Great, I think we can start. My name is Yanan Zhu. Thanks, everyone, for being here. I'm one of the analysts at Wells Fargo. We're lucky to have the management team of Regulus with us for this fireside chat session. With us are our CEO, Jay Hagan, and also Chief Medical Officer, Rekha Garg. Thank you for being here.. Thanks for having us. Thanks for having us. Great. So, Jay, could you give us an overview of the company's programs and initiatives? Sure, yeah. So Regulus Therapeutics is a company developing antisense oligonucleotides directed against microRNA, and microRNA are short, non-coding RNA implicated in disease due to aberrant expression levels, and our lead program is targeting a microRNA called miR-17. miR is a short, shortened version of microRNA, for the treatment of autosomal dominant polycystic kidney disease, and we're in the midst of a phase 1b study. We've read out three blind and placebo-controlled weight-based cohorts to date, and we have a fourth cohort that's enrolling, nearing completion, that is looking at a fixed dose of the drug, in anticipation of utilizing a fixed dose in our phase 2 study, so that's where we're at. Got it. I think it, you know, it might be helpful to bring people up to speed on the ADPKD indication. It's actually a very big indication. Can you talk more about that? That's the opportunity, obviously, you're going after. Sure. Yeah, I'll just give you a little sense of the disease landscape and then ask my colleague, Rekha, to talk a little bit about the standard of care. ADPKD is the shortened version of autosomal dominant polycystic kidney disease. So by definition, it's an inherited disease caused by a germline mutation in either the PKD1 or PKD2 genes. The predominant form of it is a truncation mutation of the PKD1 gene. That's about 80% or so of the diagnosed population. There's about 160,000 with a diagnosis in the United States, of which roughly two-thirds are in the category of a moderate to severe disease. That is typically characterized by a Mayo classification, which is a way to look at total kidney volume and adjust it for your age and your height. Because obviously, if you're taller, your kidney is going to be larger by definition, a Mayo classification of C, D, or E. So about 100,000 or so addressable, prevalent population in the United States alone. It's thought to be more prevalent, due in part due to lack of normal genetic testing that would test for this, and the lack of available treatment options up until the middle of two thousand and eighteen, when the first drug was approved in the category, a drug called tolvaptan. Maybe, Rekha, you want to talk about the treatment landscape? Yeah, sure. So currently, most of these patients are actually asymptomatic until their kidneys get bigger, and at that time, for men, you predominantly get it from a flank pain, and that's what they're complaining of and being seen from that perspective. For women, they can be diagnosed during childbearing years because they get an ultrasound and they might see a large, enlarged kidney, so currently, because it's asymptomatic and then some of the patients do have, may have hypertension, so they get treated for those types of symptoms, but as you know, the only drug that's really approved for ADPKD is tolvaptan. And it's a vasopressor, and one of the major side effects of it is patients have a lot of polyuria, so and they have to drink a lot. So although it's a proven therapy in terms of impacting, you know, your TKV and your GFR, it's really the tolerability issue is a challenge with that product. In addition to that, it also has a restricted REMS. So the patients have to get, because of liver toxicity with the product, the patients on a monthly basis have to get liver enzymes done before they can get their next prescription filled. So from that perspective, although the product is effective, the tolerability issue is probably the biggest challenge for patients. And many physicians usually, as they try to manage the patients on that, they might cut the dose. It's a BID dose, so they may not take the evening dose because they don't want to be up all night. And then also just being thirsty constantly. So it a lthough it's a product out there, I think there's still room, an unmet need for something like our product. Yeah, it's estimated to be used in less than 10% of the population. We recently completed a market research study, as part of that, looked at claims data, and it was less than 10% utilization of that. Two-thirds were at half the dose. So, significant unmet need, really nothing else out there in mid to late-stage development. Wow! Despite that, it sells for what? $1.3 billion last year- Yeah. On its fifth year on the market. Yeah. I didn't realize two-thirds were half the dose. Yeah. So the actual sales should be higher if people are taking the full dose. Correct. Yes. Yeah. Yes. A great opportunity, obviously. You know, how on target is miR-17 for treating this disease? Can you talk about the mechanism of action? Yeah. So we've been collaborating with a group at UT Southwestern for the last 10 years or so now, who first described miR-17 being upregulated in both animal models of the disease. And then, because you typically can't get tissue from patients because of bleeding risk, you really can only get it at time of explant. So this happened to be a large nephrology center, and they also biopsied tissue taken at time of explant and