Latest / The Science of Skin / Rhapsido (Remibrutinib) for Chronic Spontaneous Urticaria: Phase 3 Efficacy Data

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Rhapsido (Remibrutinib) for Chronic Spontaneous Urticaria: Phase 3 Efficacy Data · The Science of Skin

• 0:00
  SPEAKER_00: This episode is sponsored by Novartist with content independently created by the Science of Skin Podcast.
• 0:14
  SPEAKER_01: Hello and welcome to the Science of Skin Podcast.
• 0:16
  SPEAKER_01: My name is Dr.
• 0:17
  SPEAKER_01: Ted Lane.
• 0:18
  SPEAKER_01: I am a board-certified dermatologist practicing in Austin, Texas.
• 0:22
  SPEAKER_01: And my very special guest today is Dr.
• 0:24
  SPEAKER_01: Naeem Isa.
• 0:25
  SPEAKER_01: Dr.
• 0:25
  SPEAKER_01: Issa, hi, is a dermatologist practicing in Northern Virginia.
• 0:30
  SPEAKER_01: He is also on faculty as an assistant professor at both the University of Miami and George Washington University in their departments of dermatology.
• 0:40
  SPEAKER_01: Dr.
• 0:40
  SPEAKER_01: Issa is here to discuss the clinical efficacy of Remy Brutinib or Rhapsode, as today's episode is sponsored by Novartis.
• 0:48
  SPEAKER_01: Dr.
• 0:49
  SPEAKER_01: Issa, how are you doing?
• 0:50
  SPEAKER_01: Hey Ted, all is well.
• 0:52
  SPEAKER_01: Thanks for having me.
• 0:53
  SPEAKER_02: I'm excited to discuss tonight.
• 0:54
  SPEAKER_01: Oh man, we're we're so lucky to have you, Dr.
• 0:57
  SPEAKER_01: Issa.
• 0:57
  SPEAKER_01: Thank you so much for giving us some time.
• 1:00
  SPEAKER_01: As I mentioned, we are going to discuss Rhapsodo or Remy Brutinib.
• 1:04
  SPEAKER_01: And I, you know, I don't think we've ever talked about this.
• 1:06
  SPEAKER_01: Were you involved in the clinical trials at all for this one?
• 1:09
  SPEAKER_02: Unfortunately, I was not, but it was great to see it come through on the other end.
• 1:14
  SPEAKER_01: Yeah, yeah.
• 1:14
  SPEAKER_01: I mean, there's so much going on in the chronic spontaneous chronic spontaneous urticaria space.
• 1:20
  SPEAKER_01: We can't all do every trial, but it's like you said, just to get the readout of the data was amazing to see kind of this first oral targeted therapy for CSU.
• 1:33
  SPEAKER_01: What just high level, Naeem?
• 1:35
  SPEAKER_01: What would you tell people as your thoughts on this data?
• 1:38
  SPEAKER_02: I think, you know, first and foremost, before we even jump into the data, just briefly understanding like the different tiers of where you can affect the mast cell.
• 1:47
  SPEAKER_02: Because once you understand that, then the data just makes sense.
• 1:49
  SPEAKER_02: You know, it's very logical, right?
• 1:51
  SPEAKER_02: So the mast cell fires, you know, with its histamine and uh other non-histaminergic kind of pro-inflammatory mediators, that's an endpoint when the mast cell degranulates in CSU, right?
• 2:00
  SPEAKER_02: So you can block things there.
• 2:01
  SPEAKER_02: That's typically what we've done for such a long time.
• 2:04
  SPEAKER_02: But then you can block things that are external to the mast cell, all the signaling stuff that kind of binds in, such as your immunoglobulins, IgE, IgG, so on and so forth.
• 2:12
  SPEAKER_02: You can block there.
• 2:14
  SPEAKER_02: But there's also a myriad of ways that you know cells are responding, the mast cells are responding, right?
• 2:19
  SPEAKER_02: Then you have the internal component, right?
• 2:21
  SPEAKER_02: That's where you have the the way switch, right?
• 2:23
  SPEAKER_02: And that's bruton tyrosine kinase, right?
• 2:25
  SPEAKER_02: So it takes the signals from the outside, brings it to the inside, then takes it to the granules.
