Day 4 Recap EULAR 2026 Save

You're listening to a RheumNow podcast coming to you from London and you are '20 26. Enjoy. Hello, everyone. Welcome to RheumNow's daily recap from you are 2026. It's day four, the final day.

We're delighted to have been here, but even more delighted to go home. I'm gonna introduce today's panel. I'll start with myself, Doctor. Jack Cush from Dallas, Texas. Doctor.

Day?

I'm Rinalini Day, I'm a rheumatology fellow in London in The UK.

Doctor. Youssef.

Hello, my name is, Doctor. Youssef, and I'm from Leeds, and I'm actually home.

The benefits of being in London. And Doctor. Chan.

I'm Anthony Chan, I'm from Reading, United Kingdom.

Are you home?

I am about to leave now, I'm still in London. Okay.

All right, so what we do in these daily recaps is I have our faculty who've been scouring the meeting and doing a fabulous job of covering this in social media and writing and video and podcasts. I asked them to come one evening after the day and just tell me what they thought was great, even though they all have different assignments and topics that they're married to, they can freewheel and do whatever they like. So let's start with our first round with Doctor. Day.

Yeah, so I'd like to, cover one of the late breakers that were presented today. This was LB5005, JAK spare, baricitinib in early PMR, where we've got very limited treatments, although, you know, we did hear about the updated guidelines today as well. So, this was a double blinded randomized parallel group phase three study with forty six patients with early PMR randomized to baricitinib four milligrams daily or placebo alongside a rapid steroid taper from twenty milligrams to zero over eleven weeks. And essentially at week sixteen, glucocorticoid free remission was achieved in sixty five percent of the patients receiving baricitinib, as opposed to just seventeen percent who are on placebo. Baricitinib also reduced the relapse risk and lowered the cumulative steroid exposure.

In terms of safety signals, they had one serious adverse event in each of the treatment arms. So essentially, baricitinib significantly improved the chances of achieving steroid free remission in PMR, and suggests that JAK inhibition could emerge as an important steroid sparing agent. We do of course need probably larger studies though, That's the key thing. Yeah.

So let me ask the other panelists, what do you think about, is there going be a future role for JAKs in PMR? Anthony, what do you think?

I think it's great. The results were quite, good. Sixty five percent, could be quite free, and versus seventeen percent on the placebo. That's quite a significant, there's a lot of morbidity from a long term prednisolone use in these patients, and often they find it quite hard to taper. They come towards a lower doses.

So I think if we can get them off quickly, I think that's going to be a positive thing. Have to just be careful about the long term effects. They're probably older patients, older patients who are going to be using this therapy, PMR, and how that weighs on with their thrombotic and cardiovascular risks. Hughes?

Yeah, so I think there is a role for JAK inhibition, as we also see in ipadacitinib. It's just also the question will probably be asked by everyone after you receive this remission free, what happened? Because in part three of this study also, they did show that once baristinib was discontinued after six months, there is a numerically new increased frequency of relapses in those who discontinued compared to those who continued baricitinib. So we do need longer, you know, any luck in a follow-up and also like larger number like what Vinny was saying is now.

Yeah, what Yus brings up is that it was numerically higher, but the numbers at that stage of the study was small. So you can't really talk about significance, but it does say that, PMR patients, you know, need therapy for more than a year. And, what other critique I've heard, Minnie, is that, this was an eleven week steroid taper. And, you know, who in their right mind aims for eleven week steroid taper? Well, you know, the makers of this study because JAK inhibitors have a fast onset, and maybe, JAKs can take up the slack when you can get them off steroids, and maybe it's a safer kind of thing.

So I just wanna bring up something I know that you wanna talk about, Doctor. Day, and that is, right after this, or actually right before this, there was a new, PMR, GCA guidelines. And in that guideline, number three out of 12 recommendations was a new onset PMR, oral corticosteroids should start at twelve to twenty five milligrams and be tapered to ten milligrams within two months, eight weeks. But the goal being to stop steroids within a year. So the goal of this particular study was particularly aggressive, but again, they were using aggressive therapy.

So how do you think the study fits in with the new EULAR guidelines?

So firstly, I'm conflicted because I am a fellow on that guideline. However, I think one of the things we've seen is that there are limited agents for steroid sparing agents in this disease. And that was shown beautifully actually in the guideline because we suggested using IL-six inhibitors and then methotrexate has actually stayed in the guideline despite the fact that we've got limited evidence as our SLR, which is due to come out, will show. And so actually having these results is encouraging in the sense that perhaps there are more drugs on the way that we could use, just as we've seen in GCA. But, yeah, I think we need to treat it cautiously for now, because as we've discussed, the numbers are low, the time is also low in which this was tested.

