The following is excerpted from the question-and-answer section of the transcript.
(Questions from industry analysts are provided in full, but answers are omitted - download the transcript to see the full question-and-answer session)
Question: Roger Song - Jefferies - Analyst
: Thank you. Congrats for the data and then thank you for taking our question. I have a couple questions with your data. Maybe just start with the
fibrosis. Can you just give us some context why the computer, analysis even, lower than ITT for fibrosis while we see some improvement for the
mass resolution, understanding this is, tougher to hit endpoint? Thank you.
Question: Roger Song - Jefferies - Analyst
: Got it thanks.
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Question: Liisa Bayko - Evercore ISI - Analyst
: Hi there, thanks for taking the question. I just wanted to understand a little bit more, the Placebo rate and your thoughts on the methodology
you're using. I mean, we've seen some pretty extreme Placebo rates with this, sort of, [3 res] and then using the mode and rereading the biopsies
if we look at that methodology overall we've seen placebo rates as low as 7%, which really stand out and then, 20%, 25% here, which is also a very
high number. I'm just curious if you think that's the right approach, I'd be curious.
For everyone to comment on that and then, if that's something you consider, for the Phase 3, and then I guess my second question is how are you
thinking now about Glucagon adding to the mechanism of action versus GLP-1 and I'm trying to distil out sort of fat exiting the liver and the and
the liver naturally resolving itself from a direct antifibrotic effect which I think we were hoping to see within the first six months of having a profound
impact, but it seems like it's a little slower so I'm just kind of trying to understand the direct antifibrotic effect that you think you're seeing here,
versus, fats from liver? Thank you.
Question: Liisa Bayko - Evercore ISI - Analyst
: Just one follow up. What happens with the fibrosis response, on drug? I know the placebo response, goes down in phase three. I understand that
the idea and what happens with the treatment arm?
Question: Liisa Bayko - Evercore ISI - Analyst
: [technical difficulty] Oh sorry I just want to follow up in this trial, I'm sorry, what was the Placebo value for the for the fibrosis change in this trial,
and that wasn't.
Question: Yasmeen Rahimi - Piper Sandler - Analyst
: Good morning. This is Emma on for Rahimi. Thanks for taking our question. I guess we're wondering, but beyond the larger size in a Phase 3 and
duration, what are some things you can do to mitigate the Placebo response in the Phase 3, and do you think that there is an opportunity for the
regulatory like landscape to shift towards, maybe accepting AI-based histological analysis? Thank you.
Question: Yasmeen Rahimi - Piper Sandler - Analyst
: Thank you.
Question: Annabel Samimy - Stifel - Analyst
: Hi, thanks for taking my questions, and, I had a question actually about the dose. You mentioned that you are going to be pushing the dose higher
to 2.4 in Phase 3. I guess one thing I was surprised by, in certain of the measurements were the, was the reverse dose response. So I know you're
pushing dose for more weight loss. Will you actually achieve any greater, mass improvement or fibrosis improvement with a higher dose, and at
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Question: Annabel Samimy - Stifel - Analyst
: Got it thanks for clarifying.
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Question: Eliana Merle - UBS - Analyst
: Hey guys, thanks for taking the question. I guess curious for a little bit more color on how you're thinking about a potential Phase 3 design, and
what you learned from this data and how you're thinking about that, and your base case for what the design would look like in terms of like specific
doses, and, the length of the study, and then just a second one kind of on the design and prioritization just you know the timing for when you
would potentially start a Phase 3 and how you would prioritize the development in MASH relative to ALD and ALD programs.
Question: Jonathan Wolleben - Citizens - Analyst
: Hey, thanks for taking the question. Wondering if you guys had looked at responses based on F2, F3 fibrosis at baseline and diabetics and
non-diabetics, if you saw any differential responses between those two groups?
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Question: Jonathan Wolleben - Citizens - Analyst
: Do you think that you know any differential response there makes these results better or worse?
Question: Jonathan Wolleben - Citizens - Analyst
: Alright thanks, Scott.
Question: Patrick Trucchio - H.C. Wainwright & Co - Analyst
: Thanks. Good morning. The first is for Dr Noureddin. I'm just curious if you can talk about the learnings that have emerged from this data readout
in terms of informing the Phase 3 program and what you would hope to learn from the 48 week data and then, separately for the autoimmune
team, with weight loss of 6.2% at 24 weeks and no plateauing. How do you see pemvidutide positioning against Semaglutide and Survodutide as
well as [Erzepatide]?
Question: Mayank Mamtani - B Riley - Analyst
: Yes, good morning team. Thanks for taking your questions. Most of my efficacy questions are already being addressed. Maybe if I could have you
comment on, safety and tolerability. What do you guys think drove a very low discontinuation number here? Is it the GLP is mostly being mild
maybe. Not being persistent, was only observed with initial few doses, or is it just the motivation of getting, the weight loss that you get with this,
drug and then one for Dr. Noureddin with remiterro uptake going well and, semi-approval expected shortly, how do you think of allowing for, use
of background therapies? And if you could clarify in this study, was there any background GLP-1 use? I didn't see that information, as part of the
baseline characteristics.
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Question: Mayank Mamtani - B Riley - Analyst
: That is actually another important question we got like the plans for a four erotic's, is there anything formalized or are you guys still kind of
contemplating that? I don't know if Mazen want to take that or I.
Question: Mayank Mamtani - B Riley - Analyst
: Okay, thank you.
Question: Andy Hsieh - William Blair - Analyst
: Oh, thanks for taking our question. I just have one for Dr. Noureddin, and it's really a follow up on Emma's question on AI. So we know that there's
a very clear and significant delineation between various fibrosis stages and liver outcomes, progression to cirrhosis, and death, but do we have
any data to suggest that the area of fibrosis that's done by the AI in this case also has that strong correlation? And just kind of related to them. I'm
curious about how that AI is trained, what are some of the some of the training data set that they use or you basically just kind of use pay an AI
kind of what they offered. Thanks.
Question: Andy Hsieh - William Blair - Analyst
: It's really about kind of the area of fibrosis and outcomes, right? Obviously from a regulatory perspective, that's what they want to see. And so we
have that and I think the FDA accepted that as a proxy, right, for fibrosis stage and outcomes. I'm just curious about whether you can substitute
area of fibrosis as a potential alternative surrogate.
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