Amylyx Pharmaceuticals Inc (AMLX) 2025 Q1 法說會逐字稿

One. Good morning. My name is Nin and I will be your conference operator today. At this time, I would like to welcome everyone to the Amylyx Pharmaceuticals first quarter earnings conference call. All participants will be in listen-only mode.

After today's presentation, there will be an opportunity to ask questions. To ask a question, [Operator Instructions].

Please be advised that this call is being recorded at the company's request. I would now like to turn the call over to Lindsey Allen, Vice President, Investor Relations and Communications. Please proceed.

Good morning and thank you all for joining us today to discuss our first quarter 2025 financial results and business updates. With me on the call today are Joshua Cohen and Justin Klee, our co-CEOs, Dr. Camille L. Bedrosian, our Chief Medical Officer and James Frates, our Chief Financial Officer.

Before we begin, I would like to remind everyone that any statements we make or presented on this call that are not historical facts are forward-looking statements that are based on our current beliefs, plans and expectations and are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995.

These statements include, but are not limited to our expectations with respect to vexatide, AMX 35 and AMX 114, statements regarding regulatory and clinical development, the impact thereof and the expecting timing thereof and statements regarding our cash runway.

Actual events and results could differ materially from those expressed or implied by any forward-looking statements. You are cautious not to place any undue reliance on these forward-looking statements and AMX disclaims any obligation to update such statements unless required by law. Now I will turn the call over to Justin.

Good morning and thank you all for joining us. 2025 is an important year of execution at AMX as we advance three potential therapies across four clinical trials, each targeting diseases with high unmet need.

Already this year, we've achieved several meaningful milestones. Last month, we dosed the first participant in our pivotal phase 3 lucidity clinical trial of the vexatide in post bariatric hypoglycemia or PBH. We also dosed the first participant in our phase 1 lumina clinical trial of AMX 114 and ALS.

In addition, we've strengthened our financial position by raising approximately $65.5 million at the start of the first quarter, which extends our anticipated cash runway through the end of 2026.

Now, I'd like to briefly walk through each of our programs. Starting with our lead asset of exotide, an investigational GLP-1 receptor antagonist with FDA breakthrough therapy designation for post-bariatric hypoglycemia.

TBH is a chronic and often progressive condition that affects approximately 160,000 people in the United States. However, there are no approved treatment options. We believe avexotide has the potential to fill that GAAP. We are encouraged by the level of engagement from the clinical trial sites participating in our pivotal phase 3 lucidity trial.

We continue to expect enrollment completion in 2025 and topline data in the first half of 2026. In addition, we are preparing diligently to be launch ready and if approved, we anticipate a commercial launch in 2027. Later during the call, Camille will share more details about a vexotide and the lucidity trial.

Turning to AMX 35, which is an oral small molecule therapy designed to target endoplasmic reticulum or stress and mitochondrial dysfunction. AMX 35 is currently being evaluated in Wolfram syndrome and progressive supranuclear palsy or PST.

Wolfram syndrome is a monogenic progressive neurodegenerative disorder with premature mortality and no approved treatment options. This disorder is caused by mutations in the WFS1 gene.

The WFS1 gene encodes a protein called wolframin that spans the membrane of the endoplasmic reticulum, and mutations in wolframin directly cause stress and mitochondrial dysfunction. We believe AMX35 has the potential to address the urgent unmet need for the approximately 3,000 people living with Wolfram syndrome in the United States.

Last year, we reported positive topline data from the 12-person phase 2 open label Helios trial in adults with Wolfram syndrome. Participants showed improvement or stabilization across all measured outcomes at week 24.

In addition, longer term data for the subset of participants who had reached treatment through week 48 showed sustained improvement over time.

We continue to follow participants in the Helios trial and plan to present full week 48 data at the upcoming joint congress of the European Society for Pediatric Endocrinology and the European Society of Endocrinology, which is this coming weekend.

