Atea Pharmaceuticals Q3 2025 Earnings Report

Atea Pharmaceuticals EPS Results

• Actual EPS: -$0.53
• Consensus EPS: -$0.46
• Beat/Miss: Missed by -$0.07
• One Year Ago EPS: N/A

Atea Pharmaceuticals Revenue Results

• Actual Revenue: N/A
• Expected Revenue: N/A
• Beat/Miss: N/A
• YoY Revenue Growth: N/A

Atea Pharmaceuticals Announcement Details

• Quarter: Q3 2025
• Date: 11/12/2025
• Time: After Market Closes
• Conference Call Date: Wednesday, November 12, 2025
• Conference Call Time: 4:30PM ET

Atea Pharmaceuticals (NASDAQ:AVIR) is a clinical-stage biopharmaceutical company focused on the discovery and development of oral antiviral therapeutics targeting RNA viruses. The company’s lead program, AT-527, is a direct-acting nucleotide prodrug licensed from Roche and is being evaluated as a potential treatment for coronavirus disease 2019 (COVID-19). In addition to its COVID-19 efforts, Atea’s pipeline includes other small-molecule candidates for hepatitis C virus and emerging RNA pathogens, leveraging its proprietary nucleotide chemistry platform to address significant unmet medical needs in infectious diseases.

Founded in 2014 and headquartered in Cambridge, Massachusetts, Atea operates research laboratories in the Greater Boston area and conducts clinical studies across North America, Europe and parts of Asia. Through strategic collaborations with pharmaceutical partners and research institutes, the company enhances its R&D capabilities, optimizes clinical development pathways and positions its therapies for potential global commercialization.

Atea’s leadership team brings extensive experience in antiviral drug discovery, clinical development and regulatory strategy. Under their guidance, the company has advanced multiple development candidates from preclinical stages into human trials. Atea continues to expand its scientific platform through in-licensing opportunities and collaborative research, with a goal of delivering safe and effective antiviral treatments to improve patient outcomes and respond to evolving public health challenges.

Atea Pharmaceuticals Q3 2025 Earnings Call Transcript

Key Takeaways

• Positive Sentiment: Enrollment for the global head-to-head phase 3 HCV program is on track — CBONG (U.S./Canada) should finish enrollment next month with top-line results mid-2026 and C Forward (outside North America) expects enrollment completion mid‑2026 and top-line by year‑end 2026, together covering ~1,760 patients.
• Positive Sentiment: New preclinical and modeling data indicate a dual mechanism of action for bemnifosbuvir — blocking intracellular replication and inhibiting viral assembly/secretion — which may explain higher potency and activity even in the presence of NS5A resistance.
• Positive Sentiment: Clinical and PK data presented at AASLD reinforce a short‑duration, convenient profile: prior phase 2 showed 98% SVR12, modeling predicts a ~7–8 week cure time, and the commercial fixed‑dose formulation supports dosing with or without food and with H2 blockers (and shows no interaction with PPIs), a key differentiator versus Epclusa.
• Positive Sentiment: Balance sheet strength: cash, cash equivalents, and marketable securities of $329.3M provide runway through 2027 to fund phase 3, launch plans and new programs, and the company completed a $25M share repurchase (7.6M shares) earlier this year.
• Neutral Sentiment: Atea is advancing an HEV program with two preclinical nucleotide candidates (AT‑587, AT‑2490) that show ~200‑fold greater in vitro activity than ribavirin; IND‑enabling studies are ongoing with first‑in‑human expected mid‑2026, but commercial and clinical success remain speculative.

Presentation

[Operator]

Good afternoon, everyone, and welcome to the Atea Pharmaceuticals' third quarter 2025 financial results and business update conference call. At this time, all participants are in listener-lead mode. Following the formal remarks, we'll open the call up for your questions. I would now like to turn the call over to Jonae Barnes, Senior Vice President of Investor Relations and Corporate Communications at Atea Pharmaceuticals. Ms. Barnes, please proceed.

