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This is an ACR twenty twenty five podcast coming to you from Chicago. Hope you enjoy it.

Hello, everyone. My name is Youssef. I'm a consultant rheumatologist from Leeds. I'm reporting live for RheumNow at Chicago for the ACR twenty twenty five conference. Today I'm delighted to be by my colleague who is a worldwide expert in lupus, Professor Edward Vital, where we will describe about his abstract number fifteen twenty six.

Hello Ed. Hi. So first and foremost, would you please highlight to us about the objective of these guidelines and how the guideline was developed?

There have been a lot of guidelines recently for SLA and all of them consistently say that steroid doses should be lowered, shouldn't be used long term and doses should be tapered as quickly as possible. The problem is that although guidelines have said that for a long time and with good reasons, because steroids are associated with damage, in practice that doesn't always happen. Managing the lupus is quite complicated, it's difficult for the doctors and patients, and in reality steroids are not tapered in the way that guidelines say. We did a review article that showed that. The purpose of our project was to come up with a set of consensus statements and also most importantly steroid tapering protocols to try and improve adherence to good practice.

And is this like an internet expert opinion or evidence based consensus? It's expert opinion.

So we had a group of over 120 experts from across different specialties involved in the management of patients with SLA and trying to represent most areas of the world. We started with a steering committee drafted list of potential statements also of potential steroid For example, for a mild flare, start at this dose, taper down over three weeks. For a moderate flare, start at a higher dose, taper slowly. For a more severe flare, we actually took some published protocols for lupus nephritis. And then there was also a protocol for a patient who's been on long term low dose steroids and wants to get off it.

There were some other statements about other aspects of steroid use. So like a usual Delphi process, there were a couple of iterations of voting. So in the first vote, some statements were just accepted, some statements were clearly rejected, others could be refined and nuanced into repeat rounds until we got the best consensus we thought we could achieve.

So I think, out of all the, like, the statements that are there, I mean, obviously, we can't describe it all. Would you please just highlight maybe, like, two key points or statements in in the guidelines? I mean I think

really to me the core of it is to say have a plan. One of the statements is that whenever glucocorticoids are being initiated there should be a plan for how it's will be to zero. In reality, what people will often do is say start on twenty milligrams of prednisolone, come and see me in two weeks, we'll see what happens. Or maybe give some reduction plan but when the patient comes back they didn't do exactly what you expected. So our idea is if you just have a table with the dosage should be on date on certain dates it will work better especially if they're seeing different doctors.

Maybe you'll have to change from it. Maybe it'll be too fast. Maybe it'll too slow. You might deviate, but

just have a plan. And

and lastly, now that this is now established, which what we're all waiting for, I'm just wondering whether in term of dissemination, so apart from, you know, showing showcast in this conference, anything else that, you know, you and your steering committee would do so that people will, you know, uptake, you know, the guidelines?

Very good question. That's exactly what we're working on over the next year will be. I don't know exactly what they'll be yet but our plan is to develop a set of tools to help use that in the clinic whether that's simple tables, tools to work out the doses, handouts for patients, apps, there's a variety of possibilities. There's no point writing guidelines if they're not followed.

Thank you so much Ed for summarizing your work and on behalf of your committee. I hope you find the discussion interesting and hopefully you can see the protocol itself when it will come out and be published formally. In the meantime, follow me at Twitter Youssef and also other faculties at RheumNow for more content coverage. Thank you everyone.

Thank you.

Hi everybody. Mike Putman from the Medical College of Wisconsin reporting to you from ACR Convergence twenty twenty five. And today I'm here to talk about abstract eight ninety one. This is methotrexate versus tocilizumab for the treatment of giant cell arteritis, also known as the METOGIA trial. Now this is a trial that I've been waiting for for some time.

Very important clinical question. It is a open label randomized controlled trial from the French Vasculitis Study Group that pitted methotrexate against tocilizumab for patients with giant cell arteritis. Now, this is an interesting question because we have established that tocilizumab is a standard of care, had great evidence against placebo, but there's been this lingering question about whether or not methotrexate would be sufficient, and so they designed this trial. Now, the funny thing is that there's a lot of weirdnesses here and I'm going to try to highlight those as we go along. The first weirdness is that the primary endpoint for this trial was actually assessed at week seventy eight, which is fully half a year after they stopped giving the patients the medications.

