Efgartigimod in idiopathic inflammatory myopathy: Findings from ALKIVIA and ALKIVIA+

touchIMMUNOLOGY coverage of EULAR 2026

I’m Hector Chinoy, a rheumatologist based in Manchester in the UK. I work at Salford Royal Hospital, and I also run a programme of research at the University of Manchester.

Could you tell us about IIM and the unmet needs and its treatment?

Idiopathic inflammatory myopathy (IIM) is a rare autoimmune disease, classically characterized by muscle weakness. Some patients also experience skin disease, lung disease, a lot of fatigue, and Raynaud’s, so there can be a number of extra muscular manifestations. It is a rare condition; there’s probably about 15,000 cases within the UK and roughly about 80,000 cases within the whole of Europe.

What was the rationale for investigating efgartigimod in this indication?

Efgartigimod is a FCRN blocker and it’s a drug that is already licensed in a number of neurological conditions, such as myasthenia gravis and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Essentially it is a human IgG1 antibody Fc fragment that selectively reduces IgG without impacting antibody production or other parts of the immune system. In other terms, it effectively mops up pathogenic antibodies. It is a good option if you are treating a condition where pathogenic antibodies seem to be involved in manifestations of the disease.

Could you describe the methodology of ALKIVIA and ALKIVIA+, and the outcomes assessed?

ALKIVIA is a seamless phase 2/3 randomized, 1:1, double-blind, placebo-controlled, multi-centre study of adult patients with IIM. The study recruited patients with a number of different subtypes, including immune-mediated necrotizing myopathy, dermatomyositis and anti-synthetase. Participants received weekly efgartigimod or placebo. The initial results were presented at EULAR 2025, and it was a positive study. What’s happened now is after the 24-week, placebo-controlled period, which was the initial primary endpoint, patients receiving efgartigimod could continue the therapy and the patients who were on placebo could switch to the active drug. So the ALKIVIA+ has followed the patients into 52 weeks.

What were the main efficacy findings from ALKIVIA and ALKIVIA+?

With the ALKIVIA study, the primary endpoint was the mean total improvement score (TIS) at Week 24, and this was achieved in the patients with the active treatment compared to placebo. Going into Week 52 of ALKIVIA+, improvements in the TIS were maintained in the patients who are on the active treatment and also in the patients who were switched from placebo to efgartigimod; they improved and also achieved a significant TIS as well.

What was the safety profile of efgartigimod in these studies?

The overall safety profile was very favourable. There were a number of adverse events (AEs), but these were comparable generally to placebo. It was documented that approximately 1/5 of patients did experience a serious adverse event (SAE) during the ALKIVIA study, but, again, this was not statistically significant compared to the placebo group. The overall incidence of AEs remained consistent up to 24 weeks in ALKIVIA and then up to 52 weeks with ALKIVIA+.

What will be the next steps in the clinical development of efgartigimod?

These findings are from the phase 2 component of the study and the extension into week 52, but there is also a phase 3 component to the study, which is ongoing and we await these results with interest. Then we also want to know which of the myositis subtypes, dermatomyositis, antisynthetase syndrome or IMM, are most likely to benefit from the drug.