Day 4 Recap- ACR Convergence 2025 Highlights Save

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All right. Hello, everybody. Welcome to the daily recap from ACR twenty twenty five in Chicago. I'm Mike Putman. I'm a rheumatologist at the Medical College of Wisconsin, and I am very excited to be hosting the RheumNow Daily Recap Panel for day four.

This is the last official day of the meeting. This is an exciting time. It's been a great meeting, a lot of fun. I had a great time seeing all the great science, catching up with a lot of good experiences all around, and today we're going to be covering the best and most impactful presentations that we saw at the meeting today. So excited to dive right into it.

For starters, I'd like to introduce our illustrious panel. Brian, do you want to introduce yourself?

Sure, thanks Mike. Hey everyone, my name is Brian Jaros. I'm one of the adult rheumatologists at Northwestern, so didn't have to go too far for this ACR. I focus in vasculitis and medical education and I'm excited to be here and recap with you all.

Well, you for joining in. Very happy to have you. Akhil, would you like to introduce yourself as well?

Yeah, absolutely. My name is Akhil Sood. I'm a rheumatologist at Washington University in St. Louis. I have a specific interest in lupus and a background in epidemiology and clinical research.

All right, great. Well, thanks for being here, guys. Excited to have you. So the format of these is pretty straightforward. We each have picked a couple of our favorite abstracts and presentations and picked a couple of key teaching points.

We're going go round robin and give a little feedback between each other as we go along. But for starters, we're just going to get right into it. Brian, I hear you have something to say about the Yanalumab data that we presented. Yanalumab, can you tell us Yeah, all about

try saying that three times fast. Yeah, so I will kick us off with abstract late breaking 24. This is Yanalumab demonstrating significantly decreased disease activity in Sjogren's disease and it's the efficacy and safety from actually two global phase three randomized control trials, which of course are cleverly named, that's NEPTUNIS one and NEPTUNIS two. So I picked this because as most of us are familiar with, we're desperate for anything we can get our hands on for these Sjogren's patients to help with their symptoms, improve their quality of life. So I was excited to see right off the bat that this you know, improved disease activity in Sjogren's.

Yanalumab is a A FUcosylated human IgG1. It actually binds the BAF receptor. So in that way it targets B cells through kind of a dual mechanism. One is blockade of that receptor, but because of the way it's engineered, it also contributes to antibody dependent cell cytotoxicity. And there are two kinds of trials here, NEPTUNIS one and NEPTUNIS two.

The big difference is the dose of unalumab that was administered. So in NEPTUNIS one, they compared unalumab on a Q one month dosing schedule versus placebo. In Neptunus two, they compared that Q monthly dosing to Q3 monthly dosing to placebo. They recruited adult Sjogren's patients. They had to be diagnosed within the last seven and a half years.

They wanted to get people who were not smoldering for like twenty, thirty years and unlikely to have a response. They had to have an SDAI which is that Sjogren's disease activity score greater than five indicating at least moderate activity and some residual salivary flow. Again, I think trying to rule out people who just had like completely burnt out and just damaged disease. And the primary endpoint was change in that SDAI. So when you look at the results from both Neptunus I and II, you saw significantly reduced SDI in both, NEPTUNUS one and NEPTUNUS two in the Q monthly dosing regimen.

The Q three month dosing regimen did not meet the primary endpoint. So this does seem to be a dose dependent response that the Q monthly dosing is the one we're seeing in effect here. What's interesting when you kind of look at the results more closely is that actually, as is the case in a lot of our trials, placebo got also fairly high improvements in the SDAI scores.

By a lot.

Background immunosuppression was allowed and a good portion of people were on background immunosuppression, so it's possible some of this was being driven by DMARDs and other therapies that they were getting. Even accounting for the placebo, there still was a statistically significant benefit to Yanalumab, but both achieved a minimum change of at least three. I think the mean was around five to six for both of them. So they're both considered clinically significant responses. They also, I thought was interesting, did a subgroup kind of analysis of the folks who had salivary flow greater or less than 0.4 milliliters per minute.

And in those who were at the higher end of that threshold, they saw an improvement in salivary flow rate and that was corroborated by subjective improvement in oral dryness from patients taking it that they did not see in those less than point four milliliters per minute at baseline. In terms of safety, pretty comparable between groups, no major safety signals that came out of enalumab treatment. So for me-

I was surprised by that. I thought it was better than expected. What do you think?

In terms of the safety signals?

Yeah, yeah.

