Good afternoon, everyone, and welcome to the ATI Pharmaceuticals 3rd Quarter 2025 Financial Results and Business Update Conference Call. At this time, all participants are in listener mode. Following the formal remarks, we'll open the call up for your questions. I would now like to turn the call over to Joni Barnes, Senior Vice President of Investor Relations and Corporate Communication at ATI Pharmaceuticals. Ms. Vaughn, please proceed.

Thank you, Operator. Good afternoon, everyone, and welcome to Atea Pharmaceutical's third quarter 2025 financial results and business update conference call. Earlier today, we issued a press release which outlines the topics we plan to discuss. You can access the press release as well as the slides that we'll be reviewing today by going to the investor section of our website at ir.ateapharma.com. With me from Attea are Chief Executive Officer and Founder, Dr. John-Pierre Somodosi, Chief Development Officer, Dr. Janet Hammond, Chief Medical Officer, Dr. Arantia Horga, Chief Commercial Officer, John Vavrica, and Chief Financial Officer and Executive Vice President of Legal, Andrea Corcoran, all of whom will be available for the Q&A portion of today's Before we begin the call, and as outlined on slide two, I would like to remind you that today's discussion will contain forward-looking statements that involve risk and uncertainties. These risks and uncertainties are outlined in today's press release and in the company's recent filings with the Securities and Exchange Commission, which we encourage you to read. Our actual results may differ materially from what is discussed on today's call. With that, I'll now turn the call over to Jean-Pierre.

The 2020 treatment duration review that we announced today, in addition, antiviral medical need of immunocompromised patients living with hepatitis E infection. We have identified candidates derived from our nucleotide platform. IND-enabling studies are ongoing to select a clinical candidate which phase one initiation anticipated in mid-2026. More detail with today's presentation. At the end of the third quarter, we maintain a strong balance sheet with approximately $329.3 million in cash, cash equivalent, and marketable securities, providing runways through 2027. The strong cash position enables us to fully fund our phase three program, launch the new regimen, new HCV development program. I will now turn the call over to Janet to review the highlights of the presentation at the deliver meeting. Janet?

Thanks, Jean-Pierre. Let's move to slide five. I'm pleased to share with you that a few days ago we presented multiple data sets at the liver meeting. These data reinforce the strong clinical and pharmacologic profile of our fixed-dose combination of regimen of Benifostivir and Rulivir for the treatment of HCV. In an oral presentation, multi-scale modeling results predicted that our combination regimen inhibits both the intracellular replication of HCV as well as viral assembly and secretion of new HCV virions in the bloodstream. The model predicted a cure time of approximately seven to eight weeks. Because the regimen suppresses the virus at multiple critical stages, these data reinforce the potential of the combination regimen as a potent short-duration therapy for chronic HCV. We also presented two posters. The first poster was identified as a poster of distinction. It highlighted a resistance analysis from the Phase II study of our regimen, demonstrating that SVR-12 rates were not impacted by NS5A resistance variant at baseline. Viral kinetics and pharmacokinetic analyses indicated that most of the viral failures were due to treatment non-adherent and not to viral resistance. The second poster reviewed the results from a Phase I study in healthy participants, which demonstrated the high relative bioavailability of the Benifosavir and Ruzesvir commercial formulation for the fixed-dose combination. These data also support dosing of the fixed-dose combination with or without food and with homotidine, an H2 blocker, which can substantially diminish the effectiveness of oral antivirals. The six-dose commercial formulation is being used in our ongoing phase three program. Moving to slide six, we will host a virtual panel event featuring key opinion leaders, or KRLs, in hepatology, gastroenterology, infectious diseases, and Hepatitis C tomorrow, Thursday, November the 13th at 10 o'clock Eastern Time. The discussion will cover a wide range of HCV-related topics, including the needs of the current HCV patient population, the importance of early diagnosis and treatment, public policy initiatives including the test and treat model of care, and whether HCV eradication in north america is an achievable goal what benefits a new optimized hcv therapy could provide for prescribers and patients the link to register for this event can be found in our latest quarterly press release distributed earlier today and on the investor section of our website under events and presentations the virtual panel discussion will feature several hcv key opinion leaders, including Jordan Feld from the University of Toronto, Toronto General Hospital in Canada, Eric Larwitz from the Texas Liver Institute, University of Texas Health San Antonio, Anthony Martinez from the University of Buffalo Erie County Medical Center, and Nancy Rowe from Rush University Medical Center in Chicago. A live question and answer session will follow the formal discussion. We hope you can join us. I'll now hand the call over to Arantxa to review our Phase 3 program for hepatitis C. Arantxa?

