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- [00:13]
A
Welcome to Derms on Drugs, a video podcast brought to you by Scholars in Medicine, the best educational platform in dermatology and totally free. Derms on Drugs is where cutting edge derm meets hit or miss comedy. I'm Matt Cyrus and each week I'm joined by my residency buddies, Dr. Laura Faris and Dr. Tim Patton, where we use our 60 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It's everything you need to know to be on the cutting edge of derm, and it'll be the most fun you've had while actually learning something useful. New episodes drop every Friday on Scholars in Medicine, Apple Podcasts, Spotify and and any other somewhat major podcast platform where you might get them. All right, so let's go ahead and jump into our special post AAD episode where we are going to get into our favorite late breaking research and I'm going to kick it over to Dr. Farris to get us off the ground.
- [01:17]
B
All right, so I am going to talk about the iconic lead study. So this was the first release of results for the phase 3 study of the target oral peptide that blocks the IL23 receptor called ICOTRA kinra, which has something that kind of means aisle 23 in Greek. So this was all Greek for me. It was a phase three study. So I have talked before about the phase two study. I do kind of like this study, so I promise this might be maybe my last time talking about it for a while. But this is the phase three. I coach a kind of 200 milligrams once a day, which was not in the earlier phase studies, versus placebo. So primary endpoint at 16 weeks. Then patients who were on placebo did cross over to the icotra kinra. So this was adolescents and adults, but mostly adults in the study. So they actually presented week 16 and week 24 data. So these patients were kind of typical, like psoriasis clinical trial patients, BSA around 25%. About a third of them were bio experienced. So what were the top line results? PASI 90 at week 16 was 50% of patients. Interestingly at week 24 that went up to 65%. PASI 100 was 27% at week 16, but 40% at week 24. IGA 01 was 65% and then it was 74%. So kind of similar to what you saw in the phase two, but maybe a little bit, a little bit, you know, slower to get to those results. They also had scalp specific IgA, so zero or one clear, almost clear. 80% of patients who came in with scalp disease were clear, almost clear at week 24. Nothing new. Safety wise. So, you know, I think this is interesting. I think it's going to be interesting to see how this works in special sites, psoriatic arthritis, all kinds of stuff. You know, it was kind of bold to go forward with the dose that they had not looked at in phase two. But it does seem like it worked as well as bid dosing, which I think is going to be important for an oral drug.
- [03:32]
A
Do you think the results will keep getting better when we go out to 36 weeks? And at this point, what existing drug would you say it's MO if I like. Because you, I, I keep in my head like, here's how good I think. What would you think it's most at the moment? Just efficacy wise.
- [03:47]
B
Yeah. So I know we talked about the phase two data and the closest I came was cosentics, but maybe this is this data. You would say this looks like cosentics, but slower. But it's once a day oral drug.
- [03:59]
A
Yep. Okay. All right. Looks good to me. All right, Pat, go ahead. All right.
- [04:06]
C
Efficacy and safety of oral dukravacitinib in patients with cutaneous manifestations of lupus erythematosis. Results from Paisley CLE. A global Phase 2 randomized double blind placebo controlled trial data was presented by Victoria Worth. I didn't even know that there was a study in 2022 that looked at Duke or an SLE that shows you how much I'm in the literature. I'm involved. They had some skin cores in that, that study, but this study, the Paisley CLE study was specifically looking at cutaneous lupus Patients could have systemic less. Fewer than 50% of the patients did. In this particular study. Adults were randomized in a one to one to one fashion. Placebo Ducra 3mg Vid and Dukra 6mg A crossover from Placebo at week 16. So the primary endpoint was mean percent score change from the baseline in Clazy A at week 16. And for Placebo the mean percentage change was 28.4%. And for the two Duker groups it was better.47 and 50 for the 3mg and the 6mg respectively. Secondary endpoints were mean improvement from baseline and then clasi 50 and they were also better for Dukra. Clazi 70 was a post hoc analysis and that was better for the DU2 Duke groups. The classy 70 numbers were, were odd. The placebo group like 15.9% reached Clasi 70. The lower dose Dukra 3mg bid, it was 49.5. So 15.9 for placebo, 49.5 for Duke or 3mg bid. That's a huge difference. The higher dose Duker percentage was lower. It was 29.5. It was a lot. It was like 20% difference. P value was 0.273. I guess not statistically significant. So that, that 70 data was weird, but overall looks like Dukra could be a good option for CLE patients. I included a little. There was actually a review about small molecule biologics in lupus and it was like a meta analysis and Dukrit like came out on top and I mean, granted, meta analysis and all the things that go along with that. But so Duke.
