Ladies and gentlemen, thank you for standing by. My name is Yale and I will be your conference operator today. At this time, I would like to welcome everyone to the Skye Bioscience Second Quarter 2025 Financial Results and Business Update Call. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question- and- answer session. I would now like to turn the conference over to Bernie Hertel, Head of Investor Relations. Please go ahead. Hello, and thank you all for participating in today's call. Before we begin, I'd like to caution that comments made during this conference call will contain forward-looking statements under the Safe Harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995, including statements about Skye's expectations regarding its development activities, timelines, and milestones. Forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially and adversely, and reported results should not be considered as an indication of future performance. These forward-looking statements speak only as of today's date, and the company undertakes no obligation to revise or update any statements made today. I encourage you to review all the company's filings with the Securities and Exchange Commission concerning these and other matters. I'll now turn the call over to Punit Dhillon, Skye's President and CEO. Good afternoon, everyone. Today, we have most of our executive team participating in our financial results and operations update through prepared comments, or they're available to address questions during the Q&A. As we often say, we've managed the course with discipline, and we're now approaching the point where preparation becomes proof. This quarter marks a notable prelude to our reporting of Phase IIa data for nimacimab, Skye's differentiated peripheral CB1 inhibitor, in terms of execution, as well as the clarity arising from the convergence of key activities, including the progress of Phase IIa study, understanding of the mechanism of nimacimab, and planning for next steps relating to our clinical development thesis. On today's call, we'll walk through the progress we've made, the data that we've generated, and the path we're charting forward. We'll cover three key areas: one, clinical progress, where we stand on Phase IIa program and the top-line timing; two, R&D foundation, how we believe our antibody approach to CB1 inhibition is mechanistically distinct and supported by reproducible preclinical data; and three, where nimacimab fits, positioning our asset within the evolving obesity treatment landscape, including gaps we believe are overlooked and not readily fulfillable with other mechanisms. Let's begin with the clinical progress. Phase IIa cb1 trial is advancing as planned, on budget, and ahead of schedule. Enrollment was completed in February, ahead of schedule, and a 26-week visit for the last patient is projected to occur very shortly. The 26-week extension study is also now underway, with both the monotherapy and combination arms enrolling. Approximately 50% of the patients from the original study are eligible for enrollment, and we're optimistic that a majority of the eligible patients will choose to participate in the extension study. The Data Safety Monitoring Committee has now reviewed the study 4x and issued no recommendations for changes. This has been an effectively managed program, from timeline management and data capture on various endpoints to regulatory coordination, from the initial IND to the recent protocol updates to facilitate the 26-week extension. We look forward to completing treatment of our final enrolled patient for this first segment of CBIOND and then stepping into the data analysis. We remain on track to deliver top-line results by late Q3, early Q4. Next, let's discuss R&D. As a reminder, nimacimab is a fully humanized, peripherally restricted CB1 antibody designed to target a well-established metabolic pathway, but to do so without the central toxicity that has historically limited CB1 inhibitors. We differentiate from non-antibody CB1 inhibitors in two fundamental ways: one, from a distribution standpoint, and two, mechanism, both advantages that support a broader therapeutic window and target engagement in the periphery. Let's focus in on peripheral restriction. Nimacimab shows negligible brain penetration across many different species. It's confirmed through PET imaging, cerebral spinal fluid analysis, and postmortem tissue assessments. Even at high and repeated doses, the molecule remains peripherally compartmentalized. Next, let's talk about mechanism: allosteric noncompetitive inhibition. Nimacimab binds at the allosteric site of CB1, retaining potency even in the presence of elevated endocannabinoids, which is commonly associated with the obese state. This is in contrast to small molecules that bind to the orthosteric site of the CB1 receptor, which may face increasing competition to bind to the receptor and can lose efficacy in the presence of high concentration of endocannabinoids. We've evaluated this