Hi everyone, and thank you for joining us today. I'm Michelle Corral, Vice President of Corporate Communications and Investor Relations at Tenaya. Today we are excited to present initial data from Cohort 1 of the RIDGE-1 Phase 1b/2 clinical trial of TN-401 gene therapy for the potential treatment of PKP2-associated arrhythmogenic right ventricular cardiomyopathy, or otherwise known as ARVC. On the call with me are Faraz Ali, Tenaya's Chief Executive Officer, Dr. Kathy Ivey, our SVP of Research, and Dr. Whit Tingley, Tenaya's Chief Medical Officer. While the data we are disclosing will be described in full verbally, please note that during the course of today's call we will be making references to slides. A PDF file of these slides is available on the Tenaya website in the IR section under Events and Presentations. As a reminder, the information discussed during this call will include forward-looking statements which represent the company's view as of today, December 11th, 2025. These statements involve certain assumptions, and we caution investors not to place undue reliance on this information. Please refer to today's press release as well as our filings with the SEC for information concerning risk factors that could cause actual results to differ materially from those expressed or implied by these statements. In addition, I'd like to remind folks that we are unable to take questions on today's call due to the launch of a follow-on offering. That being said, we always welcome the opportunity to engage and look forward to our next opportunities to do so. Please reach out to me directly with any questions or to set up time with our team. With that introduction complete, let me turn the call over to Faraz Ali for opening remarks. Faraz? Thank you, Michelle, and thanks to everyone for joining us today. Tenaya has made significant progress in the past year across our two gene therapy programs. And while the focus of today's call is on the compelling early data generated from our TN-401 program, we also want to take a moment to share a positive update on TN-201, our gene therapy program for MYBPC3-associated hypertrophic cardiomyopathy, or HCM. We are pleased to share that the procedural clinical hold that was placed on the MyPEAK-1 trial of TN-201 has been lifted by the FDA. As you may recall, the hold was instituted following our proactive outreach to the agency to share clinical data from the TN-201 program and to discuss next steps for development. We amended the MyPEAK-1 protocol per FDA request to incorporate learnings related to patient monitoring and management of the immune suppression regimen. We were completely aligned with the FDA's suggestions, and after addressing all of their questions and concerns, the hold was lifted within about five short weeks after it was first put in place. We're now proceeding with the implementation of those changes to the MyPEAK-1 trial protocol. Where applicable, we are also proactively doing so in the RIDGE-1 protocol for this TN-401 study, although that was not formally requested by the FDA. Now, on to today's focus, which is TN-401. We are thrilled to be sharing the first look at results from Cohort 1 of the RIDGE-1 Phase 1b/2 clinical trial of TN-401 for PKP2-associated ARVC, a genetic form of arrhythmogenic cardiomyopathy. On slide three, we're jumping right into the results at a high level. First, TN-401 has been well tolerated at the 3e13 vector genome per kilogram dose. DSMB clearance has been achieved to move to Cohort 2, and Cohort 2 has been fully dosed. We're waiting for DSMB clearance. Now, from the available biopsies we have in hand to date, we see consistent evidence of TN-401 DNA reaching cardiomyocytes and consistent expression of RNA that's being transcribed. Importantly, as we look from baseline to week eight biopsy data, PKP2 protein levels have increased significantly by a mean of 10% in two of three patients. Finally, and very excitingly, we are seeing early evidence of clinical impact on electrical instability, a hallmark of the disease, with significant and clinically meaningful drops in PVC counts of 46%-89%, along with positive changes in non-sustained ventricular arrhythmias, or NSVTs. We are very encouraged by the emerging safety profile, biopsy, and initial clinical results that we can share with you today. Should our data continue in line with these encouraging early results, we believe TN-401 has the potential to make a profound difference in the lives of PKP2-associated ARVC patients. We look forward to following the patients from both those cohorts. We look forward to dosing more patients following DSMB clearance to move in the direction of the expansion cohort, and we look forward to exploring opportunities