• 2:28
  SPEAKER_02: So these are the three major areas.
• 2:30
  SPEAKER_02: When it comes to Rhapsodo, we are looking at that internal wastation, which is blockade of bruton tyrosine kinase, is the first in class in dermatology here.
• 2:38
  SPEAKER_02: So that is very exciting in of itself, right?
• 2:41
  SPEAKER_02: And so being a small molecule, it gets into the cell very quickly once it is absorbed, you know, from the gut.
• 2:46
  SPEAKER_02: And then once it's in there, it attaches with high binding affinity and specificity.
• 2:50
  SPEAKER_02: So that way it latches on real fast, very tight, right?
• 2:53
  SPEAKER_02: It's actually non-reversible.
• 2:54
  SPEAKER_02: It's a covalent binder.
• 2:55
  SPEAKER_02: So once it comes in, it sticks on, right, until the protein is recycled.
• 3:00
  SPEAKER_02: And that's actually kind of important and really kind of shows why Rhapsodel works as well as it does.
• 3:04
  SPEAKER_02: So that gives you deep efficacy, and we'll see that you know, with the results and looking at that herdary activity scores, as well as the speed of onset of that relief as well.
• 3:14
  SPEAKER_02: So the form fits the function, right?
• 3:16
  SPEAKER_02: Once you understand that, the rest of the data makes sense.
• 3:18
  SPEAKER_01: Yeah, thanks for going through that, um, Naeem.
• 3:21
  SPEAKER_01: I yeah, it's it's highly covalently bound to the uh the receptor, as you mentioned, inside the cells.
• 3:28
  SPEAKER_01: So this is a small molecule targeting the intracellular space.
• 3:32
  SPEAKER_01: And because it is so targeted to the BTK that we're talking about, as we know, there's lots of different sinus tyrosine kinases.
• 3:39
  SPEAKER_01: We had um Dr.
• 3:40
  SPEAKER_01: Jason Hawks on a previous episode where we talked about the mechanism of action of this BTK inhibitor and why we're getting such great efficacy with such beneficial safety.
• 3:52
  SPEAKER_01: Uh and some of the safety uh adverse events that did pop up make sense given the mechanism of action of this drug.
• 3:59
  SPEAKER_01: So we've we've we've spent quite a bit of time, but it's always great to have a review of it.
• 4:04
  SPEAKER_01: Uh and now let's uh, if you don't mind, let's just jump into that efficacy though.
• 4:08
  SPEAKER_01: And and you know, we've already kind of spilled the beans a little bit.
• 4:11
  SPEAKER_01: It is highly effective as this new singular oral therapy.
• 4:16
  SPEAKER_01: What really stuck out in your mind?
• 4:19
  SPEAKER_02: So the the beauty of the uh trial endpoints here.
• 4:23
  SPEAKER_02: So first and foremost, you know, patients who are on uh you know oral antihistamines, you know, first generation H1 antihistamines, who are non-responders after two to four weeks and they were put on either placebo or onto Rhapsodo.
• 4:34
  SPEAKER_02: So very nicely you see a concordance with looking at hives count, they call it the hive severity score, the itch severity score, which is a different endpoint, and then the combination of the two, right?
• 4:46
  SPEAKER_02: So when you look at the UAS uh score, your urticary activity score.
• 4:50
  SPEAKER_02: And you find that for all three metrics, you have a quick reduction within just the first week.
• 4:55
  SPEAKER_02: You have that change from baseline from whatever the scores that they they came from, to be pragmatically speaking.
• 5:00
  SPEAKER_02: So it jumped, well, rather it went down, not jumped, it went down pretty quickly, and then it continued on within uh the first couple of weeks up to the primary endpoint, which is week 12.
• 5:10
  SPEAKER_02: So the hives count went down and stayed down, the itch count went down and stayed down, and the combinatorial or combination of the two went down and stayed down.
• 5:18
  SPEAKER_02: And that's you know, again, through the logic, it made sense that that happened, and it's nice to see that in humans that actually did happen, and it is uh predictable, right?
• 5:27
  SPEAKER_02: And uh uh and uh continuous after that.
• 5:30
  SPEAKER_02: So the speed was really what I was mind blown by.
• 5:33
  SPEAKER_01: Yeah, and let me just spend a little bit of time talking about these endpoints.
