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spk04: Good afternoon and welcome to Anantha Pharmaceuticals for Fiscal Third Quarter 2022 Financial Results Conference Call. At this time, all participants are in listen-only mode. There will be a question and answer session at the end of the prepared remarks. Please be advised that this call is being recorded. I would like now to turn the call over to Jennifer Vieira, Investor Relations. Please go ahead.
spk12: Thank you, operator, and thanks to everyone for joining us this afternoon. The news release with our fiscal third quarter 2022 financial results was issued this afternoon and is available on our website. On the call today are Dr. Jay Lulli, President and Chief Executive Officer, Paul Mellet, our Chief Financial Officer, and other members of Enanta's senior management team. Before we begin with our formal remarks, we want to remind you that we will be making forward-looking statements, which may include our plans and expectations with respect to our research and development pipeline and financial projections, all of which involve certain assumptions and risks beyond our control that could cause our actual developments and results to differ materially from those statements. A description of these risks is in our most recent Form 10-Q and other periodic reports filed with the SEC. Ananta does not undertake any obligation to update any forward-looking statements made during this call. I'd now like to turn the call over to Dr. Jay Lulli, President and CEO. Jay?
spk09: Thank you, Jennifer, and good afternoon, everyone. Our vision at Ananta is to leverage our expertise in virology and liver disease to discover, develop, and deliver groundbreaking medicines as we've already done with Glicaprevir and AbbVie's Maverick for hepatitis C virus. This quarter, we made important strides toward achieving another breakthrough medicine. Today, I will start by detailing our recent positive data from the phase one trial of EDP-235 and Healthy Volunteers. As a reminder, EDP-235 is our oral antiviral inhibitor of the coronavirus 3CL protease, also known as the main protease, or mPro, which is in clinical development for the treatment of COVID-19. EDP-235 has fast-track designation and is designed to be a once-daily oral treatment without the requirement for ritonavir boosting. Our first in-human, randomized, double-blind, placebo-controlled Phase I study enrolled healthy volunteers to evaluate the safety, tolerability, and pharmacokinetics of oral EDP235 in single and multiple ascending doses for seven days along with the effect of food. A total of 72 subjects received at least one dose of EDP235 or placebo. There were 40 subjects in the single ascending dose phase and 32 in the multiple ascending dose phase. All SAD and MAD cohorts enrolled eight participants who were randomized to receive EDP235 or placebo in a three-to-one ratio. To optimize dose selections, the study evaluated a broad range of single and multiple doses in a fasted and fed state. The SAD phase included cohorts with doses of 50 milligrams, 100, 200, 400, and 800 milligrams fasted, and a 200 milligram fed crossover cohort. The MAD phase included cohorts with doses of 200 milligrams and 400 milligrams fasted, and 400 milligrams and 800 milligrams fed. Overall, ADP-235 was generally safe and well-tolerated in healthy subjects up to 400 milligrams for up to seven days. Adverse events were infrequent with headache and gastrointestinal-related symptoms such as nausea and abdominal discomfort being the most commonly reported AEs during the MAD phase. The majority of AEs were mild with the exception of three that led to study discontinuations. There was one moderate headache in the 400 milligram FASTED cohort, one severe headache in the 800 milligram FED cohort, and one grade 3 ALT grade 2 AST elevation in the 800 milligram FED cohort. The single subject with elevated ALT AST had no other lab abnormalities. and no clinically significant lab abnormalities were observed in any other patients. Furthermore, all AEs were subsequently resolved. EDB 235 exposure was enhanced with food administration of a standard meal and increased approximately proportionally with ascending single and multiple doses, with a half-life consistently ranging from 13 to 22 hours, resulting in a PK profile suitable for once daily dosing. Data demonstrated that EDP-235 had strong exposure multiples over the EC90, where EC90 is a measure of potency, namely the concentration of drug that results in 90% inhibition in vitro. Specifically, EDP-235, 200 milligrams taken once daily with food, resulted in mean trough plasma levels at steady state that were threefold and sixfold over the plasma protein-adjusted EC90 for the alpha variant and delta variant, respectively, while 400 milligrams resulted in levels that were six-fold and 12-fold over the plasma