Completely agree. I mean, we're extrapolating from other B cell targeted therapy, I would have suspected, especially with infectious risk, a higher rate of adverse events. Again, I wonder if because the placebo were also on a fair amount of DMARDs, which have their own infectious risk, if that drove some of them in that group. But I thought this was exciting. I mean, again, we're seeing a few things hot right now in Sjogren's.

I think it's a really pivotal time for the disease state. And I'm pretty excited about the idea of this coming forward as a possible treatment. I think the other interesting thing that comes out of this with that salivary flow subgroup is, do we need to be catching these people as early as possible before damage has occurred? If we do start them on this medication, will it have a disease modifying effect, which obviously we've struggled to find for salivary gland.

Yeah, big time. I love it. Akka, what do you think? Is this going to be FDA approved? Is there anything that stood out to you on the abstract?

Yeah, no, I think, yeah, no, I think that was a really interesting abstract and definitely really interesting findings. Think, definitely with Sjogren's and the ongoing, the previous clinical trials is that we haven't seen in meeting the endpoints or the placebo effect that we are concerned about. But seeing when you adjust for placebo, we are seeing it as positive response and definitely does seem like a promising drug for our patients with Sjogren's. But I think definitely it'll be things to consider like the timing of this medication, especially early Sjogren's versus long standing established Sjogren's missing that window of fibrosis, especially in those glands. I think, and especially that subgroup analysis, as Brian mentioned, was with the improved salary flow.

I think that's definitely really exciting and it'll definitely be something worth looking into, especially with Sjogren's patients when looking objectively, is that we start this enalumab and see this improve in both subjective report by patients, but also even the objective findings as really to salivary flowing as well. Definitely do think it is a promising We'll be excited to see what comes out of it with the next steps, absolutely. And I think even going back to that safety, I guess one thing was that there was comparable safety profile. I wonder if it was the bath pathway, because at least with belimumab, it does have, the previous studies have shown that it does have a pretty safe infection profile. So I wonder if there is some component that while it is a B cell pathway, the infection profile even in belimumab has been relatively safe, at least in previous days with the emulated target trial as well.

Yeah, I'm not a big science guy, but I think that it has a little less impact on T cells maybe, but I'll have to look into that one more. I got a tweet for you guys. This is from March 2019. I was talking about the preliminary preliminary data. I said failed primary endpoint, but shows significant reduction in fatigue in primary Sjogren's would be game changing, but we've been down this road before and these effects typically wash out in phase two and three.

So the fatigue did wash out, didn't hit facet fatigue so I was right but they hit on their primary endpoint so I was also kind of wrong so it'll be interesting I bet the FDA approves this but it'll be interesting to see how it goes so Akhil you're up now You were also excited about a late breaker, is that right?

Yeah, absolutely. So I think here at ACR25, we've seen a lot of abstracts related to CAR T. I think since the landmark study coming out of Erlangen, we've just seen a rapid explosion of CAR T therapies over the last few years, and especially just the different formulation, the engineering. With the landmark study was looking at cytotoxic CAR T, CD19 positive CAR T, but late breaking abstract 23 evaluated the safety and efficacy of regulatory CAR T in patients with refractory RA. So Landmark study, compared with to Landmark study, they're engineering these regulatory CAR T cells that are specific for citrullinated proteins, which is really important in rheumatoid arthritis, ACPO positive.

Compared to the standard, the landmark study, these patients also didn't receive lymphodepletion. It's a different approach in that not just one is the cytotoxic impact effect of CAR T on autoreactive B cells, but looking at the immunosuppressive effect of regulatory T cells on autoreactive B cells. They also eliminated the lymphodepletion factor. And then also they allowed patients to receive background immunosuppression up until the time of enrollment and including during the study as well. So while this is an ongoing phase one study, it was a small cohort of patients, about six total, patients with three receiving dose level one and three receiving dose level two, and they found really significant impact or reduction in disease activity measured by DAS28 CRP with four of six having decreased in their disease activity at week four but there were more rapid onset in the dose level two terms of both joint counts, tender and swollen joint counts, and they also noted significant improvement as well in HAC DI as well in terms of functional status.

But the tricky part was that after week four, we started to see some variation in terms of response. There's some patients that had sustained remission, but then there's another fraction of patients that had a rebound of their disease activity. So then it kind of leads to the question is that where is the effect, where is the major agent at play? Is it the regulatory CAR T that's the confounding or is it the lymphodepletion as well that the patients aren't receiving, even the background immunosuppression? But when it came to safety, it did overall show a pretty safe profile with no reports of ICANS or CRS.