- [06:24]
A
Yeah, maybe it's hard for me to get that, like Duke is a pretty effective drug, but like, if you're going to study something that's expensive, why not study the Jack inhibitor? That's going to be. But I, I get it. I guess I get it better, maybe.
- [06:40]
B
Better, more acceptable safety. I mean it does, it does make sense. It hits the interferon alpha pathway, right? So it totally makes sense for lupus. And looking at like I was at that late breaker, like the pictures are pretty impressive. Like, you know, sometimes you look at lupus studies, you're like, I guess, I guess that works. But you're like, oh, that looked better.
- [07:01]
A
I guess that's true. I have no sense of what classy 50 looks like. Right. You have a sense in your head what passy 90 looks like or easy 75. But yeah, classy. We're not used to any endpoints in meh. Okay. All right, we're going to move on to my first article. This was QY201 in adults with moderate severe atopic dermatitis. 12 week results from a dose finding phase 2 trial. So here's what was interesting. This is a JAK1 tick 2 dual inhibitor. So this seems that it would be the equivalent of giving somebody Both Sabinko and so TIC2. So. Right. Sabinko is highly JAK1 selective and obviously so tick 2 is a tick 2 inhibitor. So 200 patients 1 to 1 to 1 to 150 people in each arm. And what was impressive, this had by far the best results I've ever seen for any study. So if these results are reproducible in phase three, their highest dose, 20mg bid got over 80% of people to easy 75 in 12 weeks normal data. So like high dose rinvo gets about 70% of people there. So this is meaningfully better than high dose Rinvoak. They got about 70% of people to IGA01. Again, in Rinvoak, that number is more in the 50 to 60 range. So this would be the, if these numbers were real, it would turn out to be the most effective thing we've got. And it makes me think maybe some of my super challenging patients, maybe the key thing to do is have them on Subinko, which is a pure JAK1 inhibitor, and give them some so tic2 samples on top of it or something. But we'll see. But that was just most, most impressive data I've seen. Either you any comments?
- [08:59]
B
No, I think it's going to be interesting to see, you know, where these drugs end up and who knows, maybe that'll also work in things like lupus. I think we're just seeing the tip of the iceberg on what this combination, these combinations can do would be interesting.
- [09:12]
A
It's interesting just that we're not, we, we still haven't really seen a whole lot of progress in atopic derm efficacy from when Doopie came out. You know, it's just interesting different. It is from psoriasis.
- [09:23]
B
Yeah. And usually things work better in phase two than phase three. So we'll see how it does in phase three.
- [09:28]
A
True, true. All right, Dr. Faris, let's go on. You give us our tick two inhibitor update.
- [09:34]
B
Okay. Tick two, the molecule of the podcast. So this was. So I'm going to just quickly go through three. So first, one, efficacy and safety of ESK001, a highly selective oral tick 2 inhibitor, moderate to severe plaque psoriasis. Phase 2 results presented by Andy Blauvelt. And so basically the dose that they looked at was, you know, was 40mg bid sort of the pharmacokinetics behind that was that while. So tick two, you know, has partial inhibition of tick two activity throughout a 24 hour period. This, their, their claim is with this dose, you know, 24 hour and full inhibition of tick two, so maybe it'll work better. So what they see, Pasi 75 at week 12 was 64%. They did, they had an open label extension. So if we look at week 52 data, that PASI 75 response was 77.5% PASI 90, 61% PASI 139%. So how was that? You know, it's pretty good. If you look at to do the Matzyrus. How does it work? Like Sotic 2 Pazi 75 similar for Sotic 2 is 72%. So Sotic 2 Pazi 90 is about 45% versus for this drug, it was about 61%. Pazi 100 is not really published for Sotic 2. I think it's. I think I've seen it presented and it's sort of. I'm going to guess it's around. It's like around the 20% level. So don't quote me on that. So about double that. Pazi 100 of 39%. So, you know, kind of, kind of interesting that, you know, there's a lot of people working on tick 2 inhibitors. So there was another one. It was Invent bio from China D2570. So patients randomized at, you know, three different doses. And basically, if you look at Pazi 75 in that group, it was like up to 90% versus placebo was 12%. If you look at Pazi 100, they were 39 to 50%. Pazi 90, 70 to 77%. So also looking pretty good.
