Morning. I'm Eric Joseph, Senior Biotech Analyst with J.P. Morgan. Our next presenting company is Akero Therapeutics, and presenting on behalf of the company is CEO Andrew Cheng. There'll be a Q&A after the presentation. Just raise your hand and we'll get you a microphone. For the folks tuning in online, you can submit a question via the digital conference book. With that, Andrew. Thank you. Good morning, thank you, Eric. It's my pleasure to be here in person at the 2023 J.P. Morgan Healthcare Conference. Why don't we go ahead and get started. This is our safe harbor statement. Of course, given the font size, I won't be reading that, nor do you wanna hear that. I think we can, now that it's been on the screen, we can move to the next slide. When we look at our corporate highlights and we think about what's happened in 2022 and what we're looking forward to 2023, we're really pleased to be able to share some really important details. We obviously read out HARMONY, our biopsy powered placebo-controlled trial in F2, F3 NASH patients in 2022. I'll talk about that momentarily. We're looking for SYMMETRY, our F4 compensated cirrhotic study, which we announced December, will read out in Q4 of this year. We also announced in December that we're pleased to receive Breakthrough Therapy designation from the FDA. That's on top of Fast Track and PRIME, which we already have. We also announced in terms of sticking with regulatory, that we will be having a end of phase two meeting with the FDA in March of this year. Lastly, just of course, we're an investor-supported company. Our most recent cash is $374 million, and that includes a Q3 follow-on of $230 million. That gives us a cash runway into 2025. Let's turn now to some more specific. Just recognize that everyone may not be familiar with Akero's story. Just our main asset is efruxifermin, which is an FGF21-Fc fusion protein that was engineered and designed by Amgen. It was in-licensed by the co-founders in 2018. It has some important modifications, three point mutations that increase the binding and activity against Fibroblast activation protein, namely the P171 to G mutation. Just as a reminder, this is an Fc fusion protein, and activation for FGF21 is a binding to the β-Klotho ligand from the C-terminus, and with that, the N-terminus will bind the FGF receptors. Importantly, FGF21 binds the FGFR1c, 2c, and 3c, but they do so in an equal manner. There's balanced agonism between the three of them, meaning that has activity both within the liver and in the periphery, in the adipose tissue. It does not bind FGFR4 and also has a half-life in between 3 and 4 days. It's really suited for once-weekly dosing. Let's turn now to some of the regulatory interactions that I touched on earlier. Breakthrough Therapy, as you're all familiar with, is a very important designation. It commits the division which granted that to a high level of interaction and signifies a substantial improvement over available therapy at clinically significant endpoints. We're pleased to have reached and received that designation from the FDA in December. As noted at the bottom of the slide, we're the only NASH compound to receive all three designations, both Fast Track and Breakthrough from the FDA and PRIME, which also enables enhanced regulatory support, and is classified as a major therapeutic advance by the European Medicines Agency. We look forward to continuing our partnerships with regulators in both the United States and Europe to advance this important molecule to the next stage. I'll talk now about HARMONY, which is our F2, F3 study, which read out in September of last year. Importantly, we demonstrated statistically significant effects after 24 weeks for both fibrosis, 1-stage improvement in fibrosis without worsening of NASH resolution, as well as fibrosis improvement and NASH resolution. Importantly, these parameters are all regulatory defined endpoints in both the United States and Europe for approvability. I should have noted at the beginning of the slide that this deck is available on the website. It's available today, it saves those of you in the audience who wanna take pictures. You're free to do that as well. This is the clinical trial design, the schema. This is, as I mentioned, this is a randomized double-blind placebo-controlled study looking at patients with biopsy-confirmed F2 or F3 NASH with a NAS score of greater than equal to 4 and liver fat of greater than equal to 8%, a very standard inclusion for phase 2 criteria. The primary endpoint was 1-stage improvement in fibrosis without worsening of NASH, the patients were dosed for 24 weeks. There were overall 128 patients randomized, I'll talk about them in a minute. After 24 weeks, as the schema shows, the patients will continue on the randomized dose until we reach a decision with the agency at an end of phase 2 meeting, for which we will switch them and they will continue on their dose after week, the new dose out to week 96, which there'll be a second biopsy. The secondary endpoints are outlined here, and we've talked about the histology endpoints already. In addition, and I'll speak to lipoprotein, fibrosis markers, measures of glycemic control, weight change, and other liver injury markers. Moving to the next slide. This is a patient disposition. Just as I touched on earlier, there were 128 patients randomized, which we call a full analysis set. We had two patients that were misrandomized. That is, that there was clerical error at the site parse. They were ineligible, yet they were entered into the randomization system. They never received drug. 126 patients who actually received drug. 11 discontinued prior to week 24. 