The poster will be made available on the presentations page of our website next Monday, and those findings, along with our ongoing discussions with the FDA, will inform the design of a phase retrial.

Now, I'd like to turn to AMX 35 as a potential treatment for progressive super nuclear palsy. TSP is a rare, progressive and fatal neurodegenerative disease that affects an estimated 23,000 people in the US and has no currently approved treatments.

TSP is a tauopathy, which is defined by the buildup of tau protein in the brain. Based on its prior effect in reducing tau and cerebrospinal fluid in people with Alzheimer's disease, we believe AMX 35 is the first brain and cell penetrant agent that has demonstrated a significant tau reduction in CSF to be tested in TSP.

We completed enrollment in the phase 2B portion of the Orion trial in January of this year, with a total of 139 participants randomized. We expect to report data in the third quarter of this year.

Those results will guide our decision about whether to advance into the phase 3 portion of the trial.

Next, in our pipeline is AMX 114, our investigational anti-sense oligonucleotide targeting knockdown of calpae 2 for the potential treatment of ALS.

This is a novel program built on decades of academic research linking the proteate calane 2 to axonal degeneration, an early and destructive driver of ALS progression.

In pre-clinical studies, AMX 114 showed potent and durable reductions in calpae 2 levels, improved neuron survival, and reduced neurofilament light chain levels, a well established biomarker of axonal degeneration. We're excited to have dosed the first participant in our phase one luminous trial last month.

Lumina is a multinational randomized double blind placebo-controlled multiple ascending dose trial evaluating the safety, tolerability, pharmacokinetics, and pharmacodynamics of AMX 114 in people living with ALS.

We look forward to early cohort data from Lumina later this year. With strong scientific rationale, clinical momentum, and a clear path ahead, we believe we're well positioned to execute across our clinical programs.

With that, I'll now turn the call over to Camille to share more about the lucidity trial and our work with the vexide.

Thanks Justin. We are very excited about the potential of a vexotide, our investigational GOP-1 receptor antagonist. The GOP-1 receptor, a mediator of important, well-characterized biology, is an effective target to modulate this biology.

The GOP1 receptor is one of the key regulators of insulin and glucose. Unlike GLP-1 agonists, which increase insulin secretion, a GLP-1 receptor antagonist decreases insulin secretion and therefore stabilizes blood glucose levels. Aveetide has shown promised to treat post-b bariatric hypoglycemia and as a result has FDA breakthrough therapy designation.

Last month we dosed the first participant in the 16-week randomized double blind placebo-controlled phase 3 lucidity clinical trial, evaluating of exotide in approximately 75 individuals with PVH following rule on Y gastric bypass surgery.

Lucidity is designed to have similar inclusion and exclusion criteria to the previous successful phase 2 prevent and phase 2B trials of vexotide in PDH.

In addition, lucidity is evaluating the FDA agreed upon primary outcome of reduction in the composite of level 2 and Level 3 hypoglycemic events through week 16.

PBH is a debilitating condition, believed to result from an excessive GLP-1 response following bariatric surgery. PBH manifests as persistent, recurrent, and debilitating hypoglycemic events that can impose a life-altering and enduring burden on a person's health, independence, and ability to engage in everyday life.

On average, the symptoms appear approximately 1 to 3 years following bariatric surgery.

Once people have TBH, the condition is chronic and often progressive.

We estimate based on our projections from data and published literature and claims-based work that there are about 160,000 people in the US who are living with PBH today.

Additionally, bariatric surgery remains the standard of care for addressing obesity, particularly for people who require substantial and sustained weight loss. Therefore, we believe the unmet need in PBH will continue to grow.

A few weeks ago, the American Society for Metabolic and bariatric Surgery or ASMBS published new 2023 surgery data.

The results estimate that approximately 270,000 new bariatric surgery procedures occurred in 2023 in the US, including 220,000 of the two most common surgical types, Ron Y gastric bypass surgery and sleeve gastrectomy.