to transition to late-stage clinical development and pivotal studies potentially as early as 2026. However, before we go deeper into the data, I'd like to provide some context on slide four for the disease and our objectives with TN-401 gene therapy. ARVC is a rare progressive genetic familial disorder characterized by ventricular arrhythmias. During the course of the disease, cardiac muscle is replaced with fibrofatty tissue, and enlargement of the ventricle occurs. At the same time, the degradation of the tissue contributes to electrical instability, resulting in arrhythmias that endanger patients' lives and that may exacerbate the buildup of scar tissue. Now, PKP2 is the most common genetic mutation responsible for approximately 40% of cases. The PKP2 form of ARVC is estimated to affect approximately 70,000 people in the USA alone. In PKP2-associated ARVC, the average age of symptom onset and diagnosis is a young 30 years of age. Symptoms may include syncope, palpitations, and lightheadedness, but it's estimated that about a quarter of people with ARVC present with sudden cardiac death, which speaks to the unmet need. Quality of life may also be significantly impacted. Current treatments consist of beta-blockers and antiarrhythmic drugs, both of which can cause side effects. A large portion of patients receive an ICD that can shock their heart back into normal rhythm. While life-saving, the shocks themselves can be traumatic. Last but not least, patients are typically placed on exercise restrictions and warned to avoid any exertion that could trigger an event. All of these factors contribute to diminished quality of life. On slide five, we offer a closer look at the key characteristics associated with PKP2 disease. ARVC is generally divided into three distinct phases of progression. The concealed stage is primarily asymptomatic. At this early phase of disease, it may be difficult to detect irregular rhythms or structural abnormalities. In the overt electrical stage, symptoms emerge, and the risk of dangerous arrhythmias increase. Rhythm irregularities are apparent on ECG. End-stage or structural dysfunction stage of the disease is when changes to the heart, such as the distortion of the right ventricle, are visible via imaging. Patients are at risk of sudden cardiac arrest and death, and heart failure symptoms may emerge. However, it's important to point out that dangerous arrhythmias, including sudden cardiac arrest or death, can occur at any stage, including during the concealed stage, before patients are even aware that they're at risk. Data from our RIDGE natural history study of PKP2-associated ARVC tells us that genotype matters, influencing disease course and disease burden. These findings are reaffirmed in the literature that tell us that PKP2 patients are more likely to suffer consequences of electrical instability versus heart failure. In fact, among PKP2-positive patients, electrical instability and its associated risks predominate. Specifically, our data tell us that greater than 80% carry a high PVC burden despite standard of care therapies and surgical interventions, and nearly half have a history of ventricular tachycardias, whereas approximately 51% have apparent right ventricular dysfunction, but only 30% have left ventricular involvement or heart failure symptoms. We want to bear this background on disease burden in mind as it provides disease-specific insights for why we're excited by the results we're sharing at this early time point. On slide six, we provide an overview of the RIDGE natural history study, which we just referred to on the prior slide. RIDGE is now the largest known natural history study for PKP2 disease, with nearly 190 patients enrolled across 21 sites in six countries and with greater than 2,500 patient years of follow-up. We believe the insights provided by RIDGE offer us a unique competitive advantage, particularly as we head into later stages of development, providing context for how to interpret emerging results from our clinical trials, enabling us to make smarter choices about future enrollment, and enables us to have smarter discussions with regulatory agencies about trial design and endpoints for either accelerated or full approval. Underpinning the distinct experience of patients with PKP2 variants is the mutation itself. So on slide seven, we start with a closer look at the important role of the PKP2 protein. Heart muscles, known as cardiomyocytes, must be connected to one another to move in careful synchrony with every beat. The space where cardiomyocytes are linked is the intercalated disc made of different protein structures. Among the protein structures that work in the discs are gap junctions, which provide pathways for