Tenaya Therapeutics, Inc.
For the period ended Mar 31, 2026. Filed May 6, 2026.
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A company's report for each of its first three quarters. The financial statements are not audited. It shows how the business has moved since the last annual report, and what management says changed.
Mar 31, 2026 · Filed May 6, 2026
TNYA$0.36+14.0%Stored close · as of Nov 6, 2026
What changed in Management’s Discussion and Analysis?
Read the current filingPrevious report: 10-Q
Period ended 2025-09-30; filed 2025-11-10.
0001193125-25-273239
Item 2. Management’s Discussion and Analysis of Financial Condition and Results of OperationsCurrent report: 10-Q
Period ended 2026-03-31; filed 2026-05-06.
0001193125-26-209084
Item 2. Management’s Discussion and Analysis of Financial Condition and Results of OperationsThe baseline is this issuer’s latest earlier reporting period of the same form that was filed before the current report. A previous 10-Q is a different quarter, not a year-over-year comparison. Amendments are excluded.
Compared 110 previous paragraphs and 100 current paragraphs.
48 unchanged; 35 reworded; 16 added; 23 removed; 4 previous and 1 current paragraphs rearranged.
Tables are not compared: 5 previous and 3 current tables excluded. Dates, whitespace, punctuation and numbering changes are ignored; changes to financial figures remain significant.
A changed paragraph is not evidence that risk increased or decreased. An unchanged paragraph does not establish that risk stayed the same.
Added paragraphs (16)
Current report
For programs arising out of our modality agnostic drug discovery platform that address relatively rare conditions our strategy is to develop, manufacture and commercialize at least some of these programs on our own, although we may selectively consider partnerships to access technology, accelerate our progress, or improve our global reach to patients. For example, in March 2026, we entered into a multi-target research collaboration with Alnylam Pharmaceuticals, Inc. (Alnylam), to identify and validate novel gene targets for the potential treatment of cardiovascular disease. Importantly, this agreement takes advantage of our modality agnostic discovery know-how and provides reimbursement for research efforts. Where our discovery efforts lead to product candidates intended for relatively prevalent indications, our strategy is to out-license or partner such programs.
Current report
We expect to present longer-term Cohort 1 and interim Cohort 2 data in the second quarter of 2026. In the second half of 2026, one-year Cohort 2 data and two-year Cohort 1 data from MyPEAK-1 are anticipated. We are also pursuing alignment with regulatory authorities on pivotal trial plans for TN-201 and plan to provide an update on progress by year end.
Current report
In December 2025, we presented interim data from RIDGE-1, including safety, biopsy and arrhythmia results as of the October 2025 data cut-off for three patients enrolled in Cohort 1, with follow-up ranging from Week 20 to Week 40. TN-401 was generally well tolerated and no dose-limiting toxicities were observed. AEs were generally mild, asymptomatic and manageable and a majority of the AEs were deemed unrelated to TN-401. Among the AEs related to TN-401, there was a Grade 1 incidence of elevated troponin levels categorized as a serious AE due to inpatient monitoring. There were no incidents of thrombotic microangiopathy or cardiotoxicities observed and no arrhythmias associated with TN-401 occurred. Additionally, no Cohort 1 patients had experienced an implantable cardioverter defibrillator (ICD) shock post-treatment and all had tapered off prophylactic immunosuppressive medicines.
Current report
Serial biopsies taken at baseline and Week 8 post dose for Patients 1 and 2 provided consistent evidence of TN-401 transduction and expression. At Week 8, TN-401 robust mRNA expression was observed across all three patients. Post-treatment protein levels of PKP2 increased significantly in Patients 1 and 2 by a mean of 10% from baseline to Week 8 as measured by liquid chromatography–mass spectrometry normalized to myosin heavy chain, a motor protein in the sarcomere found exclusively in cardiomyocytes. Change in PKP2 protein levels for Patient 3 appeared slightly lower than baseline despite having the highest levels of TN-401 mRNA expression across Cohort 1. This confounding result for PKP2 protein level falls within the standard deviation of these methods and may be due to the inherent variability in sampling biopsies. A second post-dose biopsy will be collected and analyzed from Week 52 per protocol for all patients.
Current report
All three patients in Cohort 1 had severe electrical instability with a history of ventricular arrhythmias and had undergone a catheter ablation procedure, an elective procedure to reduce ventricular tachycardia recurrence. At baseline, each Cohort 1 patient met the enrollment criteria of greater than 500 premature ventricular contractions per 24 hours as measured over a seven-day monitoring period prior to dosing. Two of three patients experienced significant and clinically meaningful improvements in electrical instability, as measured by seven-day ambulatory monitoring of premature ventricular contractions (PVCs) following dosing. Patient 1 experienced a decrease in PVCs by 46% as of their most recent (Week 40) visit, while Patient 2 experienced a decrease in PVCs of 89% as of their most recent (Week 32) visit. Non-sustained ventricular tachycardia (NSVT) burden was eliminated or stable six months after treatment with TN-401. Patient 1 had a low NSVT count at baseline, which remained low at their most recent visit (Week 40). Patient 2 also had a substantial NSVT burden of 78 counts per 24-hour period at baseline that dropped to zero and remained stable by Week 32. Meaningful changes in PVCs or NSVTs were not expected nor observed for Patient 3 as of the data cut off, which was less than six months following treatment with TN-401. Other potential measures of clinical response including QRS duration, T wave inversions, heart function and NYHA class were in the normal range or remained stable for all three Cohort 1 patients during the post-dose follow-up period. We expect to present one-year Cohort 1 data and initial Cohort 2 data in the first half of 2026, with interim Cohort 2 results anticipated in the second half of the year. We are also pursuing alignment with regulatory authorities on pivotal trial plans for TN-401 and plan to provide an update on progress by year end.
Current report
Based on our observations of TN-301’s mechanism and evidence of efficacy for an approved pan-HDAC agent, we are also exploring the development of TN-301 for DMD, a condition caused by genetic mutations in thedystrophin gene, leading to absence of functional dystrophin protein in the heart and skeletal muscle. The muscle pathologies that underlie muscle wasting in the absence of dystrophin include inflammation, fibrosis, altered regeneration, mitochondrial dysfunction and disrupted autophagic flux – all processes that can be improved by HDAC6 inhibition.