There was a slight uptick in Roy gastric bypass and a slight downtick in sleeve. Overall, there was little or no significant change in the procedure trends from the prior year. Importantly, we believe that the biology of PBH is the same regardless of the type of bariatric surgery patients receive.

And despite dietary modifications, Rescue measures such as glucagon and off-label drugs, many people with PBH continue to experience persistent symptoms and hypoglycemic events with no sustainable management options.

Furthermore, there are no approved treatments for PBH and the current options used off label generally are are inadequate for this condition.

The lucidity trial is intended to build on the robust body of data generated to date for a vexatide, which includes five clinical trials demonstrating consistent dose dependent effects, including statistically significant and clinically meaningful reductions in hypoglycemic events.

In the phase 2V trial, a once daily 90 mg dose of vexotide led to a 53% reduction in level 2 hypoglycemic events with AP value of 0.004 and a 66% reduction in level 3 hypoglycemic events with AP value of 0003.

Avexoide was generally well tolerated, with a favorable safety profile replicated across the clinical trial. 90 mg once daily of vexotide, the dose we are evaluating in lucidity, also demonstrate a favorable pharmacokinetic profile, maintaining exposure in the therapeutic range to 24 hours, supporting daily dosing.

This characteristic translated to similar meaningful improvements in native glucose levels as measured by continuous glucose monitoring both during the day and overnight.

We are excited to present additional analysis of the vexotide phase 2 and phase 2 these studies at end of 2025 in July. These presentations will include new population PK and PD data supporting sustained effects at the 90 mg once daily dose regimen, as well as the composite rate of level 2 and level 3 hypoglycemic events.

We are encouraged by the engagement from the clinical trial sites and continue to expect to complete recruitment by the end of 2025. We're grateful we are grateful to our trial participants, investigators, and collaborators who inspire and guide us, guide our work each day.

Now I'll turn over the call to James to discuss the financial highlights from the quarter. James

Thanks, Camille. We believe we're well positioned to achieve our goals. We ended the first quarter with a cash position of $204.1 million which includes approximately $65.5 million in net proceeds from our public offering which closed in January of this year.

We believe we have the necessary cash to deliver our planned clinical milestones through the end of 2026. These milestones are top line data from the phase 3 lucidity trial of a exotide and PVH. Week 48 data from the ongoing Helios trial in Wolfram syndrome.

Topline data from the Phase 2b portion of the Iranian trial and PSP. In phase one data from our Lumina trial of AMX 114 and ALS. In addition, our cache supports the advancement of our commercial preparations for the potential first to market launch of exotide and PVH.

So, let's turn to our results. Total operating expenses for the quarter were $37.8 million down 82% from the same period in 2024.

Research and development expenses were $22.1 million compared to $36.6 million in Q1 2024, primarily due to a decrease in spending on AMX 35 for the treatment of ALS, a decrease in payroll and personnel related costs, and in pre-clinical development activities.

Selling general and administrative expenses were $15.7 million compared to $57.8 million in Q1 2024.

Primarily due to a decrease in payroll and personnel related costs and a decrease in consulting, professional and other services. We recognize $6.8 million of non-cash stock-based compensation expense for the quarter.

Compared to $9.9 million of non-cash stock-based compensation expense in Q1 2024.

We also use roughly $6 million in cash related to product rebates and the settlement of purchase commitments for Amex 35 that were established prior to the voluntary discontinuation of sales of Relibro and Albrioza in April of 2024.

We recorded $1.4 million of expense in the first quarter of 2025 related to these payments, with the remaining expense recorded in prior periods.

Going forward, the residual cash obligations related to the discontinuation of Relio and Albrioza are $3.1 million which we expect will be paid through the remainder of 2025.

We're pleased with our cash position as we progress through the year, and we're reiterating our expected cash runway through the end of 2026. With that, I'll turn the call over to Josh for some closing remarks.

