Tenaya Therapeutics, Inc.
For the period ended Sep 30, 2025. Filed Nov 10, 2025.
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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.
Sep 30, 2025 · Filed Nov 10, 2025
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 2025-06-30; filed 2025-08-06.
0000950170-25-104182
Item 2. Management’s Discussion and Analysis of Financial Condition and Results of OperationsCurrent 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 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 108 previous paragraphs and 110 current paragraphs.
68 unchanged; 33 reworded; 8 added; 6 removed; 1 previous and 1 current paragraphs rearranged.
Tables are not compared: 5 previous and 5 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 (8)
Current report
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 report
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 report
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 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.
Current 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:
Current report
Comparison of the Nine Months Ended September 30, 2025 and 2024:
Current 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:
Current 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
Removed paragraphs (6)
Previous report
In December 2024, we announced early but encouraging initial interim safety and biopsy data from Cohort 1 of MyPEAK-1, and in March 2025, we presented data from Cohort 1 in a Late-Breaker presentation at the 2025 American College of Cardiology Scientific (ACC) Sessions. Interim data presented at ACC included results from serial biopsies taken at two time points for all three patients and assessments of the first two patients at Week 52 and Patient 3 at Week 26. TN-201 was generally well tolerated at the 3E13 vg/kg dose, and treatment-emergent adverse events (AEs) were primarily mild, manageable and/or reversible. Biopsy data indicated robust transduction as evidenced by the sustained presence of TN-201 DNA in the heart (0.8 to 1.4 vg/dg) post-dose and at week 52 for Patients 1 and 2 and at Week 26 for Patient 3. TN-201 RNA expression was present at post-dose biopsies conducted in the first two patients at Week 8 and increased as much as 13-fold from Week 8 to Week 52. MyBP-C protein levels increased modestly between Week 8 and Week 52 for Patients 1 and 2, respectively. This increase, combined with the increase observed in TN-201 mRNA expression, suggests that TN-201 gene therapy is successfully being transcribed and expressed after reaching target cells.
Previous report
Promising early signals of TN-201’s efficacy suggesting clinical improvement or stability were observed across multiple parameters measured. Cardiac troponin, a biomarker of myocardial injury, was elevated in Cohort 1 patients at baseline and decreased by more than 60% in two patients to normal or near normal levels. NT-proBNP, a biomarker of cardiac strain, increased and remained elevated while patients were on immunosuppression, but returned to baseline as immunosuppressive drugs were discontinued. Two of three patients experienced improvements in one or more measures of hypertrophy, or enlargement of the heart, while other assessments remained stable. All Cohort 1 patients with objectively severe disease at baseline experienced improvements in New York Heart Association (NYHA) classification, moving from mild-to moderate heart failure symptoms that interfered in activities of daily living, Class II or Class III, to Class I, indicating no limitations to physical activities due to symptoms of heart failure.
Previous report
Research and development expenses were $17.4 million and $22.6 million for the three months ended June 30, 2025 and 2024, respectively. The year-over-year decrease of $5.3 million, or 23%, was primarily due to:
Previous report
Comparison of the Six Months Ended June 30, 2025 and 2024:
Previous report
Research and development expenses were $38.4 million and $47.7 million for the six months ended June 30, 2025 and 2024, respectively. The year-over-year decrease of $9.3 million, or 19%, was primarily due to:
Previous report
decreases of $1.6 million in other research and development costs and $1.0 million in research reflecting lower employee-related costs driven by the Workforce Reductions.
Reworded paragraphs (33)
Previous wording
You should read the following discussion and analysis of our financial condition and results of operations in conjunction with our condensed financial statements and related notes included elsewhere in this Quarterly Report on Form 10-Q and our audited financial statements and related notes thereto for the year ended December 31, 2024, included in our Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 10, 2025, or Annual Report.
Current wording
You should read the following discussion and analysis of our financial condition and results of operations in conjunction with our condensed financial statements and related notes included elsewhere in this Quarterly Report on Form 10-Q and our audited financial statements and related notes thereto for the year ended December 31, 2024, included in our Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 10, 2025.