• 5:36
  SPEAKER_01: So, what Dr.
• 5:37
  SPEAKER_01: Issa is referring to are are two endpoints.
• 5:40
  SPEAKER_01: One is called the hives severity score, the other one is called the itch severity score.
• 5:45
  SPEAKER_01: So the hive severity score, HSS, its full name is HSS seven, okay?
• 5:51
  SPEAKER_01: And it's because we we average the daily scores over seven days.
• 5:56
  SPEAKER_01: And when we're looking at the HSS seven, we we grade the severity of the hives.
• 6:02
  SPEAKER_01: Zero means no hives every 12 hours.
• 6:05
  SPEAKER_01: Okay.
• 6:05
  SPEAKER_01: One means they can you the patient has between one and six hives every 12 hours, two is seven to twelve hives, and then three, the most severe, is greater than twelve hives.
• 6:17
  SPEAKER_01: And then the itch severity score or ISS seven, um, which was a co-primary endpoint with the HSS seven, included no itch, which would be zero, and then three itch, which would be severe or difficult to tolerate.
• 6:30
  SPEAKER_01: In between, we've got mild, which of course is minimal awareness easily tolerated, and then moderate, which is definite and bothersome.
• 6:37
  SPEAKER_01: So when you add the daily scores or the mean of the daily scores together, that composite endpoint is called the urticarial activity score or UAS7.
• 6:51
  SPEAKER_01: And just it you get from well-controlled, so complete absence, so zero, well-controlled is between one and six, mild seven to fifteen, moderate 16 to 27, then above 28 is severe urticaria.
• 7:06
  SPEAKER_01: And of course, it's just a simple sum of the HSS seven and the ISS seven.
• 7:11
  SPEAKER_01: Okay.
• 7:11
  SPEAKER_01: Uh, and and those are scored over uh over the 20 over the seven days, and the max score is three per day.
• 7:19
  SPEAKER_01: And so you can imagine uh that the max uh HSS seven, therefore, is 21, the max ISS seven is 21 as well.
• 7:28
  SPEAKER_01: So those are the two co-primary endpoints, which are the HSS 7 and ISS 7, and then the UAS 7 was considered a secondary endpoint.
• 7:37
  SPEAKER_01: So now that I've thoroughly confused everybody with all of those acronyms, let's go into um Naeem.
• 7:44
  SPEAKER_01: Let's just talk about the baseline characteristics because I think it's important for us to really elucidate the type of patient that were that were in these trials.
• 7:53
  SPEAKER_01: They certainly weren't cherry-pick the easiest ones, did they?
• 7:57
  SPEAKER_01: That's correct.
• 7:58
  SPEAKER_02: So, you know, going to what you said about that combined urticary activity score, UAS 7, right?
• 8:04
  SPEAKER_02: We have the different categories.
• 8:06
  SPEAKER_02: When we look at the demographics table of who was actually included, the average UAS 7 score was hovering around 30, right?
• 8:12
  SPEAKER_02: That automatically puts them into that severe disease category, right?
• 8:17
  SPEAKER_02: So on average, these are CSU patients who have battling the disease for a number of years, actually, on average five years, who had this high burden of disease.
• 8:24
  SPEAKER_02: And on top of that, about half of those patients also had angioedema, which is another related problem in its own right, right, which is that dermal swelling in the lips and so on and so forth.
• 8:35
  SPEAKER_02: And to further layer in one more level, is that about a third of these patients were also having prior exposure to anti-IgE molecules, and these included omalismab and legalismab as well.
• 8:48
  SPEAKER_02: So this is important.
• 8:48
  SPEAKER_02: So we have these suffering patients, right, who were on previous treatments for a third of the time, and these previous treatments can possibly alter the immunology.
• 8:58
  SPEAKER_02: So the goal here was not to cherry pick patients, but to say, can Rhapsodo be used basically for all comers?
• 9:04
  SPEAKER_01: Naeem, thanks for bringing up all the additional baseline demographics and characteristics of the subjects in the trial.
• 9:11
  SPEAKER_01: As you mentioned, more than half had angioedema, um, which is part of chronic spontaneous certicaria.
• 9:17
  SPEAKER_01: But, you know, and you mentioned others had been on anti-IgE biologics.