5 due to adverse events, which I'll talk about momentarily. There was administrative discontinuations. Patients lost at follow-up, people who moved out of state, people who withdrew consent. Overall, there are 115 patients, so roughly 90% of the patients reached week 24. 2 patients, 1 on each arm, didn't receive a biopsy. Ultimately left us with 113 biopsies with the relate randomization, as you see below. Keep in mind that it was predefined that the primary endpoint was the liver biopsy analysis set. That is N equals 113 for the primary endpoint. As is common in Phase 2b studies, and it's been done by other companies throughout the industry, it's most commonly the completer set is used for the primary endpoint for Phase 2b studies. Let's turn on to the baseline demographics. Recognizing time, I won't dwell on this other than to say that approximately 70% of patients had F3, so it wasn't quite balanced between F2 and F3. That the patients were pretty standard beyond that, when one thinks about parameters for a Phase 2b study. This was all based in the United States only. Importantly, this is how we analyzed our biopsies. It seems very colorful and very complex, recognize that these are instructions that we received from the FDA. They sent us a fax in 2021, outlining what they believe to be an appropriate approach to analyzing biopsies in NASH studies. They gave us the caveat, of course, that if we had a different approach that would address both inter and intra-reader variability as well as sequence challenges with a different biopsy procedure, we were welcome to engage with them with a continued discussion to reach a consensus. We decided to accept their recipe verbatim. This is guidelines, is exactly as outlined in that correspondence. That is that it's a consensus read where two readers must come to consensus at each component. If they do not, then there's a consensus meeting. If there is consensus, then that's what the score is, and the reading is at all components of the NASH score. If there's not, then there's a third reader that brings in an adjudication. It's a three-reader trained panel to read all of our biopsies. We've adopted, without modification, what the FDA asked us to do. This is the primary endpoint. Importantly, that both doses of EFX at 28 and 50 achieve statistical significance over placebo and in just 24 weeks of dosing. This really speaks to the direct acting antifibrotic properties of our molecule to achieve this amount of fibrosis improvement in such a short period of time. When one thinks about this in context of, and of course, whenever one shows a slide like this, these were not head-to-head data. These were trials done in different times with different readers, and different patient population, as well as inclusion criteria. It is often asked, and is done in the field, to look at what other trials have read out. Some of these studies are Phase 3 studies, as the most recently reported was MAESTRO-NASH study from Madrigal, which is a longer study with two readers that was statistically combined. There are differences in between the trials, but it does show overall that the effect size seen in our Phase 2b study is among the largest seen to date in the field. Importantly, as one thinks about the duration of study, most of the trials on this slide are equal or longer in duration. Really the effects that we've seen are just seen in just the first 24 weeks of dosing. Turning now to the key secondary endpoint of NASH resolution, recognizing that this is also an FDA approved time point. Excuse me, endpoint. Recognizing that in the United States, regulatory approval per guidance is achievement of either or once it's improvement in fibrosis or NASH resolution. You see that again with both doses, we achieve statistical significance. Importantly, in the 50-milligram dose, more than three-quarters of patients achieve NASH resolution in just 24 weeks. Which is a. When one thinks about the effect size, is a 62% effect size over placebo. When one compares that to some of the things that we've seen again, with the caveats that I made on the previous slide, they still apply with cross-study comparisons. That is that this is the largest effect size that's been seen in the field to date, regardless of mechanism as well as regardless of duration. Importantly, this is what patients care about. How can I improve my fibrosis status and achieve NASH resolution. We saw this in 41% of patients after just 24 weeks compared to 29% on the 28 milligram dose. Importantly, as someone who designs clinical trials, really, we achieve a very low placebo rate of just 5%. We're 8x over placebo for the 50 milligram dose. Importantly, that helps us as we begin to think about what our phase 3 studies may look like. Importantly, this is also an endpoint that's acceptable in the European Union. This is the only endpoint that is the endpoint that considers both NASH resolution and fibrosis improvement, whether it's a composite or a co-primary endpoint, and that, it's something that we look forward and are aware that the FDA has also accepted, in a similar product as a phase 3 endpoint. We also touched a little bit on patients that achieved 2-stage improvements in NASH or 2-stage improvement in fibrosis without worsening of NASH. We saw that in