Good morning and welcome to the Cidara Therapeutics Investor Day. At this time, all attendees are in a listen-only mode. A question-and-answer session will follow the formal presentations. As a reminder, this call is being recorded and a replay will be made available on the Cidara website following the conclusion of the event. I'd now like to turn the call over to Dr. Jeff Stein, President and Chief Executive Officer of Cidara Therapeutics. Please go ahead, Jeff. Thank you, Tara. On behalf of the entire Cidara team, I want to welcome you to our Investor Day. We've been anticipating this for quite some time. We have a lot of new information to share, so let's just launch into it. Here's the agenda. I'll kick it off with an introduction and a reminder of CD388, which is the topic of today, give you a little bit of background on the program and on the company. We'll transition to Fred Hayden, really one of the global key opinion leaders in influenza. He'll provide a backdrop of this last season's influenza season. We'll provide an interpretation of how the CDC reports data. I know there's a lot of interest in what the CDC reports and how that may influence the interpretation of our phase two study. He'll provide that kind of detail. We'll then transition to Nicole Davarpanah, our Chief Medical Officer. She will provide some detail on the statistical analysis plan by which we will evaluate the Navigate phase 2B study. As several of you are aware, we've made some changes there recently, and we've achieved alignment with the FDA on how we will analyze the data. She'll also cover our current thinking on the design of the phase three trial that we hope to start early next year. We'll then transition to Rick. Rick is another key opinion leader, former head of BARDA, has a great perspective on pandemic influenza and can provide his perspective on how CD388 may be appropriate for pandemic influenza and provide a backdrop of some of the other programs that are in development. Jim Beitel, for the first time, provides some important detail on how we see the commercial opportunity. I think many of you will be surprised at how large the commercial opportunity is for a product like CD388. Jim has been leading a lot of market research and pricing research, and we look forward for the first time to share that with you today. We'll end with a wrap-up and then finally a question and answer. Let me kick it off here. Here are today's speakers. We will pretty much go in order here across the top, but also available for the Q&A. We have Les Tari, our Chief Scientific Officer, who is really the primary inventor of CD388 and the drug-Fc platform, Corina Pavetto, who is the leader of our clinical operations team and has really designed and executed on the Navigate Phase 2B study. Shane Ward can address any questions on the manufacturing of CD388. Finally, Frank Karbe, our CFO, who can address any questions on our financing plans. What you will hear today, and I hope you come away from today's session with a perspective that CD388 is really doing something that no other drug has done in influenza, and that is really to revolutionize the broad protection against influenza. We are going to focus our initial development plan, however, in a very high unmet need population, and those individuals who are most vulnerable, where the existing vaccines and antivirals simply do not adequately protect them. This is a very large population in the U.S., the way we look at it, upwards of 50 million people in the US who do not have an adequate response to influenza. The take-home message today is that we are developing CD388 to be truly universal to universally protect against all influenza strains, but also in all people. The term universal flu vaccine has been around for 20 some odd years. It has not been developed yet. Even if it were in current usage, it really only pertains to the virus, not to all people. We are developing CD388 in the broadest sense to be universal. The molecules on the lower left, CD388 is called the DFC or drug-Fc conjugate. It has two components: a potent small molecule inhibitor, which is an inhibitor of neuraminidase. This is part of an approved drug called zanamivir, also known as Relenza. We have created a dimer of zanamivir, and we have stably conjugated it to a fragment of a human antibody called an Fc fragment. This is also part of approved drugs. It is a modification of the YTE mutant, which has an attenuated effector function. There is no aspect of CD388 that requires an immune response for its efficacy. The efficacy is solely attributable to the small molecule, the zanamivir dimer. As you know, there are multiple copies of that on that Fc, and that contributes to its efficacy. We will get into more detail on that in a moment. Across the top, you see the history of this drug-Fc platform, really invented in 2018 at Cidara. We have an issued composition of matter patent that extends to 2038 and with extension potentially to 2042. We partnered CD388 at an early stage, at the preclinical stage with J &J. It was validated through that partnership. Under that partnership, we advanced it through two phase 1 studies and a phase 2 human proof of concept study. That data package was delivered to J&J. They were planning to advance it into phase 2B and phase 3 based on the results of those studies. At that point, this was the summer of 2023, they decided to exit the infectious disease space broadly. They started a series of divestitures. We, Cidara, was able to participate in that competition to get the rights of CD388. Fortunately, through the benefit of key investors, we put together $240 million financing that enabled us to not only secure the global rights of CD388, but also to advance it through the 5,000-subject Navigate Phase 2B study. On the bottom, you can see where we are. We've completed the enrollment in December, and last week we locked the database. Important to note that we told you what you're going to hear today. It's also important to note that as we have locked the database, we will not be disclosing. Obviously, we're blinded to the data, but we won't be disclosing any unblinded data since we're about a month or so away from top-line data. Just a few words on the opportunity just to level set everybody. The values you see on the left-hand side of the screen are the most recent reported ranges from the CDC on influenza illness, hospitalizations, and deaths from this last year's flu season. To give you some perspective on how that compares to perhaps some better-known ailments, kidney disease, colorectal cancer, breast cancer, and hematologic malignancies, and RSV, you can see it is quite comparable. Big burden of mortality, hospitalization, and illness in the U.S.. Currently available vaccines and antivirals simply have not been developed to adequately address this. As mentioned, in order for a vaccine to be effective, you have to mount an effective immune response. There's a broad range of efficacy of vaccines because people have a broad range of their ability to respond to a vaccine. Antivirals, by and large, have been developed for treatment or post-exposure prophylaxis. Because of the unmet need, in some cases, they are being used for more prolonged prevention in very vulnerable populations, but they simply have not been developed as such. CD388 was developed to be administered once a flu season and to provide protection against all strains in all people. We think that there's still an important role for vaccines to play. Our perspective is that CD388 can actually be complementary to vaccines in a couple of different ways. Here you can see our kind of aspirational target product profile compared to kind of the average efficacy, administration, safety, and manufacturing of the seasonal flu vaccines. We believe that the addition of CD388 on top of the repertoire of vaccines that are available can be very impactful. CD388 could be used alone, but importantly, I think it can be used in conjunction with existing vaccines. This is a theme that you will see throughout today's event. That complementarity is grounded structurally. If you look at the picture here of the influenza virus, you see two targets arrayed across the surface. Those are hemagglutinin in gray, and in pink is neuraminidase. That's the H and the N when you think about H1N1 or H5N1. These are the designations, and those are the two targets. There are about eight times more hemagglutinin on the surface of the virus than there are neuraminidase. Consequently, our natural immune response develops antibodies against hemagglutinin and to a lesser extent neuraminidase. CD388 is directed against a highly conserved active site. Actually, it's a transition state of the neuraminidase enzyme such that it is invariant and it is shared amongst all viral strains. If we take a little closer look, you can see that our natural antibody response and CD388 are hitting different targets. We believe that that is actually complementary and why CD388's activity should be additive on top of vaccines. We'll talk about that in some more detail in a moment. That broad spectrum translates to the in vitro activity. Here you can see in the kind of pink shades is the activity of CD388 compared to two other neuraminidase inhibitors, Tamiflu or oseltamivir and zanamivir, as well as another small molecule antiviral, Baloxavir, which targets viral