• 9:20
  SPEAKER_01: And you would think if that had worked, they would have stayed on them.
• 9:24
  SPEAKER_01: So maybe they were uh either not working appropriately or it's in some way failures, or excuse me, for some reason they had to stop their anti-IgE biologics.
• 9:34
  SPEAKER_01: But, you know, we could be really talking about a more resistant population.
• 9:39
  SPEAKER_01: The UAS-7 was severe.
• 9:40
  SPEAKER_01: And severity in any disease I think of as probably more resistant to treatment.
• 9:45
  SPEAKER_01: And then the fact that so many, a third of these patients had been on anti-IgE biologics, never mind the fact that the duration of chronic spontaneous certicaria in these subjects was on average about six to seven years.
• 9:58
  SPEAKER_01: So they had definitely had to deal with this for a long time, a severe patient population that had tried different therapies in the past.
• 10:05
  SPEAKER_01: So I guess the reason I bring this up, Naeem, I don't know how you how you translate this, but whenever I look at this, I think, okay, this is probably not the average patient coming into my clinic, but it's really good to know that it works on these severe patients.
• 10:19
  SPEAKER_02: Right, absolutely.
• 10:20
  SPEAKER_02: But on top of that, right, we think about you know these numbers as averages, right?
• 10:24
  SPEAKER_02: And then we have standard deviations.
• 10:27
  SPEAKER_02: So, yes, so these are severe populations, but let us not forget that we can also use Rhapsodo for your typical CSU patient as well.
• 10:37
  SPEAKER_02: And I find that because as we go on in medicine, let alone dermatology, with every subsequent clinical trial, you know, the the goalpost kind of changes necessarily because there were prior trials before the current one, right?
• 10:50
  SPEAKER_02: So necessarily it's hard to recruit.
• 10:52
  SPEAKER_02: So we get tougher patients who may not have responded to other things.
• 10:55
  SPEAKER_02: So that's gonna be a general bias.
• 10:57
  SPEAKER_02: So I urge you know our colleagues, you know, and ourselves to always remember that we can use it, you know, in this case, Rapsidone First Line for your typical CSU, as well as those patients who are truly suffering.
• 11:08
  SPEAKER_02: So I think it's a great way of uh of keeping perspective.
• 11:11
  SPEAKER_01: Yeah, it's a great point regarding kind of the increase in severity as as more and more drugs are available.
• 11:18
  SPEAKER_01: The patients that tend to be in the additional future clinical trials tend to be the hardest ones to treat.
• 11:24
  SPEAKER_01: You could see this if you look at the Atanerecept trial population versus you know the latest uh biologic trial population, they're gonna be very different.
• 11:33
  SPEAKER_01: Um, and so I I certainly appreciate that take.
• 11:36
  SPEAKER_00: This episode is sponsored by Navartis with content independently created by the Science of Skin podcast.
• 11:42
  SPEAKER_01: Let's go into kind of one of the primary endpoints, like one of the co-primary endpoints, the fast relief from hives.
• 11:48
  SPEAKER_01: And and why don't you just kind of walk us through that?
• 11:53
  SPEAKER_02: Right.
• 11:53
  SPEAKER_02: So when we're looking at the fast relief from hives, or specifically the high severity score seven, as you mentioned before, as one of those endpoints, you can see that uh, well, you can't actually the audience can't see, to be honest, but I'm looking up the graph myself.
• 12:07
  SPEAKER_02: But the the the the concept is that uh you have that that quick relief within the first week, you have that number uh decreasing, right?
• 12:14
  SPEAKER_02: So you have the the mean, it's called the the the change from baseline or CFB, and you're looking at the average number you know decreasing, and you can see that compared to placebo, that there is that sharp decrease very early in the first week, and then that kind of continues within the the the remaining couple of weeks up to week 12, which is the co-primary endpoint uh time period, and it stays on after that.
• 12:33
  SPEAKER_02: So you have a reduction in that hive score, very pertinent because the patient sees less and is experiencing less visible hives.
• 12:42
  SPEAKER_01: Yeah, uh I mean uh 40% reduction as early as week one.
• 12:47
  SPEAKER_01: And and anytime I see that kind of reduction, that kind of speed of onset, I should say, it's just it makes me think, okay, patients will stay compliant with this.