Yeah.

For those of you a little, confused at home, SLR is not a camera, it's a systematic literature review, which is a gigantic part of any guidelines effort. And, Doctor. Day was one of the people who has to put in hundreds of hours to get the literature that informs the guidelines. But yeah, I thought that was a very interesting, study. Yuz, what's your, big one for today?

Yeah, so I just wanted to present, abstract LB003 that was presented at the late breaking abstract. This is not to change our practice now, but certainly something to watch out for tomorrow or in the future. As we know, there is some limitation of CAR T cells with the conditioning, the time process, the problem with manufacturing, and also accessibility and scalability. Therefore, we need others in the therapy that can address this. One other way is to do an off the shelf therapy.

This abstract is about creating development of an off the shelf NK therapy. The compound is AB101. This was a basket study. The study overall looking at four conditions. So severe refractory rheumatoid arthritis, we have Sjogren's disease, we have severe refractory systemic sclerosis and also idiopathic inflammatory myopathy.

But the authors presented only for three diseases, excluding myopathy. I'm sure we will see that in the next conference. So in this study, they showed preliminary analysis. In order to administer this compound, this can actually be administered as an outpatient in day case unit. However, it does need a few things.

Basically, they need to receive the low dose cyclophosphamide and fludarabine, And then after that, they will then need the treatment itself, which is given seven days apart. And then after that, they also need a course of rituximab. So basically you've got these three combination therapies. And these were needed because these patients are refractory. For example, like rheumatoid arthritis, they have to fail more than two biologics.

So their preliminary results do look encouraging up to fifty two weeks. So for example, in rheumatoid arthritis, the endpoint was ACR50, so it's quite higher hurdle endpoint. And they did show about seventy one percent reduction at six months. We can't do direct comparison, but then the reflex trial in rheumatoid arthritis years ago, then at Professor Emery, so that was a failure of a one TNF inhibition. That ACR50 was around 30%.

So if you just look at that, it is quite impressive from that point of view. And certainly, did look some good signals as well in terms of Sjogren, in terms of changes in SDAI, and also the patient reported outcome improvement as well, and also the systemic sclerosis. There's no significant safety signal in the short term. They don't see any modern grade two CRS or no icons at all. Certainly, this is preliminary.

The result is up to fifty two weeks, so we don't know what happened longer term, whether the patient may relapse and whether they need redosing, whether redosing is effective. Sometimes

with

all this allergenic, you might be concerned about graft versus host rejection and so forth, but certainly something that we need to look into it. And also, they will need a comparator group. Having one in a single arm makes it difficult to interpret it. So,

can go a lot of ways here, but let me ask, the other two panelists, where are we in your head regarding CAR T? You know, and I don't want you to say what you just said, or I don't even need you to, endorse CAR T. We've had now three years of CAR T, anecdotalism. And, are you ready for this? And what do you want to see and where is this going to go?

Anthony, why don't you tackle that? Give me thirty seconds on that.

The issue is we don't have a lot of control studies in these CAR T studies. So if you had further B cell suppression, for example, in another arm, whether we would see difference with the cellular therapy. And then there is the allogeneic versus the autologous forms as well, whether there are any differences. So I think at the moment we will probably use this in our most refractory patients.

And Doctor. Day?

Yeah, no, I think we're still in very early stages, even though it feels like we've been talking about this for a long time now, but we are still in very early stages, as Dheus was saying, the longer term effects we don't quite know as well. And certainly from like, just from what I see in clinic, it is very much the very refractory ones that we are putting forward for trials and things. Yeah.

So Joost, other than learning a new tool and the many sides of this new tool in different ways, this is an off the shelf version, which is certainly unique, and learning about safety, what else has come of the CAR T cell therapies thus far?

Yeah, so I think apart from, I think that there's a way in terms of trying to improve the targets as well. Have seen the abstract presented three days ago in the first day of EULA. So we thought that CAR T will be eternity. Patient had this really intensive in the beginning, they were thus long. Certainly looking at the lupus cohort was quite impressive.