RNA polymerase. The lower the dots here, the more potent the drug. As you can see, CD388 has consistently potent activity against all the strains of influenza A and B on this slide. That translates to activity against resistant strains. When you think about it, CD388 is being administered at the beginning of the flu season and will provide efficacious protection for the entirety of the flu season. You might think that that could contribute to resistance. We have looked closely at this. We have tested CD388 against the known strains that are resistant to zanamivir and Tamiflu. On the table here, the values that are in orange reflect at least a five-fold increase in the concentration of drug needed to inhibit the growth of the viral strains. You see on this part of the table, influenza A and B, both, there are strains that are known to be resistant against Tamiflu and Zanamivir. That translates in vivo as well. What's interesting is that CD388 actually is slightly more potent in vitro against these neuraminidase resistant strains. That potency translates in vivo, as you can see on the right side of the table, the influenza B- models. With influenza B, there is no change in the inhibitory concentration of CD388 to be active in this model. With that as a backdrop, let me turn it over to Fred Hayden, who can share his perspective on this last year's influenza season and how he sees CD388. Fred? Yeah, thanks very much. And good morning to all of you online. My brief is to give you an overview of the impact of seasonal influenza and also some of the data that we have with regard to seasonal prevention strategies using antivirals. Jeff has already shared these data with you, but last season was a high severity one affecting all age groups in the United States, accounting for 47 million flu illnesses, roughly 40% of those requiring a medical visit. As you can see, 610,000 flu hospitalizations and 27,000 deaths. You'll also notice here that there are ranges given. This is quite broad, actually, in terms of deaths, where we see about a four-fold difference in the projected numbers. Part of this is because these data, again, are incomplete as of the beginning of May and are still being acquired. It also relates to how the CDC makes these estimates. This slide shows you that the data are derived from a specific network, FluSurv-NET, that comes from medical centers in 14 states that represent about 9% of the US population. They acquired these reported rates of hospitalization just for the kinds of testing that are done to get a more exact number of hospitalized and then extrapolate this both to the number of deaths as well as to the number of symptomatic illnesses across the country. This in part accounts for this variation in terms of projected impact. Of course, an important part of this is what's happening with regard to hospitalizations. These data are, I think, tighter in part because they're the basis for the estimates on both deaths and illnesses. As you're well aware, seasonal influenza disproportionately impacts in terms of hospitalizations on older adults. The dashed red line here are those 65-74 years of age. The green one, the higher one, are those aged 75 and above. You can see that there was a long period of impact throughout this past season with regard to that. In fact, we had the highest cumulative number of hospitalizations since the 2010-2011 season. Unexpectedly, we saw co-circulation of multiple influenza viruses during this last season, mostly influenza A, but about half H3N2, half H1N1, and then a small proportion of influenza B that came in late in the season as shown in the green. This is not unusual to see, again, multiple different influenza viruses circulating in a given year. This is one of the important factors we need to consider in terms of protecting against the whole range of these viruses. The CDC has also, toward the end of February, released their preliminary estimates with regard to vaccine efficacy. This is based on four networks that they have supported to acquire data both in children and adults. What I'm showing you here are just the adult data with regard to the effectiveness of vaccine on preventing either outpatient visits, that is, medically attended visits, obviously with illnesses severe enough to require attention, or hospitalizations. You can look at the vaccine effectiveness estimates across the different adult populations here of up to 64 years and then 65 and above. Note that there is a moderate level of protection seen. This is better, in fact, than many prior years, but still at best about 55% and lower. Another part of the issue here is not only the relative effectiveness of the vaccine, but also the insufficiency of vaccine uptake. As part of this test negative case control kind of analysis, they do acquire data on the frequency of vaccine uptake in the outpatient control groups who presented with respiratory illness, but that was negative for influenza. Here you see that in several of these outpatients, the highest rate of vaccine uptake was 34%. In the inpatients, it was 40%. There is clearly an inadequate response in terms of vaccine coverage, despite the fact that the U.S. has a universal vaccine recommendation for all of those six months and older. Just to remind you again about the estimated burden of influenza across multiple seasons, this is up to 2024. You can see there is a broad range for all of these different outcomes. Illness is about four-fold across different seasons and in hospitalizations, nearly six-fold and closer to eight-fold or so with regard to mortality. Another point here is that if you look at all illnesses and look at the proportion that go on to hospitalization, it's only about 1%-2%. Among those hospitalized, the case fatality is roughly 5%-7%. It is clear that it is very hard for clinical trials to actually be large enough to capture those kinds of endpoints. Almost all of the trials have focused on illness prevention in terms of both vaccines and antivirals. Let me turn then to some of the past experiences with regard to seasonal antiviral prophylaxis. This is where the drugs have been tested for a prolonged period of time in these randomized trials. The earliest one that I'm aware of really was done by Smordintsev in the then Soviet Union, institution-based study during the Hong Kong H3N2 pandemic. This was in an unimmunized population where they gave amantadine for up to 30 days and saw a significant reduction in illness, 63%. They also did serologic testing just to detect as many influenza infections irrespective of symptoms and found a more modest reduction. That is the typical pattern. When oseltamivir was first being investigated, we undertook a community-based study in households where, again, we did not have vaccine use in the enrolled individuals. Oseltamivir was given at a standard dose, either once or twice daily for six weeks, and saw a significant reduction of 74% in illness and, again, a somewhat reduced level of protection against infection. This study has many parallels with the Navigate Phase 2B study that you will hear about in more detail in a few moments. Another point here is that we used a definition of illness that was based on a temperature of only 37.2 degrees Celsius or 99 degrees Fahrenheit. If one looks at a higher temperature threshold to define influenza-like illness, 37.8, for example, what happens is that the number of events, especially in the active group, diminishes, but the relative risk reduction goes up. This is typical of influenza trials. The higher the temperature threshold, the lower number of events, but the greater the likelihood that you'll be able to see an effect with an effective antiviral. Also, oseltamivir was also studied in chronic care facilities in the frail elderly. Mean age here was 81 years. Most had received vaccines, as you can see. Again, it was a six-week trial. This showed a highly significant reduction in illness in the participants, again, supporting the point that a neuraminidase inhibitor in combination with vaccine can have an additive protective effect. Mike Icen did a difficult study in terms of looking at a high-risk population, transplant recipients who were greater than one year of age. 80% of these were solid organ transplant recipients. He looked at a 12-week period of oseltamivir prophylaxis. The children in this study did, of course, receive weight-adjusted doses and saw some protective effect that is embraced as one of the strategies in trying to protect these individuals during seasonal influenza, particularly the highest-risk stem cell transplant patients. Finally, I'd like to just highlight what I think is a very informative study of seasonal use of zanamivir prophylaxis. This was done in the community in high-risk persons. In this trial, Zanamivir was given by the standard dose of 10 milligrams per day for the four weeks. A large number of participants aged 12 years and older who had one or more risk factors for influenza complications were enrolled. Overall, compared to the placebo, the Zanamivir recipients had an over 80% reduction in influenza events, that's influenza-like illness, as well as, importantly, an 88% reduction in influenza complications and 24% reduction in overall infections. Part of this study also examined related factors. Here again, there was protective efficacy seen irrespective of which virus it was, A