saw that miR-17 is upregulated. And why that matters is that miR-17 directly controls, it binds to and recognizes the three prime untranslated region of both the PKD1 and PKD2 genes. And consequently, you have less polycystin that's being made because you have too much microRNA. And so our approach is simply to administer an antisense oligo that recognizes and binds to miR-17, thereby de-repressing or sort of taking the brake off of the, you know, PKD1 and PKD2 genes. And we've shown that this approach not only has significant impact on cystogenesis in mouse models and increases polycystin levels. We've now shown across the last two cohorts that we can see statistically significant increases in polycystin one and two at the three milligram per kilogram level versus placebo, which corresponds also with an impact on kidney volume, slowing the rate of the growth of the kidney. Right. Yeah, just a quick question to follow up on the mechanism. These patients do have a mutant allele and a normal allele, right? Because it's a, autosomal dominant- Yep disease, right? When you upregulate, is it a normal allele that is functioning, or- That's- Even a mutant allele could be functional? Well, what we measure is the full-length protein in our assay. So but theoretically, you could increase, you know, unstable mutant protein level, or, you know, polycystin one or polycystin two. But that's not what we measure in the clinic. We're measuring full-length protein. Very nice. Can you maybe talk about the data for your compound RGLS8429? The data from phase 1b MAD study that you generated so far, and maybe talk about what people might be missing from the data. Sure. Yeah. So, I would say that what we've shown to date, we developed this biomarker assay as a measure of target engagement. So specifically, we've been collaborating with a group at Kansas who had earlier published on an ability to detect polycystin levels in urinary exosomes. And so what we've done is further refine that assay and qualify it for use in the clinical setting, and have been able to show a dose response now as we step through the different dose levels of this trial, one, two, and three milligrams per kilogram are the three doses that were tested. And the dose selection was driven by first, we wanted to not have a subtherapeutic dose, and we did see a change in polycystin with our first-gen molecule at one milligram per kilogram with our first-gen molecule, and then that signal dropped off at a lower dose. And so we wanted to start with the signal and confirm you know what we'd seen with the first-gen. And then we also know, based on our extensive preclinical work, that at 30 milligrams per kilogram in a mouse, we sort of reach optimal miR-17 target engagement. And 30 milligrams per kilogram from a kidney exposure standpoint, when you scale that to a human, is about two and a half milligrams per kilogram. So the choices of the dose were driven by wanting to basically, you know, get the full shape of the dose response curve. And indeed, we saw higher levels of polycystin changes at three milligrams compared to two, and that reached statistical significance when compared to placebo. And so that assay was developed because we, you know, we never thought we'd see anything in volume in such a short study. Kidneys in patients with the disease grow on average around 6% per year. The MRI at the end of study is done one month after completion of dosing, so three months of dosing plus one month of follow-up, so four months total period of time. So you'd expect just doing linear growth model, you'd expect about 2% growth in an untreated patient. Indeed, that's what we basically saw at in the placebo arm and at the one milligram per kilogram dose level, which, you know, we thought would be subtherapeutic because of the amount of miR-17 target engagement, you know, we'd anticipate there. Then at the two and the three milligram per kilogram dose level, we were surprised to see and it was just given again the short treatment duration, that we'd have an impact on volume. It looks like we're seeing stabilization of the rate of growth of the kidney, if not some reduction. So we're excited because nobody has looked at serial MRI over just four months. You know, I think the shortest study done to date has been twelve months, is it? I think- Six. Well, there was one study that did six months. Okay. But- Yeah all of them are 12 months or longer. Yeah. Yeah. But one of our investors in the company had said as we were preparing for the study, because you do a baseline MRI anyway to qualify the patients for the study, to get a height-adjusted kidney volume. And well, might as well do a follow-up one, because if you don't look, you're never going to see anything. And lo and behold, we've now seen this repeated and you know, a stronger signal in the impact on kidney volume at three milligrams per kilogram. To your question about what people might be missing, you know, I don't want to guess why the stock markets react the way they are. Lots of different reasons. When I've spoken with all our existing investors around the financing we did in March, it was oversubscribed, a $100 million raise, at a premium. They are all generally pleased that we were able to repeat what we effectively saw at cohort two and a strengthening of the signal, and look forward to the ongoing progress of the program. Great. So you have cohort four ongoing. Mm-hmm. But cohort