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The Future of Dermatology: Innovations in Treatment · The Science of Skin

• 0:08
  SPEAKER_01: Hello and welcome to the Science of Skin Podcast.
• 0:10
  SPEAKER_01: My name is Dr.
• 0:11
  SPEAKER_01: Ted Lane.
• 0:12
  SPEAKER_01: I'm your host for today.
• 0:13
  SPEAKER_01: I'm a board-certified dermatologist in Austin, Texas.
• 0:16
  SPEAKER_01: And I have an incredible guest with me today, Dr.
• 0:18
  SPEAKER_01: Matt Zyris.
• 0:20
  SPEAKER_01: Matt, how are you?
• 0:21
  SPEAKER_01: I am great, Ted, and super excited to be here.
• 0:24
  SPEAKER_01: So Matt is not only a friend, he is uh a mentor, he is a researcher, he is a KOL, certainly an atopic dermatitis, but in other disease states as well.
• 0:35
  SPEAKER_01: And the best thing about Matt, first of all, his humor, his sense of humor is incredible.
• 0:39
  SPEAKER_01: But also he stays on the cutting edge of all of Med Derm.
• 0:43
  SPEAKER_01: So uh we're super excited to have, and you can listen to Matt Zyris along with a couple of other colleagues on Derms on Drugs.
• 0:52
  SPEAKER_01: That's his podcast, Derms on Drugs.
• 0:54
  SPEAKER_01: And I have been a guest, I'm a listener of it, subscriber, and it's a great podcast, Matt.
• 0:59
  SPEAKER_01: So congratulations on that.
• 1:01
  SPEAKER_00: Thanks, Ted.
• 1:01
  SPEAKER_00: It's uh as you know, it's a lot of fun having a podcast, and and it, it uh more work than I realized it was gonna be.
• 1:09
  SPEAKER_00: Uh, but you know, it's it's fun.
• 1:12
  SPEAKER_00: It's fun.
• 1:13
  SPEAKER_01: Well, I like it because you go through journal articles and and you really like you really dive into medical dermatology.
• 1:19
  SPEAKER_01: And if you if you listen to Derms on Drugs, you're gonna be uh hip to the latest, but you also pull out these esoteric uh articles that you know many of us have never heard of, but they're important.
• 1:30
  SPEAKER_00: Yeah, well, it's that's what I get like we don't talk about what articles Reach gonna do.
• 1:34
  SPEAKER_00: Well, those two do, because they like to review them ahead of time.
• 1:36
  SPEAKER_00: But I have no idea what they're gonna talk about whenever it comes on.
• 1:39
  SPEAKER_00: And we're always like, what the hell is that?
• 1:41
  SPEAKER_00: Like that, what is that drug?
• 1:42
  SPEAKER_00: What is what's gonna do what?
• 1:44
  SPEAKER_01: Yeah.
• 1:44
  SPEAKER_01: Wow.
• 1:46
  SPEAKER_01: Anyway, it's it's entertaining at the very least, informative and educational uh at baseline.
• 1:51
  SPEAKER_01: So I really recommend this podcast.
• 1:53
  SPEAKER_01: But but here we go, Matt.
• 1:55
  SPEAKER_01: We're gonna talk about kind of pipeline therapeutics, what we may see in 2026.
• 2:00
  SPEAKER_01: Uh you never know.
• 2:01
  SPEAKER_01: We'll talk about 2027 as well, I guess, because who the hell knows what the agency is doing these days.
• 2:06
  SPEAKER_01: Yep.
• 2:06
  SPEAKER_01: Uh, and why don't we start with your baby atopic dermatitis?
• 2:10
  SPEAKER_01: What are you most excited about?
• 2:12
  SPEAKER_00: So we are hopefully, uh, and whether it'll be 2026 or 2027 remains up in the air a little bit, but we're hopefully going to get some OX40 drugs this year.
• 2:21
  SPEAKER_00: So, right, there's the two different drugs.
• 2:23
  SPEAKER_00: There's uh Rocotinlamab, which is from uh Amgen, and then there's Amletelamab, which I think I'm saying that correct, which is from Sanafi.
• 2:36
  SPEAKER_00: Amletellamab binds to like the Ox40 ligand, and rocotinlamab binds, I think, binds to the to Ox40.
• 2:43
  SPEAKER_00: So they inhibit the same pathway.
• 2:45
  SPEAKER_00: Uh but what's fascinating about these drugs, what's so cool about them is when we think biologics, we think about stuff that's blocking a cytokine.
• 2:56
  SPEAKER_00: And and this is not a cytokine.
• 2:58
  SPEAKER_00: This is blocking a uh two stimulatory uh stimulatory molecule that two cells touch each other.
• 3:07
  SPEAKER_00: Yeah and what that allows is a much broader spectrum.
• 3:11
  SPEAKER_00: Because right, so that's those cells, the, you know, it might, if it it's kind of an antigen-presenting cell and a lymphocyte, and you know, so that lymphocyte, once it gets activated, could produce all kinds of cytokines.
• 3:24
  SPEAKER_00: And so this is like a very it's much broader spectrum than just a cytokine blocking drug.
• 3:30
  SPEAKER_00: So when it's really so we may, because that it's possible that these drugs will have very broad application and might not just be AD, they could, in a sense, be like the jack inhibitors of biologics, right?
• 3:45
  SPEAKER_00: If they're but but first they're coming out in AD, and you know, as you and I kind of have talked about, the big thing is the pig part of AD are the res skin resident T uh memory T cells.
• 4:02
  SPEAKER_01: Yeah.
• 4:03
  SPEAKER_00: And as you're on these drugs for a long time, this pathway is important for keeping them like going.
• 4:10
  SPEAKER_00: And if you're on the drugs for a long time, those skin resident memory T cells get depleted.
• 4:15
  SPEAKER_00: And it may be the like I phrase it to patients, this drug might retrain your immune system so that after you're on it for you know a year, two years, whatever, we might be able to take you off it and you'll stay better for years.
• 4:30
  SPEAKER_00: Like we don't we don't have data that the trials haven't been going on long enough.
• 4:33
  SPEAKER_00: Like I am totally like, I don't want to say, like, oh, we got data that's a but mechanistically, this might be like a you're not gonna say a cure, but we might put people into long-term remissions with AD.
• 4:46
  SPEAKER_00: Yeah, like that is super cool.
• 4:49
  SPEAKER_01: Okay, so we've got the antigen, like kind of the activated anti antigen presenting cell.