or B, and importantly, also whether they had received vaccine or not. Again, an example of where seasonal antiviral prophylaxis has been associated with additive protection when combined with vaccine. I'll just summarize some of these points for you. Seasonal influenza impact varies widely depending on the circulating strains, vaccine coverage and effectiveness, the use of non-pharmaceutical interventions, and, of course, in some cases, use of antivirals. The clinical outcome of influenza-like illness does not have a generally agreed definition, which has important implications, I think, for study design. We can talk about that further. Unlike currently available neuraminidase long-term prophylaxis regimens, which have to be given on a daily basis, CD388 may offer the possibility of once-per-season administration, as Jeff has already told you. Clinical data with inhaled zanamivir supports the potential for this intervention to prevent influenza illness in high-risk persons with prior vaccination. Thanks for your attention. All right, Fred, thanks so much for that backdrop. Great segue into Nicole's section, who will review the Navigate phase 2B study, our plans for conducting the statistical analysis of the results, and then finally, our current thinking on the design of the phase 3 study. Nicole? Thank you, Jeff. Good morning to everyone. I'm pleased to share the study design, revised statistical plan, and the expectations for the phase 2B Navigate study. The Navigate study is a blinded randomized control trial of CD388 in three doses versus placebo as a single subcutaneous administration at the start of the flu season. It evaluates efficacy, safety, and PK of CD388 in preventing symptomatic influenza. The study enrolled over 5,000 healthy unvaccinated adults aged 18 to 64 who are not at risk for complications of influenza. Fifty-eight sites were included, fifty-seven in the U.S. and one in the United Kingdom, and they were randomized equally, 1,250 subjects each to the three doses and placebo. The trial enrolled from September 2024 to early December. The primary endpoint is preventive efficacy. Preventive efficacy tells us the percentage by which a prevention method reduces the chance of getting sick compared to not using the method. The endpoint is defined by three criteria. This includes PCR-confirmed, centrally confirmed influenza, greater than two respiratory or one respiratory and one systemic sign or symptom, and a body temperature of greater than 38 degrees Celsius. These criteria were chosen specifically to reflect the mechanism of action of CD388, which Dr. Hayden nicely outlined. It does not prevent viral entry into cells, but rather viral egress and infection of cell to cell, which manifests in symptomatic infection. That is why this is an important kind of criteria to reflect the benefit of this therapy. As Dr. Hayden told us, it has been a very severe flu season. We believe that we captured that geographically in the sites that were chosen to be selected for the study. This map is a geographic map of our recruiting centers with numbers reflecting the number of enrollment sites in each state, as well as one in the U.K. It is overlain with a heat map of the severity of flu in those regions. As you can see, we believe that these centers overlapped with some of the most severe flu seasons. The enrollment in the study also allowed us to evaluate whether we could revise a statistical plan for the study. This map shows kind of the bimodal peak of the flu season for 2024. As we can see, there's an uptick of flu in week 11, which coincides with middle December, peaking in late December with a second peak in the first week of February. When we look at enrollment, this aligned nicely with enrolling all the subjects prior to the peak of flu season, which is a challenge in many influenza studies. The last enrolled subject was on December 3rd. This was ahead of our target and allowed all subjects to have been dosed and to evaluate breakthrough infections thereafter. Both of these factors combined allowed us to update and revise the statistical plan to prioritize proof-of-concept testing for the study. The new statistical plan allows a grouped dose analysis, so combining the two highest doses, 300 milligram and 450 milligram versus placebo. That will be evaluated first with an alpha of 0.05. In the hierarchical design, if that is positive, then all of the alpha will be recycled and moved down into the pairwise analysis, which is each individual dose versus placebo. To account for multiplicity, as all those individual doses versus placebo are evaluated simultaneously, the Hochberg step-up method is utilized. This allows each analysis to be grouped in order of p-value from smallest, which is most significant, to largest, which is least significant. Starting at the top, if the grouped analysis is positive and the placebo attack rate is 2%, which is how the study was originally modeled with 80% power, a protective efficacy of 58% or greater will likely result in a positive study. However, if we demonstrate a higher attack rate in the placebo arm of 3%, a protective efficacy of 50% or greater will result in a statistically significant study. The rationale for combining the two higher doses can be illustrated in this pharmacokinetic curve. This curve shows us the three different doses that were evaluated in the Navigate trial at inception. We can see on the x-axis the time of duration of exposure, and on the y-axis, the plasma concentration. We see that the curves come down as we would expect as this drug has a long half-life of approximately six weeks, and most doses afford protection throughout the kind of key period of the peak flu season. However, we would expect that some of the lower doses may lose their protection near the end of the flu season. Another thing to illustrate here is that there's not a clear dose response that may occur when subjects are enrolled at different times in the study. Here is an example of two subjects. The first on the left is dosed at 450 milligrams at the beginning of the enrollment period, and the second on the right is enrolled at 300 milligrams, but at the end of the enrollment season, approximately at week 10. As you can see, we expect the 450 milligram dose subject to have higher concentrations and longer exposure of drug and protection from the flu. However, based on this timing, the 350 milligram dose subject may actually have higher protection during the peak flu season. Because of this, it appeared apparent to us to combine these two doses to add statistical power to the study by having a larger sample size to evaluate, particularly given that these two doses have very similar exposure curves. What is the data that we expect to see at readout? Data cut off was April 30th, so all breakthrough flu cases that occurred then will be included in the primary analysis. The data will be grouped based on the hierarchical analysis. We will first look at the 300 and 450 milligram dose group. We will evaluate protective efficacy with the corresponding p-value. We will also see the protective efficacy of all the different doses grouped by most significant to least significant p-value. The primary goal of this revised statistical plan is to evaluate protective efficacy, and this data that will be available at the end of June will be the final efficacy analysis for the study. We will also see a preliminary safety analysis. The study will continue for safety monitoring and will continue also for pharmacokinetic dosing and monitoring. For that reason, the dose selected to advance to phase three may be delayed until the end of the study. What is the bar for success of the phase 2B? The population that we intend to evaluate in the phase three is a high-risk population for complications from the flu. The average vaccine efficacy for some of the individuals in this population is quite low. For immunocompromised, for example, 10%-20% is the average vaccine effectiveness, sometimes as low as 5%. In the phase 2B trial, however, we evaluated generally healthy volunteers. The average vaccine efficacy in this population is 20-60%, with an average being about 40%. This year, it appears to be in the 35%-40%, as Dr. Hayden shared with us. We believe that protective efficacy in the phase 2B above this number of approximately 50% would be clinically meaningful. As we just noted, the statistical design of the study also allows for a positive study at this level. However, ultimately, we wish to advance CD388 into multiple populations with both vaccinated and unvaccinated participants. Because of the mechanistic kind of additive effect that may occur with these two agents, the potential combined efficacy may be quite high in the 60%-90%. The phase 2B has a clear regulatory path forward. We are in ongoing discussions with the FDA, which continue to be collaborative. Per the guidance, two randomized and well-controlled clinical trials are required for the approval of antiviral drugs. We have proposed this study now as having statistical significant testing as one of those two studies. The program has been granted fast track prior to review and qualified infectious disease product designation. Navigate data will be important to discuss and review with the FDA at the end of phase two meeting. However, we believe that if it is accepted as one of two required pivotal trials, this