So I think overall it was a pretty interesting abstract.

Yeah. I like it. We're kind of getting more creative about the CAR T. I think this induction therapy part of it, or the cytoreductive therapy part of it, has always been kind of a tough sell for rheumatologists. So I think a lot of folks are focusing on ideas that are beyond that.

But we're also kind of losing the initial sort of this is all magic sauce vibes. And I'm wondering if we're kind of trending more towards a middle ground that'll be a little less inspiring, a little less harmful. I don't know. Brian, what do you think? Where does this fit for you and CAR T stuff?

Yeah, I have to say, I mean, I think this is furthering the landscape certainly, you know, into what we all want, which is hopefully curative treatment for our patients to get them off immunosuppression. I worry that, like you said, we've exchanged the cytoreduction, which I completely agree is a concern for something that seems like it might rebound and not have that strong of an effect. And frankly for me, and maybe it's definitely possible, I just don't see enough severe RA, but the type of RA patient that I would be thinking about CAR T in, we're already in connective tissue disease vasculitis thinking of very specific people, but I would have a really high threshold in rheumatoid arthritis for CAR T. So I'd want something that's really safe and works very well, which I hopefully will get to, but I don't know that we're there yet, if that makes sense.

Yeah, that's a great point, honestly. It's gonna take me exactly one person who gets grade three CRS before I'm just out, you know? And so it's kind of hard in RA. Your threshold for safety is gonna be a little bit higher. Yeah.

All right, great, Ako, I love it. All right, my turn, I'm gonna jump right in. So I'm gonna transition briefly away from the late breakers and share one that I found just a little bit ago and I watched the presentation on it and I just loved it so much, so I gotta share this. This is abstract 2,662 and this is a target trial emulation of biologic and targeted synthetic DMARDs in RA ILD. And so this is combining two of my favorite things from last year.

You know, one is target trials. And just a brief explanation of that for everyone. You know, there's a lot of funky epidemiology at the meeting this year, a lot using the TriNetX database. And some of it was great there's some and all of it was well intentioned but every once in while I just said I don't know about that and so I have been looking for some really good epidemiology to share tonight and this is rishi deci's group and this is Gregory McDermott. I'm a guy who did a really awesome presentation and a really cool study here.

So this target trial is they say, you know, we're going to do observational data, we're going to try and make it look like an RCT and we're going to try and approach some of the rigor that you have in an RCT where, you know, you have a well defined patient population, we're excluding a whole bunch of people to make sure that we're really studying the people we're interested in. We're going to spend a lot of time talking about what is day one, you know. We can't necessarily enroll someone in an observational study but we can approximate it, you know, do our best to get there and then we're gonna try and deal with all this confounding that always plagues observational data. We're gonna have well defined outcome measures. They did all that stuff and they asked a super relevant question which was in RAILD we have all these drugs that these new guidelines have recommended what about just using the normal therapies how do they perform so they said we're gonna look at Medicare A B and D and they're going get all the patients they could with RA, ALD using a bunch of validated coding algorithms and they said we're going to look at compared to rituximab how did patients do who got abatacept, tocilizumab, a JAK inhibitor, or a TNF inhibitor.

So a really cool clinical question. We're looking at all the good things for RA and we're comparing it to rituximab. Their index date was the first date after you got the ILD and you got your biologic and or targeted synthetic DMARC. And then they did the fancy propensity score matching to try and adjust for confounding. You can never fully get rid of confounding in my opinion.

There's a bunch of ways to try to measure that and this group is expert at doing it. But just so you know, it's not a magical solution, but you know it's the best effort we can do. And then they said, know, we're gonna look at hospitalizations for respiratory issues, transplantation or death so a bunch of outcomes that we really like and care about and what did they find there was just absolutely no difference on for their composite outcome measure so if you got abetacept IL-six, a JAK, a TNF, or rituximab your RAILD didn't seem to result in badness and then you differing them out. Now once you start slicing and dicing things the story got a little bit weirder and actually JAK inhibitors and Avatacin looked a little bit better than Rituximab which is completely the opposite of where some of the recommendations had come from those recent ACR guidelines. Now, EULAR is zagged and they included some of those so I think that there's some increase in awareness that some of these other mechanisms might be good.

But my summary is really from the presentation. This is what the gentleman who gave the presentation said and I really thought this was well put. He said achieving good control of disease activity is probably the key objective of treatment of patients with RA ILD. I just really like that. I think that if you're going to be treating RA ILD, your prior should be that we're going to use a drug that works for RA.