electrical signaling, and the desmosome, a collection of interdependent proteins that together provide the structural integrity by providing the velcro holding cardiomyocytes together. In addition to its mechanical role, the desmosome supports electrical firing. Now, PKP2 is a critical protein in the desmosome and serves as a linchpin for structural and electrical stability to coordinate heartbeats. This background helps set up what we are trying to do in our TN-401 program on slide eight. PKP2, as we described, is a critical protein in the desmosome, and the loss of the PKP2 protein as occurs in patients with PKP2 gene mutations results in profound destruction to the heart. TN-401 gene therapy is intended to address this underlying genetic problem. TN-401 delivers a full-length functional human PKP2 gene using a well-validated AAV9 capsid and a cardiac-specific promoter. Once delivered to cardiomyocytes, TN-401 produces PKP2 protein to restore missing protein that is caused by the mutation. Importantly, the protein produced is indistinguishable from the wild-type protein that is already there. In our three clinical studies that have been published, TN-401 reversed electrophysiological problems such as PVCs and NSVTs. TN-401 halted the progression of adverse remodeling and heart failure and extended survival in the animal model. The goal for TN-401 is to achieve a similar treatment effect in humans, and based on the data we will present today, we are off to a good start. With that, I'd like to ask Dr. Whit Tingley, our Chief Medical Officer, to tell us about the RIDGE-1 clinical trial and the first patients to receive TN-401 and the early and exciting data we're seeing thus far. Whit? Thank you, Faraz, and good evening, everyone on the line. Our RIDGE-1 Phase 1b/2 trial is designed to characterize the safety of TN-401, to identify a dose for future studies, and to assess pharmacodynamic measures of efficacy. We have completed enrollment of both cohorts and look forward to reviving the emergency data at the DSMB and potentially opening a second expansion cohort. The preliminary data that we will review today focuses on safety, biopsy, and clinical results from Cohort 1 at the 3e13 vector genome per kilogram dose. Slide 11 shows the baseline characteristics of the three participants in Cohort 1. In the shaded column on the left, we've included data for the average PKP2-positive ARVC patient based on the participants in the RIDGE natural history study that Faraz just described. The three participants in Cohort 1 have high-risk features typical of PKP2-associated ARVC. In particular, all three have undergone ventricular tachycardia ablation procedures and implantation of cardiac defibrillators to prevent sudden cardiac arrest. Despite these procedures, plus standard of care medication, they remain electrically unstable, manifest by high PVC count, with persistent risk of life-threatening arrhythmias. Each of these three participants enrolled in Cohort 1 after participating in the RIDGE natural history study. Slide 12 provides their relevant past medical histories. Among all three, we see commonalities of their disease that appear to be in line with this genotype. Patient one, diagnosed about 15 years ago, has struggled with recurrent serious ventricular arrhythmias over the last two years, requiring multiple ICD-mediated therapies, both anti-tachycardia pacing and electrical shock. Patient two, diagnosed at the young age of 16, has been living with PKP2-associated ARVC for 20 years and required an AICD at age 20. In spite of a prior ventricular ablation and multiple antiarrhythmic agents, he experienced a cluster of ICD shocks and anti-tachycardia pacing. Patient three also had a history of VT ablation and persistently high PVC counts. Elevated PVC counts are associated with the greater risk of life-threatening ventricular arrhythmia. The medical history of these three patients is generally consistent with our findings from the RIDGE natural history study overall. Standard of care medications and procedures are not sufficient to control this disease. As a reminder, the primary purpose of the RIDGE-1 clinical trial is to establish the safety and tolerability of TN-401 gene therapy. At Tenaya, we have taken a comprehensive approach to safety, summarized on slide 13. We know what to focus on from our prior experience, and we incorporate new learnings from the field. We are very thankful for the robust collaborations between sponsors, all working to optimize safety protocols for all of our patients. Safety is multifactorial, including selection of a proper capsid, design of the cassette, close attention to immunosuppression, selection of dose, and safety monitoring. Capsid selection, AAV9, has