• 12:56
  SPEAKER_01: This is a BID drug, and so which is, you know, in and of itself adds some difficulty for compliance.
• 13:02
  SPEAKER_01: But the fact that it works so quickly is really important.
• 13:06
  SPEAKER_01: And and let's hearken back to that what patients had to fail essentially or not get controlled on in order to be in the trial.
• 13:13
  SPEAKER_01: As you meant then, as you mentioned, they had to be on second generation non-sedating antihistamines, think like Claritin, Allegra, Zertex, Isol.
• 13:20
  SPEAKER_01: And they could be on them up to four times the listed dose.
• 13:23
  SPEAKER_01: So instead of one pill per day, they could take four pills per day.
• 13:26
  SPEAKER_01: And those patients in the placebo group were also on up to four pills per day of an antihistamine.
• 13:33
  SPEAKER_01: So we talk about placebo, but it's actually in some way they they were on treatment as well.
• 13:37
  SPEAKER_01: And these patients still did not have their hives controlled.
• 13:40
  SPEAKER_01: In fact, they were severe in terms of their UAS seven.
• 13:43
  SPEAKER_01: So to these patients were looking for really, they were taking so many pills already, and then to add one twice a day that 40% reduction as early as week one, 70% at week 12, 74% at week 24.
• 13:56
  SPEAKER_01: And when we look at the long-term extension, you know, we see 77% at week 52.
• 14:02
  SPEAKER_01: Not only is it incredibly fast onset, but the but the sustained durable results is incredible over 52 weeks.
• 14:09
  SPEAKER_01: I just for for our hive patients, this is just really awesome.
• 14:14
  SPEAKER_02: Absolutely.
• 14:15
  SPEAKER_02: And it's a testament to the target that was chosen.
• 14:19
  SPEAKER_02: This is truly where biology meets the clinic, and BTK is one of those solutions, right?
• 14:23
  SPEAKER_02: Especially for CSU.
• 14:24
  SPEAKER_02: And we see that here.
• 14:26
  SPEAKER_01: Now, when we look at the next co-primary endpoint, that is the ISS seven, that reduction in itch.
• 14:32
  SPEAKER_01: And probably even more important than the number of hives is the fact because itch is such a huge impact on the quality of life.
• 14:40
  SPEAKER_01: And we see pretty darn similar results from the between ISS seven and HSS seven, right?
• 14:48
  SPEAKER_02: Yes, absolutely.
• 14:49
  SPEAKER_02: And you know, it's actually kind of remarkable to see that the numbers are truly very similar to each other.
• 14:54
  SPEAKER_02: We have here 36% within the first week having that fast relief from their itch, which is very close to 40%, which well is which is what we saw for the high severity score reduction at week one.
• 15:03
  SPEAKER_02: And then similarly at week 12, we have approximately 67%, which is close to 70%, you know, in the in the highs reduction.
• 15:10
  SPEAKER_02: So we see the same pattern here for reduction in itch, which pertains to quality of life, as well as compliance here, as and on top of that, that is aligned with the high score.
• 15:19
  SPEAKER_02: So it's really nice to see the two in parallel.
• 15:21
  SPEAKER_01: Yeah, and just to reiterate, over half of the improvement that we see at week 24 occurred in the first week.
• 15:27
  SPEAKER_01: So it it you know, patients get started and they see improvement so quickly.
• 15:32
  SPEAKER_01: And of course, because UAS 7 is essentially the sum of ISS 7 and HSS 7, we should see some really nice results in UAS 7, and we absolutely do.
• 15:43
  SPEAKER_01: And and all three of these endpoints tend to mirror each other, which with about a 40% reduction and s in the change from baseline at week one, 70% at week 12, 73% at week 24, and it continues to improve through week 52.
• 15:57
  SPEAKER_01: So I, you know, this incredible data for for, you know, we didn't have anything for it besides the uh anti-IgE therapy.
• 16:07
  SPEAKER_01: We haven't had certainly no oral medication uh besides antihistamines.
• 16:11
  SPEAKER_01: And so to get an oral medication that has this kind of fast onset was really astounding.
• 16:17
  SPEAKER_01: It just kind of raises the bar of all future CSU treatments um for patients and for practitioners.
