8 to 52 weeks 3 Clinical Endpoints: Encouraging, but early • Stability—and improvement—seen in certain parameters; further follow-up needed AAV9 = adeno-associated virus serotype 9 | DSMB = data safety and Monitoring Board | mRNA = messenger ribonucleic acid | 5

MYBPC3-associated HCM is estimated to affect 120,000 people in the U.S. alone(1) A severe and progressive autosomal dominant condition affecting adults, teens, children and infants H C M H E A R T ~57%of identified genetic variants underlying familial HCM are MYBPC3 mutations1 Thickened left ventricle of genetic variants • Significant functional impairment >30% underlying childhood- • Social and psychological impacts onset HCM are MYBPC3 mutations2 • Symptoms include shortness of breath, fainting, chest pain, G A B E | A G E 1 0 fatigue, palpitations, arrhythmias Living with MYBPC3+ HCM • Elevated risk of sudden cardiac death and heart failure 1. Ho, et al, Circulation 2018 6 HCM = Hypertrophic cardiomyopathy | MYBPC3 = myosin binding protein C3 2. Marston, et al, Eur Heart Jrnl 2021

TN-201 is the first gene therapy being developed for MYBPC3-associated HCM Underlying Problem Tenaya Approach • Mutations of the MYBPC3 gene lead to lower levels of • Target the underlying genetic cause of disease myosin-binding protein C (MyBP-C) • Deliver a working MYBPC3 gene utilizing AAV9 capsid • MyBP-C is an essential structural protein in the • Produce functional protein to increase MyBP-C levels to sarcomere required to regulate the binding of myosin restore regulation of contraction and relaxation to actin and modulate contraction • Potential to halt disease progression, reverse symptoms • Lower MyBP-C protein results in increased cardiac and improve patient quality of life contractility (hypertrophy), thickening of left ventricle and impaired diastolic relaxation MyBP-C 7

MyPEAK-1 Phase 1b/2 clinical trial Open-label, multi-center dose escalation and expansion trial Study objectives DSMB endorsed dose escalation and broadening of eligibility criteria based on acceptable safety profile at 3E13 vg/kg • Safety, tolerability • Dose-finding ✓ ✓ ✓ • Pharmacodynamics Cohort 1 12 Cohort 2 N=3 N=3 Design (3E13 vg/kg) review (6E13 vg/kg) review • Open-label, multi-center, dose- Screening Patients dosed Screening Patients dosed escalation and dose-expansion sequentially DSMB sequentially DSMB • 52-week trial period with four-year safety and efficacy follow-up • Cardiac biopsies at baseline, post- Optional dose Optional dose dose and ~52 weeks (effective expansion expansion with Cohort 1, patient 3) N ≤24 Patients may be dosed in parallel Vg/kg: vector genomes per kilogram 8

MyPEAK-1 Phase 1b/2 clinical trial endpoints Seeking directional consistency across multiple parameters over time Study Endpoints Over Time Post-Gene Therapy Safety and tolerability Pharmacokinetics (PK) Guidance Cardiac biopsy (Transgene, mRNA & protein) Pharmacodynamics (PD) 2024 Plasma biomarkers (e.g., NT-proBNP, troponin) Structural/hemodynamic changes Echo parameters Functional changes Exercise capacity (e.g., 6MWT, CPET) Symptom improvement Patient reported outcomes (e.g., KCCQ, NYHA class) Today’s dataset from Cohort 1 includes assessments for Patient 1 at 52 weeks | Patient 2 at 40 weeks | Patient 3 at 12 weeks NT-proBNP = N-terminal pro–B-type natriuretic peptide | CPET = Cardiopulmonary exercise testing | 9 6MWT = 6-minute walk test | KCCQ = Kansas City Cardiomyopathy Questionnaire | NYHA = New York Heart Association

Baseline characteristics and emerging safety profile Dr. Milind Desai Haslam Family Endowed Chair in Cardiovascular Medicine, Vice Chair, Heart Vascular Thoracic Institute, and Director of the Hypertrophic Cardiomyopathy Center at the Cleveland Clinic MyPEAK-1 investigator