• 4:53
  SPEAKER_01: It's got the OX40 ligand, it presents it to the effector T cell with the OX40 receptor.
• 5:00
  SPEAKER_01: Those two combine to cause a uh essentially activated T cell population that releases tons of cytokines, but it's super upstream, right?
• 5:10
  SPEAKER_01: As you mentioned, super upstream, kind of like TNF alpha in in in storiasis too, super upstream.
• 5:15
  SPEAKER_01: And so we get maybe there can be some safety issues with that.
• 5:19
  SPEAKER_01: I think always think upstream disease modification, but more safety issues, downstream, much more specific, uh, and and maybe fewer um safety issues, but but disease specific for sure.
• 5:30
  SPEAKER_00: So first head, thank you.
• 5:31
  SPEAKER_00: I've never thought about it that way, and you are absolutely right.
• 5:34
  SPEAKER_00: That's super useful uh kind of way to think about the upstream stuff.
• 5:40
  SPEAKER_00: And so what's what's interesting with these with these drugs, so uh amletilomab doesn't there's not like any side effect that's like like oh that's an interesting one.
• 5:52
  SPEAKER_00: Rocotinlamab it is fascinating.
• 5:54
  SPEAKER_00: So about a significant number of patients will get fevers and chills with their first dose, and it's like bad.
• 6:03
  SPEAKER_00: Like what like it but you tell patients like you know, when I'm rowing them in the tri, hey, this might happen, and so they're not like freaking out, and they can take a little Tylenol, whatever, it lasts a day or two.
• 6:14
  SPEAKER_00: I don't nobody's given me a good explanation for why that happens.
• 6:17
  SPEAKER_00: Right.
• 6:17
  SPEAKER_00: And then the other thing that's interesting with Rocotinlamab is oral ulcers.
• 6:22
  SPEAKER_00: So about I think it's about 5% of patients on ROCA get aptis ulcers, and that the the patient I've I've had one or two in the trials who've gotten them.
• 6:35
  SPEAKER_00: And the thing is, their AD, they had like horribly resistant AD and they did fantastic.
• 6:40
  SPEAKER_00: And it's one of those things, it won't shock me if it turns out to be the case that the adverse events are predictive of better efficacy, right?
• 6:50
  SPEAKER_00: So kind of like the immune checkpoint inhibitors, where if you get the bad rash, it's more likely to work for your cancer.
• 6:57
  SPEAKER_00: Yeah.
• 6:58
  SPEAKER_00: I it what but there's no data to back this up.
• 7:00
  SPEAKER_00: There's Matt Zyrus like hypothesizing that like the the fevers and chills and the aptis ulcers with ROCA might be predictive of efficacy because they're they're you know showing the drug as having a a significant pharmacal, you know, an effect, it's it's doing something.
• 7:18
  SPEAKER_00: So those those are two interesting and unusual adverse uh events uh that go with these drugs.
• 7:25
  SPEAKER_00: Yeah, at least with that one.
• 7:26
  SPEAKER_00: I don't think they've been seeing with AM Litellomab, though.
• 7:28
  SPEAKER_01: Oh, that's so interesting.
• 7:29
  SPEAKER_01: I mean, when I think of aphos ulcers right now in Durham, I think of Dukra, ducrabocitinib, so tictu, because we certainly saw that in the trials and afterwards in clinic as well.
• 7:38
  SPEAKER_00: Huh.
• 7:38
  SPEAKER_00: So I'm not I'm not like I follow the psoriasis studies, but I'm not like a psoriasis guy.
• 7:43
  SPEAKER_00: So I actually didn't know that about ducra.
• 7:45
  SPEAKER_01: Yeah.
• 7:45
  SPEAKER_01: Yeah.
• 7:46
  SPEAKER_01: I think in the phase three studies, it was something like three or four percent of patients developed aptis ulcers, and and it did lead to some some patients just discontinuing from the trial.
• 7:55
  SPEAKER_01: And I've I've had a couple of patients in clinic who developed such severe aphthostomatitis that we had to just remove them from remove the drug.
• 8:03
  SPEAKER_01: Um, so that's interesting.
• 8:05
  SPEAKER_01: I wonder what the moa of that is, that those mucocutaneous kind of side effects.
• 8:09
  SPEAKER_01: I that's interesting, but but anyway, God, I I love these.
• 8:13
  SPEAKER_01: And as you mentioned, Matt, it's it seems like we may have an opportunity with these drugs for disease modification, but also this like incredibly low dosing frequency, also.
• 8:22
  SPEAKER_00: Yeah.
• 8:22
  SPEAKER_00: Yeah.
• 8:23
  SPEAKER_00: So I think they're I think they're looking at like quarterly dosing.
• 8:26
  SPEAKER_00: Wow.
• 8:27
  SPEAKER_00: Uh, and you know, who knows what we're still waiting for the data to come out if it's gonna like because you know, Lebri keeps coming out, Epglis keeps coming out with the the latest thing is their Q8 dosing.
• 8:38
  SPEAKER_00: Uh, and it it doesn't work quite as well at Q8 as it does at Q4.
• 8:42
  SPEAKER_00: Right.
• 8:43
  SPEAKER_00: And so like that's probably gonna get added to their label, but like I probably won't be like, ooh, like I don't feel like my patients are like, you know, at this once a month is just too much.
• 8:54
  SPEAKER_00: Like, can we if I could just do it every other month, then this would be like it just doesn't seem like that big of a deal to me.
• 9:01
  SPEAKER_00: But when you get out to like four doses a year, you know, Skyrizy like I think that starts to be like a a real thing.
• 9:11
  SPEAKER_01: Yeah, no, it's it's it's a real thing.
• 9:13
  SPEAKER_01: And that leads me to when we think about that lower frequency of dosing, and leads me to think about the new apogee drug, right?
• 9:19
  SPEAKER_01: The the IL13.
• 9:20
  SPEAKER_00: Oh, it's gonna be the apogee drugs are fascinating.
• 9:24
  SPEAKER_00: So like they've got basically the I'm about to start doing the they've got an IL-17 one.
• 9:31
  SPEAKER_00: And so for anybody who doesn't know, uh apogee, they're the people and I'm I'm never sure if I'm thinking of the right companies with all this stuff.
• 9:38
  SPEAKER_00: They're the ones who have the extended half-life drugs, right?
• 9:42
  SPEAKER_00: So like they've got some AD drugs and some psoriasis.