• 16:25
  SPEAKER_01: And so we're going to demand more now from future treatments.
• 16:29
  SPEAKER_01: It makes it more difficult, doesn't it?
• 16:33
  SPEAKER_02: It certainly does, you know, and again, uh it's it's a it's a remarkable feat, you know, that the biology is matching the clinic here, and you know, it just keeps us excited that uh we have now an option, which is Rhapsody, to give you that uh assurance, if you will, early on.
• 16:45
  SPEAKER_02: And that makes patients very happy, right?
• 16:47
  SPEAKER_02: And you give them hope, especially when they've been suffering for so long.
• 16:51
  SPEAKER_01: We we know from other inflammatory diseases uh in dermatology that that complete control, like for example, a PASI of 100 um for psoriasis is actually meaningful for patients versus a PASI of 99, where they may have a little bit of psoriasis on their body.
• 17:08
  SPEAKER_01: And so I would imagine the same is true for our urticaria patients, where we have you know the urticaryal activity score of zero being really important for patients versus a UAS 7 of 1, for example.
• 17:21
  SPEAKER_01: And and Naeem, could you just walk us through the UAS 7-0 data uh from one of the two pivotal trials?
• 17:29
  SPEAKER_02: Right.
• 17:30
  SPEAKER_02: Absolutely.
• 17:30
  SPEAKER_02: And what you said the this difference between let's say the POSI 90 versus a POSI 100, in this case UAS 7 of 0, which is complete absence of hives and itch, that is truly a deep and very uh patient-friendly and patient-oriented endpoint, right?
• 17:45
  SPEAKER_02: Having no hives and no itch, right?
• 17:47
  SPEAKER_02: So at that deep endpoint.
• 17:48
  SPEAKER_02: So, how did that data look like?
• 17:49
  SPEAKER_02: So at week 12, right, we see that the Rhapsody patient group, about a third of them, around 27.9%, were able to achieve that deep and complete absence of hives and itch, right?
• 18:01
  SPEAKER_02: That's just within the first three months, with the placebo group being 6.5%.
• 18:05
  SPEAKER_02: So that's a huge delta.
• 18:06
  SPEAKER_02: And then if you wanted to extend it further to the long-term extension over 52 weeks, right, and for that endpoint, the rhapsido patients had about 45.9%.
• 18:16
  SPEAKER_02: So let's put that into context, right?
• 18:18
  SPEAKER_02: So you have these suffering patients, right, and you want to get them that complete relief, right?
• 18:22
  SPEAKER_02: That UAS7 equal to zero.
• 18:24
  SPEAKER_02: Over the course of the year, right, by the end of one year of treatment with rhapsido, half of those patients are going to have that complete relief.
• 18:32
  SPEAKER_02: That is a new standard, I think.
• 18:34
  SPEAKER_01: You know, I mentioned that this was one of the two pivotal trials.
• 18:38
  SPEAKER_01: Both of them had very similar results.
• 18:40
  SPEAKER_01: So, you know, what, four times or even more patients at week 12 had a UAS 7 of zero as compared to placebo, and as you mentioned, extended out to almost 46% at week 52.
• 18:53
  SPEAKER_01: So there is an opportunity here for these, and again, in this trial, severe patients, uh, to get to the point where they have no hives.
• 19:03
  SPEAKER_01: And and remember, these patients were experiencing maybe even 20 or more hives every 12 hours.
• 19:09
  SPEAKER_01: Uh, so to go from that absolute misery with an itch severity score that was high as well, uh, to get from that to get to a UAS 7 of zero is is a complete control of uh uh chronic spontaneous urticaria.
• 19:26
  SPEAKER_01: That is just kind of mind-blowing uh to me that we could see uh 28% at week 12 and 46% at week 52, especially in this patient population.
• 19:37
  SPEAKER_01: And then when we look at uh angioedema, which I don't know Naeem, you don't have to say if you've ever experienced it, but I unfortunately I have.
• 19:45
  SPEAKER_01: And angioedema is no fun, especially when it's on your face, um, especially when you're a kid.
• 19:51
  SPEAKER_01: Uh and and we had some uh you know similar results in angioedema, right?