molecule through multiple preclinical studies using our human CB1 knock-in DIO mouse model. Based on these DIO mouse studies, we believe there are at least four distinct yet converging mechanisms that define nimacimab's action and form our platform's scientific core. One, caloric restriction via peripheral hormonal coordination. Nimacimab reduces food intake by acting on adipose and gastrointestinal tissues to modulate appetite-regulating hormones such as GLP-1, leptin, and resistin. This enables a peripherally mediated reduction in central appetite signaling without requiring brain exposure. Two, improvement and restoration of glycemic control. We see consistent improvements in fasting glucose and insulin, with significant improvements in glucose tolerance in DIO models, supporting nimacimab's relevance for patients with prediabetes or insulin resistance. Three, enhancement of lipid metabolism. Nimacimab reduces steatosis and circulating cholesterol levels, a direct benefit for patients with obesity-linked metabolic comorbidities like MAFLD or dyslipidemia. Four, reduction of obesity-induced inflammation. Nimacimab reduces the level of key serum inflammatory mediators and macrophage infiltration in liver and adipose tissue, pointing to a disease-modifying role of nimacimab related to comorbidities of obesity. These effects seen in our DIO models are robust, reproducible, and mechanistically distinct from, though complementary to, incretin-based agents. That gives us potential optionality across monotherapy, combination, and maintenance strategies. Okay, let's dive into that last point and touch on the new preclinical data that was shared today. To test how nimacimab could perform in real-world settings, we recently conducted a preclinical DIO study asking three key questions. One, can nimacimab enhance the efficacy of a suboptimal dose of tirzepatide? This is highlighted by the yellow part of this study schematic. Two, does nimacimab offer a more durable weight loss profile post-treatment? This is highlighted by comparing the yellow to the blue part of the study schematic. Three, can nimacimab act as a maintenance or rescue therapy after incretin discontinuation? This is comparing the yellow to the pink color as a clear control. Here's what we found. First, the combination efficacy. The preclinical DIO study findings demonstrated that at day 25, the combination of nimacimab and a suboptimal tirzepatide dose of 3 nmol/kg daily yielded 44% vehicle-adjusted weight loss. The combination outperformed either agent alone, with nimacimab demonstrating 21.5% vehicle-adjusted weight loss and tirzepatide demonstrating 29.7% vehicle-adjusted weight loss. The combination efficacy also exceeded an optimal dose of tirzepatide of 10 nmol/kg daily, which resulted in 38.9% vehicle-adjusted weight loss. This highlights a meaningful opportunity to develop combination strategies that achieve greater efficacy at lower doses, potentially improving tolerability, reducing cost, and expanding treatment accessibility. Now, point number two. nimacimab demonstrated durable post-treatment weight loss compared to incretin therapy after the therapy stopped. In comparison of nimacimab and tirzepatide following cessation of treatment in the preclinical DIO mouse model, nimacimab demonstrated superior durability of weight loss. Specifically, the low-dose tirzepatide group regained most of their original weight back eight days after coming off therapy, regaining 29.7% of weight by day 24 post-treatment. In comparison, the nimacimab-treated group maintained their post-treatment weight for approximately 20 days, regaining only 7.4% by day 24. This rebound effect has been well documented in animal models and clinical data and represents a major issue for patients who come off incretin-based therapies. Nimacimab's durability after cessation of therapy represents a potentially clinically beneficial and distinct outcome relative to incretin-based therapies. Let's move to the third point and now add back nimacimab. Here, we're looking at maintenance of weight loss using nimacimab alone post-incretin treatment. When nimacimab alone was used after an initial tirzepatide or combination treatment in the preclinical DIO mouse model, it greatly reduced rebound weight gain in these bottom three groups of mice: the suboptimal TRZ and NEMA combo in purple, the optimal TRZ dose in red, and the one we're going to zoom into is the suboptimal TRZ following nimacimab, which is in pink. The key takeaway, no matter which of these line graphs you're looking at, is that the data show nimacimab reinforcing its potential role as a post-incretin weight loss maintenance therapy. Specifically, when nimacimab was added following treatment with low-dose tirzepatide, the pink line, nimacimab reduced rebound weight gain from 29.7% to 12.8%. Taken together, these data suggest nimacimab has utility across a broad continuum of care, not just initiating weight loss, but also sustaining it. This continues to strengthen our thesis and bring us to the real-world setting and answering where nimacimab fits and understanding the real-world therapeutic gap. Again, we're not trying to displace GLP-1s. We believe they are foundational and they're a backbone, but they also have well-recognized limitations. 