I think there's one abstract saying there's no relapse up to four years. But altogether, with 50 patients that have been treated with the original Erlangen cohort of autologous CD19 CAR T, there were actually about twelve percent of people who had relapsed. And this was severe relapse. And then sometimes that just made me think whether this patient, whether is CD19 the right target, whether you should have targeted CD, BCMA, for example, to remove the plasma cells in the beginning, but then also you have to find the balance between in terms of long term sequelae of that with low IgG, which can increase risk of infection, vaccination response and so forth. There's a lot to ask questions, but also we also have to find the balance of this patient that's so refractory, so they fit a lot of things.

So I think cost effectiveness analysis is really important here. I think people are not really talking about it, I think is really key.

Yes, and we can't get into this because we can go forever, but Doctor. Youssef and I had a poster side conversation about this and a lot of people doing the planning haven't you know, planned for the fact that you're gonna make people hypogamma, and, you know, worrisome sort of low IgG levels so that now they need to be treated with gamma globulin. You know, so there's now an infectious risk that has an expensive solution too. So again, I I like that, you know, learning the dynamics of response and then reconstitution, you know, and learning how to do, I think these are all valuable lessons, but I think we're all anxious to start seeing controlled real trials going forward. Anthony, what's your favorite for today?

My favorite for today was the BIBO late breaking one, which is the, study between bimekizumab, the IL-17AF, head to head versus risankizumab, the IL-twenty three inhibitor. These had data at sixteen weeks and showed a fifty percent ACR 50 versus around thirty eight percent in the risankizumab. And also at four weeks, there was a threefold improvement in the bimekizumab group versus the rizanquizumab group. So I think we now have a head to head in the joints for PSA. We've had skin data before, but this is quite useful in terms of understanding the mechanism of action.

Yeah, and I think, you know, it was a great presentation by Marola, you know, first it started as a press release, then an extended press release with some data. Now we saw not just week 16 data, which was good, but week 24 data, and the ACR 50 looks great. Are you bothered by the fact that the secondary endpoints weren't significant? You know, MDA, skin, whatever, they weren't significant lead different. And there was might've been an edge, but it was not significant.

This is a pretty well powered trial. So that's one thing that makes me concerned. The other thing is why did this head to head trial work when so many other head to head trials have failed? In PSA, so many head to head trials are clearly winners in PSO, but in PSA head to head, why did this one work? So do you have an answer for either of those things?

I think the other 23, I think still has probably a bit more superiority in skin compared to joints. But if this came the other way around, the more, these people had quite low skin scores, they didn't have very high skin scores in this study. Hence they didn't probably, the MDA has a skin component to it, and probably that's why it couldn't meet all of the seven components to achieve MDA.

Yeah, And I think you're right, but there are actually now head to head, bimekizumab against 23s and the dual inhibitor has outdone the 23s. So it's little bit of an argument in the derm world, which is the better drug, when it comes to best POTSY-one hundred response. But clearly, twenty three really does very well and as does the dual inhibitors compared to the single IL-17A inhibitors without the F. So it's a really interesting study, I think it will cause a fight. If I ask you and the three of you in The UK, you wouldn't know the answer and I didn't know the answer, but, supposedly the best selling biologic right now in psoriatic arthritis in The United States is actually rizenkizumab.

Now collectively all the 17s are gonna outdo, you know, the two 23s would be my guess. The other one being guselkumab as a twenty three inhibitor. But it's a very competitive market. Companies are spending a lot of money and doctors are really confused because they got more PSA drugs than they have PSA patients. And that creates a lot of choice indifference or choice overload.

All right, so my one is, I think almost a monumental study. It is the follow-up to oral surveillance, and you're thinking, So oral surveillance, there's another one of those, are you kidding me? Well, no, there wasn't, but there was a follow-up that was FDA mandated for baricitinib to look at the VTE risk in patients taking plus a TNF inhibitor versus baricitinib and baricitinib at two or four milligrams a day. So it was a post regulatory commitment and patients were enrolled, over 3,500 patients I think, who were at risk for VTEs by either having had a prior VTE, being over age 60, and being obese. And so they had, like oral surveillance, they were trying to stack the odds for the events, but it wasn't quite the same, but then again, maybe it was pretty close.

And in the end, they had 3,600 patients enrolled, they followed them on average more than four years. And there were two studies, there was the RA Bridge and the RA Branch study. One was a global study, one was a US similar but smaller study, they combined them. And in the end, clearly baricitinib both doses individually and combined gave you significantly more venous thromboembolic events. So this mirrors the results of first baricitinib when it was first approved by the FDA and other worldwide regulators, that VTE risk was there from the start.