Good afternoon, everyone. On slide 8, let's now turn to our global Phase 3 program, which is the first head-to-head Phase 3 program for chronic hepatitis C, comparing our regimen against the current global standard of care, so phosphovir and Belpatavir, marketed as Eclusa. Our regimen includes Benifosfavir, the most potent nucleotide inhibitor, and Rusfavir, a highly potent NS5A inhibitor. Data support our regimen as a potential best-in-class treatment option for patients infected with HIV, HCD, with a differentiated profile featuring a short duration, low risk of drug-drug interactions, and convenience with no food effect. I would like to highlight that we have new study results demonstrating no risk of drug-drug interactions with proton pump inhibitors, which are estimated to be taken by at least 35% of HCD patients. These results will be presented at an upcoming scientific meeting. We view this as A-key differentiator since proton pump inhibitors can substantially decrease the effectiveness of currently approved DIA therapies for HCV. Our Phase III program is designed to confirm the efficacy, safety, and clearability demonstrated in our robust Phase II study, where we achieved a 98% sustained biological response at 12 weeks post-treatment or SDR-12. These Phase II results gave us confidence to move to our current Phase III late-stage program. Historically, in HCV development, Phase II data have proven to be highly predictive of Phase III outcomes given the well-understood biology of the virus and the reliability of SDR-12 as an established clinical endpoint for cure. Moving to slide nine, the global phase three program is composed of two pivotal trials, C-Beyond, which is enrolling across approximately 120 sites in the U.S. and Canada, and Seaforward, which includes another 120 sites across 16 countries outside of North America. Combined, these studies are expected to enroll approximately 1,760 patients. Both trials are open-label and randomized one-to-one against the active comparator, and they are stratified by cirrhosis status and genotype, including HIV co-infected patients. In non-cirrhotic patients, treatment duration is eight weeks compared to 12 weeks with the standard of care. For patients with compensated cirrhosis, patients receive 12 weeks of either regimen. The primary endpoint for both studies is SBR12, which is recognized as the definitive measure of HCV cure. Slide 10. I am pleased to confirm that enrollment in the North America Sea Beyond trial is on track for completion next month, with top-line results anticipated mid-2026 For CForward, which has a broader global geographic footprint, enrollment completion is expected mid-2026, followed by top-line results by year-end of 2026. I will now hand the call over to Jean-Pierre to review our new mechanism of action data.

Jean-Pierre? using data HCV variants in the bloodstream, significantly reducing extracellular HCV RNA, a mechanism previously inhibitors such as protein, in vitro studies conducted under another collaborative university, a mechanism of action for benifazvivir. The intracellular HCV RNA were compared with fosbivir and sofosbivir. So while both produced this similar decline in cvRNA, as you can see, benifosbivir led to a far greater and faster reduction in extracellular RNA, indicating possible inhibition into the bloodstream. At 14 now, another individual study shows that intracellular RNA, HCV RNA, the concentration of benifosvivir and NS5A inhibitors such as VELPASTAV. Important here, extracellular HCV RNA level decreased similarly to benifosvivir or VELPASTAV, demonstrating that benifosvivir or HCV assembly and secretion into the bloodstream in addition to inhibiting viral replication. In 2016, you can see this cartoon, which illustrates on the left side, the cycle, and then on the right side, the dual-mechanism fraction for beniforzbeving, showing how beniforzbeving blocks the virus from making copies inside the cell, which also blocks new virus from in terms of 2016, what the data means. Benefosivir is a potent and differentiated nucleotide prodrug with a unique dual mechanism of action, which may explain, now, the higher potency of Benefosivir as compared to Sofosivir. Importantly, even in the presence of NS5, Benefosivir will convey the differentiation and the potency of the Benefosivir and Resosivir regimen for the job for an overview of the new hepatitis E virus program.