Current report
At the Muscular Dystrophy Association Clinical & Scientific Congress 2026, we presented results from preclinical studies comparing TN-301 with the FDA-approved pan HDAC inhibitor, givinostat, in a well-established mouse model of DMD, and in human induced Pluripotent Stem Cell (iPSC)-derived cardiomyocytes from DMD patients. After five weeks of once-daily oral dosing, TN-301 showed a statistically significant increase in forelimb grip strength inmdx mice at both 3 mg/kg and 30 mg/kg compared to vehicle with both doses of TN-301 achieving wildtype levels of grip strength after five weeks. Further, TN-301 demonstrated greater efficacy at both doses compared to the 10 mg/kg dose of givinostat, which corresponds to the clinically relevant dose used in DMD patients. Notably, the effects of TN-301 at both doses approached those observed with the 30 mg/kg dose of givinostat, a level that is not tolerated in humans.
Current report
In engineered heart tissues derived from human DMD-induced iPSCs, TN-301 corrected calcium handling abnormalities, a key driver of DMD cardiomyopathy, including beat-to-beat fluctuations in calcium amplitude. In contrast, givinostat exacerbated calcium handling irregularities. In an experiment of DMD patient-derived iPSC cardiomyocytes designed to measure oxygen consumption and mitochondrial stress, both known contributors to DMD cardiomyopathy, TN-301 corrected basal and maximal respiration whereas givinostat worsened both measures. Taken together, these data support advancement of TN-301 as a potential DMD therapy with benefits for both skeletal and cardiac muscle and reduced liabilities compared to pan-HDAC inhibitors.
Current report
We plan to advance TN-301 toward clinical trials in patients in order to generate proof-of-activity data, with HFpEF and DMD being among the most promising potential indications identified to date. Consistent with our strategy, we believe that TN-301’s late-stage development and commercialization in large indications would best be led by a strategic pharmaceutical partner with global resources to explore the full potential of the molecule.
Current report
NM - Not Meaningful
Current report
Collaboration Revenue
Current report
Collaboration revenue for the three months ended March 31, 2026 was $0.2 million, compared to none in the prior year period. The increase was primarily driven by the amortization of upfront fees associated with collaboration arrangements entered into during the first quarter of 2026.
Current report
Research and development expenses were $14.8 million and $21.1 million for the three months ended March 31, 2026 and 2025, respectively. The year-over-year decrease of $6.2 million, or 30%, was primarily due to:
Current report
Based on our current operating plan, we believe that our existing cash and cash equivalents will be sufficient to meet our working capital and capital expenditure needs through at least the next twelve months following the date of this Quarterly Report on Form 10-Q.
Current report
Net cash used in investing activities for the three months ended March 31, 2026 was immaterial and consisted of purchases of property and equipment.
Current report
Net cash used in financing activities for the three months ended March 31, 2026 was approximately $0.4 million, which consisted of payments of accrued offering costs.
Removed paragraphs (23)
Previous report
We are advancing a deep and diverse modality agnostic pipeline of targeted therapies for heart conditions discovered internally using our extensive target identification and validation and genetic medicine design and manufacturing capabilities. All of our programs are currently in the clinical or preclinical stage; we do not have any products approved for sale and have not generated any revenue to date.
Previous report
Following proactive correspondence with the U.S. Food and Drug Administration (FDA) relating to future development plans for TN-201, on November 7, 2025, we announced that the FDA placed MyPEAK-1 on clinical hold requesting an amendment to the protocol primarily to standardize activities related to patient monitoring and management of the immunosuppression regimen across trial sites. We are working swiftly and collaboratively with the FDA to resolve the clinical hold and intend to resume dosing once the protocol changes have been implemented at trial sites. We do not expect this action to impact data milestones or development timelines for TN-201.
Previous report
For the production of our lead gene therapy candidates, we maintained complete ownership of process development, analytical development, and quality control and have already produced all necessary clinical trial material needed for our current clinical trials at our Good Manufacturing Practice (cGMP)-certified Genetic Medicines Manufacturing Center in Union City, California.
Previous report
Research and development expenses were $15.4 million and $20.4 million for the three months ended September 30, 2025 and 2024, respectively. The year-over-year decrease of $5.0 million, or 25%, was primarily due to:
Previous report
a decrease of $2.2 million in clinical trial related costs primarily driven by a decrease in clinical support costs, including clinical supply chain services and regulatory consulting fees;
Previous report
Comparison of the Nine Months Ended September 30, 2025 and 2024:
Previous report
Research and Development Expenses
Previous report
Research and development expenses were $53.8 million and $68.1 million for the nine months ended September 30, 2025 and 2024, respectively. The year-over-year decrease of $14.2 million, or 21%, was primarily due to:
Previous report
a decrease of $5.2 million in clinical trial related costs primarily driven by a decrease in clinical support costs, including regulatory consulting fees and lower employee-related costs driven by the Workforce Reductions;
Previous report
a decrease of $4.7 million in manufacturing costs reflecting lower employee-related costs driven by the Workforce Reductions, as well as reduced spending on supplies, materials, and facility maintenance; and
Previous report
decreases of $2.6 million research costs and $1.7 million in other research and development costs reflecting lower employee-related costs driven by the Workforce Reductions.
Previous report
General and Administrative
Previous report
General and administrative expenses were $18.7 million and $23.2 million for the nine months ended September 30, 2025 and 2024, respectively. The year-over-year decrease of $4.5 million, or 19%, was primarily due to decreases in employee-related costs driven by the Workforce Reductions and lower professional fees.
Previous report
Interest Income
Previous report
Interest income was $2.1 million and $3.9 million for the nine months ended September 30, 2025 and 2024, respectively. The year-over-year decrease of $1.8 million was primarily due to lower cash, cash equivalents and investment balances.
Previous report
Net Loss
Previous report
Net loss for the nine months ended September 30, 2025, was $70.4 million, compared to a net loss of $87.3 million for the nine months ended September 30, 2024.
Previous report
Follow-on Offering
Previous report
On March 5, 2025, we completed an underwritten offering of 75,000,000 units, priced at a public offering price of $0.70 per unit, with each unit consisting of one share of our common stock, a warrant to purchase one share of our common stock at an exercise price of $0.80 per share, which will be immediately exercisable and will expire five years from the date of issuance (a Series A Warrant) and a warrant to purchase one-half of a share of our common stock at an exercise price of $0.70 per share, which will be immediately exercisable and expire on June 30, 2026 (a Series B Warrant), under our registration statement on Form S-3 (File No. 333-266741). We received net proceeds of approximately $48.8 million, after deducting underwriting discounts and commissions of approximately $3.2 million and other offering expenses of approximately $0.5 million.
Previous report
On February 12, 2024, we completed an underwritten offering of 8,888,890 shares of our common stock at a price of $4.50 per share and, to an investor in lieu of common stock, pre-funded warrants to purchase 2,222,271 shares of our common stock at a price of $4.499 per pre-funded warrant under our registration statement on Form S-3 (File No. 333-266741). We received net proceeds of approximately $46.8 million, after deducting underwriting discounts and commissions of approximately $3.0 million and other offering expenses of approximately $0.2 million. As of December 31, 2024, all pre-funded warrants have been exercised for an exercise price of $0.001 per share.