protein-adjusted EC90 for these respective variants. These target exposure multiples were achieved without the need for ritonavir boosting and its associated drug-drug interactions. Additionally, EDP235 is projected to have four times higher drug levels in lung tissue compared to plasma, which would be expected to drive the 400 milligram multiples to 24-fold and 48-fold over the EC90 for the alpha variant and the delta variant, respectively. This is significant because an antiviral drug's potency and exposure level often translates to clinical efficacy. EDP-235's preclinical and clinical profiles suggest the potential for a best-in-class antiviral treatment for SARS-CoV-2 infection. We plan to finalize a phase two protocol in alignment with the FDA and initiate the study during the fourth quarter of this year. Looking at the COVID-19 landscape, there continue to be infections globally due to new variants, and the BA.5 variant reportedly can circumvent much of the immunity arising from prior COVID infection or vaccination. This highlights the urgent need for convenient, easily prescribed antiviral COVID treatments for patients, potentially even beyond high-risk patients. EDP-235 has the potential to fill this need as it is designed to be used once daily without ritonavir boosting and easily prescribed quickly without the need to assess drug-drug interactions associated with ritonavir. We believe a one pill once a day antiviral treatment regimen with EDP-235 can enable a true test-to-treat model to facilitate rapid treatment of COVID infections. Beyond COVID-19 and continuing with our industry-leading respiratory virology treatment portfolio, we are also advancing our respiratory syncytial virus or RSV program. RSV is another virus that represents an important unmet need. as it can result in severe respiratory infection and is associated with significant morbidity and mortality in children, the elderly, and the immune compromised. Further, there are no targeted treatments or vaccines available. Our robust RSV program includes EDP938, the most advanced N-protein inhibitor in clinical development today, as well as EDP323, a potent L-protein inhibitor. We are confident in the potential of EDP938, which has fast-track designation from the FDA. We are evaluating EDP938 high-risk populations in ongoing and planned clinical studies, including pediatric patients, adult hematopoietic cell transplant recipients, and high-risk adults, all of which have significant unmet need. Last quarter, we announced data from RSVP, a Phase IIb trial in otherwise healthy adults, with community-acquired RSV infection. In this low-risk population, which had mild, self-resolving upper respiratory tract infection, EDP938 did not meet the primary endpoint of reduction in total symptom score compared to placebo or the secondary antiviral endpoints. However, we were pleased to observe a statistically significant difference in the number of subjects achieving undetectable RSV RNA at the end of treatment with EDP938 making this the only study that has reported a statistically significant antiviral effect in an otherwise healthy adult population with community acquired RSV. Even though patients were treated within 48 hours of symptom onset, a key observation in this study was that the viral load and symptoms had already peaked and were declining at the time of the first dose, indicating RSV infection resolves quickly in this otherwise healthy population. Importantly, EDP938 demonstrated a favorable safety profile in a data set that now includes approximately 500 subjects exposed to the drug. We continue to believe that RSV and any viral treatment, including EDP938, has the greatest potential to show optimal efficacy in high-risk populations, as these patients have reduced RSV immunity, which manifests in a higher and longer duration of viral load and greater disease severity. allowing a bigger window to realize the full potential of EDP938. Moving forward, our broad clinical development plan is focused on evaluating EDP938 and populations with the greatest unmet need, namely those who are at high risk for severe disease. Our ongoing studies include RSV-PEDS, a Phase II study in pediatric RSV patients, and RSV-TX, a Phase IIb study in adult hematopoietic cell transplant recipients with RSV. Both are expected to recruit beyond 2022, subject to the reemergence of RSV in broader populations at pre-COVID levels. Also in the fourth quarter of this year, we're planning to initiate another Phase IIb study in high-risk adults, including the elderly and those who have asthma, COPD, or congestive heart failure. We believe EDP938 has the potential to deliver a potent oral antiviral treatment for all populations at high risk from RSV infection. A robust RSV antiviral portfolio also includes EDP323, a novel oral therapeutic targeting the RSVL protein RNA polymerase. We believe EDP323 