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You're listening to a RoomNow podcast coming to you from Barcelona, Spain, and EULAR twenty twenty five. Hope you enjoy it.

Hi, everyone. This is Adela Castro from Memphis, Tennessee, reporting from EULAR here in Barcelona. I wanted to, go over a representation. The abstract number is OP0102, and it's called the efficacy and safety of a new IL-17A blocker called selegepimab in patients with ankylosing spondylitis. This is a Chinese study performed in four sixty five patients with ankylosing spondylitis, and the primary efficacy was to achieve ASAS 20.

And then after week sixteen, it showed a significant proportion of patients achieved the primary outcome. And this was also noticed that this efficacy was sustained up until week forty eight in both doses of the medication. As far as safety, there was no major significant safety events. It did show a little bit of high proportion of mild elevation of LFT, but in general it seemed really safe. Something that is very interesting about this medication is that it's a fully humanized IgG4 antibody, which seems that one of the benefits is that it can last a little bit longer on the body and it can also minimize the drug antibody production.

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Hi, I'm Jack Cush. I'm coming to you from Barcelona and you are twenty twenty five. This is an early look at a new problem that we're dealing with and that is at risk RA, clinically suspect arthralgia, preclinical RA. The question is, when do you treat these folks? How do you treat them?

So we've had a few trials demonstrating the efficacy of a few drugs, but in general it's not that clear. There's a sort of a collision now of several sets of data that I think are somewhat instructive. We reported this week on RheumNow the results of a twenty twenty five ACR ULAR risk stratification criteria. This is a paper that was published that gives us some insight as to maybe who should get treated with more aggressive therapies when they just have arthralgia and maybe at risk because of ACPA or being positive, for family history. So, that paper says that the criteria, a point based system, is based on morning stiffness, patient reported swelling, inability to make a fist, C reactive protein, rheumatoid factor and ACPA levels.

And there's high and low points for low levels of morning stiffness or high levels of ACPA and that seems to be a reasonable approach but that's very different than what's being reported here at EULAR. Specifically, are two important long term follow-up studies to the Apipra study and the ARIA study. So, the ALTO study OP-four is a long term follow-up study of the Apipra study. Apipra was a two year trial where patients with at risk clinically suspect arthralgia ACPA positive but a positive MRI or ultrasound, so they didn't have synovitis, right, two hundred plus patients were either given abatacept subcutaneously or placebo for a year and then followed for a year off of that. In that study, we do know what the primary endpoint at week fifty two, six percent who received abatacep went on to develop RA but if they received placebo, it was twenty nine percent.

But after a year, another year of follow-up off of a drug, didn't seem to make much difference. It was thirty percent and forty percent, small difference. They followed those people out to as long as six years and what they found in the two year study holds true in the six year study and that is the patients who had the best responses were the ones with an extended auto antibody profile, meaning they had ACPA and rheumatoid factor, several ACPAs, and a number of different antibodies, anti acetylated protein antibodies, anti carbamylated protein, if they had all five of them, you were likely to have an extended response. In a two year study, it was fifty percent of the placebo patients went on to develop, RA but if you had this five serotype profile, only ten percent. That was at two years.

That same result is carried out to two years and four years and as long as six years and four years, the extended autoantibody, it was forty seven percent of Avatacep developed RA versus sixty seven percent. So, starts, there's still some protection is the point and that's just with one year of treatment. So, the profile being not what the ACR ULAR risk stratification said but here it's being ACPA positive and really high titer plus five other autoantibodies for RA. This is a little bit different than what was shown in the ARIA study. The ARIA study was another abatacep study, about one hundred patients were enrolled in a six month trial abatacep versus placebo and then they were followed for another twelve months.

At the end of six months, eight percent of abatacept and thirty five percent of placebo developed RA, and in this study, they followed them initially out to eighteen months where kind of the lines start to come together suggesting that the delay is being lost, thirty five percent versus fifty seven percent, but what they found in their prolonged study at five point three years, the people who never developed RA were those who had lower SED rates, lower rheumatoid factor, lower pain scores, better functional status, meaning that the opposite of that might be the people who are at high risk, and maybe those are the ones that you do want to treat and maybe that you do want to treat them with abatassa. So, from these three studies, we're getting a picture of the people that we may want to treat more aggressively with abatassa, right? So the extended autoantibody profile and maybe the people who had high risk disease, not low risk disease from the ARIA study. One more caveat and that is the treat earlier RA trial with methotrexate only showed in past publications that it worked only in seronegative, actin negative patients. So again, these are sort of rules as to who may need treatment in this hard to manage group.

Do you treat them, do you not, when they have clinically suspect arthralgia but no arthritis? Tune in for more great abstracts and presentations from UR twenty twenty five.