will potentially expedite development by two to three years and significantly lower developmental expenses. I'd like to comment on the phase three design considerations. The phase three study looks at a confluence of subjects and patients who are most at risk for complications of flu, as well as those from whom the current standard of care may not be sufficient or inadequate, combined with commercial factors. In this population, we plan to look at indication and usage prevention of seasonal influenza flu for all subjects who are at high risk for complications. The intent of the phase three population will also be to look at both vaccinated and unvaccinated subjects. Currently, we have focused in on subjects with moderate to severe high-risk comorbidities and chronic illnesses, such as heart failure, heart disease, COPD, asthma, advanced renal disease, and also severe immunocompromised status. This includes subjects with solid tumors who've had recent chemotherapy, hematopoietic stem cell transplant and hematologic malignancies, autoimmune diseases requiring therapies, solid organ transplants, as well as primary and secondary immune deficiency. Jim Beitel will speak further about some of the nuances of these populations in a few minutes. One important feature is that we do expect the phase 2B data to translate to our phase three population. This comes from precedent antiviral studies with Oseltamivir, Zanamivir, Baloxavir, which showed that there was no diminution in efficacy when you moved from a healthy population to high-risk populations. Also from the U.S. prescribing information, which is included here, there is no change in dose recommendations for these populations. The envisioned phase 3 study focuses on these individuals at high risk for severe complications. It will enroll a large population of approximately 5,000-7,000 subjects to run over two to three influenza seasons, randomized one-to-one, CD388 versus placebo. The statistical assumptions for this model are 90% power with a 1.5% placebo attack rate and 10% loss to follow-up. Due to this population's event rate being less certain from previous precedent trials, an interim analysis will occur after the very first flu season to trigger a potential sample size increase as needed. The primary endpoint has one key difference from our phase 2B, and that is that fever will be included as one of these symptoms rather than as a separate criteria. The primary endpoint will be comprised of laboratory-confirmed influenza, two or more symptoms, as well as the possibility of worsening of two or more baseline symptoms. The phase three timeline offers a path to regulatory approval. We envision the beginning of this study to be in the spring of 2026, Southern Hemisphere, starting with approximately a 5,000-subject goal of high risk and IC combined. The interim analysis will occur at the end of that Southern Hemisphere to trigger a sample size increase, which would then add a third season, which is demonstrated here. Moving forward, we have BLA prep, submission, and review with fast track timing. Base cases that are full approval from the FDA would occur approximately Q1 or Q2 of 2029. Thank you for your time. I'd now like to introduce Dr. Rick Bright, who is an international expert in biodefense and emergency preparedness and response. He's going to help us change gears here and evaluate CD388 as a potential for avian flu, H5N1. Thank you, Dr. Bright. Thank you, Nicole. Thank you to Jeff and the entire Cidara team for the opportunity to join this discussion today on CD388 and the broader landscape of influenza preparedness. As the former director of BARDA and someone who has spent over two decades in pandemic response and medical countermeasure development, I can tell you we're at a pivotal moment in how we think about influenza, and not just seasonally, but also strategically in the context of pandemics. I believe that CD388 represents the kind of innovation that we have been needing in this influenza space for many years, an opportunity to close the gaps in influenza prevention and to protect the most vulnerable from seasonal influenza and even before the next pandemic starts. There we go on the slides. Fred has already nicely covered a lot about seasonal influenza, but I want to touch on the emerging risk that we've been seeing on the global resurgence of H5N1 avian influenza. In this past year alone, we saw H5N1 spill over into U.S. dairy cattle and multiple other mammalian species. It signals that the virus is adapting, it's expanding its host range, and possibly learning how to spread more efficiently in mammals, including people. This is a warning sign. When influenza moves into new mammalian species, it's often the precursor to human adaptation. What's even more concerning is we're seeing this adaptation occur now. We're seeing more mammalian adaptive mutations, including things like changes in the PB2, this E627K. I won't go into an in-depth science discussion on these mutations, but look at this chart. You can see how the various viruses are converging, they're reassorting, they are adapting, and they're now invading and infecting a number of species that are really close to humans. What we're really seeing is that these changes are likely improving the efficient replication opportunity and transmission among humans. We're watching the virus train itself in real time. The human cases so far, luckily, have been low with the limited surveillance that we have, but that doesn't mean that the risk is low. This graph shows just how cyclical and unpredictable Zoonotic transmission can be with H5N1 influenza. From the global data that we're seeing, the question isn't if this virus will adapt now, it is whether or not we're going to be ready for it when it does. If I'm honest with you, which I will be, we're not ready. I mean, you've already seen the current influenza vaccines are inconsistent. They're short-lived. Some years they offer 40% protection, some years far less, particularly in older adults and in immunocompromised individuals. We all know that the antivirals we have today must be taken early. Many people miss that opportunity. They miss that window of efficacy. These antiviral drugs do not offer long-lasting protection. That leaves us a dangerous gap between exposure and protection. That is where CD388 is specifically designed to fill that gap. When I think about what CD388 does and what it could do differently, I mean, number one is long-lasting. You've heard about its design and what could make it long-lasting. That means it's designed for one per season prophylaxis. It doesn't rely on immunity, immune memory, which is crucial for those who don't respond well to vaccines. It can also be deployed immediately during a pandemic before vaccines were even available. That makes it a strategic asset for both seasonal and pandemic influenza. It stands out among the hundreds of different products that are in development for influenza. I mean, very few of the products, either vaccines or therapeutics in development, offer this type of durability and flexibility. CD388 is one of the most advanced, clinically advanced, long-lasting prophylactic targets in development today. It's also designed for what I call real-world use. It stands out because it's not treating the flu, it's preventing it. It has a pharmacokinetic profile that could support a once-per-season dose. In my opinion, in decades in this space, that's a tremendous leap forward for the field. For a long time, BARDA was the engine behind pandemic influenza preparedness. I mean, funding next-generation vaccines, building manufacturing capacity, and stockpiling antiviral drugs. As someone who led those programs at BARDA for a decade, I can tell you we need layered approaches. We need layered defenses. I mean, BARDA has finally evolved from funding just vaccines, primarily vaccines, into adding support now for diagnostics and therapeutics and innovative delivery strategies for influenza. I believe what they put forward now for their next-generation strategy, that drugs like CD388 fits into that space because we want to be proactive to prevent infection and disease and not have to scramble post-infection. This slide just shows you a number of the next-generation approaches that BARDA has been investing in lately, from better diagnostics and masks to stockpile modernization, and most importantly, to long-lasting antivirals. I mean, CD388 aligns with BARDA's push for simplified dosing, durable protection, and scalable deployment, all major gaps that we have in responding to seasonal and pandemic influenza. Also, we have research gaps. There is a lot of push, and you hear a lot about influenza vaccines, H5N1 vaccines. Even if we have newer technologies such as an mRNA-based vaccine, we still have significant gaps in our basic research to understand what an H5N1 vaccine needs to do. We don't have correlates of protection, and there's a long-term research plan in place for that. We don't understand cross-reactive immunity. If I have some pre-existing antibodies to H1 or N1, is it going to protect me from H5N1? We know the age and comorbidity factors and the immunological responses are different by age, with hypertension and with obesity. We haven't done those clinical trials for vaccine effectiveness in these groups. We don't really have the biomarkers. Mucosal immunity is