• 9:45
  SPEAKER_00: I think they're further on their psoriasis drugs, but so that for anybody who hasn't read about these yet, which it wouldn't have unless you're me and Ted, who's like daughter of the trials, they basically take known antibodies and replace the the FC part, the I don't know if it's the FC, not the FC, the constant part, the stem of the Y with this thing that binds to the some fetal antigen something.
• 10:13
  SPEAKER_00: And so normally the antibodies get the reason they get broken down is they get taken into a cell and chewed up in the lysosomes.
• 10:19
  SPEAKER_00: Well, with this, when they get taken into the cell, they don't get chewed up and they just get re-re pushed back out.
• 10:25
  SPEAKER_00: So they're this incredibly extended half-lives.
• 10:28
  SPEAKER_00: And the thing that I'm fascinated to see with those drugs is it may not just be that it extends dosing, it might be that if you change the pharmacokinetics, so instead of like dose and then it comes in, so you're got a little more up and downness.
• 10:45
  SPEAKER_00: If you've got a more consistent drug level, that might improve efficacy.
• 10:50
  SPEAKER_00: Uh, so it might be that these drugs just also work a lot better uh than the exact same, you know, cytokine being blocked, but it having more up and downness.
• 11:03
  SPEAKER_00: It's it's that's the other thing that's gonna be interesting to see.
• 11:06
  SPEAKER_00: Uh yeah.
• 11:08
  SPEAKER_01: I I think of you know, uh they have the same efficacy.
• 11:12
  SPEAKER_01: If you look at some of the efficacy numbers from their trials, it looks about like Lebri, like Lebrikis, like Epglis, you know, in terms of Easy75 IGA success.
• 11:20
  SPEAKER_01: But that Q3 month dosing is gonna be amazing.
• 11:22
  SPEAKER_01: And that's that's just for their IL 13, as you as their aisle 13, as you mentioned, they have other assets in A D and then and psoriasis as well.
• 11:30
  SPEAKER_01: Can we talk real quick about the antithymic stroma lymphopueten um antibody that just they halted development of it?
• 11:37
  SPEAKER_01: Was that surprising to you that it just didn't read out?
• 11:41
  SPEAKER_00: No, so there have been two that they have stopped fairly recently.
• 11:45
  SPEAKER_00: So several years ago, uh there was a drug that did TSLP, and in the phase two, it just didn't really work.
• 11:53
  SPEAKER_00: And people were like, but it should work, it should work.
• 11:56
  SPEAKER_00: So they're like, yeah, they're still, I think they're still trying to develop it.
• 11:58
  SPEAKER_00: So it doesn't surprise me because it didn't work.
• 12:01
  SPEAKER_00: Uh I was I kind of thought it should, I still think it should.
• 12:05
  SPEAKER_00: Then the other one, the J and J just stopped development on a dual, uh, it's basically it's an antibody that has bi-specificity.
• 12:14
  SPEAKER_00: It's basically half dupey and half Nemo.
• 12:18
  SPEAKER_00: And there they didn't release any actual data.
• 12:21
  SPEAKER_00: They just said it didn't, it wasn't good enough.
• 12:24
  SPEAKER_00: My bet is it's like 5% better than dupey.
• 12:28
  SPEAKER_00: And and they were like, well, we're not gonna buy like we're not gonna spend another quatrillion dollars to get something that's like a hair better than dupy and still has the same, you know, it's gonna have the conjunctivitis and the other stuff.
• 12:41
  SPEAKER_00: So it people were like, I can't believe it didn't work.
• 12:43
  SPEAKER_00: I I'm pretty sure it worked.
• 12:45
  SPEAKER_00: It probably just didn't work like that much better than dupey.
• 12:49
  SPEAKER_00: So they were like, not not worth it.
• 12:51
  SPEAKER_00: That's my guess.
• 12:53
  SPEAKER_01: Do you think I mean uh after these Ox40, Ox40 leg and drugs, do you think that's the next generation of these bi-specific, tribe-specific antibodies in I'm not sure yet.
• 13:02
  SPEAKER_00: I'm not sure yet because my experience so far has been that, and and right, there's that new test that just came out from Castle.
• 13:09
  SPEAKER_01: Yes.
• 13:10
  SPEAKER_00: Uh, where you do the little scraping and you send it in, and it will tell you this person's gonna do great on IL-13 blockade, or they're not gonna do great on IL-13 blockade, and so they're better on a jack inhibitor.
• 13:24
  SPEAKER_02: Yeah.
• 13:24
  SPEAKER_00: Uh what's been interesting in in AD so far is when I've ever put somebody who didn't do like well enough on Dupey, and then if I put them on Rinvoke or Sabinko and they don't do well enough on that, and when I try and combine them, it generally hasn't worked any better than whatever the best of the individual ones was.
• 13:45
  SPEAKER_00: And I was like, what the heck?
• 13:46
  SPEAKER_00: This does I do geez.
• 13:48
  SPEAKER_00: So I I haven't seen yet what I think the next like we haven't figured AD out to the point of like IL23 yet, where right, if you give people enough if you gave people skyresia every week, 100% of people would get 100% better, right?
• 14:07
  SPEAKER_00: We we don't have that yet in AD where there's like, here you go.
• 14:11
  SPEAKER_00: If you just block enough of that, everybody will get better.
• 14:13
  SPEAKER_00: We we don't know yet.
• 14:15
  SPEAKER_00: We don't know yet.
• 14:16
  SPEAKER_00: So it's I don't know what's coming next.
• 14:18
  SPEAKER_01: That's so frustrating.
• 14:19
  SPEAKER_01: I wish we knew for these poor patients, but luckily we have some amazing um systemic medications.
• 14:24
  SPEAKER_01: I mean, we're so far beyond prednisone at this point.
• 14:27
  SPEAKER_01: It's so well.
• 14:27
  SPEAKER_00: Yes, the other thing that's super exciting that's coming is the stat six degrader.
• 14:32
  SPEAKER_00: Oh, yes.
• 14:33
  SPEAKER_00: So, right, it's it's basically it's kind so you you almost like the way that I'm picturing it is so for again, for again, so it it intracellularly breaks down the stat six.
• 14:47
  SPEAKER_00: It doesn't actually like block anything, it just breaks it down, and so it's it's sort of a different take on jack inhibition, but probably more specific.
• 14:58
  SPEAKER_00: Yeah, so it might be jack inhibitors without the baggage, okay, right?