58% of patients discontinue before 12 weeks, 80% by year two, up to 40% of weight loss can come from lean mass, and GI side effects remain a major driver of treatment discontinuation and patient dissatisfaction. This ultimately creates a significant therapeutic gap and one that nimacimab is designed to address. There's three market opportunities: one, as a monotherapy for patients who can't tolerate or don't respond to incretin therapeutics; two, as a combination partner to amplify efficacy or reduce incretin dose burden; and three, as a maintenance therapy to sustain weight loss after a desired weight is achieved with better tolerability. As developers are racing to optimize potency, dosing, and formulation, the field is now bumping up against a real-world ceiling: tolerability. Despite their clinical efficacy, incretin-based drugs are facing significant discontinuation rates, up to 50% within the first year, and nausea is the most frequently cited reason. As illustrated here, many of the late-stage programs cluster in the high nausea, high dropout zone, trading gastrointestinal burden for marginal weight loss gains. This has created a therapeutic paradox. There are actually stronger agents, but they have a weaker persistence. We believe that this is not just a side effect problem. We believe it's a structural vulnerability in the current obesity treatment paradigm, and it's leaving a growing population of patients without sustainable options. That's where nimacimab comes in. Rather than replicate what's already been done, nimacimab is designed to potentially expand the therapeutic options in obesity treatment, not only as a well-tolerated and effective monotherapy, but as a differentiated and essential combination where the current incretin-saturated market does not provide such options. Its mechanism offers alignment to GLP-1s, unlocking the combination potential without compounding the GI burden. This positions nimacimab to potentially meet the needs of patients who discontinue using the drug due to side effects, who fail to sustain weight loss, or who require multi-pathway intervention for broader metabolic impact. For us at Skye, the opportunity is clear. nimacimab is not just an alternative. We believe it's a next-generation backbone candidate for durable, combinable, and more accessible obesity care, and it's a platform that can potentially extend beyond monotherapy to lifecycle expansion across lines of therapy and patient segments that are currently underserved by today's options. This is a key area to zoom in on, and we've been working on how best to frame it within the broader obesity treatment landscape. We believe we're entering the fourth wave of obesity pharmacotherapy, a new phase that's driven by scientific innovation still, but needs to address real-world complexity in patient care. The FDA has now approved six drugs for long-term obesity treatment, each marking a step forward in the standard of care, from short-term stimulants to safer agents like orlistat, to the rise of GLP-1 base therapy such as semaglutide and tirzepatide, which have brought us closer to disease resolution. A new chapter is unfolding. Today's obesity market is evolving beyond the singular goal of caloric restriction. The next generation of anti-obesity medications, such as the peripheral approach, is being shaped by the need for broader metabolic impact, targeting pathways related to insulin sensitivity, lipid metabolism, inflammation, and central reward signaling. This reflects a shift from weight loss alone to true disease modification, sustainable weight loss, and even addressing the other related comorbidities. With the top-line data ahead, we're preparing to potentially demonstrate how nimacimab delivers on the core needs of the evolving obesity treatment paradigm that, in our opinion, fit the definition of the fourth wave by improving quality and durability of weight loss through alternative metabolic pathways, better tolerability, and strategic combinability. Thank you again for listening to our update. I'll wrap by emphasizing that the next 90 days will be busy, and Kait's going to walk you through a few of our upcoming milestones in her remarks. Overall, for us, finishing Q2 and heading into Q3 isn't just a checkpoint. It's a culmination of disciplined execution, scientific clarity, and focused investment in a differentiated mechanism. We appreciate your continued support, and now I'll turn the call to Kait our CFO. Thanks, Punit. After the market closed today, we issued a press release and filed Skye's Form 10-Q with the Securities and Exchange Commission, outlining our quarterly financial results. We encourage you to reference our filings for the details of our financials and the risk