has the potential to be a standalone treatment or it may be used in combination with other agents such as EDP938 to potentially broaden the treatment window or range of addressable RSV patient populations. EDP323 is supported by preclinical data that demonstrates strong oral absorption and good plasma exposure across different species. Importantly, EDP323 has sub-nanomolar in vitro potency against both major subtypes of RSV, RSV-A and RSV-B. and is not expected to have cross-resistance to other classes of inhibitors. We plan to initiate a phase one study of EDP323 in the fourth quarter of this year. We also continue to pursue our respiratory discovery program in human metanemovirus, or HMPV, a virus that is similar to RSV in that it impacts a number of vulnerable populations, including the elderly, adults with underlying pulmonary disease, and those who are immune compromised. We're continuing lead optimization of potent nanomolar HMPV inhibitors and plan to select a clinical candidate in the first half of 2023. Turning to hepatitis B, we remain committed to developing a combination regimen as a functional cure for chronic HPV patients, as we believe the ultimate cure for this infection will involve combination therapy. Our commitment is based on the continued high unmet need for this disease. which is a global public health threat and the world's most common serious liver infection, making it the primary cause of liver cancer, the second leading cause of cancer deaths in the world. Last quarter at EASL, final data from two of our Phase 1B studies of EDP514 were presented. EDP514 is our HPV core inhibitor with fast-track designation, which is shown to be safe and potent in two different chronic HPV patient populations. those who have high viral load, whom we refer to as viremic patients, and those who are on treatment with a nucleoside reverse transcriptase inhibitor, whom we refer to as nuke-suppressed patients. Based on these data, we remain convinced that EDP514 has the potential to be a best-in-class core inhibitor for HPV. We believe that a core inhibitor such as EDP514 will ultimately be an important component of a successful combination regimen We continue to evaluate internal and external opportunities for additional candidates to develop in combination with EDP 514 and a NUC to create a triple drug regimen. Before moving to the financials, I want to address briefly our ongoing patent litigation in which we are seeking damages for Pfizer's infringement of our issued 953 patent in the manufacture, use, and sale of its COVID-19 antiviral, Paxlovid. We recognize the importance of Paxlovid's availability for patients, and we do not intend to seek an injunction or take other action in this litigation to impede the production, sale, or distribution of Paxlovid. In filing this lawsuit, we are taking steps to ensure that we will be fairly compensated for our intellectual property. Importantly, our 953 patent is completely separate from the patent estate covering our discovery of EDP-235 and our ongoing antiviral discovery work for coronaviruses. Indeed, we have a growing 3CL protease inhibitor patent to state, including several issued U.S. patents, one of which covers EDP-235. These patents describe compounds built on an independent and distinct chemical scaffold from the one described in the 953 patent and in Pfizer's patents for Paxlovid. At this point, I'd also like to take the opportunity to welcome our new chief medical officer, Dr. Scott Rottinghaus, who joins Enanta today. Scott is an infectious disease trained physician who has more than 20 years of experience in a broad range of therapeutic areas. He joins us from Alexion, now a part of AstraZeneca, where he was vice president, head of clinical development, hematology, and nephrology. He has also held positions at Pfizer where he worked on trials of a DNA vaccine for influenza and and on studies of anti-infectives, and continued to practice as an attending physician and assistant clinical professor in infectious diseases at Yale School of Medicine. His experience also includes multiple NDA and MAA submissions and FDA advisory committee participation. We're very excited to have Scott join us as we advance our antiviral development programs. Finally, I'd like to wrap up by highlighting our near-term milestones. We are thrilled with our Phase I results of EDP-235 and look forward to advancing the COVID-19 program into a Phase II study in the fourth quarter of this year. We're also on track to begin a new Phase II RSV study in high-risk adults in the fourth quarter of this year. And last, we're excited to initiate a Phase I study for EDP-323, our RSV-L inhibitor, in the fourth quarter of this year. as well as nominate a clinical candidate for human metapneumovirus in the first half of 2023. With that, I'll turn the call over to Paul to discuss the financials. Paul?