If you remember, tofacitinib had no VTE risk in its label when it started out. It was only after the oral surveillance that they all got slapped with it. So anyway, this data now reinforces the original baricitinib label and the extension of the oral surveillance risk for VTE to all JAK and probably tick inhibitors if you ask me. But unlike oral surveillance, the two doses, either dose of baricitinib did not increase major adverse cardiovascular events, MACE events, nor the risk of cancer, nor the risk of opportunistic infection, nor the risk of arterial thrombotic events. It did show a significant increase in serious infectious events, somewhat like the oral surveillance.

So the question is, what does this do? Does this create confidence or does it make you still worry? I'm gonna ask each of you to answer that. I'll let you think about it for ten seconds, but that's kind of where this goes, Is this data that doesn't change your prescribing, what you already know for oral surveillance, or does it make you more worried or less worried? Who wants to go first?

Minnie, why don't you go first?

Yeah, I think a couple of things. Firstly, I think it's really encouraging the results about the MACE and the malignancy, just because this was actually a population enriched cohort who supposedly had greater risk factors for both of those things. But I think, yeah, it needs, as we discussed in a separate video earlier today, needs to be treated with caution, probably the results. Of course, well, the targets of the two drugs are different, baricitinib and tofacitinib. This is only two JAKs, whereas that's three.

So, yeah, I'm not sure it would change my practice just yet, though.

Okay. Anthony?

I think

Change, change or change?

Caution, that's all. People who are above the age of 60, BMI greater than 30, previous VTE, consider whether there are alternatives, before we go use the check.

Let me just give a little perspective on what you just said. I agree with you a 100%, but it's a little bit like trying to achieve an ACR20, which is not a low level response. Getting a 20% response out of seven variables, at least five out of seven, becomes successively harder. Hence recruiting for patients go on JAKs when you restrict it to over age 60, BMI over age 30, having failed one prior. The idea is the people who are at highest risk in oral surveillance over 65 smokers with a cardiovascular event.

That's like eight percent of my Jack RAPSA audience. I think the same thing applies here. And I do think a caution is necessary, but I do also think understanding how many, you can't apply this caution to everyone, because now you've cut off a valuable treatment arm in your arsenal. Use, again, up or down.

Yeah. So I'm cautiously optimistic. I think that's what it is. Yeah. I mean, the the the risk for VTE is in line with with with the label in the safety profile that we know from vadadustat.

It's a bit difficult in terms of selection. I know you said maybe quite the same pool, but it is a bit different because this one is like you have to have one VTE risk factor, whereas in the oral surveillance, you have to have one risk factor for MACE. So it may probably intellect, but not all. So do we need another oral surveillance in varicitinib or another oral surveillance in upanacitinib, for example. So I think it's all caught up in the air there.

But I think that data give you slightly more reassurance than what it was before, yeah.

All right, so again, I will just say that I think this firmly establishes BTE and SIE risks with JAK inhibitors, over TNF inhibitors. I think it murkies the conversation considerably about cardiovascular and cancer risk, because these are two very large randomized controlled trials. Now with, you're looking at over 8,000 patients, all followed for more than four years, that's more than 32,000 patient years. I don't care what report you're going to see from some cohort, you know, from Portugal or some reconstructed, you know, claims data that's trying to, none of it matches these two studies. These two studies give you the best data from which you have to make a decision to be cautious, overly cautious, minimally cautious, it's up to you.

All right, we're gonna do one more, we're gonna do quick hits here, thirty second descriptions, a few comments, and let's move on. Let's start with Doctor. Youssef.

Yeah, so just trying to discuss about abstract LB007. So this is an extension or extrapolation of promising therapy using FC neonatal receptor blockade. The compound is nipocalimab, as we all know. So the last couple of years, have had results presented for Nipocalimab and also efagretinoin, which is another Fc receptor in Sjogren's disease, which they have now finished recruitment in phase three. So we'll probably be listening to the results in the next eighteen months.

But this one is for SLE. Basically, this is a patient with moderate to severe active SLE. They did have over 200 patients that were randomized into three groups. One is placebo, one is nipocalimab, with a five milligram per kilogram IV infusion one, and another one is fifteen milligram per kilogram. The results show that the primary endpoint, which was the SRI-four, was met in the higher dose group.

Basically, the effect size was about fourteen percent, so fifty four percent for nipocalimab and also forty percent in the placebo. Again, there's an issue with placebo response here. With the lupus trials, it should be up till thirty to fifty percent. It may be because they did try to mandate the steroid taper from week six to sixteen, and after that, you have to be less than 7.5. But after that, it's dependent on the excretion for that, as long as it didn't go up.