[Jonae Barnes, SVP of Investor Relations and Corporate Communications at Atea Pharmaceuticals]

Thank you, Oparator. Good afternoon, everyone, and welcome to Atea Pharmaceuticals' 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 Atea are our Chief Executive Officer and Founder, Dr. Jean-Pierre Sommadossi, Chief Development Officer, Dr. Janet Hammond, Chief Medical Officer, Dr. Arantxa Horga, Chief Commercial Officer, John Vavricka, 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 call. 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.

[Jonae Barnes, SVP of Investor Relations and Corporate Communications at Atea Pharmaceuticals]

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.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Thank you, Jonae. Good afternoon, everyone, and thank you for joining us. I will begin on slide three. I'm pleased to share with you the significant progress and achievements we have made this quarter, which is a testament to strong execution across our team. Our global phase 3 program for the treatment of HCV is on track, and we expect to complete patient enrollment for our North American trial, CBONG, next month. This timeline leads us to the first phase 3 top-line result in mid-2026. For C Forward, our trial outside of North America, we anticipate enrollment completion mid-2026 with top-line result anticipated by late 2026. Arantxa will provide an update on our phase 3 program.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

A few days ago, new modeling data was presented at The Liver Meeting 2025 in Washington, D.C., along with two additional data sets further demonstrating the antiviral potency with short treatment duration of our regimen for the treatment of hepatitis C. Janet will review the highlight of these data next. I'm pleased also to report that we announced today new exciting research findings, including evidence of a unique dual mechanism of action for bemnifosbuvir against HCV, further demonstrating its differentiation and potency, and I will review this data in a moment. In addition, I'm also very pleased to share with you that we are expanding our antiviral hepatitis pipeline for a major unmet medical need of immunocompromised patients living with hepatitis E infection. We have identified two new potent candidates derived from our nucleotide platform.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

IND-enabling studies are ongoing to select a clinical candidate, with phase one initiation anticipated in mid-2026. We will discuss this program in 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 equivalents, and marketable securities, providing runway through 2027. This strong cash position enables us to fully fund our phase three program, launch the new regimen, and advance our new HCV development program. With that, I will now turn the call over to Janet to review the highlights of the presentation at the Liver Meeting. Janet?

[Janet Hammond, Chief Development Officer at Atea Pharmaceuticals]

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 regimen of Bemnifosbuvir and Ruzasvir for the treatment of HCV. In an oral presentation, multiscale modeling results predicted that our combination regimen inhibits both intracellular replication of HCV as well as viral assembly and secretion of new HCV variants 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.

[Janet Hammond, Chief Development Officer at Atea Pharmaceuticals]

It highlighted a resistance analysis from the phase two study of our regimen, demonstrating that SVR12 rates were not impacted by NS5A resistant variant at baseline. Viral kinetics and pharmacokinetic analyses indicated that most of the viral failures were due to treatment non-adherence and not viral resistance. The second poster reviewed the results from a phase one study in healthy participants, which demonstrated the high relative bioavailability of the Bemnifosbuvir and Ruzasvir commercial formulation for the fixed dose combination. These data also support dosing of the fixed dose combination with or without food and with Famotidine, an H2 blocker, which can substantially diminish the effectiveness of all antivirals. The fixed dose commercial formulation is being used in our ongoing phase three program.

[Janet Hammond, Chief Development Officer at Atea Pharmaceuticals]

Moving to slide six, we will host a virtual panel event featuring key opinion leaders, or KOLs, in hepatology, gastroenterology, infectious diseases, and hepatitis C tomorrow, Thursday, November the 13th, at 10:00 A.M. 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.

[Janet Hammond, Chief Development Officer at Atea Pharmaceuticals]

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 Lawitz from the Texas Liver Institute, University of Texas Health San Antonio, Anthony Martinez from the University of Buffalo Erie County Medical Center, and Nancy Reau 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 three program for hepatitis C. Arantxa?

[Arantxa Horga, Chief Medical Officer at Atea Pharmaceuticals]

Good afternoon, everyone. On slide eight, 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, sofosbuvir and Velpatasvir, marketed as Epclusa. Our regimen includes Bemnifosbuvir, the most potent nucleotide inhibitor, and Ruzasvir, a highly potent NS5A inhibitor. Data support our regimen as a potential best-in-class treatment option for patients infected with HCV, with a differentiated profile featuring a short duration, low risk of drug-drug interaction, 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 HCV patients. These results will be presented at an upcoming scientific meeting.