spk08: Thank you, Jay. I'd like to remind everyone that Enanto reports on a September 30th fiscal year schedule. Today, we are reporting results for our third quarter ended June 30th, 2022. For the quarter, total revenue was $19.5 million, and consisted of royalty revenue earned on AVI's global Maverick net product sales. This compares to total revenue of $21.6 million for the same period in 2021. Royalty revenue is calculated on 50% of Maverick sales at a royalty rate for the quarter of 10% after adjustments for certain contractual discounts, rebates, and set-offs, which are now approximately 2% of AVI's total reported HCV product sales. You can review our royalty tier schedule in our 2021 Form 10-K. Moving on to our expenses, for the three months ended June 30, 2022, research and development expenses totaled $39.1 million compared to $47 million for the same period in 2021. The decrease was primarily due to timing of our clinical trials year over year. General and administrative expense for the court was $12.9 million, compared to $8.4 million for the same period in 2021. The increase was due to an increase in headcount in compensation expense. NANTA recorded an income tax benefit of $0.4 million for the three months ended June 30, 2022, due to the release of a state tax reserve during the period, compared to a tax benefit of $9.4 million for the three months ended June 30, 2021. when we had the benefit of federal net loss carrybacks available under the CARES Act of 2020. Ananta is still due a refund of $28.7 million for the tax losses carried back in 2021 to offset taxable income in prior years. Net loss for the three months ended June 30th, 2022 was $31.7 million, or a loss of $1.53 per diluted common share. Compared to a net loss of $24 million, or a loss of $1.19 per diluted common share for the corresponding period in 2021. And at the end of the quarter, with approximately $292.7 million in cash and marketable securities, we expect that our current cash, cash equivalents, and short-term and long-term marketable securities, as well as our ongoing royalty revenue, will continue to be sufficient to meet the anticipated cash requirements of existing business and development programs for the next two years. Further financial details are available in our press release and will be available in our quarterly report on Form 10-Q when filed. I'd now like to turn the call back to the operator and open up the lines for questions. Operator?
spk04: Thank you. We'll now begin the question and answer session. To ask a question, you may press star then 1 on your touch-tone phone. If you're 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. Our first question comes with Akash Tiwadi with Jefferies. Please go ahead.
spk11: So this is Clark on for Akash. Thanks for taking our question. First, we've seen the FDA approved vaccines on preclinical data and also pull Regeneron monoclonal antibody off the market based on preclinical data. Could you talk about the potential for an accelerated path to approval with COVID antivirals? And secondly, can you go over your current thoughts on phase two design in terms of patient population and endpoints? Given the lower event rates we're seeing with Omicron, how do you think about trial design or trial size empowering and accrual times? When can we expect EDP-235 to enter the market? Thank you.
spk09: Hi there. Thanks for the question. This is Jay Lulaid. You know, I think the vaccines and the antibodies are very different than the antivirals. demonstrated you're basically looking for, you know, generation of a species that has reactivity against the virus. And once you do that with a vaccine or an antibody, it's easy to kind of look at the neutralizing capabilities of that entity. Antiviral developments is just different. So I don't expect there to be the same sort of correlative a short path that would accelerate things. And with regards to the patient population, that's something that we're sorting out. The whole, I would say the whole, you know, design, thinking through the phase two and three in this area, it is dynamic. It's changing. The vaccination state of people is changing, both being vaccinated and then suddenly having immunity wear off either because, you know, the vaccine has sort of been short lived and or the booster or the, you know, the variants have evaded the vaccine. So, you know, again, we're in the process of designing, having our interactions with the FDA. and plan to finalize those interactions and start a phase two later this year in the fourth quarter. So stay tuned on the front of trial design in that once we've wrapped up those interactions as well as subsequent studies. But I think the plan would be to try to wrap up the phase two and hopefully be in phase three next year. And then we'll have to see what the environment of the of the virus looks like in terms of how we schedule and size that trial. Were you able, hopefully you were able to hear the answer to the question.
spk11: Yes, we were. Thank you.
spk09: Good. Good. Thank you. I'm holding my breath here.
spk04: Next question, please. The question, the next question comes with . with GMP security. Please go ahead.
spk01: Hi, thanks for taking the questions. I had a few for two, three, five. The four to one lung to plasma ratio that you guys are talking about for total drug, is that using the total amount of drug that's in the plasma or is it just the free non-protein bound drug? And then in the ISIRV poster you had last year, there was an EC90 of 33 nanomolar. Was that corrected for serum protein binding?
spk09: Yeah. So, the question regarding the 4 to 1 ratio was total drug. We measured total drug in the plasma and total drug in the blood. So, in the plasma. So, or total drug in the lung and total drug in the plasma. It's measured in the same way, so it does, it accounts for trying to think of the right way. The ratio would be the same either way you calculated it, whether you adjusted for the plasma or adjusted for binding in one tissue and the other, it would be the same sort of adjustment, the ratio wouldn't change. And then with regards to, I'm sorry, what was the other question?