Previous report
“At-the-Market” Equity Offering
Previous report
On August 10, 2022, we entered into a sales agreement (the Sales Agreement) with Leerink Partners LLC to establish an “at-the-market” (ATM) offering defined in Rule 415 under the Securities Act. Pursuant to the Sales Agreement, the Company is permitted to offer and sell, from time to time, shares of its common stock having a maximum aggregate offering price of up to $75.0 million. In January 2025, we sold 822,566 shares of our common stock under the ATM offering for net proceeds of $0.9 million, after deducting commissions and offering costs of $0.3 million. As of September 30, 2025, the Company may issue and sell up to approximately $69.8 million of common stock under the ATM offering.
Previous report
Net cash used in investing activities for the nine months ended September 30, 2024 was $13.0 million, which consisted primarily of purchases of marketable securities of $85.1 million, partially offset by proceeds from maturities of marketable securities of $72.9 million.
Reworded paragraphs (35)
Previous wording
We are a clinical-stage biotechnology company focused on discovering, developing and delivering potentially curative therapies that address the underlying drivers of heart disease. Our vision is to change the treatment paradigm for heart disease, and in doing so improve and extend the lives of millions of patients.
Current wording
We are a clinical-stage biotechnology company focused on discovering, developing and delivering potentially curative therapies that address the underlying drivers of heart disease. Heart disease remains a leading cause of death in the world. We believe the emerging insights into the genetic causes of cardiovascular conditions and increased recognition for precision medicine approaches has created an opportunity to change the treatment paradigm for heart disease, and in doing so improve and extend the lives of patients.
Previous wording
Early on in our company history, we invested in differentiated capabilities to enable modality-agnostic target identification and validation, anchored in human genetics and the use of human disease models. That proprietary expertise has directly informed the design, optimization and production of our pipeline. To support our initial focus on gene therapy candidates, we internalized expertise in capsid engineering, novel promoter constructs and manufacturing anchored on the use of AAVs as the method of delivery to the heart with the aim of increasing the safety and efficacy of our product candidates and accelerating early-stage discovery and preclinical optimization across modalities.
Current wording
Early on in our company history, we invested in differentiated capabilities to enable modality-agnostic target identification and validation, anchored in human genetics and the use of human disease models. To support our initial focus on gene therapy candidates, we also internalized expertise in capsid engineering, novel promoter constructs and manufacturing anchored on the use of adeno-associated viruses (AAVs) as the method of delivery to the heart. That proprietary expertise has directly informed the discovery, design, optimization and production of our pipeline.
Previous wording
We are primarily focused on development of our lead investigational product candidates, TN-201, a gene therapy for MYBPC3-associated hypertrophic cardiomyopathy (HCM), and TN-401, a gene therapy for PKP2-associated arrhythmogenic right ventricular cardiomyopathy (ARVC). Each candidate is currently in the clinical testing stage to establish the safety profile of two different doses in adults with disease due to pathogenic/likely pathogenic mutations. We anticipate that data generated in the next year will inform late-stage development by characterizing each candidates’ safety and tolerability profile, ability to transduce target heart cells, and produce the lacking protein underlying disease to slow – or even halt – disease progression. Where our discovery efforts lead to product candidates intended for relatively prevalent indications, such as TN-301, our small molecule histone deacetylase-6 (HDAC6) inhibitor for heart failure with preserved ejection fraction (HFpEF), our strategy is to out-license or partner with third parties.
Current wording
We are primarily focused on advancing our clinical-stage gene therapy candidates, TN-201 for MYBPC3-associated hypertrophic cardiomyopathy (HCM), and TN-401 for PKP2-associated arrhythmogenic right ventricular cardiomyopathy (ARVC). Each candidate is currently in Phase 1b/2 trials to establish the safety profile of two different doses in adults with disease due to pathogenic/likely pathogenic mutations. We anticipate that data generated to date and over the course of 2026 will support our pursuit of regulatory alignment on late-stage development for these gene therapy product candidates. A third internally discovered clinical-stage candidate, TN-301, is a highly specific small molecule inhibitor of histone deacetylase 6 (HDAC6) with potentially broad utility in heart failure with preserved ejection fraction (HFpEF) and other cardiac, metabolic, muscular and pulmonary diseases, including but not limited to Duchenne muscular dystrophy (DMD), genetic dilated cardiomyopathy (DCM) and pulmonary arterial hypertension (PAH).
Previous wording
TN-201 is our investigational gene therapy for individuals with HCM due to MYBPC3 gene mutations. These mutations result in a deficiency of myosin binding protein (MyBP-C), which in turn can cause the heart walls of affected individuals to become significantly thickened, leading to fibrosis, abnormal heart rhythms, cardiac dysfunction, heart failure and death. HCM is a chronic, progressive condition and those diagnosed with the disease often experience significant impairment in overall quality of life and may be at higher risk for serious complications and co-morbidities. TN-201 utilizes a recombinant adeno-associated virus serotype 9 (AAV9) capsid and is designed to deliver a working MYBPC3 gene to specific cells of the heart in order to produce MyBP-C and thereby potentially slow or even reverse the course of MYBPC3-associated HCM following a single infusion.
Current wording
TN-201 is our investigational gene therapy for individuals with HCM due to MYBPC3 gene mutations. These mutations result in a deficiency of myosin-binding protein C (MyBP-C), which in turn can cause the heart walls of affected individuals to become significantly thickened, leading to fibrosis, abnormal heart rhythms, cardiac dysfunction, heart failure and death. HCM is a chronic, progressive condition, and those diagnosed with the disease often experience significant impairment in overall quality of life and may be at higher risk for serious complications and co-morbidities. TN-201 utilizes a recombinant AAV9 capsid and is designed to deliver a working MYBPC3 gene to specific cells of the heart in order to produce MyBP-C and thereby potentially slow or even reverse the course of MYBPC3-associated HCM following a single infusion.
Previous wording
MyPEAKTM-1 is our Phase 1b/2a multi-center, open-label clinical trial, designed to assess the safety, tolerability and efficacy of a one-time intravenous infusion of TN-201. Enrollment and dosing in both the 3E13 vg/kg dose (Cohort 1) and 6E13 vg/kg dose (Cohort 2) cohorts are complete. In summer 2025, the independent data safety monitoring board (DSMB) for the MyPEAK-1 trial reviewed all available safety data from the first six patients dosed with TN-201. The DSMB determined that TN-201 had an acceptable safety profile and endorsed proceeding into expansion cohorts at either dose level, per protocol. We have since dosed one additional patient at the 6E13 vg/kg dose level with no new meaningful safety events associated with TN-201.