MyPEAK-1 patients younger and more severe across multiple parameters compared to average HCM patient Very Typical Abnormal abnormal for HCM for HCM for HCM Average HCM Patient Patient 1 Patient 2 Patient 3 Length of Follow-Up—12 months 9 months 3 months Gender Male (63%)1 Female Female Male Current Age (years) 501 27 43 47 21% with ICD1 ICD Implantation (years) 2 27 37 36 Average age 38 18% with myectomy3 Myectomy Age (years) 4 24 30 39 Average age 54 NT proBNP (pg/ml) 5635 1836 732 1229 Cardiac Troponin I (ng/L) 276 46 34 53 LVMI (g/m2) Female: 89 | Male: 1047 174 105 177 NYHA Class 50% ≥ Class II8 II III II 1Ho, et al; Circulation 2018 4Cui, et al; JACC 2019 7Olivotto, et al; JACC 2008 ICD = implantable cardio defibrillator | 2Rowin, et al; Circ Arrhytm EP 2020 5Neubauer, et al; JACC 2019 8Maron, et al; JACC Heart Fail 2018 LVMI = left ventricular mass index 11 3Maurizi, et al; Circulation 2024 6Okamoto, et al; Int Heart J 2013

TN-201 was generally well tolerated Reported AEs are consistent with other AAV gene therapies and known effects of immunosuppression TN-201 related-events Grade 3 AE at Week 15 Patient 1 Mitigated for subsequent patients by Reversible elevated liver enzymes occurred in all increased monitoring throughout IS tapering patients, normalized in response to steroid treatment Patient 2 Grade 1 AE at Week 1 Summary of TN-201 safety findings Grade 1 SAE at Week 2 ✓ No thrombotic microangiopathy (TMA) Patient 3 Mild elevations classified as SAE because or thrombocytopenia steroids administered in hospital ✓ No signs of cardiotoxicities Patients 1 & 2 completed IS regimen; Patent 3 tapering o No signs of myocarditis o No arrythmia-related adverse events o Stable ejection fraction ✓ No participants discontinued study On study events deemed unrelated to TN-201 ✓ Majority of treatment-emergent adverse events (TEAEs) were mild, transient or reversible o 2 SAEs unrelated to TN-201 occurred DSMB cleared dose escalation to 6E13 vg/kg | All patients remain on study AE = adverse event | SAE = serious adverse event | IS = immunosuppression 12

Biopsy Findings Dr. Whit Tingley, Chief Medical Officer 

TN-201 mechanism of action occurs in 3 stages within cardiomyocytes TN-201 Mechanism of Action TN-201 1 2 3 DELIVERY: EXPRESSION: EXPRESSION: Upon Infusion Transduction (DNA) Transcription (RNA) Translation (Protein) TN-201 enters cardiomyocytes. TN-201’s healthy copy of TN-201 mRNA is then Healthy copy of MYBPC3 gene MYBPC3 gene is transcribed converted to MyBP-C protein forms stable episome in cell by cell’s machinery to produce and taken up into the messenger RNA sarcomere, filling empty slots Biopsy samples 14

Cardiac biopsies are collected to quantify these leading indicators of TN-201 efficacy Measurement assays Anticipated result over time • Total VCN initially decreases as TN-201 DNA TN-201 TN-201 DNA is measured by ddPCR is cleared from non-CM cells Quantifies the number of TN-201 vector • TN-201 DNA delivered to CMs remains copies in heart tissue stable over time TN-201 TN-201 mRNA is measured by RT-qPCR • TN-201 mRNA increases as TN-201 DNA Quantifies expression of TN-201 stabilizes and is transcribed in mRNA specifically (distinct from cardiomyocytes endogenous) MyBp-C protein is measured by LCMS • Protein levels increase from the patient’s Quantifies abundance of total MyBP-C baseline as TN-201 mRNA is translated into (normalized to myosin). LCMS cannot new MyBP-C that is incorporated into the distinguish MyBP-C protein derived from sarcomere TN-201 vs. patient’s own gene. ddPCR = digital droplet polymerase chain reaction | RT-qPCR = reverse transcriptase, quantitative polymerase chain reaction LCMS = liquid chromatography – mass spectrometry| VCN = vector copy number | CMs = cardiomyocytes 15