factors described therein. I will now provide a brief overview of key financial results for the second quarter ended June 30th, 2025. We ended the second quarter with cash and cash equivalents and short-term investments totaling $48.6 million. Our cash flow guidance remains intact, with the expectation that our current capital is projected to fund operations and key clinical milestones through at least Q1 2027. This includes the completion of Phase IIa study for nimacimab and Phase IIb manufacturing and preparatory clinical activities, including the initial manufacturing runs needed to start Phase IIb dose-ranging study and clinical feasibility activities. In addition, our runway also includes a modest discovery research and development budget and the formulation and development work expected to support later-stage studies for nimacimab. Research and development expenses for the three months ended June 30th, 2025, were $14.3 million as compared to $4.1 million for the same period in 2024. The increase was primarily due to contract manufacturing, clinical trial costs associated with our clinical study for nimacimab, discovery research and development expenses, and salaries and stock-based compensation expense. General and administrative expenses for the three months ended June 30th, 2025, were $3.9 million as compared to $4.3 million for the same period in 2024. The decrease was primarily related to decreases in general business expenses and legal and professional fees, offset by increases in salaries and stock-based compensation expenses, consulting and advisory fees, along with investor relation costs. Our net loss for the three months ended June 30th, 2025, totaled $17.6 million, including non-cash share-based compensation expense of $4.2 million. This compared to $7.9 million for the same period in 2024, with non-cash share-based compensation expense of $4.3 million. In Q2, we maintained our track record of execution, hitting clinical milestones while managing capital with precision. We continued to build internal cadence and operational rigor, including the strategic expansion of our team to 20 employees. We made key hires in Regulatory Affairs, Quality, Clinical Operations, and CMC. Notably, we welcomed a Vice President of CMC to directly support our advancing development activities. This deliberate scaling is intended to allow us to minimize downtime between clinical trials and stay positioned to move quickly following upcoming data readouts. As we enter the second half of 2025, we remain focused on disciplined execution and are well-positioned to advance nimacimab through its next development phase. We are entering what is arguably the most crucial execution period in Skye 's history. To outline what you can expect in the coming months, on September 4th, we will host a KOL event at NASDAQ, which will be webcast live, focused on the mechanism, Phase IIa clinical data expectations, and market positioning. In addition, in the fall, we are participating in multiple investor conferences where we look forward to engaging directly with many of you. Finally, ahead of our top-line data, we are presenting the Phase I SADMAD MAFLD data at EASD on September 19th, reinforcing hepatic and metabolic benefits. In late Q3, early Q4, we expect our top-line clinical readout from CBIOND. As we have previously stated, this will be data from both the monotherapy and combo arms, with placebo-adjusted weight loss, safety, body composition, and mechanistic biomarkers. With the top-line data in hand, in Q4, we expect to finalize Phase IIb protocol, further advance CMC, initiate regulatory engagement, and external planning for next-phase studies. This concludes our prepared comments for today. Thank you very much for joining us, and we'll now open the call for questions from our covering sell-side analysts. Operator, over to you. Thank you. The floor is now open for questions. If you have dialed in and would like to ask a question, please press star one on your telephone keypad to raise your hand and join the queue. If you would like to withdraw your question, simply press star one again. If you're called upon to ask a question and are listening via a loudspeaker on your device, please pick up your handset and ensure that your phone is not on mute when asking your question. Your first question comes from the line of Ted Tenthoff of Piper Sandler. Your line is open. Great, thank you very much, and thanks for the update. Getting excited for data. I had just a little bit of a housekeeping question, but with a specific angle on it. R&D was higher. I saw that you've made some progress on the manufacturing lines. Did that account for a big part of it? In the press release, you mentioned this Arecor and a potentially higher concentration nimacimab formulation. Can you tell us a little bit about what the goal is from that and when you may be able to use that higher concentration on nimacimab? Thanks. Hey, Ted, thanks for joining the call. I'll take the first. This is Punit here. I'll take