Current wording
MyPEAKTM-1 is our Phase 1b/2 multi-center, open-label clinical trial, designed to assess the safety, tolerability and efficacy of a one-time intravenous infusion of TN-201. Enrollment and dosing in both the 3E13 vg/kg dose (Cohort 1) and 6E13 vg/kg dose (Cohort 2) cohorts are complete. A per protocol review by the independent data safety monitoring board (DSMB) of all available data from the first six patients dosed determined that TN-201 had an acceptable safety profile to proceed with dosing expansion cohorts at either dose level. We are enrolling additional patients in MyPEAK-1 to further characterize dose response and inform dose selection for late-stage clinical trials.
Previous wording
In November 2025, we presented interim data from MyPEAK-1 during the Late-Breaking Science: Main Event session at the American Heart Association’s (AHA) Scientific Sessions 2025. Interim data presented at AHA included safety, biopsy and efficacy results for the three patients enrolled in Cohort 1 with follow-up ranging from Week 52-78, and safety and available assessments for the patients in Cohort 2 who have post-dose assessments ranging from Week 12-26 as of the July 2025 data cut off. Patient 5 was lost to further follow-up after week 12. TN-201 was generally well tolerated across both dose cohorts and no dose-limiting toxicities were observed. Reversible, asymptomatic liver enzyme elevations (Grade 1-3) were the most common treatment-related adverse events (AEs) reported. There were two treatment-related AEs classified as serious either due to inpatient administration of steroids or extended monitoring; a Grade 2 transaminase elevation that responded to steroids and a Grade 1 elevation of complement factors that resolved without additional intervention. Adjustments to monitoring and immunosuppression during Cohort 1 resulted in faster tapers and lower cumulative corticosteroid doses in Cohort 2, despite the higher TN-201 dose.
Current wording
In November 2025, we presented interim data from MyPEAK-1 at the American Heart Association’s Scientific Sessions 2025, with simultaneous publication in Cardiovascular Research. Interim data presented included safety, biopsy and efficacy results for the three patients enrolled in Cohort 1 with follow-up ranging from Week 52-78, and safety and available assessments for the patients in Cohort 2 who had post-dose assessments ranging from Week 12-26 as of the July 2025 data cut-off. Patient 5 was lost to further follow-up after week 12. TN-201 was generally well tolerated across both dose cohorts and no dose-limiting toxicities were observed. Reversible, asymptomatic liver enzyme elevations (Grade 1-3) were the most common treatment-related adverse events (AEs) reported. There were two treatment-related AEs classified as serious either due to inpatient administration of steroids or extended monitoring; a Grade 2 transaminase elevation that responded to steroids and a Grade 1 elevation of complement factors that resolved without additional intervention. Adjustments to monitoring and immunosuppression during Cohort 1 resulted in faster tapers and lower cumulative corticosteroid doses in Cohort 2, despite the higher TN-201 dose.
Previous wording
Biopsy data demonstrated that TN-201 transduction and mRNA expression were robust. DNA and RNA analyses of all three patients in Cohort 1 show evidence of sustained presence of TN-201 DNA in the heart and increasing mRNA expression over time. MyBP-C protein levels also increased over time across all patients in both cohorts for whom serial biopsies were available. In Cohort 1 patient protein levels increased by an average of 4% from the first biopsy taken to Week 52. The first evaluable patient in Cohort 2 (Patient 6) demonstrated a clear dose response, and early MyBP-C expression increased by 14% after only 12 weeks post-dose. Of note, Patient 6 had a greater than 2-fold increase in cardiac transduction and expression at Week 12 relative to the averages for these measures observed across Cohort 1.
Current wording
DNA and RNA analyses of cardiac biopsy samples from all three patients in Cohort 1 showed evidence of sustained presence of TN-201 DNA in the heart and increasing mRNA expression over time. The first patient in Cohort 2 with serial biopsy data (Patient 6) had a greater than 2-fold increase in cardiac transduction and RNA expression at Week 12 relative to the average for these measures observed across Cohort 1 patients. MyBP-C protein levels across Cohort 1 increased over time by an average of 4% from the first biopsy taken to Week 52. The first evaluable patient in Cohort 2 (Patient 6) demonstrated a clear dose response, and early MyBP-C expression increased by 14% after only 12 weeks post-dose.
Previous wording
All patients with greater than 26 weeks of follow-up demonstrated improvement in at least one parameter of disease, across biomarkers, hypertrophy and heart failure symptoms. Cardiac Troponin I, a predictive risk factor of cardiac AEs such as ventricular arrhythmias, sudden cardiac death, and progression to end-stage heart failure, declined by as much as 74% from baseline, to normal or near-normal levels in all Cohort 1 patients. NT-proBNP, a biomarker of cardiac muscle strain, improved or remained stable in two of three Cohort 1 patients. Cardiac Troponin I remained within the normal range and NT-proBNP remained stable for Patient 4 from Cohort 2 at their Week 26 assessment. All three patients in Cohort 1 now have evidence of significant improvement in one or more measures of hypertrophy at Week 52, with notable reductions in left ventricular posterior wall thickness (LVPWT) of between 21% and 39%. LVPWT for Patient 4 in Cohort 2 was stable at Week 26. Greater LVPWT is an independent risk factor for reduced long-term survival after septal myectomy. Two out of three Cohort 1 patients saw reductions from baseline in left ventricular mass index (LVMI) of between 12% and 22% at Week 52. LVMI for Patient 4 in Cohort 2 was stable at Week 26. NYHA classification, a measure of the impact of heart failure symptoms on activities of daily living, improved in all patients by at least one class by Week 26, and all Cohort 1 patients are now NYHA Class I (asymptomatic). Longer-term follow-up for all patients is required to further inform our understanding of TN-201’s potential as a treatment for MYBPC3-associated HCM.
Current wording
All patients with greater than 26 weeks of follow-up demonstrated improvement in at least one parameter of disease, across biomarkers, hypertrophy and heart failure symptoms. Cardiac troponin I, a predictive risk factor of adverse cardiac outcomes such as ventricular arrhythmias, sudden cardiac death, and progression to end-stage heart failure, declined by as much as 74% from baseline, to normal or near-normal levels in all Cohort 1 patients. NT-proBNP, a biomarker of cardiac muscle strain, improved or remained stable in two of three Cohort 1 patients. All three patients in Cohort 1 showed evidence of significant improvement in one or more measures of hypertrophy at Week 52, with notable reductions in left ventricular posterior wall thickness (LVPWT) of between 21% and 39%. Greater LVPWT is an independent risk factor for reduced long-term survival after septal myectomy. Two out of three Cohort 1 patients saw reductions from baseline in left ventricular mass index (LVMI) of between 12% and 22% at Week 52. In the first Cohort 2 patient for whom Week 26 data were available (Patient 4), cardiac troponin I remained within the normal range and NT-proBNP remained stable. LVPWT and LVMI also remained stable at Week 26. New York Heart Association (NYHA) classification, a measure of the impact of heart failure symptoms on activities of daily living, improved in all patients by at least one class by Week 26, and all Cohort 1 patients were NYHA Class I (asymptomatic) as of the data cutoff date. Longer-term follow-up for all patients is required to further inform our understanding of TN-201’s potential as a treatment for MYBPC3-associated HCM.