Previous wording
We are advancing a deep and diverse pipeline of disease-modifying targeted therapies that includes both gene therapies and small molecules discovered internally and developed using our extensive core capabilities to address rare or highly prevalent forms of heart disease. All of our programs are currently being assessed in clinical trials or are in the preclinical stage; we do not have any products approved for sale and have not generated any revenue to date.
Current wording
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 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 clinical testing 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 on such programs.
Current 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.
Previous wording
TN-201 is our potential first-in-class and best-in-class gene therapy for adults and children 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 (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.
Previous 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 in both the 3E13 vg/kg dose (Cohort 1) and 6E13 vg/kg dose (Cohort 2) cohorts are complete. We plan to present initial Cohort 2 data, along with an update on Cohort 1 patients, in the fourth quarter of 2025. In July 2025, following review of safety data from the first six MyPEAK-1 patients by an independent data safety monitoring board (DSMB), the DSMB determined that TN-201 had an acceptable safety profile and endorsed proceeding into expansion cohorts at either dose level for TN-201, per protocol. We currently anticipate enrolling patients in the 6E13 vg/kg dose expansion cohort. Data from MyPEAK-1 is intended to inform dose selection and pivotal trial designs in pediatric and adult individuals with MYBPC3-associated HCM.
Current 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.
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 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. We plan to present data from MyClimb at the European Society of Cardiology Annual Meeting being held August 29 - September 1, 2025.
Current 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.
Previous wording
The U.S. Food and Drug Administration (FDA) 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 (EC).
Current wording
The FDA 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 (EC).
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. We completed dosing of three patients at the 3E13 vg/kg dose (Cohort 1) in April 2025. Per protocol, safety data from the first three RIDGE-1 patients were reviewed by an independent DSMB which endorsed both dose escalation to the 6E13 vg/kg dose cohort (Cohort 2) and expanding enrollment at the 3E13 vg/kg dose level. The first patient enrolled in Cohort 2 received TN-401 at the 6E13 vg/kg dose level in July 2025 and we are continuing to enroll patients in Cohort 2. We may also enroll additional patients at the 3E13 vg/kg dose level. Initial clinical data from Cohort 1 is expected in the fourth quarter of 2025.
Current 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.
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. Subsequent preclinical studies have shown that TN-301 addresses diverse pathological processes with a direct and systemic benefits inin vitro andin vivo studies of HFpEF. HFpEF is characterized by a stiffening of the heart muscle resulting in an inability for the left ventricle to relax and fill with oxygenated blood sufficient to meet the body’s needs. The pathophysiology of HFpEF is complex and is driven by metabolic dysfunction or oxidative stress and inflammation, with diverse conditions serving as risk factors for disease, including obesity, diabetes, aging, kidney disease and hypertension. Although HFpEF accounts for approximately half of all heart failures, there are few proven treatment options.
Current 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.
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. 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. 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 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. 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.
Previous wording
In addition to our lead product 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 heart disease.
Previous wording
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 ongoing clinical trials at our Good Manufacturing Practice (cGMP)-certified Genetic Medicines Manufacturing Center in Union City, California.
Current wording
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 wording
a decrease of $1.1 million in clinical trial related costs primarily driven by a decrease in clinical support costs, including clinical supply chain services and regulatory consulting fees; and
Current wording
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 wording
a decrease of $2.6 million in manufacturing costs reflecting lower employee-related costs driven by our workforce reductions initiated in March 2025 and May 2024 (together, the Workforce Reductions), lower costs of supplies and materials and lower facility management fees;
Current 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
Previous wording
a decrease of $3.7 million in manufacturing costs reflecting lower employee-related costs driven by the Workforce Reductions, lower costs of supplies and materials and lower facility management fees;
Current 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;
Previous wording
General and administrative expenses were $6.7 million and $8.2 million for the three months ended June 30, 2025 and 2024, respectively. The year-over-year decrease of $1.5 million, or 18%, 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 $5.6 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.