spk01: A poster from ISIRV meeting last year. Oh, the 33? Yep.
spk09: Yeah, it was not plasma adjusted. I think it was in human airway epithelial cells. Was that that cell line at the time? Yeah, so that was not adjusted, no.
spk01: Okay, and I had a question on the headache. I guess, any characterization you could make? Does it onset early, does it resolve or persist, or does it come on later in the treatment course? Thank you.
spk09: It resolved. I don't recall exactly when it came on, but, you know, any headaches that were observed, you know, resolved, so.
spk01: Okay. Thank you.
spk10: You're welcome.
spk04: The next question comes with Brian Scorny with Bayard. Please go ahead.
spk06: Hey, good afternoon. Thanks for taking my questions. I know it's reported as a low rate in trials, but it seems like the Paxlovid rebound in practice is pretty common currently. Some estimates have seen how that as much as 50%. Obviously, we saw Biden rebound on it. Just thoughts on what you think this is. Is it a Paxlovid PK issue? Do you think they don't have enough 24-hour coverage? Do you think five days isn't enough? Could it be a potential resistance issue? And just how do you think EDP 235 and sort of your program development could try to focus on ensuring that you mitigate it in your program?
spk09: Sure. Thanks. You cut out at least at our end on the beginning of the question, but I think I've intuited what it was. So the... It doesn't appear to be a resistance issue. There's no sign of resistance, you know, with regards to Paxlovid treatment. So I assume, well, this is just, you know, hypothesis right now. It could be that Paxlovid could profit from longer dosing. That's one possibility. But I think the other has to do, it does, Paxlovid does have a short half-life, even though There's ritonavir boosting involved. And our clinical half-life is longer, once a day. So, you know, that having good PK characteristics, you know, can only help you. The other characteristic of 235 is that it has good tissue partitioning and potentially into tissues that could be a reservoir of virus. And so, we think that, you know, You know, a molecule like EDP-235 with very good PK, once daily dosing, nice long half-life, good exposure, multiples, and good tissue targeting could help potentially, you know, find the virus where it might be hiding and help with that. So, that's one of the things that we're hoping to, you know, find out in future studies. The duration of treatment of five days versus seven or something longer, no one really knows the answer to that other than five days with Paxlovid, you know, isn't that bad. Can you do better with a better molecule that has different characteristics? You know, that's the possibility that we'll be exploring in the future. Does that help?
spk06: Yeah, that's very helpful. And then if I could just throw another quick question there on the ALT elevation that you So I'm just wondering if you've discussed the NOAL for ADP-235. Is the end organ tox liver here? And just I know in the protease inhibitors experience, there's sort of not uncommon ALT elevations that are mechanistically distinct from liver injury. I just wonder if you have any idea. Yeah, we haven't.
spk09: Yeah, we typically don't. describe our preclinical safety findings, if any, other than with the FDA.
spk10: Okay, thanks, Chip. Yep, you're welcome.
spk04: The next question comes with Eric Joseph with J.P. Morgan. Please go ahead.
spk03: Hi, good afternoon. This is Hannah Ong for Eric. Thanks for taking the questions, just a few from us. She just wanted to get a sense if there's any alternative mechanisms in the COVID-19 viral life cycle that you'd be looking to target, like co-target with EDP-235 to have just more of a potent efficacy profile up front. And then for the second question, just what are your current thoughts on the relationship between viral load reduction and COVID-19? Has there been a consensus reached by the scientific community on this? And is there any utility in your view in using reduction in viral load as a registrational endpoint?
spk09: Yeah, I'm sorry, you broke up on parts of both questions, but I think the first question was, are there other mechanisms that we're thinking of in COVID other than protease? Did I, was that the question?
spk03: Yeah, just any other mechanisms you're interested in and would you look to maybe look at a combination pathway or combination approach upfront just so you have that .