• 15:03
  SPEAKER_00: Without the the path here, I don't think there's mason BTE risk, but I don't know for 100% for sure there's not.
• 15:10
  SPEAKER_00: So it might take away that baggage.
• 15:12
  SPEAKER_00: That could be a big next step as well.
• 15:15
  SPEAKER_00: I think that I think they just like are going into their finishing their phase twos or something like that.
• 15:20
  SPEAKER_00: So they're still a couple years away, but that's a cool new drug, too.
• 15:24
  SPEAKER_01: Ah, awesome.
• 15:25
  SPEAKER_01: I totally forgot about that one.
• 15:27
  SPEAKER_01: Um, all right.
• 15:28
  SPEAKER_01: Well, let's let's move into psoriasis.
• 15:31
  SPEAKER_01: Matt, are you are you ready?
• 15:32
  SPEAKER_00: Yeah, oh yes, okay.
• 15:34
  SPEAKER_00: So yeah.
• 15:35
  SPEAKER_00: I'm gonna tell you my my first thought on psoriasis this year.
• 15:38
  SPEAKER_00: This is gonna be the year of oral drugs for psoriasis.
• 15:43
  SPEAKER_01: Yes, right?
• 15:44
  SPEAKER_00: Because like OTesla is not that, you know, just it's it's safe, but not that effective.
• 15:50
  SPEAKER_00: So tick to I I'm honestly, I've I was puzzled.
• 15:53
  SPEAKER_00: I don't know why so tick to didn't do better commercially than it has.
• 15:56
  SPEAKER_00: I kind of what people have told me is it's got a little bit of safety issue, and the efficacy's just not good enough to make it like taking that little bit of safety issueness.
• 16:08
  SPEAKER_00: But this year we're gonna have the the icotrokinra and zasocyt nib should both be coming out this year.
• 16:16
  SPEAKER_00: So, right, the icotrakinra, icoto, I can never say, I don't know how to say it.
• 16:22
  SPEAKER_00: Uh, but it's it's the JJ oral, it's an oral peptide that blocks IL23.
• 16:28
  SPEAKER_00: So it's quote, a biologic and a pill.
• 16:31
  SPEAKER_00: It's fat like whenever you're like, but it should get digested.
• 16:34
  SPEAKER_00: Like 99% of it does get digested.
• 16:36
  SPEAKER_00: It only has 1% bioavailability, but if you give so if you give it every day, you get it that 1%'s enough.
• 16:43
  SPEAKER_00: So that and Zasocit nib is like the next generation.
• 16:50
  SPEAKER_00: So TikTok.
• 16:51
  unknown: Right.
• 16:52
  SPEAKER_00: So it's a TIC2 inhibitor, but it's got higher specificity, higher dosing.
• 16:56
  SPEAKER_00: And so both of those drugs look really good.
• 17:00
  SPEAKER_00: So like I think they're getting passy, you know, 90 numbers over 50%.
• 17:06
  SPEAKER_00: They're getting passy 75s into like the 80% range.
• 17:11
  SPEAKER_00: Uh like so.
• 17:12
  SPEAKER_00: They're but kind of how Laura Ferris, uh, who's like my other the she's the psoriasis expert on terms of drugs, she said sort of that she thinks of uh so TikTok is kind of equivalent to Usti Stellara in terms of efficacy, and she thinks of these new guys as kind of cosentics slash talts in terms of efficacy.
• 17:36
  SPEAKER_00: And the IL-23 looks like it's probably not gonna have any safety issues.
• 17:40
  SPEAKER_00: Uh the and the Zasositnib, because it's a more selective TikTok, maybe it won't have like the little, well, maybe you should check them for TB.
• 17:50
  SPEAKER_00: Yeah.
• 17:51
  SPEAKER_00: That like was in the so maybe but it's it's certainly going to be both of these drugs are coming out with head-to-heads against so TikTok.
• 17:58
  SPEAKER_00: So we'll know that they are much better than so tick too.
• 18:01
  SPEAKER_00: You know, hope maybe this will be like when, okay, we we go back to using orals for psoriasis.
• 18:07
  SPEAKER_00: Don't know.
• 18:08
  SPEAKER_00: Don't know.
• 18:08
  SPEAKER_01: But yeah, I I totally agree.
• 18:11
  SPEAKER_01: I think I think that the so tick to quandary was you still needed labs, and the efficacy never really matched any of the biologics, right?
• 18:19
  SPEAKER_01: Yeah, the ones that we typically use at this point.
• 18:22
  SPEAKER_00: Yeah, yeah, yeah.
• 18:22
  SPEAKER_01: And though it's like no labs, easy to kind of set it and forget it.
• 18:26
  SPEAKER_01: You might get a little headache, you may get some depression, some weight loss, but you you take those risks because there's no labs, it's easy to get started.
• 18:32
  SPEAKER_01: Yeah.
• 18:33
  SPEAKER_00: And those risks are all harmless, right?
• 18:34
  SPEAKER_00: They're annoying.
• 18:35
  SPEAKER_00: If they happen, stop the drug, we'll do something else.
• 18:37
  SPEAKER_01: Yeah, yeah, exactly.
• 18:39
  SPEAKER_01: But here we have exactly I mean, uh, we're so excited about these new this new class of highly effective oral therapies.
• 18:45
  SPEAKER_01: I think it's a brand new class of drug.
• 18:46
  SPEAKER_01: I I don't want to just call them orals because then you lump them in with the others.
• 18:50
  SPEAKER_01: Yeah.
• 18:50
  SPEAKER_01: So I'm I'm trying to get everybody to call them highly effective oral therapies.
• 18:54
  SPEAKER_00: I I like that, right?
• 18:55
  SPEAKER_00: So just like in AD, our term is advanced systemic therapies.
• 18:58
  SPEAKER_00: Yeah.
• 18:59
  SPEAKER_00: Right?
• 18:59
  SPEAKER_00: Because you don't just want to say systemics.
• 19:01
  unknown: Yeah.
• 19:01
  SPEAKER_00: I like this highly effective oral uh options.
• 19:04
  SPEAKER_00: It's it somehow that has a ring to me of like extra virgin olive oil.
• 19:08
  SPEAKER_01: Yeah, exactly.
• 19:09
  SPEAKER_00: You need to get expressed.
• 19:10
  SPEAKER_00: Yeah, you need to get a V in there so you can call them like Hevos or something.
• 19:15
  SPEAKER_01: Well, I I'm very excited about so I I the Icotrochindra now has a has a trademark named it's it's icotide.