Thank you, James. As we look ahead, we remain grounded in our mission to develop novel therapies for diseases with high unmet needs. We are focused right now on strong execution across the four clinical trials, each targeting serious neurodegenerative or endocrine disorders. In the coming days, we are excited to share week 48 data from our Helios trial and Wolfram syndrome. And in the third quarter, we look forward to sharing unblinded phase 2B data from the Orion trial and PSP.

By the end of the year, we also expect early cohort data from the Phase 1 lumina trial of Amex 114 in people living with ALS, and in the first half of next year, we expect topline data from the Phase 3 lucidity trial of the vexatide and PVH.

We continue to believe we have the necessary cash to advance our pipeline and to support commercial preparations for the potential first to market launch of the vexatide and PBH.

Thank you for your continued interest, and we look forward to keeping you updated on our progress. Now, I would like to open the call up for questions.

We will now begin the Q&A session to ask a question. Please press 1 on your telephone keypad. To withdraw your question, please press 2.

Please limit your questions to one with one follow up. If you have additional questions, you may rejoin the queue. At this time, we will pause momentarily to assemble our roster. Your first question comes from Michael DiFiore of Evercore ISI. Please go ahead.

Thanks for taking my question and congrats on all the progress. Just two for me. One, on Avetide, just your recent commentary on Avetide for PBH suggests that a large patient education campaign will be required. The question is this because the 8% of symptomatic patients don't necessarily know they have PBH or will these educational efforts attempt to shore up and penetrate into less symptomatic patients have a follow up.

Yeah, thanks Mike.

Good and important question. So I would say PBH certainly among adult endocrinologists and sadly among people who are suffering with PBH is pretty well known, including the signs and symptoms.

I think sometimes it can be a bit of a connecting the dots because oftentimes takes years, on average 1 to 3 years following a bariatric surgery to manifest, but adult endocrinologists, when they can pretty clearly recognize the signs and symptoms of hypoglycemia and then of course once they actually do testing in the clinic on blood glucose, then it becomes very clear as well as at home measures.

Says like finger stick blood glucose and CGM. So I think it's certainly well recognized and unfortunately, it's quite a severe condition as well. People can have such severe events as sudden loss of consciousness or even seizures, and these are happening on a reasonably frequent basis.

I think when we talk about The education, it's because this is kind of classic rare disease. There have not been treatments before for PBH, and I think as we find with many rare diseases, there are many unmet needs throughout the community. So we see it as really our job to make sure that we're educating the medical.

Educating, advocacy and people living with PBH and then hopefully if Avexotide is approved, educating them on the potential benefits of Avexotide as well.

Very helpful.

My second question is on PSP. I just want to, as we head into the interim data, I just want to confirm the efficacy bogey on the PSP rating scale that we should be looking for in the interim. Just given that the placebo group and many prior PSB trials declined by 10 points or 11 points over 52 weeks, should we expect roughly half of that in placebo?

Furthermore, sources say that the minimally clinically meaningful difference on the PSP rating scale over 6 months is around 6 points. So taken together, should we expect maybe a flat 1% improvement in the drug treated arm.

Thank you.

Sure, so maybe first on the efficacy [bogey]. So the study has about 80% power to detect a 30% effect on the PSB rating scale and I'd say the PSB rating scales are primary endpoints, certainly going to be one of the main things we look at, but we do have other secondary endpoints and markers as well.

So ultimately our decision on the next steps for the program will be driven by all the data, not just the PSPRS. I'd say, PSP has only had so much work in of clinical meaningfulness. We have assembled some doctors and spoken to them as well, and we've heard everything from a single point.

Difference could be clinically meaningful. We've heard differences such as 20% or 30% change and I think it maybe bears in mind to discuss what is actually happening in this disease. This is a disease that often has survival of 66 years, sometimes even less and during that time these patients almost in a way, reminiscent of ALS.