[Arantxa Horga, Chief Medical Officer at Atea Pharmaceuticals]

We view this as a key differentiator since proton pump inhibitors can substantially decrease the effectiveness of currently approved DAA therapies for HCV. Our phase III program is designed to confirm the efficacy, safety, and tolerability demonstrated in our robust phase III study, where we achieved a 98% sustained virologic response at 12 weeks post-treatment, or SVR12. 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 SVR12 as an established clinical endpoint for cure.

[Arantxa Horga, Chief Medical Officer at Atea Pharmaceuticals]

Moving to slide nine, the global phase III program is composed of two pivotal trials, CBONG, which is enrolling across approximately 120 sites in the U.S. and Canada, and C Forward, 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 SVR12, which is recognized as the definitive measure of HCV cure. Slide 10.

[Arantxa Horga, Chief Medical Officer at Atea Pharmaceuticals]

I am pleased to confirm that enrollment in the North America CBONG trial is on track for completion next month, with top-line results anticipated mid-2026. For C Forward, 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?

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Thank you, Arantxa. Let's now move to slide 12. As many of you know, Bemnifosbuvir is a nucleotide NS5B polymerase inhibitor with an established mechanism of action of inhibiting HCV RNA through chain termination, thus blocking viral production and replication inside the cell. Our collaborators at Los Alamos National Laboratories, headed by Dr. Alan Perelson, have conducted HCV viral kinetic modeling using data from the phase one Bemnifosbuvir monotherapy trial. The new modeling suggested that Bemnifosbuvir may have an additional mechanism of action inhibiting HCV viral assembly secretion of new HCV variants in the bloodstream, significantly reducing extracellular HCV RNA, a mechanism previously only associated with NS5A inhibitors such as Ruzasvir and Velpatasvir. On slide 13, in vitro studies conducted under another collaborator at Loyola University confirm this dual mechanism of action for Bemnifosbuvir.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

On this slide, the study showed that the level of intracellular HCV RNA were comparable with selected concentrations of Bemnifosbuvir and Sofosbuvir. While both agents produced these similar declines of intracellular HCV RNA, as you can see, Bemnifosbuvir led to a far greater and faster reduction in extracellular RNA, indicating possible inhibition of viral assembly and release into the bloodstream. On slide 14 now, the other in vitro study shows that intracellular RNA, HCV RNA, were comparable with selected concentration of Bemnifosbuvir and an NS5A inhibitor such as Velpatasvir. Of importance here, extracellular HCV RNA level decreased similarly with Bemnifosbuvir or Velpatasvir, an NS5A inhibitor, demonstrating that Bemnifosbuvir also inhibits HCV assembly and secretion into the bloodstream in addition to inhibiting viral replication.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

In slide 16, you can see this cartoon, which illustrates on the left side the HCV life cycle, and then on the right side, the dual mechanism of action for Bemnifosbuvir showing how Bemnifosbuvir blocks the virus from making copies inside the cell, and it also blocks new virus from entering the bloodstream. Therefore, on slide 16, what the data means. The data demonstrate that Bmnifosbuvir is a potent and differentiated nucleotide prodrug with a unique dual mechanism of action, which may explain now the higher potency of Bemnifosbuvir as compared to Sofosbuvir. Importantly, even in the presence of NS5A resistance, Bemnifosbuvir will continue to block viral assembly secretion due to its dual mechanism of action. Lastly, these results further highlight the differentiation and the potency of the Bemnifosbuvir and Ruzasvir regimen for the treatment of hepatitis C.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

With that, I will now turn the call over to John for an overview of the new hepatitis E virus program. John?

[John Vavricka, Chief Commercial Officer at Atea Pharmaceuticals]

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 unmet medical need. As seen on slide 18, the WHO estimates that there are 20 million global infections annually. HEV 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 one and two 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.