I would mostly recommend looking at the week fifty two data because I think that's quite a bit more useful. And then the second weirdness here is that this was a non inferiority study. So they're saying, is methotrexate just about as good as tocilizumab? Usually

when

we do non inferiority studies, it's things like a DOAC compared to Coumadin, where Coumadin is objectively horrible. And if a DOAC is just as good then great, that's a win. In this case, Tocilizumab is objectively pretty good and methotrexate has more side effects so I was already a little bit skeptical about that. Once you get to the results you'll see more. So what did they find?

They randomized two eighteen patients to one of these therapies. Very big accomplishment. French vascular assay group does great work. I think that alone is really impressive. Week seventy eight didn't meet their non inferiority endpoint, so the trial was technically a failure for methotrexate.

But the data that I'm more interested in is the rate of relapses at week fifty two. So week fifty two, higher rates of relapse survival for tocilizumab eighty three percent versus sixty seven percent and pred free remission eighty one percent versus sixty percent. So that means if you have a patient with giant psoriasis and you say I'm going to give them methotrexate instead of tocilizumab, every fifth time you do that someone is going to have a flare. That is just not good. So I think those are pretty strong votes for atosolizumab in favor as opposed to methotrexate.

And then there's weirdness number three and this is a very weird thing. So in this study there are roughly even rate of adverse events, infectious adverse events, but the patients who got methotrexate, five of them developed PJP pneumonia and one of them actually died, which is a really horrible outcome. Methotrexate is not something we think of as causing a lot of PJP, but usually we're giving it to patients who have rheumatoid arthritis and are on maybe no steroids at all. It seems to me that the combination of high dose methotrexate in this trial and high dose steroids is actually a pretty big risk factor for PJP because we just do not see PJP in GCA outside of this trial. A very surprising finding and one that I actually think might generalize.

If you're looking to give someone methotrexate and high dose steroids in any other case, I would be very, very hesitant about that. So conclusion, don't use methotrexate for GCA. I think tocilizumab remains the standard of care. I would favor upadacitinib, abatacept, maybe even something else like glafunomide before I got to methotrexate. I already had a couple randomized trials that were of iffy on it and I think this is sort of the final nail in the coffin for my prescribing of methotrexate in giant cell arteritis.

Thanks so much for tuning in. I hope you all have a great day.

I'm Anthony Chan reporting here from ACR twenty five in Chicago. And today I want to share with you a very interesting poster, an abstract which is number O eight four nine, which looks at the, risk of cardiovascular deaths and mortality, with the use of GLP one receptor agonist in psoriatic arthritis. This was a retrospective analysis looking at a significant number of patients with psoriatic arthritis who also was started on GLP one receptor agonist for treatment of their comorbidity, namely type two diabetes. Diabetes. We know that these GLP one receptor agonists, drugs such as semaglutide and liraglutide, have been known to not only reduce weight, but also to have a protective effect in terms of cardiovascular and renal protection.

So the purpose of this study was to see whether it could also translate to reducing cardiovascular risk in patients with psoriatic arthritis. As we know, our patients with psoriatic arthritis have an increased risk of cardiovascular deaths and mortality. So this was a design where they used the TriNetX data where they had four thousand over patients with PSA who were on GLP one receptor agonist and around eighty six thousand patients who are not on GLP one receptor agonist. They matched the patient using a one to one propensity score matching on demographics, diagnosis, and medications. And the outcome were major cardiovascular events or MACE and also all cause mortality.

The after matching, the results were that the GLP one receptor agonist patients who on this treatment had lower risk of MACE and also had lower risk of overall mortality compared to those who were not on the treatment. The demographic showed that those who were on GLP one receptor agonist, they tended to be slightly older. And, also, there were more females who are on this treatment compared to those who are not on the GLP one agonist. The population was predominantly white patients in both groups. The limitations are obviously based on the study was the coding of these patients that they obviously were based on a database from TriNetX, so there's potentially, there could be potential coding errors in this, and this was highlighted in the presentation today.

I think this is an interesting, presentation because we have been looking into how GLP one receptor agonist may offer protective cardiovascular and survival benefits in our patients with psoriatic arthritis, especially those patients who have the concurrent comorbidities, namely obesity and also type two diabetes. What this study shows today is that there's potentially a potential role for not only management of inflammation in psoriatic arthritis, but also management of the metabolic phenomenon that also happens together in these patients with psoriatic arthritis. So I think further research certainly would be important firstly to understand the mechanisms behind the metabolic and also inflammatory and vascular connection between these mechanisms. And secondly, to study how this long term comorbidity can be reduced by the use of GLP-one receptor agonists. I'm Anthony Chen reporting here for RheumNow in ACR twenty five in Chicago.