about 15% of patients. We talked in for our Phase 2a BALANCED study about NAT-MRI-PDFF, which was the primary endpoint. When we think about liver fat reduction, after 24 weeks, we saw that roughly similar levels of NASH resolution or NASH fat reduction were achieved at 64% in the 50 milligram dose. Most importantly, when one thinks about normalization of liver fat, that is the percentage of patients who achieve less than 5% liver fat is roughly half of patients on the 50 milligram dose. What we've also done is that in additional analyses, we found that patients that achieve normalization of liver fat have a greater than 4-fold likelihood of achieving NASH resolution. When one looks at non-invasive markers, we find once again that they all go in the same direction. They correlate with what we saw histologically, which uses statistical significance in multiple non-invasive markers, whether it's markers of collagen formation like PRO-C3, the Enhanced Liver Fibrosis score or FibroScan, that we continue to see statistical significance when it comes to changes from baseline. Similarly for markers of liver injury, ALT and AST, we see sustained and rapid reductions in those parameters that were maintained throughout the 24 weeks. When one turns to safety, we found that overall this compound is well-tolerated with just 5%, 2 patients in each of the treated doses, discontinuing for adverse events. Really, the if I was to look at the adverse event profile, I would say that these are GI adverse events that are mild to moderate and mostly transient in nature. Despite 1 looking at, let's say, diarrhea, which is occurs in about a third of patients, really, there was only 1 patient that discontinued for diarrhea in the entire study. Looking at parameters of glycemic control, you may ask why are we speaking about that? I think it's important to recognize that more than half of NASH patients have type 2 diabetes, and unfortunately not all type 2 diabetics are at their target of less than 6.5%. When 1 focuses on the type 2 diabetic subset, after adding on either efruxifermin at either dose, they saw significant reductions in their hemoglobin A1c. A nice orthogonal mechanism which lowers insulin resistance, that is it increases insulin sensitivity, and that's a feature that's particularly desirable for these patients. You see that the benefits this compound has on the panel on the right, when one thinks about markers of endogenous insulin secretion, the byproduct C-peptide, we see significant declines in that parameter as well. The declines in A1c are correlating well with decreases in insulin secretion. When one turns to lipids, I would say when one looks at this, that is significant decreases in LDL, increases in HDL, as well as decreases in triglycerides. It really is a very heart-friendly profile. It'd be ideal for a cardiologist to look at this kind of profile, keeping in mind again that it is cardiovascular mortality that is the number 1 cause of death for these patients, not liver mortality. A compound that is heart-friendly is really, again, highly desirable for these patients. Lastly, weight. Nearly all the patients with NASH suffer from obesity. Anything that lowers weight is certainly desirable, and patients on the 50 milligram dose saw a statistically significant decrease of about 3%. Again, not the magnitude that you see with some other agents, but also recognizing that the magnitude of fibrosis improvement is not driven by this degree of weight loss. With that background, one, you know, that was last year and, you know, we're moving forward with the agency, but really the biggest readout this year is in the F4 population. For us, that's in the fourth quarter with SYMMETRY with the patients with compensated cirrhotics. People, I often get a question is, "Why do we think this is gonna be successful?" I think the short answer is that we have proof of concept data where we saw 58% of patients in a very, very small proof of concept study demonstrated either one stage improvement of fibrosis or NASH resolution after just 16 weeks of dosing. I'll talk about that momentarily. I do wanna remind everyone this may look similar, but this is a like Harmony, it's a randomized double-blind placebo-controlled trial. Symmetry only involves patients with biopsy-proven NASH F4, and the primary endpoint is cirrhosis reversal. That is one stage improvement in cirrhosis. Now, the similar secondary markers are being followed in the secondary endpoint, fibrosis markers and other liver injury markers. The biggest difference is the duration. It's not a 24-week study, but a 36-week one. Why the increased duration? I think it's just the recognition of how difficult it is to treat compensated cirrhotics and to achieve any degree of improvement. It will take quite a long dosing period. We completed enrollment last month. We're looking forward, as I mentioned, in the fourth quarter. I think we can all get our phones out and think of a 36 endpoint about when in the fourth quarter that might be. I'm turning to the proof of concept study. This was what we used to call Cohort C. This is a study, a cohort that came out of the BALANCED study. It was a study that when we saw the results of the trial, this was usually designed to be a non-invasive study. Patients with compensated cirrhosis, how would they respond, what markers would they changes would we see in those markers after 16 weeks? After the BALANCED study results became available, we were requested by