So I don't know, what do you guys think? Do you feel good about that? How do you feel about observational data to answer causal questions? Akhil, I'm going go to you first. What do you think Akhil?

Yeah, I think that's really interesting. Mean I think definitely when you think of the sequence of therapies you think like rituximab is going to be the superior, the later line agent but then when we're seeing these findings of the abatacept and the JAK inhibitor in RE ILD, I think it really then boils down to is just treat the target and getting the disease under control. And then if you can control the rheumatoid arthritis aggressively within joints, you can avoid progression outside the joints. And even when you have RA associated ILD, it'd be interesting to see where exactly yeah, think that it was really interesting just how they can get the treat to target within control, and that's better the similar outcomes. Yeah.

Brian, what's your where are you at on this? What do you think?

So reminding, like and you may have mentioned this. When they're propensity matching, are they matching also based on, like, severity of ILD in these folks? Like, do we know where they balance between treatment arms groups? Because presumably, if you're getting rituximab, you have, you know you're thinking of like people with sicker disease

yeah the plot thickens right so in their abstract they went over their propensity so the nice thing about propensity match is you can look at a whole bunch of variables they have like over 40 or some but this is Medicare data. You don't have like really granular FVC. You don't have a six minute walk test for these people. And so, yeah, I mean, you found the fly in the ointment here. This isn't the kind of data that you can be like 100%.

We knew exactly what these patients have. And when I said you can't always fix things with propensity matching, part of the problem is you don't, you can't always match, or if you use inverse probability weighting, which is a similar approach, you can't always have all the variables you know. I always joke about acai berry consumption and you know yoga participation like we never know how much people participate in yoga but maybe it's really bad on one side and the beauty of randomization is that you fix all of those and I think you keyed in on a key point which is that you know there's some things they couldn't really fix and maybe that's part of the problem here so good epidemiology coming from Brian here all right I'm gonna throw it back to you after you sorry

I was gonna say a phrase I don't know if I've ever heard before. No.

You got right to the crux of the matter and rained on my little target trial parade, which is very appropriate. I think you I think that's a very important limitation I forgot to mention. Alright. So let me throw it back to Brian here. Tell me about your next abstract.

What are you excited about, Brian?

Yeah, so actually somewhat in the same vein when we think about propensity matching and observation. So this is abstract 2689it was in the psoriatic arthritis abstract session today. It's comparison of incidence of PSA in patients with psoriasis treated with a variety of different agents: IL-seventeen inhibitors versus 23 versus twelve and twenty three versus TNFs. And this was a retrospective study by April Armstrong and their group. So, of course, this tries to address or give us information about a really interesting question, which is who with psoriasis progresses to psoriatic arthritis?

Are there certain treatments that we should be giving people or dermatologists should be thinking about upfront that will prevent progression to psoriatic arthritis or maybe just treat the joints better. And so this was a retrospective study. They tried to capture a very specific patient population. So they had to have a diagnosis of psoriasis without having ever started any kind of biologic treatment. So they were biologic naive and the chart was scanned for no diagnosis of PSA.

They gave a fourteen day grace period. So if within fourteen days after the index date, they were diagnosed with PSA, it was accounted for that they may have just not seen a rheumatologist yet or something like that. And they basically matched cohorts compared to the last group, which where rituximab kind of served as the comparator IL-seventeen served as the comparator here. And they reported the results as percent time with psoriatic arthritis per agent exposure. So, in all of the groups, numerically speaking, IL-17s seemed to perform the best.

They had numerically less time with psoriatic arthritis that only reached statistical significance when IL-seventeen was compared to the twelve-twenty three combo or versus TNFs, not versus 23, though it came close. And similar to what you were mentioning before, tried to control for confounders with propensity matching based on psoriasis extent, the subtype of psoriasis that they've had, the disease duration, background DMARDs, again, not perfect, but at least trying to take some of these other factors out of it. What's, you know, I think a big limitation here and was definitely mentioned in the presentation is that these patients are often with psoriasis PSA not staying on one agent for a very long time. And when they switch to another agent, they're automatically, they drop out of this study. And so you see, they start with really large numbers at the beginning in the first year, there's like around a thousand people, for example, in each arm by year one that gets cut at least 50%.