Thank you, Jean-Pierre. As shared earlier by JP, we are expanding our pipeline of oral direct acting antiviral candidates to include hepatitis E virus, or HEV, a virus with no approved therapies and high on medical needs. As seen on slide 18, the WHO estimates that there are 20 million global infections annually. HIV is an inflammation of the liver caused by the hepatitis E virus. It is a growing public health challenge in both the developed and developing world. In developing countries, genotypes 1 and 2 are most prevalent, and the virus is transmitted primarily through contaminated water. In developed countries, genotypes three and four are most prevalent, and the virus is transmitted primarily through contaminated foods such as undercooked meat. Moving to slide 19, however, in recent years, there's been a growing incidence of chronic HEV genotype three and four infections in immunocompromised individuals, a population that includes solid organ transplant recipients, hematopoietic stem cell transplant recipients, as well as patients with hematological malignancies and preexisting liver disease. In these patients, HEV may not resolve spontaneously resulting in chronic HEV infections, which left untreated can quickly lead to liver inflammation, rapid fibrosis progression, and, in some cases, cirrhosis within three to five years of infection. Currently, there are no approved therapies anywhere in the world for HEV. For at-risk populations, clinicians can reduce immunosuppression, which risk organ rejection or relapse of underlying disease. Some clinicians also use ribavirin, an older antiviral therapy, approved for other viral indications, off-label for HEV, which yields inconsistent efficacy results and is often poorly tolerated and poses risk of significant toxicities. This leaves clinicians and patients with a significant unmet need for a safe, orally available, direct-acting antiviral that can achieve sustained viral clearance or cure. Let's move on to slide 20. The number of immunocompromised patients continues to rise each year in the U.S. and Europe. There are approximately 450,000 cases of solid organ transplants, hematopoietic stem cell transplants, and hematological malignancies per year across these markets. While advances in modern medicine, especially in transplantation and oncology, have led to an increased survival, it may likely also explain why more HEV is being observed in these at-risk populations. Approximately 3% of these at-risk patients go on to develop chronic HEV. While the overall prevalence of HEV is high in the general population, a relatively smaller proportion of immunocompromised patients are at risk for poor outcomes. As such, there is the potential to seek an orphan drug designation, which can have development and regulatory advantages. Okay. These light-saving procedures continue to expand the population of immunocompromised patients that could be susceptible to chronic HEV infections. Using other viral infections, such as hepatitis C virus, as a guide to pricing, this HEV market opportunity could translate into roughly between $500 to $750 million per year or more. I will now turn the call back to Jean-Pierre to review preclinical data for our two candidates for HEV. JB?

The in vitro data on this slide and AT2490 antiviral platine, antiviral activity in vitro, HEV, and that's how we do HEV activity, AT587 and AT2490 led us to advance. It's interesting to point out in the sugar, AT9067, AT587 and AT2490 as compared to to AD9010, which is the active triphosphate. Candidates efficiently convert to the active triphosphate form in human hepatocytes. Clinical safety profile to date, positioning them as leading candidates for first-in-class. Select the clinical candidate. We would be presenting more in each EV program at a scientific meeting early next year.

Thank you, Jean-Pierre. As Jonay mentioned in her introductory remarks, earlier today we issued a press release containing our financial results for the third quarter of 2025. The statement of operations and balance sheet can be found on slides 24 and 25. In the third quarter of 2025, R&D expenses increased compared to the same period in 2024. This increase was principally attributable to increased spend in 2025 in our HCV Clinical Development Program. For G&A, expenses in the third quarter of 2025 decreased in comparison to third quarter 2024. The decrease was primarily driven by lower 2025 stock-based compensation. Interest income in Q3 2025 decreased compared to the third quarter of 2024 due to lower investment balances. For the remainder of 2025, we expect our R&D expenditures will be driven principally by the conduct and advancement of our global Phase III HCV program. As Jean-Pierre mentioned at the beginning of the call, at the end of third quarter of 2025, our cash, cash equivalent, and marketable securities balance was $329.3 million. dollars. Continuing our strong financial discipline, we project our cash guidance runway through 2027. With respect to other matters, I would like to note that we continue to evaluate options to maximize shareholder value. As announced, we completed our share repurchase program after having repurchased the full 25 million dollars of shares authorized by the board. Under the program, we repurchased a total of 7.6 million shares of common stock at an average person price of $3.26 per share. All repurchased shares were retired and returned to authorized but unissued status. Regarding our strategic process, as we've previously stated, we believe the HCV Phase III clinical development results will drive the shareholder value and catalyze business development discussion. While our discussions to date with potential counterparties have been positive, positive Phase III outcome would further significantly de-risk the program, strengthening our ability to maximize the value of this asset and to secure attractive terms. For this reason, today we announced the conclusion of our formal engagement with Evercore. While we now focus principally on the execution and completion of the Phase 3 trials, which we believe is the best path forward at this moment to drive shareholder value, we remain open to all opportunities to drive shareholder value, including a potential strategic transaction. I'll now hand the call back to Jean-Pierre for closing remarks.