patients and physicians to consider a second paired biopsy after week 16. We reconsented some of the patients. Those that elected to do so were only 17 out of 30. Again, a subset of a not a big population to begin with, but I think the results are somewhat enlightening. The short answer is that a third of patients, that is 4 out of 12 on the arm, compared to 0 out of 5 on the placebo arm, achieved one stage improvement of fibrosis, which after 16 weeks, if you would ask me beforehand, is a remarkable number just to see a third of patients. Again, recognizing that it's not a large sample size, but I think 16 weeks of dosing to see any improvement of fibrosis is remarkable given the unfortunately very poor results of past studies in this population. When we look at this again with this slide of cross-study comparisons being what they are, we see that most compounds, regardless of mechanism, regardless of duration, have a placebo-like outcome when one thinks about treating this population, even though the medical need is the greatest, recognizing that the 5-year mortality is roughly 50% for cirrhotics. This is the NASH resolution data, about a quarter of the patients, so again, 3 out of 12 achieved NASH resolution. They're not the same patients. If one looks at the box on the right, we can see the improvements in NASH score from baseline to week 16 after a short period. Again, where this is a small number of patients, it's pretty stark, 7 to 1, 6 to 1 in a short period of time. It gives us a lot of encouragement as we move to SYMMETRY that we're likely to see a meaningful impact. When one looks at non-invasives, now, given the fact that this was only a subset of patients had the biopsies, when we look at the totality of the patients, all 30 patients, we have a much bigger N, and the non-invasive all go in the same direction. We see statistical improvements across markers of collagen formation, ELF score, as well as liver stiffness. And when one looks and compares that to what we saw in HARMONY after 24 weeks, again, we see very similar effects despite the fact of a different population. Again, that gives us encouragement that as we dose out to 36 weeks, we perhaps will see a similar histologic change that we saw in HARMONY. Lastly, in this quarter, we'll read out on Cohort D, which is a data readout in a small number of patients. These are patients who are all Type 2 diabetics who are receiving a GLP-1. We don't have a preference, any marketed product. We're combining that with 50 milligrams of efruxifermin. The real question here is why do we do this? I think it's recognizing how much GLP-1 use is in Type 2 diabetics today, and it's likely to continue, especially with the approval of some of these agents for obesity. Given the physiology, it's as a drug that increases insulin sensitivity, it's a natural pairing for the drug with a, like, an incretin that increases a secretion from the pancreas. We're eager to look at the safety and tolerability. There are no biopsies in this study. It's an entirely non-invasive trial, but we look forward to the results in Q2 of this... or Q1 of this year. Q2, sorry. Lastly, just on finances, I mentioned earlier, I think we're well-capitalized at $375 million as of last reported, following our $230 million fundraising in September of last year. Just as a highlight, we have cash until beginning part of 2025. With that, maybe I'll stop here and turn it back over to Eric. Great. Thanks, Andrew. certainly, 2023 is the year of SYMMETRY. A number of readouts that we're all, of course, looking forward to. That being said, HARMONY is on... There is a continued evaluation of subjects on HARMONY. In particular, some additional biomarkers being gathered over the course of, I guess, 48 weeks. Any expectation of readouts from HARMONY short of additional biopsy data that we might expect over the course of the year? Sure. I think just as a reminder, there is a 96-week biopsy plan for HARMONY, so that won't be until later this year. At the same time, we are continuing to follow biomarkers. And one thing we're looking at is that we'll be looking at DEXA data at week 48. I think there are additional data points that will be available, and that's something once we cross those time points, we look forward to sharing them at an upcoming scientific conference. Oh, there's a question in the audience. Why don't you hold on. The microphone's coming. One second. Maybe you can just ask your question, I'll repeat it so that everyone can hear. Oh, there's the microphone. Here it is. Small. Yeah. Thank you very much for presentation. Yeah. I have a couple questions. Did you use or did you take into consideration diet of patients in control and treatment group? Yes. As part of the study entry criteria, all patients were counseled to encourage to adopt perhaps a lower calorie as well as additional exercise. If you're asking whether we control for caloric intake per patient, that was not controlled for in the study. I think overall, a movement towards healthier eating is encouraged and counseled at every study visit. Okay. The second question, I'm just wondering, in terms of enrollment... Yes. how you deal with this and how many patients per site you have, and what is the cost per patient? You know, those numbers are actually, it varies from patient to patient, site to site. In terms of the cost per patient, I'm not sure I have that at my fingertips. If you wanna follow up with me later, we'll see. Okay, great. The