four is a little different. It's not an escalated dose, right? Can you describe cohort four and what are you trying to achieve? Yeah. Yanan, we went to the FDA in December to confirm what has been stated publicly and what's in the guidance for industry in terms of surrogate markers suitable for accelerated approval. And total kidney volume is listed in there. There is a precedent of Sanofi, who had a program, was following a similar paradigm. And so we've confirmed that with them. And so therefore, if our next study is potentially registrational with accelerated approval pathway, we need to introduce the commercial presentation now, so it'd be part of your NDA filing. And we don't envision a commercial product that's, you know, a vialed physician-administered as being as attractive as a prefilled syringe. We are in the midst of this fourth cohort, which is a fixed dose, where we're again looking at safety and tolerability and want to see a continued trend in terms of impact on polycystin and how to adjust the total kidney volume. To date, we have safety margins that support dosing at this level. So it's really finding that sweet spot where we know everyone's gonna be at roughly 3 mg. If you're under 100 kg, you know, 220 lbs, you're gonna be getting 3 mg per kg or more of drug. And that conveniently fits in a 2-mL prefilled syringe. We formulated 150 mg per mL. So the purpose of this is to get some experience with the fixed dose, show that it's got That it's safe and well-tolerated, can reconfirm the signals we've seen to date, and then be in a position to introduce that into our phase II program, which could start mid-next year, where patients then could, after they learn how to utilize the device, will be able to, dose at home, which makes, you know, fewer clinic visits, makes your phase II, more streamlined and sets you up for, you know, including that in your NDA. Got it. So, this cohort is open-label? Yes. Is there a reason to design this cohort this way? You could speak to it, as well as I, but you know, we've got enough blinded safety data thus far, and it's much more attractive to enroll an open-label study where everyone knows their own active. That's a big part. Yeah, I think that's pretty much it. It's pretty much it. And it also is an opportunity to, you know, have the 300 mg fixed dose available as an open label, where patients are able to get the drug. And that's-- there's a lot of demand in terms of interest from that patient population, 'cause the advocacy group is very engaged and for this disease state. So, this provides an opportunity for them, and it just validates-- we can just validate what we've seen with the three mgs per kg cohort anyways, because it's a slightly higher dose that seems... So it is slightly going up, but not to the same level. Yeah. Yeah. Okay. So, in other words, in terms of dosing, at the individual patient level, do you expect in people with lighter body weight, could you have a higher effective dose or not so much? It remains to be seen. Some subjects will be at 4 mg or higher, 4 mg per kg, you know, equivalent. If you're 75 kg or less, you'll have a higher dose in this study, and it remains to be seen if we see, you know, incremental benefit in the form of the biomarker changes and the kidney volume changes. But I would say that, you know, our base profile here in terms of, you know, what kind of commercial profile resonates with physicians and payers is to have similar efficacy to tolvaptan, but be safe and well-tolerated and, you know, without a black box warning for the potential for drug-induced liver injury. That's what's available right now. And the feedback from, in terms of, you know, intent to prescribe is very high- Got it with just that baseline profile. So, in other words, we don't need a lot more impact on volume from where we sit today to have an attractive product for patients. Right. So how is the enrollment going, and what's the data timeline, and how many patients is- Yeah. So we have said that. So when we did the financing, we upsized this fourth cohort because we had the time and the interest from patients. So we said we upsized it up to 30. It's an imperfect science, so we won't probably land right at 30 because once they're in screening, you know, ethically, you want to include them in the study. So we'll shut down screening when we know we're gonna get close to our target here of enrollment. It's going very well. You know, we've guided that we'll have data from a significant number of subjects from this fourth cohort early next year, and we're trying to put that together with an overall program update around the you know when we've received the meeting minutes from the FDA meeting as well, the end of phase I meeting. That's targeted towards the end of this year. That would put it early next year for meeting minutes if they stick to their thirty-day clock. Got it. Got it. Can you describe what would be considered a positive outcome from Cohort IV? You know, I think, you know, again, safe and well-tolerated. We did see a few injection site reactions in Cohort II. Now, they weren't dose limiting, and they're characterized by, like, five to ten minutes of pain and tingling at the injection site. But seeing that you don't have any worsening of a tolerability profile would be great. And then again, seeing consistent effects on polycystin and kidney volume, I wouldn't expect much more than what we've seen at three, just