[John Vavricka, Chief Commercial Officer at Atea Pharmaceuticals]

However, in recent years, there's been a growing incidence of chronic HEV genotype 3 and 4 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 pre-existing 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 risks organ rejection or relapse of underlying disease. Some clinicians also use Ribavirin, an older antiviral therapy approved for other viral infection indications, off-label for HEV, which yields inconsistent efficacy results and is often poorly tolerated and poses risk of significant toxicities.

[John Vavricka, Chief Commercial Officer at Atea Pharmaceuticals]

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 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.

[John Vavricka, Chief Commercial Officer at Atea Pharmaceuticals]

As such, there is the potential to seek an orphan drug designation, which can have development and regulatory advantages. These lifesaving procedures continue to expand the population of immunocompromised patients that could be susceptible to chronic HEV infections. Using other viral infections, such as hepatitis E virus, as a guide to pricing, this HEV market opportunity could translate into roughly between $500 million-$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. JP?

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Thank you, John. Moving to slide 21, the in vitro data on this slide shows the potent nanomolar antiviral activity of AT-587 and AT-2490 against hepatitis E virus genotypes 1 and 3, and underscore why HEV represents a compelling extension of our antiviral platform. Our two candidates demonstrate approximately 200-fold higher antiviral activity in vitro as compared to Ribavirin, which, as John mentioned, is used off-label for the treatment of hepatitis E virus. While in vitro and in vivo activity of Bemnifosbuvir was also shown against HEV, and that's how we start to understand that our platform could have some anti-HEV activity, the 10-fold higher activity for AT-587 and AT-2490 led us to advance these two promising candidates.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

On slide 22, it is interesting to point out that only a fluoratom in the sugar ring differentiates the active triphosphate metabolite AT-9068 from the two analogs AT-587 and AT-2490 as compared to AT-9010, which is the active triphosphate of bemnifosbuvir. Of particular importance, these two candidates efficiently convert to their active triphosphate form in human hepatocytes and have a clean preclinical safety profile to date, positioning them as leading candidates for first-in-class hepatitis E antivirals. IND-enabling studies are ongoing to select the clinical candidate for phase one evaluation. We are also pleased to announce that we will be presenting more information on our HEV program at an upcoming scientific meeting early next year. I will now turn the call over to Andrea to discuss our financials. Andrea?

[Andrea Corcoran, CFO and EVP of Legal at Atea Pharmaceuticals]

Thank you, Jean-Pierre. As Jonae 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 three HCV program.

[Andrea Corcoran, CFO and EVP of Legal at Atea Pharmaceuticals]

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. 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 a full $25 million of shares authorized by the board. Under the program, we repurchased a total of 7.6 million shares of common stock at an average purchase 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 three clinical development results will drive shareholder value and catalyze business development discussions.

[Andrea Corcoran, CFO and EVP of Legal at Atea Pharmaceuticals]

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 III 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 potential strategic transactions. I'll now hand the call back to Jean-Pierre for closing remarks.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Thank you, Andrea. Slide 26. In closing, the significant progress and achievements we have made within the last quarter reflect strong execution across our team. We are on track with patient enrollment in our global phase III program for the treatment of HCV, and we look forward to the top-line phase III result from the U.S. and Canada trial CB Young in mid-2026, followed by top-line result expected for the outside North American trial C Forward at the end of 2026. We continue to present new data supporting the potential best-in-class profile of Bemnifosbuvir and Ruzasvir for the treatment of hepatitis C. If approved, we believe it can become the most prescribed treatment for hepatitis C and disrupting and expanding the current global HCV market of approximately $3 billion in annual net sales.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

The new data reviewed today demonstrates a new and unique dual mechanism of action for Bemnifosbuvir against hepatitis C, highlighting its unique and differentiated profile as compared to Ruzasvir. This data now can explain in part 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 along with the expansion of our antiviral pipeline. These compounds may help to address the unmet needs of the many immunocompromised patients living with hepatitis E virus infection. We look forward to providing more updates soon on this program. Before opening the call to your question, I would like to thank our talented and dedicated employees.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Our team's relentless pursuit of excellence drives our dedication to advancing all antiviral therapeutics for patients worldwide affected by severe viral diseases. With that, I would turn the call back over to the operator.