And by year two, you're talking like double digits of the number of people. And a lot of the time when you get to year two, that's when you start to see the separation curves of people who are getting PSA between the two treatment arms. And so you wonder like how much is all this dropout and treatment switching, you know, creating an effect that is not actually, you know, causal, but, associative. So anyway, I think it's interesting. I think I'm always trying to ask the question of anecdotally see when patients come from Durham, what biologic they're on and trying to make my own associations of what I see the most of.

But I'm curious to hear from you all, and I know Mike, you probably have some thoughts on this from your own work, what your takeaway from this is.

Yeah, I'll let Akhil jump in first and then I'll share some thoughts on that. Akhil, what do you think about this? Do you have a favorite? Do you believe it? Where are you here?

Yeah, no, that's a good question. I mean, I think for me, I I think when I see patients, I guess with psoriatic arthritis, we often think of the TNFs first, but I think it's interesting when you're seeing that this IL-seventeen is having better data compared to the TNF versus IL-twelve 23. And I think Brian, you brought up a really good point is that within this window, there's lots of switching, discontinuation, and that could be a factor that is kind of confounding this. And I think definitely the timing or switching of medication could be one thing. And then think also thinking about which biologics work best on the skin domain is also a big factor as well.

I mean, IL-seventeen, I think does work well. IL-seventeen and TNF work well for joints versus, like, twelve twenty three, you know, that could be a component that could be, you know, confounding it, but definitely it's interesting as well.

Yeah. So Brian was joking because I have done work in this area before. Published, I was a co author on paper with Sheikha Singlo that looked at this particular question. We saw that IL-17s were not better than TNFs, but the 23s and 1223s might be. So this goes back to what I started with a little while ago about the perils of observational research for causal inference.

You know, just need randomized controlled trials. And the nice thing about this area is that there actually are enough trials. It'd be kind of neat if we could pool all that data and kind of get into it. But yeah, it's going to be an ongoing debate and I think this is a research group. They know what they're doing and so this is definitely gonna throw some gasoline on that fire.

That was a great one, Brian. Thank you. Akhil, you're up with another one looking at lupus nephritis. I love it. What's going on in the world of lupus nephritis?

Yeah. Yeah. So there are two abstracts in the SLE treatment session earlier today, it's really interesting that they're looking at the use of tacrolimus versus MMF plus tacro or MMF alone in lupus nephritis. There's abstract 2,697 and abstract 2,698. So abstract 2,697 was a prospective randomized control trial that looked at the efficacy and safety of tacro versus mycophenolate, in both cases receiving glucocorticoids and the induction and maintenance remission for proliferative lupus nephritis.

And the primary endpoint was looking at sustained renal response by week ninety six. The sustained renal response was defined as at least 50% reduction in proteinuria and twenty four hour urine protein less than one gram and no rise in creatinine at least 15%. And they also evaluated the safety as well. This was a trial that's composed of 130 patients, sixty five in each group. And so when they're comparing tacrolimus versus mycophenolate, both groups actually showed similar rates of sustained renal response at sixty percent in tacrolimus versus seventy percent by week ninety six in the mycophenolate group, and then the time to renal adverse events were actually similar in both groups at a rate about seventy percent.

And then there's another abstract, 2698, that took a different approach and alluding to the target trial emulation nicely described by Mike that was comparing tacro versus tacro and mycophenolate combination in patients with proliferative lupus nephritis. And so this one, they looked at the primary outcome was the total renal response, which is complete or partial renal response by twelve months. And they also looked at the safety as well. And so in this one, they actually showed that compared to the combo mycophenolate plus tacrolimus group had a much lower rate of total renal response at thirty three percent versus sixty percent. And both in the intention to treat and per protocol analysis, or the equivalent that they use in an emulation of a target trial, the tacro plus mycophenolate showed simply a higher total renal response.

So And I think just overall, which is really interesting is that the one abstract was showing that tacro alone versus mycophenolate, there was similar efficacy. But when you look at the combination of mycophenolate plus tacro, it was much superior in terms of efficacy and similar safety and so kind of alluding back to the guidelines that were released last year I think I would still say in terms of guidelines I would still favor the triple therapy of mycophenolate plus CNI if the patient has elevated protein in urea but curious to hear your guys' thoughts as well.

And I gotta say this made me uncomfortable and here's why. Because voclosporin was fine, but it wasn't really this good. Is it possible we've picked the wrong horse and it should have been tacro all along? I don't know, I've always been kind of excited about tacro. I like tacro for myositis.

I've kind of long thought that it'd be maybe a good addition in lupus. And then the VocalSpout trial, they confirmed that. But then we went Voclo, and it wasn't that strong. So I I don't know. It gives me the heebie jeebies.