a large safety track record through its commercial use for spinal muscular atrophy and is also the best validated for cardiac gene therapy at low doses in the 3e13 vector genome per kilogram range. Immunosuppression, we use common prophylactic immunosuppressive agents, prednisone and sirolimus, which have served us well across both of our gene therapies, TN-201 and TN-401. The timing of immunosuppression initiation and tapering regimen matters, and we have been able to refine these to reduce the total dose of prednisone, as we shared last month at the American Heart Association. We have never needed to use a complement inhibitor. Dose, we are encouraged by the signs of efficacy we are seeing in both programs at a dose of the 3e13 vector genome per kilogram and do not need to escalate into the E14 dose range where safety can be more problematic, and finally, monitoring, frequent monitoring of safety laboratories is the key to safely managing the immune system's response to AAV in the days to weeks after infusion. Slide 14. For the data readout today, we are focusing on Cohort 1. These patients have had 20- 40 weeks of follow-up. We are very encouraged by the positive safety profile emerging for TN-401 that has been well tolerated to date. For Cohort 1, the majority of related adverse events have been mild, asymptomatic, and manageable. Transient mild elevations of transaminases have been easily managed. One mild, Grade 1 out of 5 troponin elevation is classified as an SAE only because it was monitored in the hospital. It resolved spontaneously without treatment and had no sequelae. Importantly, there has been no evidence of cardiac inflammation by imaging and cardiac biopsy and no evidence of proarrhythmic effects. There have also been no clinical TMA events, and complement inhibitors have not been used. All patients in Cohort 1 have tapered off immunosuppressants and remain on study. Cohort 2 patients, dosed more recently, are at various stages of the taper now. I will now hand over to Dr. Kathy Ivey to go over the encouraging biopsy results from Cohort 1. Thank you, Whit. I'm glad to be here today to share the data we've obtained from each of these precious biopsies. Turning to slide 16, in RIDGE-1, biopsies are taken at three junctures. These are pre-dose or baseline, week eight, and week 52. Using a catheter, a small snip of tissue about the size of a peppercorn is taken from the cardiac septum. Six to eight of these tissue samples are collected in the cath lab and receive an initial visual inspection for quality, and then each of these precious tissue samples is preserved and earmarked for specific quantitative analyses of DNA, RNA, or protein. The measurements collected during these biopsy sample analyses allow us to affirm that our gene therapy is reaching the heart, entering the cardiomyocytes and producing messenger RNA, which ultimately provides instructions needed for the cell to produce more PKP2 protein. Results on slide 17 provide evidence that TN-401 DNA is consistently reaching cardiomyocytes and being robustly transcribed into PKP2 mRNA. The bar chart on the left side shows the effective transduction of TN-401, which is achieving robust vector copy numbers per host genome of 3.4 and five vector copies per cell for patients one and two, respectively. On the right-hand side of the slide, we see clear evidence of RNA expression, which is measured as transcript copies per microgram of RNA. As a reminder, the PCR assay used here detects only mRNA produced by TN-401 with high sensitivity and specificity. Preclinically, the TN-401 RNA levels continued to increase over the first year, and we look forward to results from future biopsies of these patients. On slide 18, we can see protein levels from biopsies taken pre-dose and at week eight. Since PKP2 protein from TN-401 is identical to the patient's endogenous PKP2 protein, total levels of PKP2 are reported. Following the TN-401 treatment, PKP2 protein in the heart increased by 11% and 9% in patients one and two. All patients' baseline PKP2 protein levels were below normal, consistent with PKP2 haploinsufficiency. As with mRNA, we would expect protein levels to increase somewhat over time based on pre-clinical and clinical experience, and we are very pleased by the magnitude of increase we are seeing at this early time point. Turning to slide 19, we note that patient three's protein change is within the noise of the assay. Based on the extent of TN-401 mRNA expression we detected in this patient at eight weeks, we believe this protein result is simply attributable to the inherent variability between samples, and we look forward to the opportunity to analyze future biopsies from this individual. On slide 20, we