Hi, my name is Akhil Sood reporting for RheumNow. Today I have the pleasure speaking with Doctor. Melanie Hagen from Erlagen, discussing abstract fifteen thirty seven which describes a new reported adverse event in patients who received CAR T. Doctor. Hagen, could you tell us a little bit more about, LICATs?

Yeah, thank you for invitation. So LICAT stands for local immune cell, affected toxicity syndrome, which means that we have observed a transient inflammation and worsening of symptoms of priorly affected organs in autoimmune disease that were treated with CD19 CAR T cell therapy.

That's very interesting.

And can

you tell us about the onset of LICATs? When do you expect to see this adverse effect?

Yes, so we had a median of fourteen days, but referring to different organs, for example, patients with lupus nephritis showed an earlier onset of worsening of the creatinine or the proteinuria, earlier than for example skin manifestations who occurred at about three weeks after treatment. So maybe there's also a difference in the ability from the CAR T cells to migrate into the tissue in a different speed in different organs.

That's very interesting. And, what would the management involve in, for LICATs?

Yeah. So we graded it referring to the treatment and grade one for example was just a watch and wait approach, so we didn't do exactly nothing and just be patient and brave and see what happens. And grade two were the use of steroids, only short term. And grade three for example would be steroids and prolonged hospitalization. We only see that in three patients and we define grade four as ICU treatment, but there were no patients fortunately, who, were experiencing a grade four like kids.

So most of the time it's self limiting and it's very mild.

That's really reassuring to hear. And have you seen similar reports of LICATs in oncology?

Yeah, that's a pretty good question. So when we did all the observations and did the research and literature, it's interesting because for lymphoma patients there were big trials reporting after CD19 CAR T cell therapy and then doing the follow-up PET CT scan, they saw an increased uptake of the tracer in this lymphoma patient. They were really afraid that this is progression or this is a secondary malignancy. And then they did a lot of biopsies showing this is just inflammation or necrosis. And we have also performed biopsies showing that we see only inflammation and we had no signs of the disease.

For example, in the skin, we could not see, immunocomplexes, that were specific for lupus because someone were afraid that these are relapses and not only a new adverse event that, is self limited.

That's really interesting. And should we be worried about this, new reported adverse event in CAR T?

No. Totally not. As I mentioned, it's only mild, and we can treat it, very easily, even with doing nothing or just short term cause of steroids. On the other hand, it's very important to report it because we don't want to use unnecessary immunosuppressions in these patients. Because if you say, it's a relapse and I want to treat that, I think that would be, it's not necessary and I think that's a key point of the whole, like its description.

And we should report it in all the ongoing trials and, yeah, state it like a new side effect.

Absolutely. And what would be some of the labs or parameters that we should use for monitoring of LICATs in the trials?

The labs? Yes. You mean if there was any correlation?

Some more in terms of the disease monitoring

Yeah, that's a good question. So for example, in the lupus patients who then showed new transient worsening of manifestations, we couldn't see any serological marker for they already were seroconverted and had normal complement levels. And we couldn't observe any increase of inflammation markers. So that's definitely also the difference between LICATs and a systemic like CRS.

Oh, that's really interesting. Thank you so much for sharing and discussing your abstract highlighting this new adverse effect that's been reported in CAR T and discussing the management and manifestations. This is Akhil Sud reporting for RheumNow. Thank you.

Thank you.

Hi. Welcome. I'm doctor Janet Pope here at RheumNow, ACR twenty twenty five in Chicago. I wanted to talk about the connective tissue diseases and, and rheumatoid arthritis and interstitial lung disease. And, hopefully, with this, we'll be breathing more easily and so will our patients.

So the first abstract was number zero one five four. And what it did was they combined data from market scan and Optum looking at people with either a label of CTD and specific ones in particular or rheumatoid arthritis. And they had between the two datasets nearly 30,000 patients. So the mean age, depending on the dataset, was anywhere from 56 to 65. And as expected in, these autoimmune connective tissue diseases, three quarters were women.