• 19:56
  SPEAKER_01: What was it, 46% of patients um had primary had prior angioedema uh in one of the the trials, and in terms of the cumulative number of angioedema free weeks, it was over, it was almost nine weeks out of the 12 versus uh less than seven weeks in placebo.
• 20:17
  SPEAKER_01: So not only are we taking care of the hives and the itch, but we're also taking care of the some of the soft tissue swelling that we see with angioedema, um, which we do see as part of CSU as well.
• 20:29
  SPEAKER_01: In terms of the definition of CSU, angioedema is there.
• 20:32
  SPEAKER_01: So um it doesn't matter what we're talking about, does it?
• 20:35
  SPEAKER_01: Whether itch, hives, angioedema, uh composite endpoints, we see some very, as you mentioned, Naeem, very deep results that that look like they last for a long time.
• 20:46
  SPEAKER_01: Now, in terms of safety, everybody, we we have uh another podcast that reviews the safety.
• 20:52
  SPEAKER_01: The the uh primary goal of this podcast tour was to do an overview of the efficacy in the phase three clinical trials, which I think we have we you know, Dr.
• 21:02
  SPEAKER_01: Issa has done a wonderful job at at contextualizing that and making sure everyone understands, you know, the kind of patients that we had, the deep results that we saw early, and over the long-term extension through week 52, which of course was not placebo controlled, uh, but we do see some really nice results there.
• 21:20
  SPEAKER_01: Uh Naeem, any any final thoughts here as as we kind of wrap up the these efficacy results with the nice bow?
• 21:29
  SPEAKER_02: So I'll leave our audience with one additional thought.
• 21:32
  SPEAKER_02: While we this evening we've talked about the pivotal trial data, for those who are very astute learners and are excited to see have we gone beyond?
• 21:41
  SPEAKER_02: The answer is actually yes.
• 21:42
  SPEAKER_02: There is some new data that has been pumped out uh in in conjunction with our allergy friends.
• 21:48
  SPEAKER_02: Uh, when we have some posters that came out in the allergy conferences and soon in the dermatology conferences, where we are looking at even uh shorter time frames to see just how fast Rhapsodel works.
• 22:00
  SPEAKER_02: And I think a lot of us can predict that it worked pretty darn fast.
• 22:03
  SPEAKER_02: And I would say look for those data in the near future.
• 22:06
  SPEAKER_01: Thank you for that.
• 22:07
  SPEAKER_01: Absolutely.
• 22:07
  SPEAKER_01: When you see that kind of result at week one, you're you gotta be thinking, gosh, maybe as early as day one, we're seeing some significant results for patients.
• 22:15
  SPEAKER_01: So um, yeah, that was my thought process.
• 22:18
  SPEAKER_01: And and I'm I'm happy to hear that some of that data is being published.
• 22:21
  SPEAKER_01: So uh everyone, thank you uh so much for listening.
• 22:23
  SPEAKER_01: My name is Dr.
• 22:24
  SPEAKER_01: Ted Lane.
• 22:25
  SPEAKER_01: I've been your host for today, along with uh my esteemed colleague, Dr.
• 22:28
  SPEAKER_01: Naimisa, who is a board-certified dermatologist practicing in northern Virginia.
• 22:33
  SPEAKER_01: Um, everybody, if you enjoyed this podcast, if you like the material that we presented, please give us a five-star rating.
• 22:38
  SPEAKER_01: Um, subscribe.
• 22:39
  SPEAKER_01: And we found that the growth of our podcast really occurs because of word of mouth.
• 22:43
  SPEAKER_01: So if you don't mind telling your colleagues about what we're trying to do here, we're really trying to keep you at the cutting edge of dermatology, whether it's skincare, medical, or aesthetic, we're trying to be right there.
• 22:52
  SPEAKER_01: So uh thank you so much for listening, Dr.
• 22:54
  SPEAKER_01: Issa.
• 22:55
  SPEAKER_01: As always, um, I appreciate you sharing your wonderful knowledge.
• 22:58
  SPEAKER_01: Thank you.
• 22:58
  SPEAKER_02: Thanks for having me.
• 23:00
  SPEAKER_01: Yeah, thank you.
• 23:00
  SPEAKER_01: And for Naimisa, my name is Dr.
• 23:02
  SPEAKER_01: Ted Lane.
• 23:03
  SPEAKER_01: Thank you so much for listening.