the first, or I'll let Kait take the financial questions relating to R&D. I can jump in and just explain the Arecor relationship. At the moment, we have a concentration of 200 mg per 2 mL, or 100 mg per mL is our current concentration, and that's what we're using in the clinic. Our goal here from a target product profile is to increase that concentration to allow for a longer dosing period or less frequent dosing. Ideally, it would mean even considering 200 mg per ml. We're basically looking to increase our concentration to go higher than 100 mg per mL, and Arecor is supporting that effort. Just so we are clear about that, that's a separate kind of R&D track. It doesn't interfere with our clinical development strategy. As you know, our clinical development strategy and CMC efforts continue on track to support the advancement of nimacimab. As we consider additional lifecycle management, that's where we are looking for ways that we can improve concentration. Kait, do you want to answer the financial piece? Hi, Kait. The question really is, does with the step up in R&D, the $14 million in the second quarter, was that largely due to this manufacturing line or more clinical trial line? Yeah, sure. There was approximately $9.1 million that we spent during the six months ended on contract manufacturing costs, and that related primarily to Phase IIa resupply for the extension study and the supply for Phase IIb trial as well. Great, thanks. Excited for more data in the opportunity this fall. Thanks, Ted. Your next question comes from a line of Jay Olson of Oppenheimer. Your line is open. Oh, hey guys, this is Matt on for Jay. Thanks so much for taking our questions and congrats on all the progress. As we near CBIOND data, just curious, I guess, what you're thinking for nimacimab's weight loss efficacy potential at week 26. Should we expect to see something around 8% or if it's slightly below that, would the range of around 5% to 8% be potentially compelling? Additionally, beyond weight loss and obviously safety, what other key metrics will you be paying attention to and what biomarkers do you believe could be informative as well? Really appreciate it. Hey Matt, thanks for joining and taking the call on behalf of Jay. Yeah, we are looking at Phase II, the CBIOND trial, Phase IIa, really as a proof-of-mechanism study. It was originally designed to detect an 8% placebo-adjusted difference in weight loss with 80% power over 26 weeks. Our goal here is to demonstrate a really clear, clinically meaningful weight loss separation from placebo. As you alluded to, we believe that if we're seeing 5%- 8% range placebo-adjusted, that's really a strong signal of biological activity of nimacimab. Importantly, the study was not powered to detect a smaller difference with any statistical significance. That's an intentional component because otherwise we would have required a way larger study. The objective here is to validate the mechanism, establish a really strong safety and tolerability profile, and proceed to a definitive dose-ranging study to identify the optimal dose and then the ultimate regimen for nimacimab in a Phase III setting. Our goal here is to deliver, obviously, consistent weight loss, improve GI tolerability profile. I think we alluded to that today in terms of where there's a lot of white space in the market, and that's where we feel we have really the upper hand and obviously a clear safety signal without any neuropsychiatric side effects. All of those three parameters we would consider CBIOND a success, and it really puts a strong foundation to move forward Phase IIb for us. Okay, got it. That makes sense, Punit. Really appreciate it. Just a quick follow-up, if you have any expectations on the potential discontinuation rate within 26 weeks and also how, you know, based on your expectations, we believe that could translate into an advantage versus GLP-1s in the real-world setting. Also, just to clarify, as you previously said, you expect about 50% of patients from the original study to be eligible for the extension study. If you could just walk us through your thinking there, that'd be great. Thank you so much again. Yeah, Dr. Arora, you can take the 50% approximate on the extension study. Let me walk you through the other pieces of your question. In terms of discontinuation, we're expecting the similar kind of trends that we're seeing in most obesity studies. Now, keep in mind, in the last two years, I think overall in almost all obesity studies, we've seen probably about 25%- 30% discontinuation. I don't think that's a factor of always the drugs. It's also a factor of a very competitive landscape and the accessibility of just commercial drugs and access to new modalities. A lot of patients are looking for that access. We haven't seen any unusual trend in terms of discontinuation in our study and definitely not seeing anything related to safety. In terms of the real-world situation, as I alluded to in the presentation, there's a really large opportunity here