- [11:50]
A
And then finally, it's hard to understand. So if, if the idea is that the one right before this, this, the ESK drug is above the whatever threshold for 24 hours, how the hell can another drug be meaningfully more effective?
- [12:10]
B
Yeah, it's hard to know. I mean, I don't know if it's hitting. I. You know, one could argue one might be less selective, one might be more selective. You know, I think they're all allosteric inhi. But yeah, bioavailability, I mean, you know, who knows? Like, those are generally in vitro things. So. So that was kind of interesting. And then the not last one was, I know care pharma, which is also Chinese ICP488. And so they had, you know, Pazi 75 results that were like 78. Their Pazi 90s were like 35 to 50%. Pazi 100 was more like 11. So I would say this is just a little bit more like so Tick two in efficacy. So lots of, you know, development around Tick two. We'll see which one wins.
- [12:59]
A
Yeah, that's it. So it'll be an interesting race. Hopefully it's not a race to the bottom. Hopefully it's finish line.
- [13:07]
B
It's a lot of energy.
- [13:09]
A
A lot of energy, A lot of investment. Yes. All right, Dr. Patton, let's go on to the the doopie for BP. Yeah.
- [13:18]
C
Efficacy and safety of dupilumab in patients with bullous pemphigoid Results from Liberty BP Adept Phase 23 study data presented by Frederick Carr. I'm not sure if you pronounce that X. He was French. He was very French. The design of this trial was published in Advances in therapy in March 24th. And so that's kind of what I would show during the slide. It's a double blind placebo controlled 52 week study of dupy plus steroids. I think it's very important mentioned it was doopie combined with steroids dosed in a very specific and well controlled way in adults with moderate to severe bp. Primary endpoint was proportion of patients achieving sustained remission at week 36. It was a tough endpoint. Right. Patients had to be in complete remission. So no active disease at week 36. No steroids after the initial taper at week 16. No relapse once steroids were discontinued. No rescue therapy through week 36. They had to meet all of those endpoint and it was reached by 20. About 20% of patients on DUPY versus 4 on placebo. So that doesn't seem like a huge number, but I think that primary endpoint was challenging.
- [14:26]
A
Were they using any topical steroids?
- [14:28]
C
What?
- [14:29]
A
Do you know if they were using any topical steroids?
- [14:32]
C
I don't, I, I want to say it was probably not allowed, but I don't know that for sure.
- [14:39]
A
Yeah, probably not, but I couldn't, I couldn't find it anywhere I looked. Yeah, yeah, yeah.
- [14:44]
C
There were other endpoints greater than 90, improvement in BPDI, peak pruritus scores that the doopie group did better at. Cumulative prednisone dose was mentioned. It was kind of interesting. In the DUPY group it was 1678 milligrams lower over 36 weeks. That works out to 6.6 milligrams a day if I did my math right. I like it doesn't seem like that much of a difference, but maybe over 36 weeks that, that would be a huge difference. I don't know the average.
- [15:13]
B
Do you know what the average prednisone dose would was for the people who were not on it? Like how much of a reduction was that?
- [15:20]
C
Yeah, they did present that, but it wasn't in the little abstract. And I'm not one of those persons that takes a picture of every slide.
- [15:29]
A
When they put up the thing. Not a nerd like Ferris.
- [15:32]
B
I love that my camera roll is full.
- [15:35]
C
It's very, it's very odd looking. I don't know, it's dystopian to me. Everyone's.
- [15:40]
B
I Have that confidence. We're good.
- [15:43]
C
So I think doopie will help physicians manage BP patients. But you know, when you have BP patients, you're like, steroids will get this under control. We know this. How do we get them off steroids? These are old people. They have comorbidities. If 80 of the patients are still on steroids, did you really, like, kind of get you to your main goal and you know, with rituximab out there, which may allow us to do it better? I don't know. But doopie's easier to administer. Side effect profile is nice. I think more people will use it. It'll be interesting to see where Doopie fits in for the treatment of bp. I, I just, I don't know. I think it will help us manage these patients. But.
- [16:20]
A
Yeah, but people know how, like a.
- [16:23]
B
High enough dose to clear and then say, now let's taper. Or did you have to. They did do that. They didn't come to totally clear on steroids.