Overview of initial biopsy findings TN-201 has been delivered to the heart with evidence of expression in Patients 1 & 2 1 2 3 DELIVERY EXPRESSION RESTORATION Is TN-201 DNA getting Is TN-201 DNA getting Is TN-201 RNA Objective of Biopsy into the heart? expressed in the heart? translating into protein?  Baseline biopsy Patient 1 Week 8 biopsy ✓ ✓ ✓ Week 52 biopsy  Baseline biopsy To be confirmed Patient 2 Week 8 biopsy ✓ ✓ ï,¨ Week 52 biopsy with Week 52 biopsy  Baseline biopsy Patient 3ï,¨ Week 26 biopsy Baseline and Week 26 biopsy to be analyzed together ï,¨ Week 52 biopsy 16

TN-201 demonstrates robust and durable levels of cardiac transduction at 3E13 vg/kg dose Vector copy number (VCN) exceeds preclinical expectations TN-201 Cardiac Transduction Cohort 1 results to date 2.5 • Consistently high VCN >2.0 vg/dg at Patient 1 efficacy Patient 2 Week 8 for P1 and P2 2.0 • Expected drop of VCN to 0.8 vg/dg at Number clinical Week 52 for P1 1.5 pre Preclinical comparison for Copy 1.0 • TN-201 VCN results in humans exceeds threshold range in preclinical studies in homozygous Vector knock-out mouse model 0.5 VCN 0.0 Week 8 Week 52 17 

TN-201 cardiac transduction compares favorably with clinical data from other cardiac gene therapies TN-201 VCN and published results from peer cardiac GTx program1* 6.0 Patient 1 (3E13 vg/kg) • Higher VCN achieved at a 4.8 Patient 2 (3E13 vg/kg) 5.0 higher dose AAV9 Peer (6.7E13 vg/kg) 4.0 AAV9 Peer (1.1E14 vg/kg) • VCN declines over 1st year, Number without loss of expression Copy 3.0 2.7 • VCN remains stable at least 3 years post-dose 2.0 2.1 2.1 TN-201 performs similarly to Vector 1.1 1.0 0.6 peer low dose at >2x lower 0.8 dose. Expect similar dose 0.6 0.6 response and durability with 0.0 2 Months 12 Months 36 Months TN-201 Time Post-Dose 1Greenberg, NEJM 2024 GTx = gene therapy Comparison with peer programs is not intended to indicate *Peer values represented as means for given timepoint 18 likelihood of TN-201 clinical benefit

TN-201 RNA expression in cardiomyocytes confirmed TN-201 RNA expression increases over time; performs similarly to other sponsors’ data TN-201 RNA Expression Cohort 1 results to date • RT-qPCR assay is TN-201 specific • P1 and P2 clearly show expression at Week 8 • P1 expression increased +75% from Week 8 → to Week 52 Contextual comparisons • mRNA expression at 3E13 vg/kg dose was lower in humans than achieved in preclinical models (Expected based on species-to-species variability) • Magnitude of expression similar to peers’ clinical data1,2 1Greenberg, NEJM 2024; median number of mRNA transcripts per μg RNA Comparison with peer programs is not intended to indicate from 6.7E13 vg/kg and 1.1E14 vg/kg patients at latest timepoint 19 2Thomas, WORLD Symposium February 2024; n=1 patient at Week 26 likelihood of TN-201 clinical benefit

MyBP-C protein levels vary between healthy and MYBPC3+HCM populations and between individuals Range of MyBP-C protein levels in 1 MyBP-C protein in MYBPC3-associated HCM MYBPC3-associated HCM and healthy controls Max = 109% • MYBPC3-associated HCM patients exhibit 100% Mean = 100% ~40% lower MyBP-C protein levels on average vs. healthy controls Max = 79% Protein 80% • No apparent correlation between MyBP-C C Min = 78% protein level and markers of disease severity; —Mean = 60% suggests differing sensitivity to protein levels on 60% MyBP an individual basis 40% Min = 47% • Treatment goal with cardiac GTx: Increase Normal each individual’s protein levels from their of baseline; modest restoration has achieved 20% % measurable benefit in cardiac gene therapy (n=18) (n=21) clinical trials 0% MYBPC3+ HCM Adults Healthy Controls Comparison with other GTx programs is not intended to 1O’Leary, et al; J Mol Cell Cardiol 2019 (updated) indicate likelihood of TN-201 clinical benefit 20