• 19:23
  SPEAKER_00: Oh, yeah, I hadn't heard that.
• 19:24
  SPEAKER_01: Icotide, I can see that I can say you could say that, right?
• 19:28
  SPEAKER_01: Because the other one's really difficult.
• 19:30
  SPEAKER_01: There's too many syllables and way too many vowels.
• 19:32
  SPEAKER_01: Yes.
• 19:32
  SPEAKER_01: Um, but icotide we could say, and it leans into the the ico for iconic and and tide for the peptide, the small peptide.
• 19:40
  SPEAKER_01: Oh yeah.
• 19:41
  SPEAKER_01: So we're we're excited about ikotide coming out.
• 19:44
  SPEAKER_01: I think the PSA data will be really interesting as well, right?
• 19:47
  SPEAKER_01: We we think of that small molecule as being able to penetrate into the synovial tissue maybe at a greater concentration than the antibodies and so do you buy that story?
• 19:56
  SPEAKER_00: Like I've I've heard it over like a number of times, and it sounds good, and it's 100% could be true.
• 20:02
  SPEAKER_00: I'm not like that.
• 20:03
  SPEAKER_00: Sounds like crap.
• 20:04
  SPEAKER_00: Sounds very true to me, but there's a lot of stuff that sounds good and then it's kind of baloney.
• 20:09
  SPEAKER_00: Yeah, what do you what's your guess that we're gonna see for the for the arthritis stuff?
• 20:14
  SPEAKER_01: I think it's gonna be good.
• 20:15
  SPEAKER_01: I really do.
• 20:16
  SPEAKER_01: I I've I've I've heard from phase two.
• 20:18
  SPEAKER_01: I haven't reviewed all the PSA data, um, but from my understanding, phase two data is is quite good.
• 20:23
  SPEAKER_01: And so it it may not be, you know, different differentiated itself um you know greatly, but I think it's gonna be good enough for us to say, you know what, we can get both the the skin and joint disease with this drug.
• 20:35
  SPEAKER_00: And is it that it has to be taken, it's on an empty stomach, right?
• 20:39
  SPEAKER_00: It's you you have to.
• 20:42
  SPEAKER_01: It's right, it's on an empty stomach.
• 20:43
  SPEAKER_01: I mean, you get one percent bioavailability.
• 20:46
  SPEAKER_01: Uh look, if we draw if you take it with food and you get 0.8% bioavailability, like how much do you actually need?
• 20:52
  SPEAKER_01: I guess we'll find out.
• 20:53
  SPEAKER_01: Yeah.
• 20:54
  SPEAKER_01: And how many patients in clinical trials actually took it on an empty stomach as well, right?
• 20:59
  SPEAKER_01: So I don't know about it.
• 21:02
  SPEAKER_01: It it is supposed to be taken on an empty stomach, but come on now.
• 21:06
  SPEAKER_01: You know, I think we know what our subjects do at home.
• 21:08
  SPEAKER_01: Yeah, exactly.
• 21:09
  SPEAKER_00: They're also they also agree that they're not gonna how often do you enroll someone in a trial who's like, I'll be abstinent.
• 21:14
  SPEAKER_00: That's how I'm gonna, and you're like, uh-huh.
• 21:18
  SPEAKER_00: Uh-huh.
• 21:18
  SPEAKER_00: Okay.
• 21:20
  SPEAKER_01: Yep.
• 21:21
  SPEAKER_01: Um, so okay, great.
• 21:22
  SPEAKER_01: So we just talked about the uh the Takeda drug, the J and J drug, and then we've got Medi, uh, which has got the PDE four inhibitor, MEGI Seca has got the PDE four, the PASI 75 at week 16, and phase two is above 60%.
• 21:36
  SPEAKER_01: So that's an interesting one.
• 21:37
  SPEAKER_00: So that one I hadn't heard about at all.
• 21:39
  SPEAKER_00: Does it were they able to overcome it all the GI stuff?
• 21:45
  SPEAKER_01: Yeah, I think I think it was okay.
• 21:47
  SPEAKER_01: They were just waiting for, in my understanding, we we helped them out with a phase two.
• 21:50
  SPEAKER_01: I think they're just waiting for some investment to move forward with a phase three.
• 21:54
  SPEAKER_00: Uh, because I tell you what, what's fascinating about PDE four?
• 21:57
  SPEAKER_00: So I'm a big like reflumelast guy.
• 22:00
  SPEAKER_00: Because you can use it for everything, right?
• 22:01
  SPEAKER_00: Everything, right?
• 22:02
  SPEAKER_00: Oral reflumolasts, connective tissue disease, lycumplantis, GA, whatever.
• 22:09
  SPEAKER_00: And so I've gotten into that data, and it is so uh PDE4 inhibition systemically is just generally good for you.
• 22:17
  SPEAKER_00: So it it substantially improves cardiovascular uh stuff.
• 22:21
  SPEAKER_00: But what's most interesting, it makes people smarter.
• 22:24
  SPEAKER_00: So even even young, healthy people like me and you, they have done studies where they like do cognitive testing, then like put them on oral reflumolast for a week and repeat the cognitive testing, and they do better.
• 22:39
  SPEAKER_00: And there's there's some mechanistic like reasons, what like into PDE4 and neurons and blah blah blah, which is above me.
• 22:46
  SPEAKER_00: But so a PDE4 drug that works because reflumolast is like it's a little more effective than O Tesla, maybe it's just as much GI, maybe even worse, but it's super cheap.
• 22:59
  SPEAKER_00: Uh, but it but one that actually works really well, and if it gets a little less GI-ness, uh like there's a lot of ancillary benefit.
• 23:11
  SPEAKER_00: It's kind of like with Dupey, where now it's like, hey, if you go on dupey, uh there's now some data that your risk of getting cancer goes down because we've we've shifted your immune system to TH1, TH17 dominant.
• 23:23
  SPEAKER_00: Well, hey, if we put you on this PDE4 orally, we may reduce your risk of dementia long term.
• 23:29
  SPEAKER_00: Like that's you know, because we we like when you've got such good drugs, it becomes more like what are the little nuances of like why I should pick this one over that one, right?
• 23:42
  SPEAKER_00: And so then it's like, do I do I is the data good that dupey reduces can no?
• 23:46
  SPEAKER_00: There's one like trinetic study, but hey, makes sense and now okay, maybe it protects you from cancer, right?
