Tenaya Therapeutics, Inc.

Previous wording

Our lead investigational product candidates are TN-201, a gene therapy for MYBPC3-associated hypertrophic cardiomyopathy (HCM), TN-401, a gene therapy for PKP2-associated arrhythmogenic right ventricular cardiomyopathy (ARVC), and TN-301, a small molecule for heart failure with preserved ejection fraction (HFpEF).

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 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.

Previous wording

MyPEAK-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. We have completed Cohort 1 dosing at the 3E13 vg/kg dose with no unexpected events or toxicities associated with TN-201 observed. Following review of safety data from the first three MyPEAK-1 patients by an independent data safety monitoring board (DSMB), the DSMB endorsed our plan to escalate to the 6E13 vg/kg dose, per protocol and broaden eligibility criteria. In December, we dosed the first patient in the sentinel phase of Cohort 2 at the 6E13 vg/kg dose and we remain on track to complete Cohort 2 enrollment in the first half of 2025. We plan to present initial Cohort 2 data, along with an update on Cohort 1 patients, in the second half of 2025.

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 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.

Previous wording

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 has been 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) at post-dose and week 52 for Patients 1 and 2 and baseline to 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 post-dose. MyBP-C protein levels increased from 56 to 59% and from 62 to 64% of normal 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.

Current wording

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 wording

Promising early signals of TN-201’s clinical impact 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, whose levels are now normal or near normal. 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 and mild-to moderate heart failure symptoms that interfered in activities of daily living experienced improvements in New York Heart Association classification and achieved Class 1, indicating no limitations to physical activities due to symptoms of heart failure.

Current wording

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 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 in the second half of 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 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.

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.

Current 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).

Previous wording

We dosed the initial patient in RIDGE-1, 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 November 2024. We have activated multiple clinical trial sites at leading cardiology centers in the U.S. with ARVC expertise and intend to expand enrollment of RIDGE-1 to the United Kingdom. We expect to complete enrollment of the first cohort of patients at the 3E13 vg/kg dose in the first half of 2025. An independent safety review will then inform plans for dose escalation to 6E13 vg/kg and/or enrollment of additional patients in the first cohort. Initial clinical data from the first cohort of patients is expected in the second half of 2025. 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

Current 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.

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 Heart Rhythm 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

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.

Previous wording

TN-301 is our small molecule inhibitor of histone deacetylase-6 (HDAC6), initially being developed for the potential treatment of HFpEF. HDAC6 is a cytoplasmic enzyme known to regulate diverse cellular processes. TN-301’s multi-modal mechanism addresses diverse pathological processes and has shown 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. 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.

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, and based on TN-301’s multi-modal mechanism of action, TN-301 may have future potential in a number of related cardiometabolic conditions. 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. 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.

Previous wording

a decrease of $1.0 million in manufacturing costs reflecting lower employee-related costs driven by our workforce reduction initiated in May 2024 (the 2024 Workforce Reduction), lower costs of supplies and materials and lower facility management fees; and

Current 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;

Previous wording

a decrease of $1.9 million in clinical trial related costs primarily driven by a decrease in clinical support costs, including clinical supply chain services and regulatory consulting fees.

Current 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

Previous wording

a decrease of $0.7 million in other research and development costs reflecting lower employee-related costs driven by the 2024 Workforce Reduction.

Current 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.

Previous wording

General and administrative expenses were $6.5 million and $8.7 million for the three months ended March 31, 2025 and 2024, respectively. The year-over-year decrease of $2.2 million, or 26%, was primarily due to decreases in employee-related costs driven by the 2024 Workforce Reduction and lower professional fees.

Current 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.

Previous wording

Interest income primarily consists of interest earned on our cash, cash equivalents and investment balances. The interest income was $0.6 million and $1.5 million for the three months ended March 31, 2025 and 2024, respectively. The year-over-year decrease of $0.8 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 $0.8 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.

Previous wording

Net loss for the three months ended March 31, 2025, was $26.9 million, compared to a net loss of $32.2 million for the three months ended March 31, 2024.

Current 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.

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 March 31, 2025, we have funded our operations primarily from the sale and issuance of our equity securities. As of March 31, 2025, we had cash, cash equivalents and investments in marketable securities of $88.2 million and an accumulated deficit of $541.3 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 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.

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. In April 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 six months ended June 30, 2025, the Company received $0.6 million from CIRM in connection with the grant.

Previous wording

On August 6, 2024, we entered into a Loan Agreement with Silicon Valley Bank (SVB). As of March 31, 2025, under the Loan Agreement, we have the right to draw down $22.5 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 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.

Previous wording

Based on our current operating plan, we believe that our existing cash, cash equivalents and investments in marketable securities, along with the $22.5 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.

Current wording

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.

Previous 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 of 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.

Current 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.

Previous wording

Net cash used in operating activities for the three months ended March 31, 2024 was $28.7 million, which consisted primarily of a net loss of $26.9 million and a net change in operating assets and liabilities of $3.6 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 $3.1 million and a decrease in operating lease liabilities of $1.1 million, partially offset by a decrease of prepaid expenses and other current assets of $0.4 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 $4.2 million and depreciation and amortization of $2.2 million.

Current 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.

Previous 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.

Current 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.

Previous wording

Net cash used in investing activities for the three months ended March 31, 2024 was $4.5 million, which consisted primarily of purchases of marketable securities of $23.6 million, partially offset by proceeds from maturities of marketable securities of $19.7 million.

Current 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.

Previous 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.

Current 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.

Previous wording

Net cash provided by financing activities for the three months ended March 31, 2024 was $46.8 million, which primarily consisted of net proceeds from the follow-on offering of $46.8 million.

Current 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.

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 months ended March 31, 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 six months ended June 30, 2025.