Increase in MyBP-C protein levels observed in Patient 1 Changes in both mRNA and protein levels suggest TN-201 is being transcribed and expressed MyBP-C Protein Levels in Patients 1 & 2 and MYBPC3+ HCM and Healthy Controls Protein levels over time 80% • 3% increase may not 79% 78% represent total change in protein levels due to lack of Protein 70% C baseline—62% • Baseline biopsies (plus 59% MyBP 60% 56% post- dose and Week 52) 60% +3% are now in protocol starting with Patient 3 Normal 50% • Patients’ clinical state of 47% anticipated to be sensitive % to changes in protein over 40% time MYBPC3+ HCM Patient 1 Patient 1 Patient 2 * Healthy Controls Adults (Week 8) (Week 52) (Week 8) * Patient 2 52-week biopsy not yet taken 21

Biomarkers and clinical impressions Dr. Milind Desai, Director at the Cleveland Clinical HCM Center and MyPEAK-1 investigator

Circulating biomarker levels overall stable at this early time point NT-proBNP Levels Cardiac Troponin I Levels 3000 100 52 40 5240 Baseline Week Baseline Week Baseline TBD L) 80 Baseline Week Baseline Week Baseline TBD 2000 (pg/mL) (ng/m 60 cTnI 40 1000 proBNP 20 ULN—ULN NT 0 0 Patient Patient Patient Patient Patient Patient 1 2 3 1 2 3 Baseline to Last Visit Post-IS Baseline to Last Visit Post-IS • MyPEAK-1 baseline NT-proBNP levels are higher • MyPEAK-1 baseline troponin I much higher than than levels in other nonobstructive HCM trials1,2 those in other nonobstructive HCM trials1,2 • Immunosuppression known to influence NT- • Patient 1 remains elevated, however Patient 2 has proBNP levels; upon completion of IS regimen, normalized since TN-201 treatment levels return to baseline 1. Ho, et al; JACC 2020 ULN = upper limit of normal (values per MyPEAK-1 central laboratory) 2. Masri, et al; JCF 2024 23

Encouraging early clinical signals More follow-up, more patients, and data from higher-dose cohort needed Clinical Snapshot Patient 1 Patient 2 Domain at Week 52 at Week 40 • Initial improvement and/or NT-proBNP stabilization observed across Biomarker several domains Troponin I • Seeking directional Hypertrophy improvement in multiple Imaging parameters over time Diastolic Function • Overall clinical picture will Functional Capacity Unavailable/not yet interpretable become clearer with time, more follow-up, and more patients NYHA Symptoms KCCQ * * Confounded or unavailable at last timepoint Improved Stable Declined/Mixed due to AEs unrelated to study drug 24

Closing remarks and Q&A Faraz Ali, Chief Executive Officer

Summary • Safety: TN-201’s emerging safety profile is consistent with other AAV gene therapies and known effects of immunosuppressives o Immunosuppressive regimen has been successful in preventing and managing immunologic reactions to TN-201 o No cardiac AEs, including myocarditis or arrhythmia o Ejection fraction remained within the normal range o DSMB endorsed dose escalation; 6E13 vg/kg dose cohort now enrolling • Biopsy: Evidence of robust cardiac transduction and TN-201 RNA expression and protein level increase o Vector copy numbers of TN-201 DNA are within range associated with significant efficacy in preclinical studies; compare favorably to published rates of other sponsors o TN-201 mRNA quantities increasing over time; expression levels at similar ranges as peers o Protein levels increase from Week 8 to Week 52 for Patient 1, consistent with mRNA changes o Relationship between dose, VCN, RNA and protein expression and clinical endpoints are not yet known for TN-201 • Clinical parameters: Modest, but encouraging early signals in key parameters o Circulating biomarkers stable overall, but likely confounded by IS regimen o Improvements and/or stability observed in key measures of disease o More time and data points needed 26

Study status and next steps • Cohort 1 readout anticipated in 1H 2025 o Continued focus on safety o Biopsy data - Patient 2 at one year and Patient 3 at baseline and post dose • Cohort 2 enrollment ongoing o Initial readout anticipated in 2025 27

Thank you