Eventually locked in the progressive motor impairment, progressive, walking impairment, the speech and swallowing difficulties, so the ability to make that go a meaningful percentage slower, I think our view and certainly many of the KOLs view we've spoken to would be highly meaningful. So, won't put a specific line on it. We're going to look at all the data as it comes, but I, maybe just remind we're 80% power to see a 30% effect.

Very helpful. Thank you.

Your next question comes from Mark Goodman of Lyric. Please go ahead.

Hi, good morning.

Thank you for taking my question. This is Basma on formark. We have a question on PBH, regarding the prevalent population of 160,000 patients. Reminding us again how many are seeking treatment. So this is basically a follow-up question. The previous one, so all of these patients again are symptomatic and also if you can provide any color on new incidents, so we know that like 200,000 to 300,000 surgeries per year, should we still assume that 8% of the surgery of the patients who undergo the surgery will eventually develop TBH in like 3 year to 40 year time frame or or should we assume something else?

Thank you very much.

Yeah, thank you for the great questions on the TBH population. So starting with your first question on the 160,000, are those people seeking treatment, I'd actually say there's a larger group seeking treatment and I can walk you through that. If you look at the number of people who have hypoglycemia following bariatric surgery, in any form and any frequency, it's it's as 30%, 40%, 50% of the population depending on the methodology you use.

Now people with hypoglycemia following bariatric surgery are counseled to use medical nutrition therapy, sometimes off-label prescriptions like aarbocerri, so that if you if you look at just even over the past decade of people, you're looking at a population of 500 to a million people in that group. When we're talking about PBH, we're talking about the people who have tried those things and yet still have persistent hypoglycemia.

That's how we get to about 8% or about 160,000 people.

So this is pretty rare. We're talking single digit percentage of people who get bariatric surgery and again years to manifest, but it's a single digit percentage of a population of millions of people who have had bariatric surgery.

So in terms of seeking treatment, as you might imagine, people who have such a debilitating condition where they're having sudden and from what they can tell, unexplained drops in blood glucose that lead to neuroglycopenia, which means their brains aren't functioning as they're supposed to are certainly seeking medical attention.

Back to the first answer, I think with rare disease what often happens if you don't have a treatment then. And hopefully we can deliver one with Avexitide, then I think suddenly you have options that weren't there before and I think as we were able to do with ALS, access is certainly important and education is very important as well.

Your second question on should we continue to model 8% in the population, we certainly think. So I think as Camille mentioned, the new the 2023 numbers from the ASMBS on bariatric procedures came out still well in 270,000 procedures in the year and we know that with these upper GI surgeries that there is a portion of people, again single digit percentage but a portion of people who will develop persistent hypoglycemia.

So we think that one of the major drivers of that is that the body seems to have a potentially accelerated GLP-1 response.

We think that's why a GLP-1 receptor antagonist makes a lot of sense in this condition, and we see that continuing. But again, I'd remind this is a single digit percentage, so it's not everyone, but it's a very large population of people who are getting bariatric surgery.

And I just have one smaller detail. What we've observed in the literature and talking to KOLs is usually PBH appears 1year to 3 years following surgery. So it's, possibly a little sooner than the 3 years to 4 years, you mentioned.

Got it. Thank you so much. It's very helpful.

Your next question comes from Tim Anderson with Bank of America Securities. Please go ahead.

Hi, good morning. This is Susan on for Tim Anderson. We're really looking forward to the upcoming QE datata next week. My question is on the ongoing discussions with the FDA on trial design. What are some of the remaining questions or debates that you guys are having with the FDA on trial design and what are we expecting to learn from the 48 week data that will help inform one way or the other, some of the decisions that will need to be made on trial design.

Thank you.

Yeah, thank you for the question. This is Camille.

We too are looking forward to presenting the week 48 data next week at the end of scientific medical meetings, and what I'm going to answer your second question first, what to expect, I.