last question. Oh. What is your vision? Are you focusing on one product at the moment, or you plan to become a bigger company with a big pipeline? I think that's something as we have other assets that we're investigating, but it's not something we've publicly shared at this time. We're very pleased to have the asset that we have, given its profile. Thank you. There's a question. One more question in the back. Thanks, Andrew. Nice talk. On the F4 study, two questions. Would you consider extending it if maybe your biomarkers showed an indication but your biopsies didn't? Because I know it's such a tough area to meet, and I still am curious about the heterogeneity of the liver itself. You know, is biopsy really the best tool? Another question I'll just ask at the same time, do you see the FDA softening on that a little bit and going to these different diagnostics in the future since more and more people are showing a very good correlation between the biopsies and the other non-invasive technologies? That's a good question, Kent, or questions. Let me take the FDA since I remember that and then. I would say that the FDA is very aware of the science and is looking forward to, Whenever we speak with them, they've been very encouraging us to partner with them and advance the non-invasives, recognizing that biopsy has some morbidity to the procedure. In terms of predicting what they'll do, which is sort of what you're asking, that's always a tough one to predict what a federal agency will do. I'm gonna demur on that. In terms of the first question, I think we recognize where the medical need is and where there are no hard and fast rules of what we'll continue to do in that F4 population. We're gonna look at the totality of the results. What I mean to say is that let's say the trial comes out and the significance is P is great, 0.52. I don't know that that obligates us to terminate the program. I think we need to look at the totality of what the results are overall and, move, you know, decide to move forward. I think more likely than not, given the really there are no options for these patients, I think we're biased towards trying to do everything we can. Oh, one more question. Yes. I've seen you have done liver stiffness measurements and show very good effect before and after. Have you done any measurements on inflammation from the fatty liver? We have some biomarkers with regards to inflammation that, we plan on sharing at an upcoming scientific event. While the mic makes its way up to the front. What's been the incremental physician feedback in the wake of the MAESTRO-NASH read with resmetirom? Any sort of I guess now that you have what seems to be additional modality. I guess any feedback on sort of the importance delivery modality might play in the treatment of NASH, EFX being a sub-Q injection, resmetirom being an oral? Sure. Let me just say that I wanna congratulate Becky and Paul on the results from their Phase 3 study. I for one and Akero overall are thrilled that another agent for NASH will be available. I think this is a field that has not had an excess of success. Anything that provides more opportunity to treat patients is fantastic. To answer your question more directly, Eric, I think that physicians are encouraged that there's more availability because there are no NASH products. I think when people ask sometimes perhaps on a competitive nature, I don't think there's a competition. The medical need is enormous in this field, there's plenty of room for multiple agents. Overall, we're pleased. Nice talk. Nice data. Thank you. It's great to see everything moving in the same direction. As far as the newer study that you talked about with the patients that are on the GLP-1s, are you including people on tirzepatide, or is it only strictly GLP-1? I think at the time when the enrollment was done, it was, there wasn't a lot of tirzepatide out there. A priority, we didn't exclude them, but it's a small study. I'd be very surprised. I haven't seen the full breakdown of agents, if any patients were receiving tirzepatide in the study. Along those lines, as you think about your mechanism of action, I mean, I think that was a great idea because it's already out there in this population. What other combinatorial things are you considering other combination therapeutics? Well. Is that a nod to this? Given what happened in December with Madrigal's compound, it's certainly something we're considering, but it's remains an investigational agent. I think that's the advantage of why the other study could have been done so easily because GLP-1s are so prevalent and widely used, so it allowed us to do so. Certainly once the Madrigal's compound will be approved, it'd be something that we'd be interested in learning more about. There's another question. Yeah. Just, going back to the Madrigal results. Sure. There's been a little bit of a controversy. Mm-hmm. Argument about NASH with an S versus NASH with an H. Any take on that? You know, this is. I'm aware of that. I've received some of the analyst reports. I've received questions from that. I think it's something that I've that I don't have a lot of insight into as the statistics and how we're designed. I've been aware from other reports that the distinctions were discussed with the agency, and I think that's. I can't really say much more. I don't have much more insight, is what I would say. There's a clinical distinction between non-cirrhotic and cirrhotic patients. You know, F4, 3 and