I think because of that, it's still a bit lenient. If you compare it to other trials that are more successful, for example, the Yanaluma phase two, they did ask to go all the way down to five milligram per day. Then they see a lot of margin difference and reduced placebo response, and that may be the case. So in this case, it did show the primary endpoint was demonstrated. And also they did do some subgroup analysis where they did say if you stratify them in patients with high interferon in very active antibodies, you will get better response.

So I just want to highlight one thing potentially. So in terms of safety, they did see about twenty three percent people had low IgG, although they did say that this patient didn't have any serious infection. But certainly this is something to look out for in the longer run. And I think there were two patients also had pneumonia and things, but certainly it will go to phase three. And one thing that I quite like, just quickly one, is I like the name.

Woah, woah, woah. Mean, is I like the name. First Yeah, so the name is like, this one is called Jasmine and the phase three, which currently undergoing is called Gardena. There you go.

Yeah. Well, again, there's a lot of buzz around FcRn receptor drugs, and they do a really good job of lowering autoantibodies, but that isn't necessarily an endpoint. It shouldn't be an endpoint. In B cell driven disease like lupus, it might pan out, so this is encouraging. But I don't know that it's going to, again, there's a number of these that are in development, a number of disorders, and I'm very cautious about interpreting, but I like this result.

Let's go on to the next one. Doctor. Day, what's your last one?

So I'm actually not going to talk about an abstract, but I'd like to draw attention to the plenary sessions, which are available to rewatch and particularly the rheumatoid arthritis one today, which was a really good overview. It was by Doctor. Nicky Foroo, a good overview right from the beginning of where we started in terms of treating RA several years ago, right up until the current day with the trials that we've had on potentially preventing the onset of RA, and really highlighting the landmark papers that have happened in between on difficult to treat RA and the comorbidities in RA. And it was really a good reminder of, well, essentially of how far we've come, but also I can recommend it to people who weren't able to come to EULAR, a really good overview of, all things rheumatoid arthritis.

Is there a proof that all these great advances actually has done anything really important? Like, you know, ACR twenty, fifty, 70, who cares? They all look the same, in the end. And I know we're very good at managing RA and we're very good at patting each other on the back, but RA is still a deadly disease. What proof did she say that these really have changed the

outcomes? Well, she was talking about how perhaps we are in our drive to develop new drugs, we are forgetting the other aspects around the drugs which matter. So we are better at managing comorbidities, but we still got a long way to go. Then there's also the bits that I'm interested in, the health equity, the social determinants, that side of things as well, which we're maybe not so quite so good at looking at, things like fatigue, pain syndromes, what do we actually

Mental health, mental health, yeah.

Yeah, mental health. So all of that as well. And I was having a conversation earlier in the Congress with somebody saying that perhaps we've forgotten a little bit about RA in our drive to try and improve the treatments in other areas as well. So I think there's more work to be done in RA actually. I don't think we've quite reached our peak as yet.

Well, again, I think the evidence is also that mortality rates are down and have trended down since the biologic era and surgeries are way down. Hospitalizations haven't really changed all that much. But you know, the question is, is that because of biologics and advanced therapies, and I think we assume that, and I think it's, I assume that, but I can't prove that. But here's my worry. My worry is we all think we're pretty darn good at RA, which means that there's no urgency on RA.

And I think you just need to have one or two of your RA patients die prematurely to be reminded that we're not as good as we think we are. Doctor. Chan, what's your last one?

My last one is, the sonolizumab, the nanobody IL-17AF. We've heard about it in PSA today, we've heard about it in XBA, both radiographic, non radiographic. This is a phase 2B. It's a single arm study, so there were no controls, but it showed positive response in ASAS forty. And also they had PET scan results.

They had a fluoride PET scan which measured the uptake and they had reduction in the overall uptake and also in the sacroiliac joints in this study. So more from a mechanistic point of view rather than a sort of true efficacy because we don't have a control in this study, but I thought it was interesting that the size of this molecule maybe has a role to play in terms of its long term benefit.

So that's like the thing that companies will do, right? You know, they'll take a drug that looks like another drug. You know, this is a dual IL-17AF inhibitor, like another one that was just talked about in the B BOLD study. That looks really good, but this one's new because why? It's a nanobody.