still a mystery. To be honest with you, after 100 years of dealing with influenza, about 80 of intense research and development and vaccine availability, we still don't really have a lot of those assays in place. When I think about responding quickly to a pandemic to H5N1 with a vaccine, we just don't have it. There's a lot of work that needs to be done. What comes off the shelf or out of the stockpile is not going to be the most effective approach to stopping the spread of influenza. There are a number of other products in development. I mean, let's take a step back, look at the progress. We have Flumas V2 of this and other mRNA-based vaccines. They sound promising, but they're unproven in their durability. They're still a vaccine that would have to be redesigned as the virus shifts and changes. You saw from the earlier slide how quickly even H5N1 is shifting and changing within one year or one season. Monoclonal antibodies are also short-lived, short-acting, and very tuned into a specific part of the virus that we saw with the COVID and SARS-CoV-2, how effective monoclonal antibodies appeared to be at the start of the pandemic, but how quickly they became ineffective because of how the virus changed. We have things like Molnupiravir, which was developed as a broader spectrum antiviral, they believe, but it also has safety issues and concerns about mutagenicity and modest efficacy if we're honest about it. CD388, by contrast, I think offers this protection. It's a fusion antiviral, as Jeff described, once-per-season prophylaxis, and it does not have to be updated as the virus changes. You saw that it has activity against the broad spectrum of influenza viruses, both seasonal and pandemic, and influenza A and influenza B. The limitation, of course, is, as Nicole described, we're in clinical studies. The early data look very promising, and we're getting ready to go into the larger phase three study, which I think is going to be validating to this type of approach for a new long-lasting therapeutic. To me, this is the time to invest forward, not retrospectively. If we wait until H5N1 adapts to humans, we'll be scrambling to catch up. CD388 gives us a head start, gives us a way to protect people while vaccines are in development, gives us a solution for people who don't want to take vaccines. In this day and age, there are more and more people who are anti-vaccine or vaccine-averse, risk-averse. This is the moment, I think, that CD388 can fill that gap and make sure that we're ready not only for seasonal, but also pandemic influenza. I do want to address just real quickly a recent announcement you saw from HHS about the major investment, $500 million, a major, into this compound or vaccine approach called BPL1357. Unfortunately, it is not a look forward. It is, I would, I think, something that is slipping backwards. You may have seen the announcement. It's an investment in an old whole virus inactivated flu vaccine approach being developed at NIH. And to be direct with you, this is an approach that Jonas Salk and Thomas Francis started with in influenza in 1943, 1945. It was all we had for the longest time, but it was abandoned in the 1970s because of the significant reactogenicity we saw in children with high fevers and even seizures in some cases. It certainly wasn't long-lasting immunity. It certainly wasn't broad-spectrum immunity. It is not a next-generation vaccine. In my opinion, it's a retreat to the past. It's repackaged with political gloss. I think we can do much better. I think we are doing much better. Comparing, I don't think I have to belabor this point, but here I've put together side by side. CD388 is a modern, scalable approach already in phase two. BPL1357 is legacy technology with uncertain performance, known reactogenicity. I don't think the contrast could be any clearer. We need to prioritize tools that match the speed and the complexity of modern threats. Just in closing, just to remind you that the next flu pandemic could start with the spillover effect that we won't be able to detect, especially that we've shut off most of our surveillance and we're certainly not sharing data within the U.S. or around the world as we should. It'll be limited time to think about developing and deploying an effective vaccine. We need a long-lasting antiviral like CD388 that can serve as a frontline pre-exposure prophylaxis, especially for people who are at highest risk and those exposed population. We need a bridge strategy to protect before vaccines arrive and to complement vaccines where immune response is uncertain or can be delayed. I think of CD388 as a multi-layered biosecurity net, coming from my background. It's not just for seasonal influenza mitigation, but also very important for pandemic containment. I'll stop there and thank you, Nicole and Jeff. Rick, thanks so much for your observations. We'd like now to close today's session to talk about the market and pricing work that we've been doing. That work has been led by Jim Beitel, our Chief Business Officer. Jim? Yeah, thanks, Jeff. First, I'd like to share some highlights of our patient segmentation work, as you can see on the next slide here, which really aims to answer the question, how many subjects have moderate to severe comorbidities and IC status? The ones that Nicole mentioned will be the focus of our registrational program. As you can see from this data, subjects with advanced forms of cardiovascular disease and chronic lung diseases are the largest segments, both when looking at the most severe forms and also when adding in the moderate forms. Renal disease is another large segment. Shown here is CKD stage 3A and 3B as moderate, also a very large subsegment. We can add in additional patients with moderate to severe IC, and also the advanced ages here shown as 85 and above. The big picture here is that there's very large populations with advanced forms of these comorbidities. While there's considerable diversity, the segments are well defined and can be readily identified using criteria that physicians use every day to manage these patients. Moving on to burden, we used hospitalization rate as a barometer for identifying those populations at greatest risk. There's good reason for that. Hospitalization is associated with a lot of different health consequences, as you can see on the left-hand side. When we look at hospitalization rate, we can see that patients with 65 and above, all comers, these are individuals that are healthy or have comorbidities, most certainly have an elevated hospitalization rate relative to background, otherwise healthy individuals of younger ages. What's really fascinating is when you look at these individuals that we intend to focus on for the registrational program, these individuals with cardiovascular disease and pulmonary disease, these are the individuals that are at even greater risk of hospitalization from flu. This is why we're very excited about this population. Again, these are populations regardless of age. Based on the CDC data, they have these background conditions. When you do the math and calculate the hospitalization rates, you see elevated rates versus the 65 and above all comers population. What's even more exciting when you think about the benefit that we can bring to these patients is that this includes all subjects, whether they have mild, moderate, or severe forms of these background comorbidities. We are confident when you look at the moderate to severe subjects, as Nicole described, we have the opportunity to see an even higher hospitalization rate and demonstrate even greater benefit in these populations. Lots of ways to think about CD388 development. We went through a pretty exhaustive process, honestly, to reach these conclusions. There are a lot of populations we looked at that are not on this slide, but the ones that floated to the surface in terms of hospitalization rate are the ones that we are focusing in on for our registrational program and the ones that are shown on this slide. The other thing I wanted to speak to is the diversity of this patient population and ways to reach them effectively commercially. I mean, we need to be honest here. This is a very large and diverse population, right? It spans several different physician specialties. We have to think about whether or not we can engage physicians effectively and generate demand for CD388. Although the population is quite diverse and large, I wanted to just impart upon you that there absolutely are pockets of concentration here. If you look at the cardiology and pulmonology segment alone, there are approximately 40 million high-risk subjects in the United States with these conditions that are managed by these specialists and are frequently seeing the specialists for these conditions. Certainly a lot of diversity, but opportunities through thoughtful market segmentation to focus in on the areas where concentration exists. Within these specialties, honestly, I have never seen a physician segment that did not play by the 70-30 rule, meaning that 30% of the physicians drive 70% of the business. We're expecting the same will prove true as we acquire the physician-level prescription data and do the more detailed launch planning during the course of the phase three program, that we can focus in on those high-volume, high-decile physicians and group practices, those that have standardized procedures