spk09: Okay, you cut out right there, but the, So the short answer is, you know, there are other mechanisms where we're, you know, looking at a couple of other ones in house. Again, not lacking any confidence in 235 against the COVID world as we know it now. But, you know, just sort of doubling down with our strengths in protease, thinking about the future and if the virus were to take any twists and turns. Maybe there would be the need for combinations in the future. Again, no sign of that offering benefit now, but we're thinking, you know, long term here. So, since the beginning of the pandemic, we've been working on multiple different mechanisms in-house. The second one, I heard the tail end of the question. I thought it was asking, you know, was it possible to have a virologic endpoint in registration? Was that the question?
spk03: Yeah, just what is the utility of a virologic endpoint in COVID currently?
spk09: Well, you know, it's a little confusing in part because, you know, remdesivir, you know, seems to have good data in terms of, you know, prevention of hospitalization and death in patient populations, but yet it hasn't demonstrated an effect on viral load reduction, yet other mechanism such as protease inhibitor has demonstrated viral load reduction. So, it's a little bit It's not the only thing that you can measure that matters. And in fact, you know, the viral load reductions that you sometimes see in COVID when you do see them are fairly modest. I think that's in part based on the area that you can readily sample, which is through, you know, a nasal pharyngeal swab. So, you know, where that goes in terms of endpoints, I think you want to certainly if you can demonstrate an antiviral effect or a trend wherever you can look for it. But beyond that, that doesn't always appear to be necessary. And I would put nukes in that category or at least remdesivir. Is that helpful?
spk03: Great. Very helpful. Yeah. Thinking about outside of COVID and outside of respiratory viruses, just wondering if there's any potential for an antiviral acute treatment approach in something like monkeypox, considering it does seem to hang around a little bit longer than respiratory infections. Is this something of interest for you guys?
spk09: I'm not sure. I don't know. You know, hopefully vaccines will be ultimately very helpful there, but to the extent they're not, We have our eyes on any viruses where vaccines leave a void. So, if there's a need, we would be thinking about it.
spk04: Okay. Very helpful. Thanks for the question.
spk10: You're welcome.
spk04: The next question comes with Brian Abraham with RBC Capital Markets. Please go ahead.
spk07: Thanks. This is Steve. I'm from Bryan. Thanks for taking our question. You shared EC90 multiples for the alpha and delta strains, and with some difference between those strains, can you comment on your expectation for multiples with the Omicron variant, and maybe whether you expect time to steady state or other PK parameters to be important for current or future strains that might be faster replicating to assess efficacy or predict efficacy there? Thanks.
spk09: Yeah, sorry. I hate to do this to you, but part of the first part of the question broke up, and part of the the back end of it. I'll ask you to repeat the beginning, but I think the Omicron I heard was the tail end. We have Omicron studies in process right now. We don't have the data. We'll get it later this year. But just speaking about it in general, when you're talking about protease, the protease mutations across all the different variants and even subvariants, you know, all the different variants of concern like Omicron and then you drill down and look at whether it's BA.2 or 2.1.2 or 4 or 4.6 or 5. The protease itself is highly conserved and any mutations if they do occur, are distal, they're far away from the active site of the enzymatic activity where our drug works. And so that's important actually for the virus's own survival is to not radically mutate that site. So what we've observed is up and down the line with every variant that we've tested, first thing we do is look at biochemical test for enzymatic inhibition and very, very tight data. You can see some of that data in our slide deck. So we believe that, you know, for all the variants of concern, the subvariants that have followed and very likely future variants, that by targeting the protease mechanism, 235 will continue to have very, very strong activity. And I apologize, I missed the beginning of the question.
spk07: I think you covered it there. That was pretty comprehensive. Thanks.
spk09: Good. Great. Thank you.
spk04: The next question comes with Rana Ruiz with SVB Security. Please go ahead.
spk02: Great afternoon, everyone. So I was curious if you have any thoughts on whether an EUA filing for EDP-235 is still on the table for the FDA, or at some point do you think it would be more strategic to go for a full NDA approval for the product?
spk09: Well, right now we don't know that an EUA is not available. I think it's going to be, you know, again, as we get closer to that time, it's going to be facts and circumstances on the ground with regards to what the virus is doing. The FDA, I'm not aware that they've given indication yet that for new drug therapies in the antiviral category that it's not available.
spk02: Got it. Thanks. And a quick one on RSV as well. Have you heard anything on the ground about the RSV infection rates in the northern and the southern hemispheres, and how are you monitoring enrollment for your ongoing studies there?