outline the challenges of accurately measuring and comparing PKP2 protein levels in patient biopsies and why our carefully developed method provides a reliable and consistently quantifiable result. As a result of fibro-fatty replacement associated with disease, ARVC cardiac tissue is highly heterogeneous with variable cardiomyocyte content in different samples. Since PKP2 is expressed primarily in cardiomyocytes, overall PKP2 levels in individual biopsies will be inherently variable based on cardiomyocyte composition in any given biopsy. The image on the left shows a section of cardiac tissues from an ARVC donor heart with two encircled areas that could each represent a 1-2 millimeter biopsy. The area on the left in the dark blue circle contains a higher proportion of cardiomyocytes than the area on the right in the red circle, which contains more fibro-fatty replacement. A key step built into our protein analysis accounts for this difference in composition by normalizing PKP2 levels to levels of the cardiomyocyte-restricted protein, myosin heavy chain, or MYH. The graph on the right shows PKP2 levels measured from the same five normal donor hearts, but using three different methods: liquid chromatography mass spec, or LCMS, with normalization to MYH, or Western blot with a standard curve to calculate absolute PKP2 levels, or normalized to the ubiquitously expressed protein, GAPDH. Without normalization to the myocyte-specific protein, Western results show up to seven-fold difference between these five normal donor hearts. In comparison, LCMS normalized to MYH results in a twofold difference in PKP2 protein between these same five hearts. The variability that occurs when cardiomyocyte composition is not taken into account may be further intensified in samples from diseased hearts due to their higher degree of heterogeneity. A KOL webinar we conducted in August 2025 with Dr. Mike Previs, an expert in cardiac protein quantification methods, provides a more fulsome explanation of our methodology and its merits and is available on our website. On slide 21, we have representative images of the changes we've observed in PKP2 protein levels following gene therapy treatment. Using multiplexed immunofluorescence, we can visualize not only PKP2 protein, but also N-cadherin and the gap junction protein connexin 43, co-localized at intercalated disc. We know that in the setting of PKP2 haploinsufficiency, such as this patient's pre-dose biopsy, not only are PKP2 protein levels decreased, but as a result, desmosome structures are degraded, and there's a decrease in the levels of other intercalated disc proteins. Patient one's eight-week biopsy shows both an increase in PKP2 protein compared to baseline, as well as more structured intercalated discs with a higher degree of connexin 43 and N-cadherin and co-localization. Together, these data provide visual confirmation of what we are observing by LCMS. I'd like to invite Whit back to tell us about observed clinical changes at this point in the trial. Whit? Thank you, Kathy. While today's readout was always intended as an early look to focus on safety and biopsy results, we are pleased to be able to share promising clinical data on arrhythmias as well. As mentioned in PKP2-associated ARVC, electrical instability is the hallmark of disease, and sudden cardiac arrest due to ventricular arrhythmias is the most feared consequence. Across the top of slide 23, we share the continuum of ventricular arrhythmias based on frequency and severity. The most severe arrhythmic event, ventricular fibrillation and sudden cardiac arrest, are thankfully rare compared to other ventricular arrhythmias. At the other end, there are premature ventricular contractions, single abnormal beats, and non-sustained ventricular tachycardia, runs of fast arrhythmias lasting up to 30 seconds. These can be symptomatic. They cause significant anxiety, and they're frequent, hundreds to thousands of times per day in the case of premature ventricular contractions. These are valuable indicators of electrical stability that can be monitored in real time in our trial. PVCs and non-sustained VT are also direct measures of disease severity and risk of life-threatening arrhythmias. High counts are associated with high risk. PVCs and NSVTs can directly trigger the more severe ventricular arrhythmias. The values, the numbers of PVCs and the presence of non-sustained VT are used to calculate risk in ARVC patients and make decisions about implanting cardiac defibrillators. The goal of TN-401 is to stabilize the PVCs, reduce NSVT, and prevent life-threatening ventricular arrhythmias. Slide 24 shows initial PVC data from Cohort 1. Clinically meaningful reductions in PVCs were observed in the first