where we're seeing 50% of patients not continuing incretin therapy after a year, right? That's where this maintenance data really showcases. Here we can essentially capture those patients and continue on with drug and allowing patients to have that long-term sustainable weight loss. I think there's a really clear market opportunity there where nimacimab's not really competing for that initial weight loss that incretins do, but it's designed to really lock in those losses that once the incretin therapies do their work, then we can see that there's an application there in a really large market. Obviously, there's still an opportunity there in the monotherapy setting too, because there's patients that don't respond. I hope I answered those two questions. I'll turn it over to Dr. Arora to just talk about the extension study and those expectations. Thank you. The extension study enrollment has started. I'll just start with the good news. We've been enrolling for the last month or so patients in the combination arms, and we're also now enrolling patients in monotherapy. Just between the logistics of starting the extension and allowing patients to roll in, as you know, we didn't initially plan for an extension, but we've been able to execute on it. Between that and the natural early terminations that you get in an obesity study, we still believe that approximately 50% of our original patient target will be eligible to roll over into extension. It's just started, so I can't give you any precise numbers, but just based on the enthusiasm of the sites and from what we hear, we're very optimistic that a majority of these patients are going to roll over because we see a lot of interest in it. Okay, got it. That all makes sense. Really appreciate the questions again. Thank you so much. Thanks, Matt. Your next question comes from a line of Jon Wolleben of Citizens. Your line is open. Hey, thanks for the update and taking the questions. Punit, you kind of laid out a nice optionality between, you know, maintenance, monotherapy, combo. How do you think about what we'll see in CBIOND and how that might guide development and the different utility in those three different modalities for nimacimab? Yeah, so that's a great question. Thanks, Jon. Look, I think there's a significant opportunity for a broader maintenance franchise really taking place, and that's probably really underappreciated in the market because let's face it, we're dealing with a very rapidly moving market. You know, just this week we've seen some highlights from other obesity developers and drug developers, and everyone's kind of adjusting to where does everything shake out. I think that there's a clear opportunity for nimacimab in all three settings. In the monotherapy, we've quoted about 10%- 15% of patients based on our primary research that don't respond to GLP-1 therapy, so there's a pretty large capture rate of those patients. In the maintenance setting, we've pointed to some really important stats there, about 50% discontinuing after one year, 80% discontinuing after two years. There's really a clear need for a drug that can kind of capture that patient population with minimal GI side effects, and we're not expecting to add on to any of the tolerability concerns that we're seeing with incretins. The third opportunity, in terms of combination, I think that's really going to come down to evidence-based data. So far, this data that we pointed to today really is another important development because now we've shown with a suboptimal dose of tirzepatide in combination with nimacimab that we actually get a deeper weight loss. Apply that to the real world, then we expect that a patient may be able to take a more tolerable dose of an incretin therapy, and we can make up that delta in terms of weight loss with another modality. It really points to a separation of the different biology here and pathway that CB1 is acting on versus GLP-1. Tu has been doing a lot of the market access research, so I want to give him a few minutes here to just maybe elaborate on anything I've said. Yeah, no, I think, thanks Punit. I think you've hit all the highlights. I think what's important is when we speak to KOLs, they make it pretty clear that they are very excited at the prospects of new modalities that are beyond just incretins. I think they want the option to be able to provide their patients with additional mechanisms of action that may be more tolerable, may provide different benefits, and may provide different options for patients that may not need to lose significant amounts of weight, but may need to manage other areas of their health. These are important things that I think the market needs to understand and is beginning to understand that weight loss as a bottom line number is no longer going to be the most important endpoint as these new drugs, new therapies, and particularly these non-incretin drugs, new data is coming to the fore, and that these other complementary mechanisms and other endpoints are going to be