Previous wording
To support our development efforts for TN-201 we are conducting two noninterventional studies: a study evaluating seroprevalence to AAV9 antibodies among adults with MYBPC3-associated HCM, and MyClimb, a prospective and retrospective global natural history study focused on pediatric patients with MYBPC3 mutation-associated cardiomyopathy. The seroprevalence study has completed enrollment. Initial data from the seroprevalence study indicated that antibodies to AAV9 in the majority of participants were below the eligibility threshold that would allow for participation in MyPEAK-1. The MyClimb natural history study is following patient medical history to characterize the outcomes, burden of illness, risk factors, quality of life, and biomarkers associated with disease progression in pediatric patients. MyClimb complements existing disease registries focused primarily on adult patient HCM populations and may support and expedite the development of TN-201 in the pediatric patient population. Initial data from MyClimb indicated that 93% of participants had the nonobstructive HCM phenotype, for which there are currently no approved treatment options and that genotypic status was a significant predictor of risk. The data also revealed that left ventricular mass index may serve as a surrogate marker for poor long-term outcomes and as an appropriate marker to evaluate the early effectiveness of TN-201’s potential in a future pivotal trial.
Current wording
Despite advances in the treatment of the obstructive HCM in recent years with the approval of cardiac myosin inhibitors, there are no approved treatments for those with the non-obstructive form of disease or those diagnosed before the age of 18. Recognizing the urgent medical need among pediatric patients, we initiated MyClimb, a retrospective and prospective natural history study of pediatric patients to characterize the outcomes, burden of illness, risk factors, quality of life, and biomarkers associated with disease progression in pediatric patients. MyClimb complements existing disease registries focused primarily on adult patient HCM populations and may support and expedite the development of TN-201 in the pediatric patient population. MyClimb completed enrollment of more than 200 individuals and is believed to be the largest study of pediatric individuals with MYBPC3-associated HCM ever conducted. Initial data indicated that 93% of participants had the nonobstructive HCM phenotype, for which there are currently no approved treatment options and that genotype was a significant predictor of risk. The data also revealed that LVMI may serve as a surrogate marker for poor long-term outcomes and as an appropriate marker to evaluate the early effectiveness of TN-201’s potential in a future pivotal trial.
Previous wording
RIDGETM-1 is our Phase 1b multi-center, open-label clinical trial, designed to assess the safety, tolerability and efficacy of a one-time intravenous infusion of TN-401. In July 2025, safety data from the first three RIDGE-1 patients dosed at the 3E13 vg/kg dose (Cohort 1) were reviewed by an independent DSMB which endorsed both dose escalation to the 6E13 vg/kg dose cohort (Cohort 2) and expanding enrollment in Cohort 1. Enrollment in Cohort 2 is now complete and we may enroll additional patients at the 3E13 vg/kg dose (Cohort 1). Additional enrollment at the 6E13vg/kg dose (Cohort 2) will be considered following a review of all available safety data by the DSMB. Initial clinical data from Cohort 1 is expected before year end.
Current wording
RIDGETM-1 is our Phase 1b/2 multi-center, open-label clinical trial, designed to assess the safety, tolerability and efficacy of a one-time intravenous infusion of TN-401. Enrollment and dosing in both the 3E13 vg/kg dose (Cohort 1) and 6E13 vg/kg dose (Cohort 2) cohorts are complete. In January 2026, the DSMB for RIDGE-1 reviewed all available data from Cohort 1 and Cohort 2, determined that TN-401 had an acceptable safety profile and endorsed proceeding into expansion cohorts at either dose level, per protocol. We are enrolling additional patients in RIDGE-1 to inform dose selection for late-stage clinical trials.
Previous wording
In February 2025, we were awarded a Clinical Grant (Clin2) of $8.0 million from the California Institute for Regenerative Medicine (CIRM), a state of California Agency that funds regenerative medicine, stem cell, and gene therapy research. Proceeds from the grant will help fund clinical trial costs for our ongoing Phase 1b RIDGE-1 clinical trial of TN-401 gene therapy. RIDGE-1 is being conducted at multiple clinical trial sites with ARVC expertise at leading cardiology centers in the U.S. and United Kingdom.
Current wording
In February 2025, we were awarded a Clinical Grant (Clin2) of $8.0 million from CIRM, a state of California Agency that funds regenerative medicine, stem cell, and gene therapy research. Proceeds from the grant will help fund clinical trial costs for our ongoing Phase 1b/2 RIDGE-1 clinical trial of TN-401 gene therapy. RIDGE-1 is being conducted at multiple clinical trial sites with ARVC expertise at leading cardiology centers in the U.S. and United Kingdom.
Previous wording
In support of our development efforts for TN-401, we initiated RIDGE, a global noninterventional study to collect natural history and seroprevalence to AAV9 antibodies data among ARVC patients who carry pathogenic or likely pathogenic PKP2 gene mutations. Interim data from RIDGE, believed to be the largest natural history study of adults with PKP2-associated ARVC was presented at Heart Rhythm Society’s annual meeting in April 2025. Adults with PKP2-associated ARVC experience a high burden of arrhythmias despite treatments with anti-arrhythmic medications, beta blockers and the anti-arrhythmic flecainide, as well as surgical interventions such as ablation and ICD placement. Further, current treatments appeared to do little to halt or prevent progressive structural changes to the heart that occur as a result of PKP2 mutations. A large majority of adults with PKP2-associated ARVC would be eligible to participate in our ongoing Phase 1b RIDGE-1 clinical trial of TN-401 gene therapy based on low levels of antibodies to AAV9.
Current wording
To support our development efforts for TN-401, we have initiated RIDGE, a global noninterventional study to collect treatment history and seroprevalence to AAV9 antibodies data among ARVC patients who carry pathogenic or likely pathogenic PKP2 gene mutations. Interim data from RIDGE, believed to be the largest natural history study of adults with PKP2-associated ARVC, was presented at Heart Rhythm Society’s annual meeting in April 2025. Adults with PKP2-associated ARVC experience a high burden of arrhythmias despite treatments with anti-arrhythmic medications, beta blockers and the anti-arrhythmic flecainide, as well as surgical interventions such as ablation and ICD placement. Further, current treatments appeared to do little to halt or prevent progressive structural changes to the heart that occur as a result of PKP2 mutations. A large majority of adults with PKP2-associated ARVC would be eligible to participate in RIDGE-1 based on low levels of pre-existing antibodies to AAV9.