They looked at the frequency of interstitial lung disease by a diagnostic, algorithm from these databases. And what they found was as a, for instance, systemic sclerosis, ILD, that seemed clinically relevant was about fifteen percent. Now we have found that in an old study that we published as an Ontario, incident study over about ten years. Obviously, ILD is even higher if you're gonna look, more thoroughly. That leads me to talking about scleroderma, and ILD.

So there was a whole session devoted to systemic sclerosis, of which a lot was talking about ILD. So the first question was, can we predict who will progress? And the answer is not so well, but SCL 70 is a risk. Men, certain racial characteristics such as in The US, people who identify as black. But we don't really have a good prediction model.

So two different studies looked at k l six, which is used in Asia as a prediction, and they also looked at other, factors. K l six and in the other studies, some other factors, MIG, etcetera, were predictive, but they're not strongly predictive. So the answer there is you have to keep following and screening your patients. The next thing was how common is ILD in our patients with the limited subset? So we you might have think of it before as being called CREST, but it's limited cutaneous systemic sclerosis.

And in that group, up to a third had interstitial lung disease. And if you followed for the time of the study, in the database that they had, a good one in six patients will progress. So the take home from all these studies are we have to be vigilant. There is ILD in our patients with connective tissue disease. Within scleroderma, we don't have a good biomarker that says who will progress.

So in scleroderma, because the incidence and prevalence is so high of CTD as a complication that you have to screen regularly. The other good news is you can breathe more easily because there are treatments. Nirandelomast will be approved at some point as a p d e four inhibitor in the treatment of progressive pulmonary fibrosis, and it was well tolerated. That's the Fibronir, ILD study, and there are other treatments on the horizon. There's immune suppressive treatments in early diffuse scleroderma and in limited as well where ILD is relevant.

So please follow us at RheumNow. Thank you very much.

Hello. I'm Jonathan Kaye reporting from ACR Convergence twenty twenty five in Chicago, Illinois. I'm here with doctor Shreya Shaktevel, who's a third year internal medicine resident from Anne Arundel Medical Center in Washington DC. And Shreya is here at the ACR meeting intending to become a rheumatologist, but has presented a fantastic poster number thirteen sixty nine looking at SGLT2 inhibitors and GLP one agonists and their effect on rheumatoid arthritis flares. Now, SGLP-two inhibitors are drugs like that little pill with the big story to tell, and GLP-one agonists are increasing popularity.

They have anti inflammatory effects. And, Trey, you looked at the TriNetX database, which is a large database with over twelve thousand patients with rheumatoid arthritis, You came up with a definition of a surrogate for rheumatoid arthritis flares.

Yes.

You looked at about three twenty patients on GLP-one agonists and about two twenty patients on SGLP-two inhibitors. You found that there was an effect on the incidence of flares.

Yes. Yeah.

Tell us a little bit.

Sure. Because we didn't have access to a DAS28 scoring system, I had to kind of make my own. We looked at the increases in ESR CRP from their baseline, number of times they got prednisone, IV methylpred, steroid injections, and DMART escalation. And so we kind of broke it down to, two different analysis. So the first one was we looked at the RA composite flare score, and we found out that GLP-one users had the highest, composite flare score.

So then we looked further and looked at pre and post initiation of these two drugs.

So by having the highest composite flare score, is that the greatest reduction in flare or the more flares?

Flares.

Most flares. The GLP-one agonists are inducing flares?

No. So they just had a total from the whole study had the most flares.

So the GLP-one agonists had the most flares of their Counting. Patients. Looking at the SGLP-two inhibitor and GLP-one treated patients, not of all rheumatoid arthritis patients.

So we had three different groups. We had a DMARD only group, a DMARD SGLT-two, and a DMARD GLP-one. So then the GLP1 group had the most flares. So I wanted to look further into like what exactly does that mean? So we looked at pre and post initiation of these drugs and we found that at the patient level, both had a reduction of RA flares.

But when we look more of a chi square analysis, we found that SGLT2s had a statistically significant reduction and GLP-one, while they still had a robust reduction, it wasn't statistically significant.

So the increased number of flares were probably mostly before they initiated therapy?

That's what I'm thinking. I'm thinking that, you know, we consider obesity as an inflammatory state, so patients who are obese are usually prescribed GLP-1s. Or I can say the other way around, GLP-one users are mostly obese people or with diabetes as well. And so that's kind of why I think, like, the GLP-one group had the most flares is because they're already in an inflammatory state.