spk09: Yeah, we're kind of between sort of traditional seasons. I think next up would be, I don't want to say hopefully, you know, but the next season would be northern hemisphere, Starting, you know, later in the, it's been very quiet in the northern hemisphere of late, which is not unexpected, generally speaking, at this time of year. So, you know, as you get into late Q4, that's the traditional time when it would perk up again. And so that's currently what we're, you know, planning and expecting.
spk02: Got it. Helpful. Thanks.
spk10: You're welcome.
spk04: Thank you. Once again, if you have a question, please press star 1. The next question comes with Jay Olson with Oppenheimer. Please go ahead.
spk05: Oh, hi. This is Chung. I'm live for Jay. Thanks for taking all the questions and congrats on the progress. Just maybe a follow-up on a question asked previously. Can you share a little bit more color on the discovery programs on COVID-19? And is that more specific or more potent against some emerging variants? And where do you see the need to combine EDP-235 with another mechanism or with another molecule? Thank you.
spk09: Sure. We see no reason to combine now. Again, there's no signs of resistance as it relates to patients who are treated with protease inhibitors. It's an acute treatment, acute infection. You know, we're talking about five or so days. And so, if you put lots of pressure on the drug, which we do, or on the virus, which we do, you know, a trough, we see great multiples of a very potent drug with a long half-life and good tissue uptake. So, don't see the need for it. But as I said before, you know, if a more serious variant came along, someday you may want to have as many weapons as you could possibly have. And this is no different, by the way, than any virus we've taken on. When we went after Hep C, We went after multiple mechanisms, even though it looked like probably a couple would be enough, but you don't know at the, until you're done, you're always wondering. Same with Hep B, same with RSV. When we get into an area, we're going to mine as many different mechanisms until we know we don't need them. As long as we possibly might in the future, We want to be at the cutting edge with everything that we can. So I would say, you know, EDP-235 being sort of the cornerstone at Enanta, you know, we'll continue to do research in this. And maybe someday combinations will be necessary. You know, hopefully they won't. And hopefully 235 is all we'll ever need or anyone will ever need.
spk10: Great, thank you so much. You're welcome.
spk04: The next and final question comes with Akash Tiwadi with Jefferies. Please go ahead.
spk11: Hi, this is Clark again for Akash. Thanks for taking our additional questions. First, could you comment on the potential costs for the trials for the EDP-235? And secondly, in your phase one healthy volunteer study for EDP through 3.5, what percentage of patients reached EC90, and can you comment on the PK variability across patients? Thank you.
spk09: So, you broke up on the question, and it's quite frustrating, at least at our end. I hope you can hear at your end. So the cost, I think at the end of the day, we'll need to wait and see how we've sized the trials. Really hard to project on that until we see how big they are. And that's going to be dependent on all kinds of design factors that we haven't finalized yet with the agency. So stay tuned on that. I think generally speaking, the concept on the phase two piece would be fairly small. And then we would head into the to the larger portion, which would be registration obviously. And ultimately, you know, keeping in mind all of that, our ultimate plan is to be teaming up with a, you know, larger company that can more effectively help with the, you know, global launch and distribution of the drug. So, you know, stay tuned on that front. And then I missed the other part of your question. Sorry.
spk12: Hello.
spk11: Oh, sorry. The second part of the question was, in your phase one healthy volunteer study for EDP-235, What percentage of patients reached EC90, and can you comment on the PK variability across patients?
spk09: I think I'll let Tara take that question.
spk13: Sure, no problem. Hi, Clark. This is Tara Keeper speaking. So we actually saw pretty low variability in our Phase I study. It was about 15%. And so we would expect down the road we would have the vast majority, greater than 95% of the patients above that EC90 value.
spk11: Great. Thank you.
spk04: Sure. This concludes our question and answer session. I would like now to turn the conference back over to Jennifer Vieira for any closing remarks. Please go ahead.
spk12: Thank you everyone for joining us today. Serious apologies for the technical glitches. If you do have any follow-up questions, feel free to contact us by email or call me at the office. Thanks again and have a great evening. Goodbye.
spk04: This conference is now concluded. Thank you for attending today's presentation. You may now disconnect.
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