less. Sorry, F3 and less, and then F4 patients. In terms of just how you're planning for your phase 3 program, to perhaps address both segments, do you anticipate as having to run a sort of sequential or parallel phase 3 trials, or would you be able to kind of adopt an integrated, comprehensive phase 3 strategy? Yes, Eric. I think, of course, I have to preface this, is that we're having an end of Phase 2 meeting in March. We have proposals, but we haven't reached consensus with them as the meeting hasn't taken place. I would say overall, we plan an integrated approach in that there'll be a potential development pathway. It's available on YouTube. I can give the link for anyone who's interested. Where one where there would be a subpart H approval in F2, F3. There would be a sort of confirmatory study in the F4 population, all of whom would add up to the safety database. They wouldn't all start at the same time. We wouldn't start the confirmatory study until we had SYMMETRY results in the fourth quarter. I think overall, the drive is to move this compound as quickly as possible to the clinic. Okay. In terms of just sort of resources to begin the phase 3 program and, I mean, as it is right now, just where does your runway kind of get you in terms of initiating and running the a phase 3 trial? How would you seek to additional capital in order to run the program to completion? Yeah. That's tricky. I think the answer to that is that we've mentioned that our cash, you know, gets us into 2025. At the same time, it's hard to answer how far and how much cash we'll need because we don't have the final designs on a phase 3 program with the agency. At the same time, I think it's fair to say that it's clear to everyone that the drug won't be approved in 2025. Given it's 2023 already, you know, additional capital will be needed, but the magnitude of which still needs to be determined. Suffice it to say that we have a very innovative capital structure, and we're considering multiple options in order to how to reach commercialization. You know, it... The options as to which slots and where, are sort of to be determined. Okay. Maybe just coming back to the HARMONY data, and really on the safety side. I guess some conversations that we have with investors kind of point to certain of the AEs, treatment-related AEs that led to perhaps discontinuation, esophagitis, pancreatitis. I guess how concerning is that potential or How are you able to delineate whether those results might, in fact, be treatment related? Do you have a sense of whether those patients were also on background GLP use, which I believe also emerges as a treatment-related AE for that product class? I guess, how do you kind of rule out risk of pancreatitis with EFX going forward? There are multiple levels to that question. Why don't I just start at the last point since, you know, pancreatitis is a known, one of the risk factors for it is obesity, and that's a well-established risk. I think when one looks at it, you know, obviously one looks at any adverse event in any of our study subject patients, we're concerned. We want our patients to have no adverse events in an, you know, ideal world. This is an extremely well-tolerated drug. That being said, this class and metabolic agents in general are known to have some adverse events related to the gastrointestinal system. Each adverse event we look at extremely carefully and working with the physician. The pancreatitis was assessed as being not related per the physician for the patient with esophagitis, they had a long history of gastroesophageal reflux disease and when they had some degree of nausea, there was a mild tear. I think that's how the investigator assessed that. We've not seen that in the past. It was the only esophagitis we've reported as a SAE in our development program, but it's something we're keeping on track of. Like everything else, this is a compound in development, and as we continue to move forward, we'll have a better idea of its safety profile. Are F4 patients, perhaps more at risk from a safety perspective versus, earlier stage NASH? Absolutely. I think the F4 patients, why the medical need is so great is because, frankly, their disease is so advanced, their liver, the amount of functioning hepatocytes is quite low. The amount of fibrosis is taken up a large portion of the liver. There's their synthetic app capability and their overall liver function is diminished, so they're much more susceptible to any number of insults. I think one of the risks of cirrhosis is not just hepatic decomposition, but hepatocellular carcinoma, as well as other components of decomposition, such as ascites. I think overall when one thinks about it's, they're a very fragile group of patients. Well taken. I guess my point really was as a result of, perhaps some of the GI sensitivities that are related to efruxifermin and/or GLP-1s. What I would say is based on the small proof of concept study that we have, the overall safety profile didn't seem that dissimilar. N is small, but in the 30 patients, the profile seem very the percentages seem, actually a little bit less than the Phase 2a study that it was part of. About the same as the Phase 2b. We haven't seen an increase in severity in that population. Of course, the SYMMETRY data with the larger sample size and longer dosing duration will tell us more. Yeah. Okay. All right. I think we'll leave it there for time. Thank you very much, Andrew. Thanks for Thank you. Thank you all.