And when they lost the weight so this was cross sectional data, and you didn't really have times, associated with the flare.

Yeah. So I didn't look too closely into the the weight loss. So we just picked anyone who had a BMI above thirty. I think the next step definitely is to see if if those who are on that GLP ones or SGLT twos, as they're losing weight, are their RA flares also reducing? Because it seems like there are non responders out there that could have been mixed into our data.

And so breaking that down further will kinda give us a little bit more clarity.

And there was another poster adjacent to yours that looked at the predictive signature Mhmm. That suggested that the addition of a GLP one agonist to TNF inhibitor in people with a body mass index greater than thirty

Yes.

Actually, those that were not responding before the GLP one agonist was added might respond better with the addition of a GLP one agonist.

Yeah. I actually went by that poster as well and talked with him. So it was very interesting. We're gonna try to collaborate in the future to see if we can get more data out

of

it.

That's fantastic. In addition to the anti inflammatory activity and the weight loss activity, there might actually be a measurable reduction in flares in patients with rheumatoid arthritis. Absolutely. So should we as rheumatologists be prescribing GLP-one agonists to rheumatoid arthritis patients even if their BMI is slightly less than thirty?

I definitely think that's like the number one question now. So I think we're kind of headed in that direction. Obviously, data needs to come out about that. But based off of, like, it being GLP ones are such a trend nowadays, as as like, rheumatologists haven't really, you know, started prescribing GLP ones or SGLT twos. That might be a thing in the future, once we get more data.

So there are a couple of take home lessons from this that we as rheumatologists need to become familiar with the prescribing of GLP one agonist and probably should take responsibility, not just deferring this to primary care providers, but to provide to prescribe GLP-one agonists to our patients to facilitate weight loss and especially to reduce the incidence of rheumatoid arthritis flares and perhaps to improve responsiveness to TNF inhibitors if that actually is an effect of these medications. Well, congratulations.

It's a

third year medical resident to have such a terrific poster.

Thank you.

There's lots of work that can be done. And as a rheumatology fellow, I hope you continue this and take this further. Thank you. This might be a niche for you to look at bariatric medicine and rheumatology in that intersection.

Thank you so much.

Congratulations. Thank you. Is Jonathan Kay from ACR twenty twenty five Convergence in Chicago with doctor Shriya. Your last name, I apologize.

Totally fine. Shak Devell.

So for this and more information about other topics at ACR Convergence twenty twenty five, go to roomnow.com. Hi.

It's doctor Arti Kavanaugh coming to you from American College of Rheumatology Convergence, ACR Convergence twenty twenty five in Chicago. I'm gonna talk about psoriatic arthritis, talk about some concepts, new concepts, hot concepts. Some of these are being covered in sessions here at the ACR, and you'll see them on RheumNow as well. Some of them are abstracts, you'll see those covered also. The concept that I would like to talk about now is prediction, and a number of interesting aspects to that.

One is what do we want to predict? An important one is the progression of psoriasis to psoriatic arthritis. As we know, about twenty five percent of people with skin psoriasis ultimately develop psoriatic arthritis. Most of them have skin psoriasis for a period of time before the psoriatic arthritis develops, often eight or ten years. A key question then is, who are those people that are ultimately going on to develop psoriatic arthritis?

A lot of work has been dedicated to this because the flip side could be, if you treated the group of people with psoriasis who are going to go on and develop psoriatic arthritis, maybe you could prevent the psoriatic arthritis. We want to treat diseases early in almost all diseases, certainly in many rheumatologic conditions. The earlier you treat, the more successful you are. So if you had such a start that you could treat people who had a higher likelihood to develop psoriatic arthritis, you might be able to prevent the disease. It makes sense.

There's not a consensus on whether or not that works, and that's been the subject of some analyses here at this meeting, but also at other meetings. A lot of work has gone into that. Genetics haven't really played a role such that they're going to be something useful to us to use in the clinic, where we need something that has a pretty good predictor. You want to take that twenty five percent and say, No, this patient did have a twenty five percent chance. This psoriasis patient did have a twenty five percent chance for ulcerative arthritis.

They have a seventy percent chance. That's a patient you treat. If you say, Well, it's a twenty five percent chance, and these data give me a thirty percent chance, you're still not that that much better off. So an important area, a great and super interesting area, and one that we see some incremental developments in. One of the things that I think is exciting, and we've seen it in the past couple of meetings, the ACR meeting and the UR meeting, is epigenetics.