for identifying patients at risk of flu and administering flu vaccines. It's a matter of, of course, adding CD388 to vaccines. We're not asking physicians to really change anything with respect to vaccination. There is an opportunity for sort of seamlessly adding CD388 to what's going on in these high-volume cardiology, pulmonology, and nephrology practices already. We are expecting endorsement from physician societies. Each one of these physician verticals has a medical society, and in most cases, they have guidelines in place for flu vaccination already. We envision during the course of the phase three program, working with those organizations to get CD388 endorsed and bringing sort of clear use guidelines through these medical societies to the various segments that are applicable here. Another thing we need to think about that you might have thought about as well is the seasonality of the promotional effort. That's an exciting opportunity, actually, because while there certainly will be personal promotion involved in the CD388 launch effort, combined with non-personal promotion efforts, it's a seasonal promotional effort. That creates capacity to promote other products for the remainder of the season. We absolutely envision commercial relationships with other companies that are operating in these spaces to both leverage the commercial capacity that we have on other products, as well as bring our excess commercial capacity to bear on their products. Lots of opportunities as a business development veteran to get excited about what we can do as it relates to maximizing the reach and frequency of promotional effort through business development as we get further along. Next, I want to ask or sort of pose the question and get the answer for you related to whether or not these specialists acknowledge flu burden in their high-risk patients. Also, do they themselves see themselves playing an active role in managing it? This was an open question. Honestly, we were not sure if we could focus in on the specialist and sort of anchor there for demand generation. We were very pleased to see that these specialists acknowledge a very high flu burden in the subjects with moderate to severe comorbidities. That is shown by the dark orange in this chart here. They also actually see considerable burden in the mild patients. This is really exciting when we think about growth opportunities beyond the populations that we're focusing in on for the registrational program and launch label. We also asked physicians, "Okay, so you acknowledge a burden in these patients. Do you yourself take responsibility for preventing it?" They came back with very strong marks here as well. These specialists rated themselves highest of any other physician specialty, including pharmacy and PCP, as being the primary party responsible for preventing flu in these high-risk patients. As evidence for that, we found that about 80% either stock and administer flu vaccines in their clinics or in adjacent infusion centers if they're operating in a hospital. Those two data points on the right were very encouraging to see because, A, they acknowledge that they themselves play a primary role, the primary role, actually, and they're following through by taking action and administering flu vaccines in their practice. You can see how CD388 can come in and fit on top of what's being done already in these specialty clinics. Another question we posed is, of course, as you would in market research, what's the response to the CD388 target product profile? What kind of recommendation rates and utilization rates can we expect? The data that you see here, the light green is the physician recommendation rate based on the CD388 target product profile. This is for individuals with moderate to severe comorbidities and IC status. Very high and strong responses based on the physician's review of the target product profile. We tested a range of efficacy assumptions and sort of sensitivities in the target product profile as well. Strong responses across the board. I also want to point out that you might be aware that physicians often overstate sort of how they might actually use a product in market research versus what ends up happening at launch. We have reduced these numbers to account for that. These are actually the downward adjusted numbers. This is not sort of raw data coming from the market research. Even with those downward adjustments, we see very strong responses by physicians and expectations of recommendation rates. Patients have a voice too. We also ask physicians what% of their patients with these conditions would they expect to accept their recommendation. That is shown by the dark green line here. Also, very high. This is driven by sort of the patient self-awareness. Even though vaccination rates are not this high across the board, when you look at these higher-risk comorbidities and IC status, people are aware of their health condition and more likely to accept a recommendation from a specialist who they have been seeing for perhaps many years managing the condition. Exciting to see the strong response from physicians and expectations of patient acceptance. Moving on to the payer side of the equation. We also wanted to understand what kind of pricing opportunity and access opportunities we can expect with CD388 in these populations. We saw very similar things, actually. Payers also perceive influenza to create a high clinical and economic burden in patients with moderate to severe comorbidities and IC status. That is shown by the data on the right. The economic burden is a little higher for the comorbidities, a little lower for IC. That is really just driven by the differences in the size of the patient populations that you saw on the slide that I presented earlier. In terms of pricing and access levers for CD388, in addition to the burden that payers acknowledge, we also found that they responded very well to the expected reductions in symptomatic influenza. As Dr. Hayden pointed out, we may not see hospitalization reduction in our registrational program. We wanted to make sure that we did not overstate the target product profile that we put in front of payers or physicians. We made the claim that that would come later in post-marketing studies. They were very receptive to that. They understood the practical considerations, and they viewed symptomatic reduction in flu as being an endpoint that mattered and one that they could have confidence that translates into economic value as well as clinical value. We also, I think, with payers can expect to leverage endorsement from the medical societies that I mentioned. That is going to be important. We do need the backing of the medical community. We imagine during the course of the registrational program, going much deeper and broader with our key opinion leader development efforts into these various physician specialties. We do expect medical benefit access with office-based administration. This is what payers said they would do. It was, I think, maybe expected on the front end. It was nice to see payers not sort of push it in a different direction. This is important because, again, we are imagining a demand creation model here that is driven by creating demand mostly through office-based administration, perhaps a little different than vaccines, which are a little more of a pharmacy-driven play. We expect no issues with buy and bill for CD388 with these specialty clinics. By focusing in on these high-risk patients, we also expect that there is feasibility of demonstrating economic value sufficient to have commercial feasibility in XUS markets. We're excited about that. Remember, it's not just about hospitalization. There are considerable health consequences downstream of the hospitalization, step changes in health status as a result of COPD patients that just never really recovered to where they were before. There also is a well-documented increased rate of heart attacks in individuals with underlying cardiovascular comorbidities that experience flu. Moving on to price. Just to give you a little color for how we approach the discussions with price in our payer market research. Again, this, as well as the previous slides, refer to U.S. commercial payers. This is sort of employer-provided healthcare as well as managed Medicare and managed Medicaid. What we did is we found the most relevant commercial analog we could, which we believe is Beyfortus. As you may know, it's a long-acting antibody being developed and commercialized by Sanofi and AstraZeneca. The price point there is about $560 for the season. This is for protecting infants from RSV. We just use that as a reference point. It's not a perfect analog. There are differences, but it's the best available one. We use that as a starting point. We asked them what kind of restrictions would they expect if we priced CD388 at $560. As you can see on the left, we found very low expectation of restrictions. We then moved on to a higher price point range, north of $560 but south of $750 for the season. Here we began to see payers start to pull out an occasional restriction in their responses to us. In some cases, it was not a prior authorization. It was just, "Okay, we'd like the physician to certify that this patient actually has one of these comorbidities or is immune compromised." In some cases, it was a PA. This is when we began to see