- [16:30]
C
Right. So six weeks of, of of corticosteroids, like at a, at a moderate dose to, to shut BP down. I can tell you from seeing a bunch of BP patients that have been managed by other dermatologists. Nobody does that. Nobody keeps their, their patients on 30 or 40 milligrams of prednisone for six weeks. That was how the study was done. And then they, they tapered it more rapid than I think what you would have done in clinical practice. But I think they had to, to see if doopie worked, you know what I mean?
- [17:00]
B
So maybe there's room for this, like with slower tapers and.
- [17:05]
A
Well, do we have any idea how doxycycline and minocycline work in bp? Like is. Because that would be the obvious combo is put them on that and doopie and it's all very safe and blah, blah.
- [17:18]
C
Inflammatory matrix, metallo protein 9 inhibition by DOCS. I mean, I don't think we know.
- [17:26]
A
Okay, fair, fair. So do you think this will be like, seeing the picture? I don't know if they had pictures of the thing or whatever, but they're going to show you the best pictures. So who, who the, who the heck knows so far, have you used much dupy off label in. In bempigoid?
- [17:40]
C
A decent amount. It's, it's plus minus. I mean, some people absolutely respond and other patients, you know, they come back and they're like, I stopped that shot. It wasn't doing anything. Like, I still have all these blisters.
- [17:54]
B
And yeah, it'll Be the OTESLA of.
- [17:57]
A
BP or maybe they'll find biomarkers. So in the urticaria space it looks like there are, it's going to be definable. Like this will be a good doopie patient. This won't. That data should be coming out pretty soon. Yeah. All right, we're going to jump onto mine which I love this idea. So three phase adaptive clinical trial to evaluate the human factors of patient LED patch testing protocol for the diagnosis of allergic contact dermatitis. So this is one of the most timely, interesting things I think I've seen somebody really try and do. So the basic idea here is they have this thing called the patient journey which is like the patient, I don't know what they're doing, answering question something and it helps individualize allergen selection. And then rather than putting like 80 or 100 or 120 patch test allergens on somebody's back, you put 20 on, on both, you know, 10 on each of their volar forearms. And then they developed a app that the patient then after they take them off in two days, two days later they do this AI deep learning visual thing to interpret the patch test spots. And so and I will tell you literally nowadays with Camp 2.0, the Contact Allergy Management Program for the Merit Contact Derm Society and AI between those two things, most patients, once they figure out what they're allergic to, can probably figure it out themselves. And this, you know, if you're just testing people to 20 allergens you could literally be like hey, put this app on your phone, you know, do the stuff for the next month, then come back. It'll tell us what to test you to. We'll put the tests on and go on your way. You don't have to come back again. It could make it so much more patient friendly. Now you're not gonna get into like occupational cases and stuff like that. But for routine patch testing this could be a really big breakthrough. And I did go back and look cause as a patch tester you always talk about, well you wanna put it on their back because that's where we developed all the allergens for. And your skin's different in different places. There have been a few studies looking at that and it not a ton, but a few, like literally two or three. And it does look like putting allergens on your volar forearms is fine, that you don't get too many false positives or false negatives. So this, this is feasible. I'm interested to see where it goes. Don't you know, I don't think it's something you go out and start doing tomorrow, but next year this could have developed to the point where we're able to do it.
- [20:35]
B
So one question from this, because I sat through this and I was like, I thought it was kind of cool for the AI aspect but like half of these patients had an allergy to propolis.
- [20:46]
A
Yeah.
- [20:46]
B
So what's up with that?
- [20:49]
A
So that was the, with propolis, which for our listeners, propolis is a component of beeswax. It's basically theoretically processed out of the beeswax and whatever comes from the pollen, that kind of stuff. But you see a ton of propolis patch test reactions. If you're patch testing full panel. And in my opinion the vast majority of them are false positives. They are real positives, meaning there is clearly a reaction on your arm and it clearly looks like allergic contact dermatitis. But I just, I, I never saw clinical relevance to it. It can be a marker for fragrance allergy in theory can be a marker for beeswax allergy. But, but I never really saw any clinical relevance to it, meaning I didn't see the people get better. But that's, you're right on the money. It's it, it. You saw a lot of positives, but I think they were not truly indicative of allergic contact dermatitis. All right, all right, let's go on to our next one. Dr. Faris.