two patients for whom we have the longest follow-up beyond six months, specifically reductions of 46% and 89% at their most recent visit. Patient three remains essentially unchanged at this early time point. Given the relatively early stage of this trial, we are excited by the emerging evidence of TN-401's potential to impact disease, promote electrical stability, and reduce this critical risk factor for life-threatening ventricular arrhythmias. Slide 25 shows NSVT rates for Cohort 1. Patient two had a very high burden of NSVT at baseline, 78 per day. Importantly, we measure arrhythmias over the course of a full week, and 78 was the average daily number, so this patient was experiencing a very large number of NSVTs. It is great to see that fall to zero at week 32. Patients one and three had lower burdens of NSVT at baseline, so we would not expect to see a large signal. Other measures of clinical response, including QRS duration, T-wave inversion, heart function, and New York Heart Association class, were in the normal range or remained stable. In all, we are thrilled by the data emerging from the 3e13 dose of TN-401. To date, the safety profile looks promising, and biopsy data has been robust, as Kathy described. Most importantly, the clinical data show meaningful evidence of reduced arrhythmia burden and improved electrical stability, which are expected to substantially reduce the risk of sudden cardiac arrest. We are grateful to the trial participants and their families, to our investigators and the clinical site teams, and to our own Tenaya team, who have all been working tirelessly to advance these gene therapies for patients with severe genetic cardiomyopathy who need better options. I'd also like to recognize the important support provided by the California Institute for Regenerative Medicine, which has provided financial support for the TN-401 trial. Faraz, your closing thoughts? Thank you, Whit. Sorry, I was on mute. Thank you for that important update. Now, we're aware that we're not the only company that is operating in this space, and data has been presented by other gene therapy programs earlier this year. To place the results that we've just shared with you into context, we believe that across those measures where data can be compared, such as safety, DNA transduction, mRNA expression, and clinical measures of electrical instability, such as PVCs and NSVTs that Whit just shared, our results look quite favorable as compared to our peers working in the other gene therapy programs. That is even more so the case if you recall that we are operating at doses of only 3e13 vector genome per kilogram in this first dose cohort, which is less than half the dose of a peer program. Also important in that these data are at least at less than one year's follow-up for all patients with the opportunity to improve as more patients followed longer. We will now close with slide 27 that captures our progress and our future milestones. It has truly been a remarkable year of execution and momentum for Tenaya. Approximately this time last year, we were presenting our very first look at safety and biopsy data for TN-201. And just last month, we provided an exciting update for that program at the annual meeting of the American Heart Association, showing early but significant and clinically meaningful improvements for all three patients in the first dose cohort. That data was also concurrently published in Circulation Research. Today, with the presentation of these results for the TN-401 program, we now have shared evidence of disease modification in two programs and with internally consistent performance across multiple clinically significant parameters. This is the promise of genetic medicines such as TN-201 and TN-401, and we hope you'll agree that the data we shared for each of our gene therapy programs in the last month have been compelling. We're optimistic that they will continue to get even stronger over time. Executing on expressive milestones each year is in Tenaya's DNA, and as we end the year of 2025, this year is no exception. With the presentation of TN-401 Cohort 1 data, we will have accomplished everything we had set out to do this year and then some, including dosing patients and presenting data from our natural history studies and our clinical studies. We are now looking forward to a similarly productive 2026 as we drive each of these programs forward. We plan to share new meaningful data for TN-201 and TN-401 at key junctures throughout the year, with the goal of engaging with regulators in the pursuit of alignment on endpoints and trial design for late-stage and potentially pivotal studies. Thank you for joining us on the call, for your engagement, and for your support.