• 23:52
  SPEAKER_00: PDE4, the new drug comes, maybe it helps you with the like it's it's maybe maybe okay.
• 24:00
  SPEAKER_01: We'll have to keep our eye on it.
• 24:03
  SPEAKER_01: Let's let's do this, let's jump into HS, hydratinitis.
• 24:07
  SPEAKER_00: Okay, have you are you doing the obsolera trial?
• 24:13
  SPEAKER_00: Yes.
• 24:14
  SPEAKER_00: So we've I just have like my first two patients, and so far I've been surprised, like it's it's working on the lesions that we used it, but like they're coming in with like, okay, the three that I had are better, three of the four are better, one of them's getting better, but I got like two new ones in other places.
• 24:34
  SPEAKER_00: Yeah, I I think it's going to end up this this right.
• 24:39
  SPEAKER_00: I've had two patients, right?
• 24:40
  SPEAKER_00: So it's not like, oh, I know.
• 24:42
  SPEAKER_00: Uh I bet we're going to end up saying to patients, okay, all the areas that you get HS lesions, like put it on three times a week, like even if you don't have anything.
• 24:56
  SPEAKER_00: And then when you start to get a lesion, put it on twice a day.
• 24:59
  SPEAKER_01: Oh, that's interesting.
• 25:00
  SPEAKER_00: Like something like that is how I bet we're gonna end up using it.
• 25:04
  SPEAKER_00: That that won't be the indication because they, you know, they didn't design the trial that way.
• 25:09
  SPEAKER_00: But what what have you because I I was surprised how well it worked on the lesions that we put it on.
• 25:15
  SPEAKER_00: Like it it was good.
• 25:16
  SPEAKER_00: Like what's what have you what's your bidden take been so far?
• 25:20
  SPEAKER_01: Yeah, I I agree.
• 25:21
  SPEAKER_01: I think obsolera surprises me uh all the time, honestly.
• 25:24
  SPEAKER_01: Um, for a non-steroidal to work as well as it does hand and foot eczema or other kind of really difficult lycentified eczema tends to work well, and then you start putting it in these intergenous areas where you know you you might get some greater absorption just because it is intergyous and yeah, and the barrier is totally gone, you know.
• 25:43
  SPEAKER_01: Yeah, I I was surprised.
• 25:45
  SPEAKER_01: Um, but again, you're right, it doesn't stop new disease from coming, and so you've got to kind of continually use it.
• 25:51
  SPEAKER_01: But I I could see it as adjunctive therapy with something else too, you know, or for that early stage one where it's pretty easy, it only happens in the right side of my groin dock and and it happens every couple of months and only with my period, that kind of thing.
• 26:04
  SPEAKER_01: I can see it being really good for that.
• 26:06
  SPEAKER_00: Yeah, that that makes absolutely that's a good thing I hadn't I hadn't thought about it like that, but you're right.
• 26:11
  SPEAKER_00: Because the if we can get people from not going to hurly two, where we can prevent them from getting some of the scarring and therefore like persistent recurrent lesions, uh it it could be really interesting if we can get to a point where like the people who are already hurly two were cleaning them up, meaning we've we stopped them from getting new ones, then maybe we do a procedure on the three or four scarred lesions that they have, you know, excise them or whatever.
• 26:40
  SPEAKER_02: Yeah.
• 26:41
  SPEAKER_00: And maybe we can push people, you know, back to being not such a bad disease.
• 26:47
  SPEAKER_01: That would be the holy grail, right?
• 26:49
  SPEAKER_01: If we could disease modify like that.
• 26:51
  SPEAKER_01: But but if you look at what's coming in the pipeline, Matt, I mean, for for something that we haven't had much before Humyra, now now you've got, I mean, I guess it's keeping with insight, which which makes obsolero, they've got Povor, which is a Jack 1 inhibitor.
• 27:05
  SPEAKER_01: Yeah.
• 27:06
  SPEAKER_01: And that's that's probably the one that's coming out the soonest, right?
• 27:09
  SPEAKER_00: Yep.
• 27:09
  SPEAKER_00: And I I that drug has been really good.
• 27:12
  SPEAKER_00: Uh some of the patients I have who had like the big, you know, you can never get it any better.
• 27:21
  SPEAKER_00: It's like swollen.
• 27:23
  SPEAKER_00: You can't tell if it's like all fibrotic tissue or some of its lymphedema, and if it's gonna go.
• 27:29
  SPEAKER_00: I have been shocked at some of what has gone away.
• 27:32
  SPEAKER_00: Like it wasn't like, hey, you came in for your second visit and you're back, but like over, you know, okay, you're better, you're like everything is calmed away down, and then slowly seeing this stuff like shrink.
• 27:43
  SPEAKER_00: It's been it's been crazy.
• 27:46
  SPEAKER_00: Uh and I would love to see a head-to-head against you know, one of the IL 17s.
• 27:53
  SPEAKER_00: My gestalt is I think it's better, uh, like meaningfully, but you know, you never know.
• 27:59
  SPEAKER_00: You don't need like HS is a is a tough disease.
• 28:03
  SPEAKER_00: Like psoriasis, I feel like you get a new drug, you see it like five people, and you're like, okay, I know where that goes now.
• 28:11
  SPEAKER_00: HS is is harder.
• 28:12
  SPEAKER_00: It's it's harder.
• 28:14
  SPEAKER_01: So difficult.
• 28:15
  SPEAKER_01: It's also difficult, if I'm gonna be honest with you, I so difficult as an investigator to assess HS.
• 28:21
  SPEAKER_01: Oh, oh it's the it's just the high score is so tough.
• 28:24
  SPEAKER_01: The is that a draining tunnel?
• 28:25
  SPEAKER_01: Is that an abscess?
• 28:26
  SPEAKER_01: Is that a flammatory nodule?
• 28:27
  SPEAKER_01: Is that a non-draining tunnel?
• 28:29
  SPEAKER_01: I don't know.
• 28:29
  SPEAKER_01: If I press over here, I think there might be some drainage.
• 28:31
  SPEAKER_01: Does that mean it's draining?
• 28:32
  SPEAKER_01: It's just tough.
• 28:33
  SPEAKER_00: Oh, it it and and each trial, like it's one of the only diseases that like I actually like carefully watch the video of like the how you're gonna do the assessments because some of them, well, if it's a plaque, you count it as this, and it's and you you you push one centimeter, and I'm like, Well, that's not what I'm doing for the other three HS trials.