Epigenetics, of course, changes to the DNA not related to its structure, but to its expression. So how the DNA strands are acetylated, how the histones decorate them, which affects the transcription of the RNA, and then ultimately translation of RNA into protein. So those epigenetic changes can vary depending on environmental influences, things like the diet, things like your microbiome. A super hot area, of course, and one that's gotten a lot of attention. I think these things, in the future, I bet when we look back, if we're at ACR convergence two thousand and thirty five, I bet there'll be a lot more information, and we'll be able to say, Oh yeah, we should have known back then that this is the group of people who are more likely to develop disease.

They should make these changes perhaps environmentally, dietary wise, and also they are more worthwhile to treat. And then, as in many areas of rheumatology, our ability to look at biomarkers has also expanded very dramatically. We're seeing incredible techniques now with the ability to sequence RNA, look at the expression of many, many, many proteins, look at the genes, look at the epigenome. These are big data, and I think along with the explosion of data, almost too much data, we're seeing the application of artificial intelligence to try to say, where is the meaning? Where can we take the meaning out of this to answer an important question, not only like which psoriasis patient is going develop psoriatic arthritis, but which drug is the right drug for that next person that we see in the clinic?

Personalized medicine. So it's always been a buzzword. It's been, I think, at the top of our needs list, and it's something I think we're beginning to see some information that will hopefully prove useful and give us something in the clinic. So here for RheumNow at ACR twenty twenty five is doctor Arty Kavanaugh. Thanks for watching.

Hello, everyone. My name is Youssef. I'm a consultant rheumatologist from Leeds. I'm reporting live from Chicago to cover the ACR two thousand twenty five conference. As we all know, Sjogren's disease is a condition where it affects predominantly the glands leading to symptoms such as dryness, but it also can affect other organs as well as can lead to patients' symptoms burden such as fatigue and also having pain.

There is significant unmet need in Sjogren as currently there is no licensed therapy. So many drug trials have failed phase three, and for the first time at ACR conference, we see positive light for a drug called yanalumab. So this was presented in the late breaking abstract number l b 24. Yanalumab is a B cell drug where it works by inhibiting the buff receptor, but it also has anti dependent cytotoxicity mechanism, which leads to complete B cell depletion. So it's very attractive because it does two job.

One is inhibiting the B cell survival factor, and second one is doing depletion. So in this phase three trial that were presented, it was actually two trials, one called Neptunus one where they compare two arms, one with the drug yanalumab subcutaneous versus placebo, and the second is Neptunus two where they compare three arm. One is the placebo, one is Neptunus monthly injection, and another one is to be given a three monthly injection with placebo in between. An interest so in term of patient characteristic, so this patient had a moderate to severe systemic activity as measured by SDI. And interestingly, about thirty percent of patient had a high less severe disease activity as defined by SDI more than 13.

So in term of the results, is it still resounding yes? So the primary endpoint was a change in SDI, and this was consistent in both trial, Neptunus one and Neptunus two. And you can see the effect of Yanalumab from week twenty onwards. So what about other key secondary endpoints? So the results also showed that the face the patient the physician global assessment also improved significantly over placebo in the Yanaluma group and also patients global assessment as well.

How about other objective measures? So when they did a sub analysis, they found that in patient who had some residual of saliva, which is more than naught point four mil per minute, they have significant improvement in objective salivary flow rates as well. However, other with other trials in Sjogren, we didn't see significant improvement in terms of a fatigue, although there is some new numerical changes there. It will be interesting to know because the drug company is also now about to start the trial for patients with high symptom burdens to see whether this can also help this group of population as well. Lastly, in terms of safety, there's no significant adverse events or any major safety signals comparing ayanalumab versus placebo.

Although I did not see any data about immunoglobulin, but certainly serious infection rates are comparable. It'll be interesting to see, like, you know, the whole paper, you know, with with that regards. So, really, this is really a promising therapy. So first time, we now have a drug which have two trial that's supporting, that the drug is effective and also provided some clinical meaningful, improvement to the patient. And now we're just gonna wait for for the drug to undergo FDA approval, and, hopefully, we will have an option now to treat our patient with moderate to severe activity.

And so thank you for listening to my summary, and follow me at u six Youssef and my colleague at RheumNow for more content coverage. Bye bye.