based on our understanding of, as I mentioned earlier, dose level, kidney exposure, miR-17 engagement. We think we're kind of at the flat part of the curve in polycystin, and so I. You know, maybe you're going to see more consistent response. The error bars shrink even further. That's what we saw at three mgs, that the error bars shrunk. That's why we hit statistical significance. And the magnitude, I think, would be fairly similar and perhaps a little bit more, again, more consistent response. Got it. Great. So it sounds like you will have this meeting with the FDA end of phase one, that's after the Cohort Four data. Is that right? We, you know, the meeting planning is all in motion, and we've guided around year-end. Those meetings, you know, you request a meeting 70 days before the meeting takes place. So, you know, that whole process of preparing a briefing book is well underway. You know, draft protocols being fine-tuned and collection of all the data that you're gonna include in that submission. So all the blinded data to date thus far in patients, the tox data that we have thus far, and we've completed the mouse study last year. We've got other smaller studies that are ongoing in the non-human primate. We finished dosing in that. We should have a draft report in time for that meeting. It won't be the final report. We'll submit that to the IND after we get the final report, but it's not rate limiting to having the meeting and having the discussion around the suitability of the protocol and the evidence to date. Got it. Got it. Will you announce the outcome of this, the meeting with FDA? Would that also be around the time you have Cohort Four data? Yeah, that's... So Cohort Four is continuing on. What we'll do is we'll take a cut of the data that we have available for a general program update when we have the meeting minutes and can characterize the outcome of the meeting. You usually wait till the thirty days after your meeting, get the meeting minutes, you know, before you disclose the outcome of it. Got it. Right. I think earlier on you did mention something about FDA's comfort around using total kidney volume as a biomarker, right? So can you talk about the correlation for that biomarker with renal outcome? Yeah. So, Otsuka has, you know, has led the charge in developing much of the evidence that total kidney volume is correlated with GFR and, and 'cause they showed in their studies that they can slow the growth of the kidney by about 50%. So instead of growing at 6% per year, on average, they grew around 3%. A little bit small. It was, like, five and a half- Yeah three or something, but for easy math, they cut the growth rate in half, and that ultimately led to a reduction in the rate of decline in GFR of approximately 30%. But you need a longer period of time. You need more data points to hit statistical significance on that separation between placebo. But ultimately, they were able to show that they're linked. And so we had, and I think we've talked about this, with you in the past, we had a Type D meeting with the FDA in December of last year to review, you know, just to, discuss the suitability of total kidney volume, make sure they hadn't changed their mind of what they've said publicly at a variety of different forums, as well as it's in the Guidance for Industry and, there was no difference there. But included in that was our own analysis around showing the correlation between GFR and kidney volume over time and how that predicts benefit. So in the eyes of FDA, you know, in this discussion, that a statistically significant impact on reducing the rate of growth of the kidney is reasonably likely to predict clinical benefit in the form of GFR. And very, very analogous to the FSGS and IgAN space, where, you know, you have a proteinuria endpoint and the GFR in the postmarketing setting. Got it. Got it. Can you talk about the pivotal path, given that accelerated approval based on total kidney volume and then, you know, longer-term confirmatory trial? Like, what's the patient number? Yeah, we're still fine-tuning the exact protocol and doing various sensitivity analysis. But, you know, it's somewhat similar to what Sanofi had presented for and disclosed for venglustat. If you assume again that you have that target product profile that I described, that you can reduce the rate of growth by 50%. So instead of growing at 6% over a year, you grow at 3% per year. And assume you enroll a similar patient population, then you'd be able to detect that with around 300 subjects at one year. You'd be able to see that effect with 90% power. And so that's kind of our base assumption, that sort of profile. And then, depending on the number of data points you have, GFR is something that bounces around. Historically, sponsors, some have, you know, measured at three and four months, GFR. So over the course of a year, that would be only three to four data points. If you measure every other month, for example, you're gonna have six data points, seven data points in a year. And the more the number of data points when you're trying to determine a slope, the smaller the sample size required. But there's a balancing act. You don't want them to come in every day, right? So, but GFR does bounce around, which, you know, is out there in the public domain. So we're fine-tuning, you know, the visit schedule because the patients can administer at home. We're looking at something like probably every other month visits, 300 subjects for a year. With that sample size, you need roughly that same number. What you do is enroll 300. When they reach one year of treatment, unblind the TKV endpoint, and if you hit it, file for accelerated approval. Those same 300 continue in the study in a blinded fashion for GFR at two years. Then you get, you know, then you look at that data set and file that for full approval and update the label. Got it. Got it. So, with that, powering assumption is based on 50% reduction in total kidney volume- Yeah at one year, right? Yeah. Remind me. 30% at two, and 30% GFR at two years. 