Previous wording
TN-301 is our small molecule HDAC6 inhibitor initially discovered and validated as having cardioprotective qualities in preclinical studies of a rapidly worsening mouse model of BAG3 mutant dilated cardiomyopathy (DCM). HDAC6 is a cytoplasmic enzyme known to regulate diverse cellular processes. Based on TN-301’s multi-modal mechanism of action, TN-301 may have future potential in a number of cardiometabolic conditions.
Current wording
We are also advancing TN-301, a highly specific HDAC6 inhibitor that has potential utility in HFpEF and other cardiac, metabolic, muscular and pulmonary diseases. TN-301 was initially discovered and validated as having cardioprotective qualities in preclinical studies of a rapidly worsening mouse model of BAG3 mutant DCM. HDAC6 is a cytoplasmic enzyme known to regulate diverse cellular processes. Based on TN-301’s multi-modal mechanism of action, that includes reductions in inflammation, oxidative stress, fibrosis, and metabolic dysregulation, as well as improvements in autophagy, protein quality control, mitochondrial metabolism, and lipid metabolism, TN-301 may be well suited to the treatment of HFpEF, as well as other cardiac, metabolic, muscular and pulmonary disorders where there is strong alignment between TN-301’s mechanism and the pathophysiology of disease.
Previous wording
We shared positive data from our Phase 1 clinical trial of TN-301 in healthy participants at the 2023 Heart Failure Society of America Annual Scientific Meeting. TN-301 was generally well tolerated across the broad range of doses studied. Pharmacokinetic results showed overall dose proportionality with a half-life supportive of once-daily dosing. Increasing doses and exposures with TN-301 correlated with increased pharmacodynamic effects. There were no changes in histone acetylation with TN-301 underscoring the selectivity of TN-301 for HDAC6 and potentially reducing the risk of off target effects. Taken together, these data support continued development of TN-301 as a potential treatment for patients with HFpEF and other severe diseases - including those outside of cardiology- in which inflammation, fibrosis and metabolic dysregulation may be implicated. We believe late-stage clinical development of TN-301 for more prevalent indications is best suited for development by or with a well-resourced partner.
Current wording
We shared positive data from our Phase 1 clinical trial of TN-301 in healthy participants at the 2023 Heart Failure Society of America Annual Scientific Meeting. TN-301 was generally well tolerated across the broad range of doses studied. Pharmacokinetic results showed overall dose proportionality with a half-life supportive of once-daily dosing. Increasing doses and exposures with TN-301 correlated with increased pharmacodynamic effects. There were no changes in histone acetylation with TN-301 underscoring the selectivity of TN-301 for HDAC6 and potentially reducing the risk of off target effects. Extensivein vitro andin vivo studies have also shown that TN-301 addresses diverse pathological processes with direct and systemic benefits in models of HFpEF. In comparative studies, selective HDAC6 inhibition as a single agent has been shown to have similar efficacy to empagliflozin, an SGLT2 inhibitor which is approved for the treatment of HFpEF and co-administration of our HDAC6 inhibition with a SGLT2 inhibitor in a HFpEF mouse model demonstrated additive benefit. Taken together, these data support continued development of TN-301 as a potential treatment for patients with HFpEF and other severe diseases including those outside of cardiology in which inflammation, fibrosis and metabolic dysregulation may be implicated.
Previous wording
In addition to our clinical-stage candidates, we have multiple early-stage programs using various therapeutic approaches, including gene addition, gene editing, gene silencing, and cellular regeneration to address other forms of rare and/or prevalent heart disease.
Current wording
In addition to our clinical-stage candidates, we have multiple early-stage programs using various therapeutic approaches, including gene addition, gene editing, gene silencing, and cellular regeneration to address other forms of rare and/or prevalent forms of heart disease. We do not have any products approve for sale and have not generated any product revenue to date.
Previous wording
We expense all research and development costs in the periods in which they are incurred. Costs of certain research and development activities are recognized based on estimates from a number of factors, including an evaluation of the progress of the activities, as well as input from external service providers.
Current wording
We expense all research and development costs in the periods in which they are incurred. Costs of certain research and development activities are recognized based on estimates derived from a number of factors, including an evaluation of the progress of the activities, as well as input from external service providers.
Previous wording
The process of conducting the necessary research to advance through the clinical stages and ultimately obtain regulatory approval is costly and time-consuming, and the successful development of our product candidates is highly uncertain. As a result, we cannot reasonably estimate or know the nature, timing or estimated costs of the efforts that will be necessary to complete the development of, and obtain regulatory approval for, or when and to what extent we will generate revenue from the commercialization and sale of any of our product candidates. The level of our research and development expenses over the next twelve months will be subject to operational decisions made following data generated from our MyPEAK-1 and RIDGE-1 clinical trials.
Current wording
The process of conducting the necessary research to advance through the clinical stages and ultimately obtain regulatory approval is costly and time-consuming, and the successful development of our product candidates is highly uncertain. As a result, we cannot reasonably estimate or know the nature, timing or estimated costs of the efforts that will be necessary to complete the development of, and obtain regulatory approval for, or when and to what extent we will generate revenue from the commercialization and sale of any of our product candidates. The level of our research and development expenses over the next twelve months will be subject to operational decisions made following data generated from our MyPEAK-1 and RIDGE-1 clinical trials and our ability to achieve regulatory alignment on our pivotal trial plans for our TN-201 and TN-401 programs.
Previous wording
a $1.6 million decrease in research expenses, reflecting lower employee-related costs driven by our workforce reductions initiated in March 2025 and May 2024 (together, the Workforce Reductions) and reduced lab supply and service costs; and
Current wording
a $3.0 million decrease in research expenses, reflecting lower employee-related costs driven by the workforce reduction implemented in March 2025 (the 2025 Workforce Reduction) and reduced lab supply and service costs; and
Previous wording
a decrease of $1.0 million in manufacturing costs reflecting lower employee-related costs driven by the Workforce Reductions and lower facility maintenance fees;
Current wording
a decrease of $2.0 million in manufacturing costs reflecting lower employee-related costs driven by the 2025 Workforce Reduction and lower facility maintenance fees and depreciation expense.
Previous wording
We will continue to incur legal, accounting, insurance and other expenses in operating our business as a public company, including costs associated with regulatory and compliance activities. As with our research and development, the level of our general and administrative expenses over the next twelve months will be subject to operational decisions made following data generated from our MyPEAK-1 and RIDGE-1 clinical trials.