- [21:54]
B
All right. My last one that I wanted to talk about was totally different. This was laser assisted drug delivery to treat non melanoma skin cancer. So I just thought this was cool. This was not like. And this was, you know, sometimes like you get all these pharma studies. I also like, this was sort of a single center training program where they present, they did this study and presented it so biopsy proven basal and squamous cell carcinomas that were under 2 centimeters. They had 30 cancers in 23 patients. This was not a randomized study. But what they did was they had this dual wavelength and I'm not a laser person, but not ablative laser, which I kind of know what that means. And so they treat, they did like a little pulse with the laser and 1550 and 1927 nanometers and then with a one to one and a half centimeter margin. Then they put turbinebulin, which is clay Siri on first dose in the office. Then they had them do it for four more nights at home. And then they saw them back and like re biopsied and reevaluated at 1/6 and 12 months. And so what was kind of cool was like there was a 100% response rate. These were, you know, there's their skin cancers that were lower risk. They ben shave biopsied. But they did like and they showed pictures like the cosmetic outcome looked really good. And you know, the moderator said, well you should have done, you know, laser alone, clyceri alone and then the two together. It should have been a three arm study. I totally get that. But you know, kind of an intriguing idea that maybe there are ways that we can deliver drugs into, we can do things more creatively to deliver topical agents into skin cancers, whether it's laser or injection. And I think deserves more work. And also kudos to people in training for doing clinical trials. It's not always easy. And being up there against the big pharma companies.
- [23:57]
A
Why the hell did they have to use a laser? Why couldn't they have just used or hyphricator like zap, zap, zap, zap, zap. Okay, here's some turbanabule to put on there.
- [24:07]
B
Yeah, I mean I think that the idea is that that kind of targets your, your you know, like these little, like not like little holes but not, you know, not ablative into like you get an epidermal and dermal penetration. So it sort of lets you open up and target drug into those areas. Yeah. Could, could you maybe get this another way? Like, like the little smallpox vaccine things that they used to use. Like maybe there's another way to do.
- [24:33]
C
It, but probably a bunch of that laying around.
- [24:35]
B
You got a bunch exactly.
- [24:39]
C
Measles coming back. Smallpox is probably gonna come back.
- [24:42]
B
I'm the only one old enough to have gotten vaccinated against smallpox.
- [24:45]
A
My mom said she tried so hard to get a find a doctor to give me the smallpox vaccine, but they weren't giving it anymore.
- [24:51]
B
She was actually just trying to give you smallpox.
- [24:54]
A
She could tell early on.
- [24:55]
B
Yeah, exactly.
- [24:57]
A
All right, Patton, what do you got?
- [24:59]
C
All right. Also skin cancer E PD1 directed intra tumoral immunotherapy for cutaneous carcinomas. Interim results from an ongoing study of Intacil Ph762 data presented by Mary Spellman. What is Intell Ph762? It's a proprietary compound by phyopharmaceuticals. It delivers a silencing. Is that how you say it? Silencing RNA Silence.
- [25:26]
A
Yes.
- [25:27]
C
To cells through some sort of spontaneous delivery. Which I guess is kind of a unique for SIRNA technology. The self delivering molecule enters the cell. In this case, it would be a T cell, binds to an RNA silicing complex risk R, I, S, C, which then goes and finds the messenger RNA that is going to make the cell make PD1 and it destroys that messenger RNA, so the T cells won't express PD1, so it would serve the same function as a PD1 blocker. Patients got four doses of intratumoral injection over three weeks and then underwent surgical excision two weeks later. Six patients with SEC two complete responses, two partial, one of which was like a 90% and two non responders. So for intra tumoral stuff, is this good, is this bad? I don't think we really know. Small study, one patient with metastatic melanoma had no response. So just a kind of a neat molecule, I guess. But you know, I don't think we have any big intratumoral data out of the PD1s or anything like that to see how these numbers compare.
- [26:34]
A
No, we just have.
- [26:35]
B
You have ongoing trials and there's been some like, early phase data for intralesional simiplimab for basal cell carcinoma and squamous cell. So yeah, I think that the response rate was better than this for intralesional semiplumab. But.
- [26:54]
A
And we got that TVEC and then tumor TVEC stuff coming. Yep, that's, that's. But yeah, I got a little stuck on one of the slides. I was reading it and I was like. Because it shows the two strands of DNA and then it's. One is the guide strand and I'm saying guide, I've never seen what squid. And then turns out it's just the guide strand.
- [27:16]
B
Yeah. And it's rna, but.
- [27:17]
A
Yeah. Okay, moving on to our last two here.
- [27:25]
C
It's, it's getting late in the, in the podcast.