Ask you to recall the ISA data that were presented for the week 24 data for Wolfram in the Wolfram study last year, and now we have twice as much time for those participants in the study. So we will be looking at the similar end points and change in AUC and the C peptide response to a mixed meal tolerance, as well as other glycaemic measures such as hemoglobin A1C, as well as visual acuity.

And overall global global impressions have changed. So I invite you to look at those data and see how things have evolved over an additional 24 weeks, recalling that these are adults with this genetic disorder, and it is a neurodegenerative and beta cell degenerative disorder where progression is expected in these folks. Your first question was regarding the phase 3 and the FDA.

So we really do not go into the details of our interactions and discussions with the FDA. Having said that, for sure the week 48 data will inform and is informing our phase 3 program and when we have additional information in alignment with the agency on the Phase 3 protocol, we expect to.

Be able to share that information. Just to remind also, this is the very first clinical trial of a of a agent to potentially impact Wolfram syndrome. So the design, there's no template for the design of a trial on Wolfram syndrome, and so we're having those discussions with the FDA.

Well.

Thank you. I think next question.

All right. Our next question comes from Greg Savanna of Muzo. Please go ahead.

Hi, this is SAM on for Greg. Thanks for taking my question. Maybe a couple on the vexatide. First, will there be any kind of subgroup analysis within the study, separating level of severity of PDH in terms of number of episodes and such, and then also assuming approval, do you anticipate any kind of step up or restrictions from a payer perspective that would limit access based on Either severity of the disease or or any type of surgery or anything like that.

Thank you.

Good questions. So I'd say maybe first, our kind of focus on the study is, in the full study population. We are enrolling a population, all of which are required to be having during, a run-in period, we have a three-week run-in period. And people have to be having at least one level 2 or level 3 event per week.

So we are enrolling a population that is having frequent events, so all of the patients we have will have that, characteristic as well. In terms of, step therapy, there are no currently approved therapies for PBH, so I would say we do not anticipate, step therapy in this indication and certainly as we get closer to launch, we'll spend time, interacting and educating pairs, but we do believe we have a, quite exciting and differentiated approach here, we have FDA breakthrough therapy designation, 5 prior trials showing.

Differences in patients who are already trying their very best to reduce these symptoms, and we're still seeing, those differences, even in that context.

Yeah, and I would say that, access is very important to us. If we believe if you have a treatment that can help people, you need to make sure that people can access it efficiently.

So our team's already working on that, and I just remind for what I was saying earlier that we're already talking about people who have been on medical nutrition therapy, which is really standard of care right now and yet still have these persistent hypoglycemic events which are very debilitating and I think that's important because it's we're talking about a population that really needs help and from a physician and payer perspective, these are people who have to regularly seek medical attention for very dangerous events. So I think those will be very important messages as we do our market access education.

It's helpful call.

Thank you so much.

Your next question comes from Joel Beetti of Baird. Please go ahead.

Thanks. My question relates to a vexotide, GLP-1 agonists seem to have many favorable short term and long term health effects.

So, with that in mind in that context, what it gives you confidence that GLP1 antagonists like a vexide won't cause some type of safety issue, and then I have a follow.

Up.

Sure, great question. So one, we do have a good amount of safety data both non-clinically and clinically on Avexotide and to date Avexa has generally been well tolerated. So it's a first empirically what we've seen is a good, safety profile thus far.

I'd also maybe add that Avexotide is a competitive antagonist, so it's not running the GLP-1 receptor in reverse, it's attenuating, the GOP one that you have endogenously. And so I'd add with that, we don't really see or we haven't seen weight gain, hyperglycemia, any of the things you might think about in that context.

So maybe I Say that overall we've seen, a good safety profile to date and just kind of highlighting as well in the animal studies we even dosed manyfold above from a human equivalent dose perspective, manyfold above what we're dosing in the human clinical trials, and even there, we don't see, particularly adverse events of concern.

Okay, that makes sense. And then as a follow up, I'm just, how are you currently thinking about potential business development activities?