some restrictions. It was not until we got north of $750 that we saw most payers begin to mention prior authorization as a restriction that they would expect to deploy. This is all based on the target product profile of having a reduction in symptomatic influenza in the launch label when the price decision is made and payer access is requested. Obviously, over time, with additional data in post-marketing studies, or maybe even seeing medical resource utilization reduction in our registrational program, we expect to end up with additional pricing leverage in the United States. I'll also remind you that Medicare operates differently. Traditional Medicare is a bit different there. We expect coverage to label without any restrictions across the range of price points. I also want to point out that it's well known that payers overstate restrictions that they report in market research. While we did make downward adjustments in the recommendation rate you saw earlier, here we have not made any adjustments. This is the verbatims and expectations of payers based on what they told us in market research. We do expect it to be a conservative look on the relationship between price and restrictions and access. Overall, this is really exciting. It is clear that as a result of the product profile and the fact that CD388 is not a vaccine, it is a long-acting antiviral, and it is not even passive immunization either, that payers really think about it differently. It really creates an opportunity for differentiated pricing relative to what you see with vaccines and a very compelling commercial opportunity. In summary, I hope I have given you some reasons why we believe that the registrational program that we will be running will unlock a very compelling commercial opportunity. It is a large, diverse population, but it is well definable. The CD388 product profile is very unique and differentiated, both with respect to commercially available options today as well as anything in the clinical stage pipeline that's out there. The target physician universe is quite large, but there are absolutely strategies to successfully engage them, and they do respond well to the CD388 target product profile. Importantly, they are administering vaccines today in these high-risk patients in their office, as I mentioned, about 80% stocking and administering vaccines today. We believe very confidently in the opportunity for favorable pricing and access. We're also excited about utilization beyond these high-risk individuals in the United States. Remember the data I shared on physician perception of burden in the more mild patients and also the opportunity for utilization and commercial reach outside the United States. Overall, very excited about the commercial opportunity. It's been a real pleasure to work with our business partners on the analytics and also Nicole, Corina, and other members of the team here to arrive at these conclusions. We considered a pretty wide range of development strategy alternatives. Honestly, there's a lot of things on the page we didn't share with you, but this is clearly where the value is at for the initial registrational program, and it's very exciting. With that, I'll pass it back over to Jeff. All right. Thanks, Jim. Everyone, we'll take it home here. We'll end with a prophetic target product profile for CD388. I hope you can appreciate why the Cidara team is very excited about the opportunity to have a product profile, as you see here on this slide, is truly an exciting prospect. We look forward to continuing with our development plan, starting with the potential announcement of data approximately one month from today, assuming that the data turnout anywhere close to what our expectations are. We'll be planning on an FDA end-of-phase two meeting as soon as possible afterwards. That would put us on a path to potentially start our phase three program as outlined today in the spring of 2026, starting in the Southern Hemisphere. With that, let me turn it back over to Tara, and we can take it into Q&A. Thanks. Great. Thank you, Jeff. Yes, at this time, we'll be conducting a question-and-answer session with our speakers. Our first question comes from Eric Schmidt at Cantor Fitzgerald. Please go ahead, Eric. Thank you for the opportunity to ask the question and congrats on a really informative webinar. This is a textbook A to Z rundown of CD388 and why it's a critical therapy. Question maybe for Nicole. You laid out two powering assumption scenarios in the phase 2B Navigate trial. I think one assumption was that the attack rate might be around 2% in the placebo arm and the other about 3% in the placebo arm. Do you have rationale or justification for why the attack rates may be in that range, I guess? Hi, Eric. Thanks for the question. We had a model to a 2% because that has been the average over previous flu seasons and previous flu studies. As we saw from Dr. Hayden's presentation, and we were, of course, receiving this news as well, watching Flu View and hearing from colleagues, this has been a more severe flu season, the most severe flu season in 15 years. I think thinking back, we can look back at, for example, the VIR data, that I think the attack rate there was about 1.7%. We'd expect it to be a little bit higher. I think there's an important point there is that our criteria for what is an event is also more strict. The fever endpoint would necessarily bring down the number of events. I think we're not sure where we're going to end up, but we think it's going to be higher than we had modeled or anticipated. That gave us enough confidence to change the statistical design to move forward with powering. That's great. Thanks for the answer. I assume you're not willing to share with us the blinded attack rate in the trial. Nice try, Eric. Yeah, we locked the database last week, so it would not be appropriate for us to be sharing the blinded attack rate at this time. Great. Thanks very much. Thanks for the questions, Eric. Our next question comes from Seamus Fernandez at Guggenheim. Please go ahead, Seamus. Oh, great. Thanks for the questions. Can you guys hear me? I just want to make sure there was a little glitch there. Yes, we can. All right, great. Can you just clarify a little bit the differences between the phase two primary endpoint and then the prospective phase three primary endpoint? I think there were some differences there that might need clarification, including, I think, a somewhat lower assumed attack rate over multiple seasons. That's my first question. Go ahead, Nicole. Thank you. Hi, Seamus. Thanks for the question. Yes. The phase two essentially has very strict criteria. The fever temperature of 38 degrees and then two respiratory or one respiratory and one systemic symptom, as well as PCR-confirmed influenza. The same is in the phase three. We also have centrally confirmed PCR-positive influenza. We also will have two symptoms, but we will not have the fever cutoff. That is the main difference. The fever instead will be moved as an option for the respiratory or systemic symptom category. The reason is that this population, the IC population in particular, as having immune deficiency, may not manifest fever at all. We did have a discussion with, actually, the FDA about this as well. We want to be able to capture changes in symptoms, but previously, when that has been used, fever cutoffs have been used, the trials have not been able to demonstrate a difference between those populations and placebo. The attack rate was also lowered for that same reason. These are populations that have other conditions, other health conditions, and we expect higher loss to follow up, also a change in symptom and illness presentation. We are providing a buffer for that. That is why the attack rate is going to be lowered for that study. Great. In terms of the recycling of the alpha, I think you talked about it makes a huge amount of sense. Great powering assumptions and combining the 300 and the 450 makes a ton of sense. As you recycle the alpha, can you talk about the power that you have in the individual arms or would be assumed in the individual arms for a potential p-value of less than 0.05? Yes. It still models to 80% powered to show. It actually kind of follows similar numbers. Approximately 58%-60%, if there's a 2% attack rate, would be 80% powered by modeling. If it's 3%, it'll be closer to 50%, would allow 80% powering. Okay. Maybe just one last question. As you looked at the commercial opportunity in the landscape, I think one of the things that really does influence the responses that you get from the providers is the target product profile that was presented. Can you just help us understand the target product profile that was presented to the payers, the physicians, the patients in terms of the assumed efficacy or the presumed efficacy, as well as the patient population that's presumed, again, to kind of drive that payer analysis? Thanks. Jeff, would you like me to take that one? Yeah. Please do. Very good. Yeah, it's great. Great question, Seamus. We approached it open-mindedly. We tested a range in our market research. The high end, we anchored around 80% reduction in symptomatic influenza. That correlates to the study that Dr. Hayden mentioned with zanamivir in flu prevention in subjects with COPD and other comorbidities. That was the high end of the range. In that study, you