Previous wording
Interest income primarily consists of interest earned on our cash, cash equivalents and investment balances. Interest income was $0.8 million and $1.4 million for the three months ended June 30, 2025 and 2024, respectively. The year-over-year decrease of $0.6 million was primarily due to lower cash, cash equivalents and investment balances.
Current 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.
Previous wording
Net loss for the three months ended June 30, 2025, was $23.3 million, compared to a net loss of $29.4 million for the three months ended June 30, 2024.
Current 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.
Previous wording
a decrease of $3.0 million in clinical trial related costs primarily driven by a decrease in clinical support costs, including clinical supply chain services and regulatory consulting fees; and
Current wording
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 wording
decreases of $0.9 million in other research and development costs and $0.6 million in research reflecting lower employee-related costs driven by the Workforce Reductions.
Current wording
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 wording
General and administrative expenses were $13.2 million and $16.9 million for the six months ended June 30, 2025 and 2024, respectively. The year-over-year decrease of $3.7 million, or 22%, 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 $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 wording
Interest income was $1.4 million and $2.8 million for the six months ended June 30, 2025 and 2024, respectively. The year-over-year decrease of $1.4 million was primarily due to lower cash, cash equivalents and investment balances.
Current wording
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 wording
Net loss for the six months ended June 30, 2025, was $50.1 million, compared to a net loss of $61.7 million for the six months ended June 30, 2024.
Current wording
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 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 June 30, 2025, we have funded our operations primarily from the sale and issuance of our equity securities. As of June 30, 2025, we had cash, cash equivalents and investments in marketable securities of $71.7 million and an accumulated deficit of $564.6 million.
Current 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.
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 six months ended June 30, 2025, the Company received $0.6 million from CIRM in connection with the grant.
Current 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.
Previous wording
On August 6, 2024, we entered into a Loan Agreement with Silicon Valley Bank (SVB). As of June 30, 2025, under the Loan Agreement, we have the right to draw down $7.5 million at our discretion, up to an additional $2.5 million upon the satisfaction of a clinical milestone orthe receipt of specified proceeds from equity financings and other qualified funding, 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 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.
Previous wording
Net cash used in operating activities for the six months ended June 30, 2025 was $38.7 million, which consisted primarily of a net loss of $50.1 million and a net change in operating assets and liabilities of $2.4 million, partially offset by $13.3 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 $3.0 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 $7.4 million and depreciation and amortization of $4.7 million.
Current 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.
Previous wording
Net cash used in operating activities for the six months ended June 30, 2024 was $52.3 million, which consisted primarily of a net loss of $61.7 million and a net change in operating assets and liabilities of $5.6 million, partially offset by $14.2 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 $4.9 million and a decrease in operating lease liabilities of $2.2 million, partially offset by a decrease of prepaid expenses and other current assets of $1.1 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 $8.8 million and depreciation and amortization of $4.3 million.
Current 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.
Previous wording
Net cash provided by investing activities for the six months ended June 30, 2025 was $47.3 million, which consisted primarily of proceeds from maturities of marketable securities of $36.9 million and sales of marketable securities of $11.0 million.
Current 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.
Previous wording
Net cash provided by investing activities for the six months ended June 30, 2024 was $17.1 million, which consisted primarily of proceeds from maturities of marketable securities of $52.2 million, partially offset by purchases of marketable securities of $34.5 million.
Current wording
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.
Previous wording
Net cash provided by financing activities for the six months ended June 30, 2025 was $49.8 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 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.
Previous wording
Net cash provided by financing activities for the six months ended June 30, 2024 was $47.3 million, which primarily consisted of net proceeds from our February 2024 follow-on offering of $46.8 million.
Current wording
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.
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 six months ended June 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, 2024. There were no material changes to our critical accounting policies and estimates during the three and nine months ended September 30, 2025.
Rearranged current paragraphs (1)
Current report — wording carried from 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.
Rearranged previous paragraphs (1)
Previous report — wording carried elsewhere
Based on our current operating plan, we believe that our existing cash, cash equivalents and investments in marketable securities, along with the $7.5 million of funds available under our Loan Agreement with SVB, 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.