[Operator]

Thank you. We will now begin the question and answer session. To ask a question, you may press star, then one on your touch-tone 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 two. At this time, we will pause momentarily to assemble our roster. The first question comes from Maxwell Skor with Morgan Stanley. Please go ahead.

[Selena Zhang, Equity Research Associate at Morgan Stanley]

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 Epclusa?

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Janet, you want to address the question, please?

[Janet Hammond, Chief Development Officer at Atea Pharmaceuticals]

Definitely. Thank you. Thank you, Selena, for the question. I think we know that there is in the label for Epclusa a contraindication to the concomitant use of H2-reducing therapy with Epclusa, 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 10-20% 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. This is a clear problem for patients when they're taking therapy because it can reduce the levels of antivirals that are achieved, and this can compromise efficacy.

[Janet Hammond, Chief Development Officer at Atea Pharmaceuticals]

We see this as a really important differentiator. Thank you.

[Selena Zhang, Equity Research Associate at Morgan Stanley]

Great. Thank you.

[Operator]

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

[Andy Shea, VP and Equity Research Analyst at William Blair]

Thanks 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 one and genotype three, with three showing a more rapid time to undetectable. I'm curious if there is 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.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Yes. Maybe I can address the first, and after we go over the second one. Thanks for looking at the slide of the presentation at the liver meeting. Indeed, you're correct. The modeling suggests that there is a more rapid decline with genotype 3. I think that we know that Bemnifosbuvir is, interestingly, more potent in vitro, actually, against genotype 3 than genotype 1A or 1B. When we did the in vitro study about 10 years ago now, that's another differentiation with sofosbuvir, for example, where sofosbuvir is less potent on genotype 3. It's possible related to the dual mechanism.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

As Andy had suggested and wrote in one of his reports a few months ago, at least in the phase two, we had a 100% cure in our genotype 3 non-cirrhotic patient, which definitely, at least as compared historically to other regimens, we have very high rate of very high cure rates.

[Andy Shea, VP and Equity Research Analyst at William Blair]

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. 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 is not optimized for protide. I'm curious if you can comment on that as well. Thank you.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Sure. It is. I can tell you that we did not include the chemical structure, but it is exactly the same prodrug that we have used for BEM, which is a phosphoramidase. It is identical. We feel very comfortable with the PK and the safety and the efficacy as well. As you have seen, interestingly, it is only the fluoratom at the four-point position that differentiates between 587 and BEM, for example. What is interesting is that while we are 10 times more potent with 587 and 2490 as compared to BEM in hepatitis E, these are less potent as compared to BEM in hepatitis C by about the same magnitude, about tenfold.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Here we have a very specific inhibition of hepatitis E with this active triphosphate, and we are evaluating now really the molecular rationale of the binding of the polymerase, why we are more potent, but definitely has to be a better binding with the presence of the four-point fluoratome.

[Andy Shea, VP and Equity Research Analyst at William Blair]

Oh, great. Thanks for that, JP. Great. Good luck with the phase three readout, and look forward to additional information from the hepatitis E program.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Thank you so much for your questions.

[Operator]

Thank you. This concludes our question and answer session. I would like to turn the conference back over to Jean-Pierre for any closing remarks.

[Jean-Pierre Sommadossi, CEO at Atea Pharmaceuticals]

Again, thank you all for joining us to our third quarter earnings conference call, and thank you for your continued support.

[Operator]

Thank you. The conference has now concluded. Thank you for attending today's presentation. You may now disconnect. Thank you.

Participants

Executives

• Jonae Barnes, SVP of Investor Relations and Corporate Communications
• John Vavricka, Chief Commercial Officer
• Arantxa Horga, Chief Medical Officer
• Andrea Corcoran, CFO and EVP of Legal
• Jean-Pierre Sommadossi, CEO
• Janet Hammond, Chief Development Officer

Analysts

• Selena Zhang, Equity Research Associate at Morgan Stanley
• Andy Shea, VP and Equity Research Analyst at William Blair