might remember about two-thirds of the individuals were vaccinated. At the low end of the range, we assumed 40%-50% efficacy. At the low of the range, we did see some softening of expected use, especially when you got into the more moderate individuals or mild subjects. In the severe patients, and I might remind you in that dark orange data in the first slide I presented, there are tens of millions of those. The severe population itself is a very interesting opportunity. You can imagine if, for some reason, we end up on the lower end of the range, we might focus there commercially. Really, positive feedback across the board with respect to efficacy ranges. Trying to think of other things. We told them that approximately 80% of the subjects in the study would be vaccinated. We thought that would be reasonable. It is a little bit higher than vaccination rates in these populations. In a clinical trial situation, we might see slightly higher vaccination rates. That is where we landed on that one. Hopefully, that answers your question. Just to echo Eric's responses on this, I think it was a fantastic presentation. Really, again, you guys, high marks on efficiency. Jim, I apologize if I cut you off there. No problem. Thanks, Seamus. Thanks for the question, Seamus. Our next question comes from Greg Renza at RBC Capital Markets. Please go ahead, Greg. Great. Thanks, Tara. Good morning, Jeff and team. And let me add my congrats on really a very productive event from our and the viewers. Maybe, Jeff, just keeping with Jim's commentary and the elaboration of the commercial opportunity, a lot of interesting work here to build on. Jim, I just wanted to maybe have you expand a little bit about the demand generation that you're commenting on. Just given your experiences as you've laid out some of the tactics and the overall strategy, how does this compare? How does the feasibility and practicality compare to your experiences as you think about comping it to other launches and other go-to-market strategies? Maybe you can just talk a little bit about sort of the incentivization that you're thinking about when it comes to prophylaxis treatment. Yeah, thanks for the question. It's one reason why I sort of proactively put that slide in the deck on commercialization strategies and how we can think about being effective commercially. We have to acknowledge this is a heavy lift, right? It's a fairly large population. We're talking about multiple physician specialties. I feel very confident in saying that focus is going to be the key. There are large pockets of concentrated business in any specialty. I'm sure we're going to see that here as we get into the more granular physician segmentation. I'll just bring you back to the comment I mentioned with 40 million subjects in cardiology and pulmonology alone. If we could set aside and just commercially ignored everything else, which we won't do, you can imagine it's not difficult to think about a salesforce and also non-personal promotion being deployed effectively to reach a population of physician specialties. There, it's about 28,000 physicians, cardiology and pulmonology. That's a pretty manageable number. Again, within that, there's going to be high deciles. There's going to be group practices. That hopefully gives you some confidence that this is commercially feasible. I absolutely believe additional leverage can come from commercial relationships with parties that are in this space already. Yeah, that's really helpful. Thank you. Jeff, I think in that last slide on the near-term milestones and maybe just building on even Jim's mention of leverage here, I think you've got in parallel business development discussions. Just wanted to give you an opportunity to elaborate on what you're prioritizing, what can help with the leverage of CD388 and getting it to progress. What exactly is in mind in order to optimize the value? Yeah, I think consistent with what Jim laid out, we have initiated a number of discussions with parties along the lines of what Jim has indicated. Clearly, as a seasonal drug, there's a great opportunity to co-promote other products. Given the commercial opportunity provided by CD388, we think that that could be very commercially attractive for other companies that have complementary products in this space. Jim, anything else you want to add to that? I think that's right, Jeff. Certainly, we feel very confident in a standalone strategy, but that may be suboptimal, and there could be additional leverage in these commercial relationships that we will explore over time. I think in the short term, I just add we've been actively engaging for quite some time and exploring options already. There is the potential for relationships that are more focused on additional development leverage to more broadly develop the product and sort of accelerate additional studies that might be useful to sort of build product value and demonstrate that. I mentioned those post-marketing studies with real-world evidence, right, being post-launch. There is, I would say, upside in our commercial thinking if we're able to pull that forward. There could be opportunities for more development-focused relationships in the near term. That's great. Thanks so much. Congrats again, and looking forward to late June. Thanks for the questions, Greg. Our next question comes from Joey Stringer at Needham & Company. Please go ahead, Joey. Hi, good morning. Thanks for taking our questions. Technical one on the phase 2B primary endpoint. What qualifies as a respiratory symptom and what qualifies as a systemic symptom? Maybe just to clarify for us, is there a difference in how FDA or CDC defines these? Yeah, Nicole, do you want to field that, or Corina could do so as well? Yes. Essentially, the respiratory symptoms were nasal congestion, cough, or sore throat, and the systemic were headache, body aches and pain, feeling feverish, and fatigue. There are some differences. These are traditional kind of endpoints that the FDA has accepted in previous studies. I think Dr. Hayden also did a nice job of showing that different endpoints have existed prior to this. The most common has been the different temperature cutoffs. The FDA does not necessarily require you to have a fever cutoff as one of your primary. CDC does, and WHO also does have a high fever cutoff. I think those are the main differences. I hope that answered your question, but I think the reason that we wanted to emphasize why we chose our endpoint was that we do believe the high fever cutoff is important for demonstrating the mechanism of action of this particular therapy, which prevents kind of symptomatic severe infection. Sorry, Joy, but we only have a short amount of time left. I wanted to make sure that Roy had an opportunity to ask a question before we close the sessions today. Yeah, sure thing. Thank you for taking our question. Sure. Roy? Okay, great. Thanks for the presentation, and thanks for taking the questions. I guess a couple probably for Dr. Hayden. Just in looking at placebo event rates from prior trials, correlating the CDC data for illness depends on the rate that the patient who has illness goes to seek care and then that they within care that a test is performed. I guess can you just maybe characterize those rates for the season for RSV antibody 2022 to 2023 versus this last season that we just went through with CD388? I have to go back and look at the VIR data in more detail. I just point out that, again, the CDC definition is 37.8 degrees Celsius, 100 degrees Fahrenheit with cough and/or sore throat. WHO, as you heard, is a little bit higher at 38 degrees Celsius, 104 degrees Fahrenheit with cough. Those are epidemiologic definitions that they use for monitoring. It obviously does not capture nearly all the flu that is going on. As you on the call know, up to half of seasonal influenza infections and almost that proportion of human pandemic flu infections can be subclinical or paucely symptomatic. The level in the VIR study was 37.8, but it was not in the primary definition. It was one of the systemic components, so they did not have to reach that threshold. There was only one where there was a threshold that was introduced, either using the CDC definition or the WHO definition, that we actually started seeing some separation between the control group and the high-dose antibody group. I hope that clarifies your— okay. That's great. If I could ask one follow-up, just going from the 37.8 to the 38-degree threshold, based on historical data, what proportion of patients do you think you'd lose? Is 20% reasonable? I showed you the one slide going from 37.2 to 37.8. I cannot recall if you then bump it up again to 38, what the losses would be. But I point out in the Navigate phase 2B, you have a population that's not immunized, that's otherwise healthy for the most part. So I think you'll see a fair number that will have a more classic influenza illness. The nice thing is you can obviously look at other temperature thresholds as well. With that, that brings us past the end of our session today. I want to thank everybody for participating. I know there must be a number of other questions. Feel free to reach out directly to us. Just as a note, today's slide set will be made available on the Cidara website. Again, thank you very much. We look forward to reengaging, hopefully, in about a month or so. Thank you.