- [27:29]
A
All right, so initial results from the SIGNAL AA study, randomized placebo controlled phase 2, a trial of ichabart.
- [27:42]
C
You got it.
- [27:42]
A
Novel IL7TSLP, bifunctional receptor antagonist in patients with severe various, severe alopecia areata. So basically this is a monoclonal antibody that blocks. That binds to one thing, but kind of like stelara blinds to one thing, but blocks two. This binds to one thing but blocks both IL7 and TSLP. And basically it turns off autoimmune T cells without having much effect on normal T cells is the basic idea. So it does seem to have some element of blocking response to a totally new antigen, but it doesn't really immunosuppress you. You don't see people getting opportunistic infections. This is a very small study, 44 patients, kind of a proof of concept in the salt 20 scores were not great. But I can tell you that as an investigator it was really hard to enroll this trial because the JAKS had just come out. So everybody with alopecia areata was going on jacks and what was really shocking was that they had a number of patients who continued to regrow, get better and better for six months after the end of the study. So this could be our first biologic for alopecia areata. And it could be something that really has a long term effect of turning around this autoimmune process. So it's an interesting new mechanism of action. They're going to be pursuing it a number of other things including vitiligo. So Right. Two diseases we don't really have any biologics in yet, but just an interesting. The long term effect was what was coolest. And then the other study, similarly a very. The long term. This is what's important here. So this is rokatinlumab. This is an Amgen molecule. And so rocatinlumab significantly improved clinical signs and symptoms by targeting OX40 receptor positive T cells in patients with moderate severe atopic dermatitis. Results from the phase three Rocket Horizon trial. And so this is a monoclonal antibody that targets the OX40 receptor and blocks OX40 and OX40 ligand from CO. Stimulating each other reduces memory T cell populations. This was basically a normal atopic DE study except the end point was 24 weeks instead of the usual 12 or 16. And the results were not like mind blowing. So easy. 75 they got about 33% of people at week 24. IJ01 versus placebo got 13% IG01, they got 19.3% versus 6.6 for placebo. Got to tell you, my experience on the trials, I thought the drug worked better than this in the trial. So. But the big takeaway is it had not plateaued at 24 weeks and there are because of its depleting memory T cells. There is real belief that this could be long term disease modifying where you take this for six months or a year and then you're able to be off therapy for long periods of time, perhaps indefinitely. So that's kind of the interesting thing. The other cool thing with this drug or interesting thing, small number of patients, when I say small, maybe 20% will get fevers and chills after the first dose. And it's pretty impressive. Like whenever they come back in and tell you about it. They're like curled up in bed, like shaking and sweating, which I'm, I'm wondering if that's a marker for efficacy, if those people, you know, have a better outcome. But nobody's cut the data that way yet. But. So that's just an interesting new pathway that will be on the, that's on the horizon. Free topic derby term. And again, the main benefit doesn't seem to be rapid efficacy. It seems to be potential for long term remission. Is the, is the big takeaway. I don't either of you have any comments on either of these.
- [31:43]
B
I, I think that's, I, I thought the, the pickup art or however you say it study was super interesting and it's tslp. So you could imagine like it's maybe not just atopic or, you know, that could work in. Atopic derm. That could work in, you know, it's interesting for the safety look good. And you know, again, like we talked about Jackson and aa, like six months is still kind of an early endpoint. Right.
- [32:08]
A
So, yeah, no, I agree. And this. And you're right. So this has both. Because IL7 is more in the TH1E pathway. So this has got kind of a TH1 and TH2 slant to it. And so it really is broad what it could work in. I think they're going after some pulmonary indications as well. Maybe eosinophilic esophagitis, that kind of stuff.
- [32:30]
B
Maybe bp.
- [32:32]
A
Maybe bp. Maybe we'll finally get something.
- [32:34]
B
All right.
- [32:35]
A
All right. Well, that sums it up for the late breakers that we here at Derms on Drugs thought were the most interesting this year at the aad. So thank you for joining us. If you've got questions, comments, ideas for topics we should cover on the show, shoot us an email. Questionsourmsondrugs.com Again, questionsrmsondrugs.com and we hope you learned a few things. We hope to laugh once or twice and mostly we're hoping you're planning to join us next week. Until then, I'm Matt Zyrus.
- [33:06]
C
I'm Tim Patton.
- [33:08]
B
I'm Laura Farris. And we are Derms on drug.