• 28:54
  SPEAKER_00: Like, what am I gonna like?
• 28:56
  SPEAKER_00: Yes, it's it is incredibly hard disease.
• 29:00
  SPEAKER_00: The first HS trial I ever did, uh I then didn't do any for like two or three years because the the drug didn't work and the assessments were awful.
• 29:11
  SPEAKER_00: Uh and but now that we've got drugs that actually work, it's it I was like, I you know, these people need help.
• 29:18
  SPEAKER_00: And if people are coming to me and say, hey, we've got trials with new drugs, like the patients that are getting into the trials are really it's making a huge difference for them.
• 29:28
  SPEAKER_01: I completely agree, but but I do think for the people listening, just knowing how difficult it is to assess HS severity as part of the trials as an investigator, I I would really look at pain um reduction as an endpoint.
• 29:40
  SPEAKER_01: Uh, I know that's not the primary endpoint in the trials, but pain reduction and patient satisfaction is such a huge component of of the efficacy and success of these drugs.
• 29:50
  SPEAKER_01: Look at that data.
• 29:51
  SPEAKER_01: That would be my recommendation because that's a way that you can truly compare um kind of between trials in terms of what the pain reduction is for these poor patients.
• 30:01
  SPEAKER_01: Um, and that's what's most meaningful, I think.
• 30:03
  SPEAKER_00: No, I I agree completely.
• 30:05
  SPEAKER_00: I think the the the pain reduction is number one for them.
• 30:08
  SPEAKER_00: Number two is the drainage.
• 30:10
  SPEAKER_00: Yeah.
• 30:11
  SPEAKER_00: Uh it's get, you know, those are but but pain is some right.
• 30:14
  SPEAKER_00: If I think if we said to these people, because I always think that way about like in psoriasis, if you said I can get your rash better or your itch better, they would all take the rash.
• 30:24
  SPEAKER_00: In A D, if you said I get your rash better or your itch better, they would all take the itch.
• 30:28
  SPEAKER_01: Yeah.
• 30:29
  SPEAKER_00: HS said I get your pain better or your drainage better.
• 30:32
  SPEAKER_00: I think the 90% of them would take the pain and 10% of them would take the drainage.
• 30:38
  SPEAKER_01: Like a good point.
• 30:39
  SPEAKER_00: It's it's oh, it's just such an awful.
• 30:42
  SPEAKER_00: I just I feel so bad for people who have that.
• 30:44
  SPEAKER_00: Well, it's just it's tough.
• 30:46
  SPEAKER_01: I say the same thing to my coordinators every time I see one of our poor Hurley III patients.
• 30:50
  SPEAKER_01: Oh just be thankful you don't have that.
• 30:52
  SPEAKER_01: Yeah.
• 30:53
  SPEAKER_01: Um, but you know, there's another drug I want to talk about.
• 30:55
  SPEAKER_01: That's Sonalocamab by Moon Lake.
• 30:58
  SPEAKER_00: That's the new IL36, right?
• 31:01
  SPEAKER_01: This is this is 17 ANF nanobody, so it's an inhibitor of nanobody.
• 31:05
  SPEAKER_01: Yeah, okay.
• 31:06
  SPEAKER_01: So this has gone through phase two, high score 50 of 52 percent, which is pretty darn good.
• 31:12
  SPEAKER_01: And then for phase three, their primary endpoint is high score 75.
• 31:16
  SPEAKER_01: Okay, they're raising the bar.
• 31:18
  SPEAKER_00: That's right.
• 31:18
  SPEAKER_00: And I have great, because this is the one, the nanobody idea, again, penetration into the tissue better.
• 31:26
  SPEAKER_00: Uh, yeah, that's for the moon lake, and they yeah, that's right.
• 31:29
  SPEAKER_00: They bought so they bought some of that that could the name change.
• 31:32
  SPEAKER_00: Yes.
• 31:33
  SPEAKER_00: Uh it's gonna be like it's it's I wonder because it's it's interesting to me that Bimzelix is like drum spectacular in psoriasis, right?
• 31:47
  SPEAKER_00: Like it's it's like cosentics and talt are really effective drugs to start with, but like it is meaningfully better than either of those.
• 31:57
  SPEAKER_00: Yeah I'm not convinced like it's it's not as obvious, it's not as big of a jump from cosentics to bimzelex in HS.
• 32:08
  SPEAKER_00: And that has made me wonder like, is is IL 17 like not the answer?
• 32:15
  SPEAKER_00: Right?
• 32:15
  SPEAKER_00: Where which if it's not if it's just that IL 17 is part of the disease, but not like then more, you know, better penetration may it may or may not matter.
• 32:26
  SPEAKER_00: Yeah, like it's gonna be it's gonna be fascinating to see whether it will or not.
• 32:32
  SPEAKER_01: All right, we've only got a couple of minutes left, but uh I want to take advantage of our time.
• 32:36
  SPEAKER_01: What about CSU, Matt?
• 32:38
  SPEAKER_01: What are you excited about?
• 32:39
  SPEAKER_01: CSU?
• 32:40
  SPEAKER_01: I mean, you pick them, CSU or Vitiligo.
• 32:42
  SPEAKER_01: Which one do you want to talk about?
• 32:43
  SPEAKER_00: So Vitiligo can be really quick.
• 32:45
  SPEAKER_00: Uh so far, doing the oral jack trials for Vitiligo, they're just so slow.
• 32:51
  SPEAKER_00: They are so slow.
• 32:54
  SPEAKER_00: Yeah, like they work, but it is slow.
• 32:58
  SPEAKER_00: That's it.
• 32:58
  SPEAKER_00: That's that's everything I gotta say about Vitiligo.
• 33:01
  SPEAKER_00: Uh CSU, it is gonna be so Barzo, yeah, uh, right, which is the C kit inhibitor.
• 33:10
  SPEAKER_01: That's right.
• 33:10
  SPEAKER_00: So first, that drug is unbelievably effective, like stunning, hard to hard to get like I don't have a ton of people in the trial, but everybody I've got in the trial, it's like as soon as they get like trials they're right, because it it's the first drug we have that literally like gets rid of the mast cells, right?
• 33:31
  SPEAKER_00: So it basically kills depletion.
• 33:34
  SPEAKER_01: Yep.
• 33:34
  SPEAKER_00: Right.
• 33:35
  SPEAKER_00: What's gonna be fascinating about that drug?
• 33:37
  SPEAKER_00: It's also been the case that these patients who are doing spectacularly well, the depigmentation or hypopigmentation, right?