Current wording
We will continue to incur legal, accounting, insurance and other expenses in operating our business as a public company, including costs associated with regulatory and compliance activities. As with our research and development, the level of our general and administrative expenses over the next twelve months will be subject to operational decisions made following data generated from our MyPEAK-1 and RIDGE-1 clinical trials and our ability to achieve regulatory alignment on our pivotal trial plans for our TN-201 and TN-401 programs.
Previous wording
General and administrative expenses were $5.6 million and $6.4 million for the three months ended September 30, 2025 and 2024, respectively. The year-over-year decrease of $0.8 million, or 12%, was primarily due to decreases in employee-related costs driven by the Workforce Reductions and lower professional fees.
Current wording
General and administrative expenses were $5.4 million and $6.5 million for the three months ended March 31, 2026 and 2025, respectively. The year-over-year decrease of $1.0 million, or 16%, was primarily due to decreases in employee-related costs driven by the 2025 Workforce Reduction and lower professional fees.
Previous wording
Interest income primarily consists of interest earned on our cash, cash equivalents and investment balances. Interest income was $0.7 million and $1.1 million for the three months ended September 30, 2025 and 2024, respectively. The year-over-year decrease of $0.4 million was primarily due to lower cash, cash equivalents and investment balances.
Current wording
Interest income primarily consists of interest earned on our cash and cash equivalents balances. In prior period, interest income also included amounts earned on marketable securities. Interest income was $0.8 million and $0.6 million for the three months ended March 31, 2026 and 2025, respectively. The year-over-year increase of $0.2 million was primarily due to average higher cash and cash equivalents balances.
Previous wording
Net loss for the three months ended September 30, 2025, was $20.3 million, compared to a net loss of $25.6 million for the three months ended September 30, 2024.
Current wording
Net loss for the three months ended March 31, 2026, was $19.3 million, compared to a net loss of $26.9 million for the three months ended March 31, 2025.
Previous wording
Since our inception, we have not generated any revenue and we have incurred significant net losses and negative cash flows from operations. From our inception through September 30, 2025, we have funded our operations primarily from the sale and issuance of our equity securities. As of September 30, 2025, we had cash, cash equivalents and investments in marketable securities of $56.3 million and an accumulated deficit of $584.8 million. We believe that savings from the Workforce Reductions and future cost containment initiatives to be taken as necessary, combined with existing cash, cash equivalents and short-term investments as of September 30, 2025, along with the $10.0 million of funds available under our Loan Agreement with Silicon Valley Bank (SVB), and the $1.9 million of proceeds from warrant exercises in October 2025, will be sufficient to fund our operations for at least the next twelve months following the filing of this Quarterly Report on Form 10-Q.
Current wording
Since our inception, we have generated limited collaboration revenue and no product revenue, and we have incurred significant net losses and negative cash flows from operations. From our inception through March 31, 2026, we have funded our operations primarily from the sale and issuance of our equity securities. As of March 31, 2026, we had cash and cash equivalents of $80.9 million and an accumulated deficit of $624.3 million.
Previous wording
In February 2025, we announced we were awarded an $8 million grant from the CIRM to support RIDGE-1. The award is payable to us upon achievement of certain clinical milestones. Additionally, if CIRM determines, in its sole discretion, that we have not complied with the terms and conditions of the grant, CIRM may suspend or permanently cease disbursements. Funds received under this grant may only be used for allowable project costs specifically identified with the CIRM-funded project. Such costs can include, but are not limited to, salary for personnel, itemized supplies, consultants, and itemized clinical study costs. Under the terms of the grant, we will co-fund the research project with CIRM and the amount of our co-funding requirement is predetermined as a part of the award. For the nine months ended September 30, 2025, the Company recognized $1.5 million in connection with the grant.
Current wording
In February 2025, we announced we were awarded an $8.0 million grant from the CIRM to support RIDGE-1. The award is payable to us upon achievement of certain clinical milestones. We expect this grant to provide funding for a portion of our research and development activities, subject to the achievement of applicable milestones and compliance with the grant terms.
Previous wording
On August 6, 2024, we entered into a Loan Agreement with SVB. As of September 30, 2025, under the Loan Agreement, we have the right to draw down $10.0 million at our discretion, and up to an additional $20.0 million that may be available at SVB’s discretion, subject to specified conditions.
Current wording
On August 6, 2024, we entered into a Loan Agreement with Silicon Valley Bank (SVB). As of December 31, 2025, all of the term loan commitments expired under the Loan Agreement and no term loans were outstanding. The Loan Agreement provides that an additional loan of $20.0 million may be available at SVB’s discretion, subject to specified conditions.
Previous wording
continue to advance our lead gene therapy product candidates, TN-201 and TN-401;
Current wording
continue to advance our lead product candidates, TN-201, TN-401 and TN-301;
Previous wording
In order to complete the development of our product candidates and commercialize our product candidates, if approved, we will require substantial additional funding. Until such time as we can generate significant revenue from sales of our product candidates, if ever, we expect to finance our operations through public or private equity offerings, debt financings or other capital sources, which may include strategic collaborations or other arrangements with third parties, or other sources of financing. We may not be able to raise additional capital on terms acceptable to us or at all. To the extent that we raise additional capital through the sale of equity or convertible debt securities, the ownership interest of our stockholders will be or could be diluted, and the terms of these securities may include liquidation or other preferences that adversely affect the rights of our common stockholders. Debt financing and preferred equity financing, if available, may involve agreements that include covenants limiting or restricting our ability to take specific actions, including restricting our operations and limiting our ability to incur liens, issue additional debt, pay dividends, repurchase our common stock, make certain investments or engage in merger, consolidation, licensing or asset sale transactions. If we raise funds through strategic collaborations, partnerships and other similar arrangements with third parties, we may be required to grant rights to develop and market product candidates that we would otherwise prefer to develop and market ourselves. If we are unable to raise additional capital on acceptable terms when needed, our business, results of operations, and financial condition would be adversely affected.
Current wording
In order to complete the development of our product candidates and commercialize our product candidates, if approved, we will require substantial additional funding. Until such time as we can generate significant revenue from sales of our product candidates, if ever, we expect to finance our operations through public or private equity offerings, debt financings or other capital sources, which may include strategic collaborations or other arrangements with third parties, or other sources of financing. We may not be able to raise additional capital on terms acceptable to us or at all. To the extent that we raise additional capital through the sale of equity or convertible debt securities, the ownership interest of our stockholders will or could be diluted, and the terms of these securities may include liquidation or other preferences that adversely affect the rights of our common stockholders. Debt financing and preferred equity financing, if available, may involve agreements that include covenants limiting or restricting our ability to take specific actions, including restricting our operations and limiting our ability to incur liens, issue additional debt, pay dividends, repurchase our common stock, make certain investments or engage in merger, consolidation, licensing or asset sale transactions. If we raise funds through strategic collaborations, partnerships and other similar arrangements with third parties, we may be required to grant rights to develop and market product candidates that we would otherwise prefer to develop and market ourselves. If we are unable to raise additional capital on acceptable terms when needed, our business, results of operations, and financial condition would be adversely affected.