important. Yeah, and just to add to that, you know, looking at the orforglipron data today, there's still a clear opportunity here that orals are not necessarily going to save the day in a maintenance setting. They don't necessarily add any more substantial weight loss, but here we've now pointed to a completely different biology, a peripheral mechanism may be enhancing that weight loss. I think from a competitive positioning snapshot perspective, there's clearly room from an efficacy standpoint. We'll see what that data looks like in the clinical setting now. There's a maintenance franchise, which we're starting to, I think, understand better, and there's a really clear safety mode, right, with the peripheral exclusion on the neuropsychiatric side, as well as the tolerability profile to date. Those three things I think really stand out from a competitive positioning perspective. That's really helpful, guys. I appreciate it and looking forward to the event in September. Thanks, John. Your next question comes from a line of Kristen Kluska of Cantor Fitzgerald. Your line is open. Hi, this is Ayan on Kristen's line. Congrats on the progress here and thanks for taking our questions. First, regarding the independent board that oversees the trial for safety, could you just remind us what the protocol is here? What types of adverse events would they report? I know you touched on this already, but I just wanted to get some clarification around the enrollment eligibility in the extension study and how about 50% of the patients from the original study made the cut. Sure, thanks for joining today. I'm going to let Dr. Arora, Chief Medical Officer, take both of those questions. Yes, thank you, Ayan. As far as the DMC is concerned, on a routine basis, they meet quarterly, and we actually provide them all of the data, safety data of the study. We give them the complete listing of all adverse events, all serious adverse events, and any AESIs that are reported. They also have complete information on all of those patients, any narratives, all the labs. They have a complete store of unblinded information with which they work when they review the data for the study. They are in a position to come back and ask us for clarifications, to ask us if they want us to monitor anything or they want to know about an individual patient. At this point, frankly, we've had four reviews completed. The last one was on July 18, barring some minor clarifications and some questions where they wanted to know about an individual patient and were curious about certain things. There really hasn't been anything too significant, and after each meeting, they've indicated that they are comfortable with the study continuing exactly as it is. Thank you for that. The second question is just the clarification around the enrollment eligibility in the extension study. Yeah, so the enrollment eligibility, and we were talking about this earlier, so patients who complete their dosing for 26 weeks are eligible for enrollment into the extension study. Anyone who does not complete 26 weeks of dosing is not. Primarily what's happened here is that because we designed the extension study somewhat belatedly after the original study was started, it's taken us a while to get it going, to get all the approvals, to get all the sites set up. We did lose a certain number of patients who would be otherwise eligible to roll over into the study. When we say 50%, it doesn't mean that 50% would not, the remaining 50% would not necessarily have been eligible. A lot of those patients are not eligible simply because they had already completed the study before the time for rollover came. There is a certain amount of dropouts as well, as we've been seeing them with all obesity studies. As seem to be in line with what you see, when you combine those two things, what we are looking at now is that we think it'll be about 50%, about 50% are eligible. Got it. Thank you for that. Your last question comes from a line of Albert Lowe of Craig-Hallum. Your line is open. Hi, thanks for taking my question. Just a quick one from me. I know the original study design had the 13 fo llow-up period to track for durability of weight loss. I was wondering if the follow-up period after the extension study still has this follow-up period to look for durability and rebound weight gain. In either case, when might we see this data from either portion of CBIOND? Hey Albert, thanks for joining the call today. Yeah, that's a great question. We're going to continue to have that 13-week follow-up, but that probably won't be available until the first- half of 2026 in terms of that part of the data readout. Now with the extension, we will finish the 52 weeks, and then all those patients will be tracked for a follow-up 13 weeks, and then that data would be available. That's more of a 2026 event now. All right, got it. Thank you. There are no further questions at this time. This concludes today's conference call. We thank you for your participation. You may now disconnect.