30% at year. Remind us of your Cohort III effect size over four months? We, I mean, the mean was a reduction in kidney volume, but it was with 11 active? Yeah, eleven. You know, we theoretically could say we were having a much more dramatic impact, and you could detect that mathematically if you were just to say, "Okay, what if we stop the growth of the kidney?" You could see that in as little as 150 subjects at six months. We may be overpowered, but that's not prudent to plan your study that way. You wanna make sure that you're planning to win on a base case scenario that's, you know, attractive for physicians and patients. Having a safe and well-tolerated drug that doesn't have a black box warning, that similar efficacy is a big opportunity. Right. Well, given, you know, this 300 patient number is much larger than what you have done so far, right? How you plan to recruit the study in a timely manner? Yeah, so it'll be a global study or multinational. So we'll have sites around the world. I think some things that have changed in the market, if you look historically, these orphan kidney disease studies enroll typically around 0.25 subjects per site per month. So based on that, it would take us around 15 months to enroll 300 subjects. There are pockets, though, with socialized medicine, you know, where there's a lot more awareness of where patients are, where tolvaptan has been tried and not tolerated, like it was available in Europe for ADPKD a lot longer than the U.S. So we've gone now already. We were at ERA earlier this year. A lot of enthusiasm to participate in the study. But we're just basing our assumptions on enrollment based on, you know, historical norms. Although those historical norms have included competing trials, you know, since those studies, bardoxolone is no longer in development, I think venglustat's no longer in development. So we don't think we're gonna be competing for patients in a significant way, and perhaps there'll be potential upside to enrollment from that. Got it. Once you start the pivotal trial, how long does it. I think you mentioned this two-year, how, you know- One year for the primary endpoint on kidney volume- Right for accelerated approval. So that would be from study initiation. If we started mid-next year, you'd have data in, late 2027. Got it. Got it. And, will we have any visibility or any interim update? Good question. You know, an interim analysis would result in alpha spend. So, you know, I think our current thinking, and it, you know, continues to evolve and we look forward to discussing with FDA, is instead to do a blinded sample size re-estimation, which, you know, you don't spend alpha on those, and they can tell you, you need more or you don't need as many to look at the primary endpoint, or you need to enrich for GFR. And so that would be conducted, you know, at an earlier time point than just waiting till the dataset. Got it. I guess one gating factor to do the pivotal study, which is long-term dosing, is a chronic tox study. Yes. Can you tell us about where you are? Yeah. We completed the in-life portion of the dosing of the non-human primates, and the takedown has occurred. No gross findings of concern, and we should have the histopath in the next month or so. And so we'll have draft reports, you know, as we go into that FDA meeting. Got it. And we, I think I mentioned earlier, you know, we completed the mouse chronic tox last year. They take a lot less drug, and they're a lot less expensive than non-human primates. So while our balance sheet was a little thinner, you know, we did that when we could. Non-human primates, and they're a longer study, too. But the mice are more sensitive species, and the top dose of three hundred milligram per kilogram was the NOAEL. So we have a tenfold margin to our therapeutic dose- Okay with the most sensitive species. Right. So, all the tox studies does not turn up any signal so that- No. We got to wait till we get the final reports, but yeah, we haven't seen anything to date. Okay. Okay, great. You know, maybe, let's think a little more about commercial. You, you've laid out the opportunity, the Unmet need, obviously very high. So how... You know, in terms of competing with tolvaptan- Yeah I guess safety alone is a great factor, but you also can slow the growth or instead of, I mean, stop the growth, sounds like, maybe? We haven't even tested that profile in our market research. Like, to stop the growth, you know, I think that's, let's just let that be upside. You know, physicians state a very high intention to prescribe with just that base profile of being something that's tolerated. When you look at the utilization patterns, you know, over half of potential subjects have tried it and just discontinue pretty rapidly. Those that remain on the drug, which is less than 10%, they're