Brian, what do you what do you think?

Man, I have to say I am not a tacrolimus lover. No. For me, I mean, listen, I think in lupus, it's just hard because it's not treating a lot of good stuff in lupus other than the kidneys. And so I like that CellCept, know, mycophenolate gives you much broader coverage. I agree with Akhil, you know, this is mirroring our guidelines of triple therapy.

And I think that's reassuring to see like another trial that, supports what we're doing. But between Tacro and Voclo, I think I'm still on board with the Voclo train. I haven't sold my ticket yet.

Calcineurin non exciter guy or whatever. I get it, I get it. Would not favor Attackro over MMF or just monotherapy. That's for sure. All right, I'm gonna end with a quick hit here.

This is a late breaker number 20. This is important data. This is the efficacy and safety of ducravacitinib up to week fifty two. This is from the POETIC trial program. Ducravacitinib is a TYK2 inhibitor.

It's kind of a cool mechanism. You know, we had our whole run of JAKs and now we're all kind of bored of JAKs and we're moving on to the newer, fancier, shinier things. And I think that ticks are kind of coming on strong and ducravacitinib is, I think, the first of the party really. And so they're investigating psoriasis. They're approved in 2022.

And then this is their TYK2 inhibitor, ducaracitinib, that was showing their data of fifty two weeks for psoriatic arthritis. Now the trial only ran for sixteen weeks in a blinded fashion. At first I kind of like looked askance at that, but then I remembered that you can't untreat people for fifty two weeks for active psoriatic arthritis. So, you know, sixteen weeks seems like a reasonable time point. It looked pretty good.

Over sixteen weeks, pretty nice benefit. Patients in the ducravacitinib group had higher PASI75s. That's a skin score, as you would expect. But DAS28 CRP scores were better and there's about a 20% difference in the ACR20s, you know. So you have about number number three or five people to get an ACR twenty at sixteen weeks.

Not bad. They did an open label and everyone just sort of drifted up and found their little happy place. So overall it looks pretty good, pretty encouraging. I bet they get the label for psoriatic arthritis. And then we're gonna have to decide what to do with it.

So you guys have any early hot takes on where tick twos are gonna fall into your treatment paradigm? It's a pretty crowded place. We've got jacks, 17s, 23s ish, TNFs. Where you gonna put it guys? Brian, I'll go to you first.

What do you think?

Yeah, I imagine so I don't think we're seeing the same safety signal that the Jack saw. So I imagine this is not coming with the black box warning that the Jack has. So I'm wondering if the place is gonna be a patient who prefers an oral agent, hasn't necessarily failed a TNF or something allowing us to get a Jack, but this is maybe in our armamentarium as a potential first line that we can use for those patients who really just do not wanna take an injection or infusion.

Pretty sharp hot take, I like it. Hako, what do you think?

No, I completely agree with Brian is that I think definitely an individual that prefers an oral formulation over injectable or infusion, I think is definitely one thing. And then even looking at the JAK inhibitors, I think just the safety profile, the black box warning, and then the strong association of metabolic comorbidities in psoriatic arthritis or psoriasis as well, I think I would definitely place a TYK2 above a JAK, but definitely each is a case by case and risk versus benefits. But I think these findings are really promising and really exciting as well. And definitely, I think there's some problems with the TYK2, and I think it'll be a great option for our patients as well, especially those looking for an oral option too.

I love it. Very promising and some great options for patients. I think that's kind of a good theme for today. We had a lot of interesting new drugs and kind of a lot of good reports, observational studies, kind of reporting on some of the older drugs, whether or not who knows which ones were correct. I think that wraps up our day four coverage.

Thank you to everyone who tuned in. I really appreciate y'all following our coverage at RheumNow for the last day of the meeting. This does not end our coverage though, so if you're looking for a very spooky way to stay connected to ACR25, Artie and Jack will be hopping on the podcast Halloween. That'll be this Friday. I certainly expect them to be wearing costumes.

And then next week we'll have a lot more great content. There'll be a bunch of content panels, the Axe Boss, RheumNow, CR T of course. And then most importantly, if you are available, please sign up for RheumNow Live in Dallas, TX. That'll be February. I will be there talking.

I would love to see you all in Dallas, TX. It would be a lot of fun to have a big crew at that meeting. You can register now at roomnow.live. That's the last thing I've got. Want to thank both of our panelists thank you brian thank you aqua thank you for joining us appreciate having this conversation with you all

awesome thanks mike great to be here thank

you thank you thanks everybody