And they gotta market the heck out of that, telling you that that means something. What exactly does that mean other than the size? You know, show me the money, you know, as Cuban Gooding Jr. Said, which is, I don't care about your PK, your human versus chimeric versus I don't care what, versus, you know, 12 microns versus 400 microns, show me that it works. One of the things that I liked that I heard from, you know, all the people that you run with Anthony in the, spondyloarthritis world, was that the supposition that maybe this would be better at penetrating entheses and getting to enthesitis and these diseases being really enthesopathies at their origin, which would either result in less enthesitis or maybe better outcomes, better But again, that's all talk.

Well, I mean, do you have any different perspective now? Because this is a phase three trial, there's been a few trials of this. I think it's good, think it's gonna get to the market, I think we're gonna hear these discussions when we talk to our colleagues or to the companies.

Yeah, I think we will have to see when it gets to phase three and whenever a, you know, comparator, another head to head, that would be interesting.

So my last one is born of, you know, walking the poster floor. And it's hard for me to do because so many nice people wanna do selfies and talk about RheumNow, and that's all great, but I gotta learn something. And then even worse, I see my friends, you know, and I'm walking by and there's Atul Diadar standing talking to some gal about something and he starts, you know, waving at me and waving me over and I, oh, you know, I'm gonna go over because he's a great guy, he's a great teacher, I learn from him all the time. And I don't really wanna look at his poster because it's about, it's a drug company study and I don't really, I don't know. Anyway, it was an interesting study.

It's actually a poster on the SELECT AXIS-two study, which was a phase three randomized control trial of seven thirty four patients with radiographic or non radiographic XBA who were treated with upadacitinib fifteen or placebo, and it worked really well. But of the seven thirty four patients at the end of the trial at week one hundred four, one hundred and ninety four were in remission. And then they were randomized, I think to either continue or to stop. No, actually I think they all stopped and they followed them. And the interesting thing was that seventy eight percent of them flared.

So obviously you don't wanna stop, you know, a powerful JAK inhibitor like upadacitinib that was working, because seventy 8% are gonna flare, but the other, there's two really interesting caveats to here. One, that when you retreated them, almost 90% of them regain their low disease activity status within six months. So that's encouraging that you could stop and always go back to the thing that worked before. But then there's this crazy story of twenty two percent went off the drug and maintained drug free remission for more than forty eight weeks. Who are these people?

They were bad enough to get into AXIS II with active axial spondyloarthritis, they benefited from it and then you stopped it. So I told the story and there was two people there along with Doctor. Deidar, put three or four rheumatologists together, you'll get seven opinions. And they all agreed with me. The story is that's a young male with ankylosing spondylitis in the non steroidal era.

He didn't wanna go on a TNF inhibitor. He kept saying, Dude, dude, try it, it's a silver bullet, you'll feel fabulous. And finally they do it, and they come back and say, Why didn't you make me do this? I feel so good and I'm doing great. And then the interesting happens is that after a year or two or three, they stop the drug that was working, but then they stay in remission and they don't want to go back on whatever drug it was you put them on.

So does this mean that there's something about spondylitis that it needs a big hammer to knock it down and maybe that can have long term benefits in one out of five patients? Anthony, what do you think?

There are some patients who stay on NSAIDs for long periods of time and the disease seems to be very well controlled. There's no structural change. Think probably this group of patients who are now on top of that are also probably getting JAK inhibitors when their scores went up. It could be that group who in the past would have maybe maintained them on long term NSAIDs. Because there was another, the FASTLAIN study also presented here, which also showed that if you went with NSAIDs plus, Jack, you do better than the NSAID alone.

So we are probably looking at this group of people who would have responded quite well to any anti inflammatory type treatment hard at the start.

Alright, any any other comments on on this one?

Okay. If

not, let's

go. Use go ahead.

Any was Was any the difference in term of disease duration? Was was it like shorter disease duration or these patients, do you know?

I don't know that that was not available in the poster. I think that's certainly a reasonable thought that maybe shorter duration disease might have been self limiting in some way, as opposed to someone who's had disease for ten, twelve years, which is often the case in patients enrolling in axial spondyloarthritis trials, they usually have long disease durations. But that's an interesting thought. Don't be, I guess the point is don't be surprised when this happens. And I'm glad that, I got stopped by a major character like, Atul Diador.

Alright, everyone. Thanks so much for all your hard work this week at ULAR. Get some rest. Enjoy each other's coverage and next week we're gonna, once we're all back home and rested, we're gonna do a few panels, topic discussions and the audience can watch those. I think it starts next Tuesday at the same time as this program.

All right, folks. Thank you so much. Bye bye.

Thanks. Bye.