at, you know, the majority of them are at half a dose, so it's questionable. I think physicians in the back of their mind are probably thinking, "That hasn't been studied. I don't know if it's how efficacious it is." So there's a real unmet need here. And so in terms of commercialization, unlike other categories, where you might have multiple modalities as well as you know me-toos of the same modality, multiple antibodies approach, and you know maybe a slightly different tissue distribution or you know binding characteristics. Here, there's really not much else. tolvaptan loses exclusivity in the United States next year, and so you know we'd expect it to be genericized. And so you know I question how much promotion will still be behind it. So share voice, I think, is less of a concern than it is market development. You know there are many large academic centers which have patients who respond very favorably to the profile, and they're the ones that are typically the first to prescribe. Then you've got market development in the community nephrologists who may have a patient on ADPKD. Their awareness level, you know, of knowing whether there's something new that's approved, you know, will take time to build awareness just because there hasn't been things available. But it seems to me, you know, based on the work we've done to date and looking at the marketplace, that it's wide open. Got it. Yep. You know, when you decile out physicians, you know, and current prescribing, rather than building the prescriber base, just thinking about current prescribing, you know, you can do this with a targeted sales force. Got it. Got it. Is there an argument to be made on reimbursement difficulty based on an accelerated approval rather than a full approval? You know, I think you're gonna see some payer groups wanna see a step at it, right? But stepping through, I mean, if people have tried it and they can't tolerate it, it's more administrative than it is, you know, practical. And so you might expect some of that until you get the GFR data in the label. But there are patient assistance programs to work to bridge through that, and I think the timing that I described in terms of 300 subjects, you unblind, you know, at one year of treatment, you submit, that usually takes you, you know, close to six months, and then hopefully we'll have a priority review. By the time we get to the point where we have potential approval, you're getting approaching the GFR endpoint, right? And so while that still will take time to unblind, file a, you know, supplemental NDA and get your label updated, because you'll have all of the new data, right? Because it's more than just the GFR data that's gonna go on the label. It'll be two-year safety data as well. That takes some time before you get in the label, but you'll have it published. There'll be awareness and on its impact on GFR, not far behind your accelerated approval date. So, you know, there are techniques that are used to bridge from a reimbursement standpoint. And the reimbursement is really good, actually, quite good for tolvaptan right now. Because keep in mind, if you can delay your time to dialysis, we know what dialysis costs, just in direct costs alone. So, you know, that price point in terms of quality of life and the outcomes in dialysis is well understood by payers. Got it. Got it. Can you, in terms of financials, can you remind us of the runway and how do you plan to fund the pivotal study? Yeah. So right now, you know, at the conclusion of that financing we did in March, that gave us over two years of cash. We've guided, you know, into the first half of 2026, and that assumes initiating and commencing that 300-subject study, one-year study. Now, it's not enough to get through the end of it, but what we said is, we wanna get through this end-of-phase 1 meeting, and have alignment with FDA on the exact size and duration of the study, before we, you know, determine the incremental amount of cash we need, to get through the primary endpoint on that study. And so, as I said, we're on track for that meeting at the end of the year. We'll know next year, you know, the exact nature of it. Meanwhile, we have BD discussions looking at opportunities. If there's, you know, compelling strategic opportunities to partner, say, outside the United States, that could offset the cash needs we'd have. Balancing, obviously, there is... That's not completely non-dilutive. You know, there's, you're giving up on a level of earnings, perhaps not issuing as many shares, but cognizant in evaluating whether there's a compelling BD opportunity that's less dilutive than just raising straight equity capital. Got it. Could you comment on whether there has been inbound interest in partnership? Yeah, we have discussions ongoing, and we're trying to investigate if there's something interesting there, and we have a timeline on that too. A timeline, meaning? Timeline, meaning through the end of phase one meeting. You know, when FDA says you're good to go with this study and, and your, all your supporting, you know, talks and safety data, you're ready to start. If there's something compelling to do, we'll do it on the heels of that. Otherwise, you know, we'll look for alternatives to finance the remainder. Got it, got it. I think with that, we, we're out of time and, you know, thank you for a very helpful and enlightening session. Thank you. Thanks for having us. Great. Thanks, everyone.