• 33:44
  SPEAKER_00: It's it men, and it's been interesting.
• 33:46
  SPEAKER_00: The the people I have in the trial have all been men, which is weird uh for CSU since the vast majority of patients are women, but the beard is what hits first.
• 33:55
  SPEAKER_00: Uh, and then maybe hair and maybe skin.
• 33:59
  SPEAKER_00: Now it's all reversible, and my patients have been like, I don't nothing like I don't care.
• 34:04
  SPEAKER_00: I am so happy that I am no longer getting hives.
• 34:09
  SPEAKER_00: That's what's so Barzo, I think, is gonna be our by far most effective drug, but I think it's going to have this, yeah, you're probably gonna lose pigmentation.
• 34:18
  SPEAKER_00: And like, do you it it?
• 34:21
  SPEAKER_00: I think it'll be interesting how many patients because it's not like it's dangerous and it's reverse.
• 34:25
  SPEAKER_01: It's not like it's every patient either.
• 34:27
  SPEAKER_01: So so yeah.
• 34:28
  SPEAKER_00: But yeah, telling them there's a real risk of that, uh, you know, it's okay.
• 34:33
  SPEAKER_00: You maybe you're become a silver fox, you know.
• 34:36
  SPEAKER_00: Uh something like that.
• 34:38
  SPEAKER_00: But that that's the big thing coming in.
• 34:41
  SPEAKER_00: And then there's also these MGPRX2.
• 34:45
  SPEAKER_01: Yeah, Evan Mun has got EVO756.
• 34:48
  SPEAKER_01: It's just it's in phase 2B and and uh inducible.
• 34:51
  SPEAKER_01: They're focusing on chronic inducible first, they'll grow into CSU later, I'm sure.
• 34:55
  SPEAKER_00: Yes.
• 34:56
  SPEAKER_01: Uh and that that just essentially stops mast cell degranulation.
• 34:59
  SPEAKER_00: Yes, and that's good, you know, it's it's so it remi, right?
• 35:03
  SPEAKER_00: Which I mean, Rhapsodo.
• 35:05
  SPEAKER_00: I freaking love that name.
• 35:06
  SPEAKER_00: It is such a good, cool drug.
• 35:09
  SPEAKER_00: Uh, right, how fast it works for CSU is just stunning.
• 35:15
  SPEAKER_00: Uh it's one of the few drugs that I'm like, look, you give people a sample, it have them call you back in a week or two weeks, and if they're no better, give it the two weeks.
• 35:24
  SPEAKER_00: If they're no better, it's probably not the drug for them.
• 35:26
  SPEAKER_01: Or it may not be the right diagnosis, honestly.
• 35:29
  SPEAKER_00: Yeah, that's very true as well.
• 35:31
  SPEAKER_00: Right.
• 35:31
  SPEAKER_00: So it's and it's gonna also be interesting to see if if there are other uses, right?
• 35:38
  SPEAKER_00: So I could imagine uh Rhapsodo working in rosacea, right?
• 35:43
  SPEAKER_00: I could have met 100%.
• 35:45
  SPEAKER_00: You know, I it's I could imagine it.
• 35:47
  SPEAKER_00: There's there's data that it helps in HS.
• 35:49
  SPEAKER_00: And I'm like, why the hell would it help in HS?
• 35:51
  SPEAKER_01: We're doing the trial.
• 35:52
  SPEAKER_01: We're doing the trial, Remy and HS right now.
• 35:55
  SPEAKER_01: Yeah.
• 35:56
  SPEAKER_00: Like it's but and the day, the prelim data was good.
• 35:59
  SPEAKER_00: Like it's like it's it's one of those deals where we're we're learning something new because we got a drug, and it's like, son of a gun that works.
• 36:09
  SPEAKER_00: That's a which which actually reminds me, there was just data uh that a sick there's a tick, another tick two inhibitor out there that they just released data in AD, and it was like really effective, like Jack inhibitor level effective.
• 36:23
  SPEAKER_00: Uh, which like maybe that's uh, you know, so tick two or the other, you know, the the zestocit nib, maybe those are gonna end up being like, hey, we can get jack efficacy.
• 36:38
  SPEAKER_00: Maybe they're better drugs for AD than there are for psoriasis.
• 36:41
  SPEAKER_00: Like this, like, yeah, you you don't really learn until you like try this stuff and see.
• 36:49
  SPEAKER_01: Love it.
• 36:50
  SPEAKER_01: Well, I mean, Matt, thank you so much around the world in 30 minutes and dermatology, right?
• 36:55
  SPEAKER_01: Um, this is what's we're looking into your future, dermatologists.
• 36:59
  SPEAKER_01: Um, so thank you so much.
• 37:01
  SPEAKER_01: Brilliant, Matt.
• 37:02
  SPEAKER_01: Um, just really took us through all these different drugs.
• 37:05
  SPEAKER_01: Thank you again.
• 37:06
  SPEAKER_01: That was wonderful.
• 37:07
  SPEAKER_00: Uh, thanks for having me on, Ted.
• 37:08
  SPEAKER_00: This was it's it's it's really fun to get to talk with somebody else who's uh on the cutting edge in an investigator and like because you know, unless you live and breathe this world, yeah, like you just uh derbs who aren't doing trials, like they know what's on the horizon and they know what's out there, but unless you're doing the trials, you just you don't have the same uh interest.
• 37:30
  SPEAKER_00: Yeah, interest, right?
• 37:31
  SPEAKER_00: Because it doesn't matter on a day-to-day, it's not like it helps seeing tomorrow's patient to know that there's a drug coming out in 18 months.
• 37:38
  SPEAKER_00: That you know yeah, yeah, it's awesome.
• 37:41
  SPEAKER_00: But th thanks for having me on.
• 37:42
  SPEAKER_01: Oh man, it's our it's our pleasure.
• 37:44
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• 37:45
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• 37:50
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• 37:51
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• 37:54
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• 37:56
  SPEAKER_01: Uh, otherwise, give us a five star rating if you have a chance.
• 37:59
  SPEAKER_01: Subscribe as well, and uh, we'll see you at the Science of Skin Summit September 17th through the 20th, 2026, here in beautiful Austin, Texas.
• 38:07
  SPEAKER_01: Otherwise, thank you very much, everybody.
• 38:09
  SPEAKER_01: Thank you, Dr.
• 38:10
  SPEAKER_01: Zyris, and goodbye.