It was in the last quarter, reflect, you know, a global phase three program for the treatment history results from the U.S. and Canada trials C-B-Yong in mid-2026, top-line results, a side North American trial C-Forward at the end of 2026. to present new data supporting the potential best-in-class profile of Benefosbivir and Rezazivir for the treatment. The new data we view today, a unique fraction for Benefosbivir against hepatitis C, highlighting its unique and differentiated profile as compared to Sofosbivir. And this data now can explain the potency of our regimen for the treatment of hepatitis C. In addition to our HCV program, I'm really pleased to share the information today about the potential of our proprietary preclinical candidates derived from our nucleotide platform with the expansion of our antiviral pipeline. may help to address the unmet needs of the many immunocompromised patients living with hepatitis E virus infection, providing more updates soon on this program. Opening the call to your question, I would like to thank our talented and dedicated employees. Our team relentless drives our dedication to advancing all antiviral therapeutics for patients worldwide affected by severe, the call back over to the operator.

Thank you. We will now begin the question and answer session. To ask a question, you may press star, then 1 on your touchtone phone. If you are using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed and you would like to withdraw your question, please press star, then 2. At this time, we will pause momentarily to assemble our roster.

The first question comes from Maxwell's call with Morgan Stanley.

Please go ahead.

Hello, this is Selena on for Max. Thank you for taking our question. How does your recent data set at the liver meeting showing no interaction with famotidine in addition to your prior data showing no interaction with PPI increase your differentiation from EPCLUZA?

Certainly. Thank you, Dina, for the question. So I think we know that there is in the label for Ectusa a contraindication to the concomitant use of H2-reducing therapy with Ectusa. And the recommendation in their label is for there to be at least a four-hour window of separation between dosing of the one and dosing of the other. Proton pump inhibitor use is widespread in the U.S. I think I said on the last call about 10 to 20% of the U.S. population apparently uses this type of therapy, generally over the counter. But it's actually even higher in patients with hepatitis C, and it's estimated to be around 35% of HCV patients use acid-reducing therapy. So this is a care problem for patients when they're taking therapy because it can reduce the levels of antivirals that are achieved and this can compromise efficacy. So we see this as a really important differentiator.

Thank you.

Great, thank you.

The next question comes from the line of Andy Shea with William Blair. Please go ahead.

For taking our questions, I have two. One is from the modeling poster that you presented at AASLD. There is a chart basically showing time to undetectable. And interestingly, there is a separation between genotype 1 and genotype 3, with 3 showing a more rapid time to undetectable. I'm curious if there's any significance in that, and also maybe the observed trend. Does that have to do with the dual mechanism that you announced earlier? So that's question number one. Question number...

Maybe I can address it first, and then after we go over the next slide. Indeed, the modeling, we know has put on a mechanism. And as I suggested a few months ago, that at least in the percent, you know, genotype 3 non-serotic patients compare...

Yeah, that's correct. Okay. Great. Thanks for sharing that perspective. The second question has to do with the compound that you outlined in the slides for hepatitis E. you know, maybe more of an academic question, but it doesn't employ the protide technology. So I'm curious if that's kind of a deliberate decision, or maybe in this context, protide doesn't, you know, is not optimized for protide. I'm curious if you can comment on that as well. Thank you.

We have used for BAMPK 10 times more for 90 as compared to BAMP in hepatitis E, hepatitis C by about this magnitude of about 10-fold. So here we have a very specific hepatitis E with this active triphosphate, and we are evaluating now really the molecular rationale of the binding of the polymerase, why we are are more potent, but definitely has to be a better binding with the presence of the four-prime flu.

Oh, great. Thanks for that, JP. Great. Well, good luck with the Phase 3 readout and look forward to additional information from the Hepatitis E program.

Thank you so much for your questions. Thank you.

This concludes our question and answer session. I would like to turn the conference back over to John Pierre for any closing remarks. Thank you. The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.