Previous wording
Net cash used in operating activities for the nine months ended September 30, 2025 was $54.3 million, which consisted primarily of a net loss of $70.4 million and a net change in operating assets and liabilities of $3.3 million, partially offset by $18.6 million in non-cash charges. The change in net operating assets and liabilities was primarily due to a decrease in accounts payable and accrued expenses and other current liabilities of $2.6 million. Cash flows from operations are generally impacted by the timing of payments to vendors and vendor payment terms. The non-cash charges primarily consisted of stock-based compensation of $10.3 million and depreciation and amortization of $6.6 million.
Current wording
Net cash used in operating activities for the three months ended March 31, 2026 was $19.2 million, which consisted primarily of a net loss of $19.3 million and a net change in operating assets and liabilities of $4.6 million, partially offset by $4.6 million in non-cash charges. The change in net operating assets and liabilities was primarily due to a decrease in accounts payable and accrued expenses and other current liabilities of $4.1 million. Cash flows from operations are generally impacted by the timing of payments to vendors and vendor payment terms. The non-cash charges primarily consisted of stock-based compensation of $2.2 million and depreciation and amortization of $1.8 million.
Previous wording
Net cash used in operating activities for the nine months ended September 30, 2024 was $72.1 million, which consisted primarily of a net loss of $87.3 million and a net change in operating assets and liabilities of $6.9 million, partially offset by $21.0 million in non-cash charges. The change in net operating assets and liabilities was primarily due to a decrease in accounts payable and accrued expenses and other current liabilities of $5.3 million and a decrease in operating lease liabilities of $3.2 million, partially offset by a decrease of prepaid expenses and other current assets of $1.0 million. Cash flows from operations are generally impacted by the timing of payments to vendors and vendor payment terms. The non-cash charges primarily consisted of stock-based compensation of $12.7 million and depreciation and amortization of $6.4 million.
Current wording
Net cash used in operating activities for the three months ended March 31, 2025 was $23.1 million, which consisted primarily of a net loss of $26.9 million and a net change in operating assets and liabilities of $3.4 million, partially offset by $6.9 million in non-cash charges. The change in net operating assets and liabilities was primarily due to a decrease in accounts payable and accrued expenses and other current liabilities of $2.3 million and a decrease in operating lease liabilities of $0.7 million, an increase in prepaid expenses and other current assets of $0.5 million. Cash flows from operations are generally impacted by the timing of payments to vendors and vendor payment terms. The non-cash charges primarily consisted of stock-based compensation of $3.7 million and depreciation and amortization of $2.7 million.
Previous wording
Net cash provided by investing activities for the nine months ended September 30, 2025 was $56.2 million, which consisted primarily of proceeds from maturities of marketable securities of $45.7 million and sales of marketable securities of $11.0 million.
Current wording
Net cash provided by investing activities for the three months ended March 31, 2025 was $22.2 million, which consisted primarily of proceeds from maturities of marketable securities of $11.7 million and sales of marketable securities of $11.0 million.
Previous wording
Net cash provided by financing activities for the nine months ended September 30, 2025 was $50.2 million, which primarily consisted of net proceeds from our March 2025 follow-on offering of $48.8 million.
Current wording
Net cash provided by financing activities for the three months ended March 31, 2025 was $50.3 million, which primarily consisted of net proceeds from our March 2025 follow-on offering of $49.3 million.
Previous wording
A summary of our critical accounting policies and estimates is presented in Part II, Item 7 of our Annual Report on Form 10-K for the year ended December 31, 2024. There were no material changes to our critical accounting policies and estimates during the three and nine months ended September 30, 2025.
Current wording
A summary of our critical accounting policies and estimates is presented in Part II, Item 7 of our Annual Report on Form 10-K for the year ended December 31, 2025. There were no material changes to our critical accounting policies and estimates during the three months ended March 31, 2026.
Previous wording
See Note 2, Summary of Significant Accounting Policies, to our unaudited interim condensed financial statements for more information about recent accounting pronouncements, the timing of their adoption, and our assessment, to the extent we have made one yet, of their potential impact on our financial condition of results of operations.
Current wording
See Note 2, Summary of Significant Accounting Policies, to our unaudited interim condensed financial statements for more information about recent accounting pronouncements, the timing of their adoption, and our assessment, to the extent we have made one yet, of their potential impact on our financial condition or results of operations.
Previous wording
If we are a smaller reporting company at the time we cease to be an emerging growth company, we may continue to rely on exemptions from certain disclosure requirements that are available to smaller reporting companies. Specifically, as a smaller reporting company we may choose to present only the two most recent fiscal years of audited financial statements in our Annual Report on Form 10-K and, similar to emerging growth company’s smaller reporting companies have reduced disclosure obligations regarding executive compensation.
Current wording
If we are a smaller reporting company at the time we cease to be an emerging growth company, we may continue to rely on exemptions from certain disclosure requirements that are available to smaller reporting companies. Specifically, as a smaller reporting company we may choose to present only the two most recent fiscal years of audited financial statements in our Annual Report on Form 10-K and, similar to emerging growth companies, smaller reporting companies have reduced disclosure obligations regarding executive compensation.
Rearranged current paragraphs (1)
Current report — wording carried from elsewhere
The FDA has granted both Orphan Drug and Rare Pediatric Drug Designations to TN-301 as a treatment for DMD.
Rearranged previous paragraphs (4)
Previous report — wording carried elsewhere
Extensivein vitro andin vivo studies have shown that TN-301 addresses diverse pathological processes with direct and systemic benefits in models of HFpEF. In comparative studies, selective HDAC6 inhibition as a single agent has been shown to have similar efficacy to empagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor which is approved for the treatment of HFpEF and co-administration of our HDAC6 inhibition with a SGLT2 inhibitor in a HFpEF mouse model demonstrated additive benefit.
Previous report — wording carried elsewhere
The following table summarizes our results of operations for the periods presented:
Previous report — wording carried elsewhere
The following table summarizes our research and development expenses for the periods presented:
Previous report — wording carried elsewhere
Net cash provided by financing activities for the nine months ended September 30, 2024 was $47.4 million, which primarily consisted of net proceeds from our February 2024 follow-on offering of $46.8 million.