So I would say one, we're very excited about our pipeline. We have major milestones across each of our 4 clinical trials over the next 12 months to 15 months, which is which is very exciting, and each is in a disease where there's no treatment or substantially inadequate treatment.

So we're very excited. Potential in each one of these programs we, are always our mission is to help people who have unmet medical needs and so with that, we're always making sure that we stay on top of what's what's promising, but our focus right now, as I was mentioning in my remarks, is really on execution because we have some very exciting milestones ahead.

Thank you.

Your last question comes from Ananda Gush of HC Wainwright and Company. Please go ahead.

Hey, hi comrades on the quarter. Maybe, one question with respect to the ALS trial, given the importance of NFL in this trial and especially with the pre-clinical data showing the effect of knocking down CAA2 on NFL, can you remind me if the Inclusion criteria for the trial, like during the inclusion criteria of the trial, did you consider the NFL levels of the ALS patients, which might be higher compared to the natural history, or how did you think about the trial given the focus on NFL?

Yeah, that, that's a great question. It's actually something we discussed a lot as we were planning and designing the study as well. We do not have a, inclusion criteria that requires, particularly high NFL levels going into the trial.

I think a couple of things went into that. One, just to put context on it as well. In the CSF and ALS, NFL levels are often 10 times as high as normal and it's quite a stark separation as well. So you can generally expect in IS that particularly when you're measuring CSF, you're going to see pretty high levels.

And then additionally, given that this is our first, in human with the drug, we didn't want to oversubset and potentially miss populations or signals that could be quite important. So we definitely will be looking at that, looking at those patients who may come in with higher as compared to lower neurofilament, but we didn't want to exclude them from the trial, in the initial trial.

Got it. Makes.

Sense. Thanks.

Thank you. We still have one question from Dan Akschuti of Pareto Securities. Please go ahead.

Hello everyone and thank you for taking my questions. Congrats on the progress. I'm excited for the heli readout next week. Just a more general question how you compare it Avexitide to other drugs that could enter the space that are more inhibiting insulin and COP1 secretion like summato in analog and how you see the placebo response with impulse bariatric hypoglycemia for the face.

Thank you.

Yeah, good questions. So maybe first I'd remind, we're in phase 3 with vexotide. We have breakthrough therapy designation built on 5 prior successful trials. So we, think the profile of Avexitide is quite strong both in terms of what we've seen thus far in terms of say.

And efficacy. I think all, any other programs in the space are quite a bit earlier and have a number of hurdles, I would say to overcome. And so, we're focused on Avexitide that at this time and do believe that as the best profile we've seen thus far.

Yeah, and I just reiterate too, the reason that Avexitide was granted FDA breakthrough therapy designation is because PBH has a high unmet need and because of the promising data from the phase 2s, breakthrough therapy means benefit over existing treatments and of course right now there are no existing treatments or approved treatments for PVH.

So we're very excited about the potential and that's why we're focused on rigorous execution in this study.

Yeah, and I realized you also asked. About placebo rate. So, in the phase 2 study, there was a placebo period as well, and we did not see a meaningful difference between the run-in and the placebo. So I'd say purically we haven't really seen much of a placebo effect in this indication. That being said, when we did the powering analysis for the study, we certainly thought about that, and we do believe our power is robust, that even if there is some degree of placebo effect, we should have enough power, regardless of the study.

Yeah and I this is Camille, I would just also comment that these individuals have tried and are trying everything to manage this very debilitating condition and that really isn't going to change whether they're in a clinical trial or not. So they're.

Their Daily life is, will not be changing because of being in a clinical trial.

There is no question at this time. I'll turn the call back to Mr. Lee.

Thank you, operator, and thank you all for your time. If you have any follow-up questions, please reach out to Lindsey. We hope you have a great rest of your day.

Ladies and gentlemen, this concludes today's conference call.

Thank you for your participation. You may now disconnect.