Artiva Biotherapeutics (Nasdaq: ARTV) reported that its allogeneic NK cell therapy AB-101 (AlloNK), combined with rituximab, produced a 71% ACR50 response rate in refractory rheumatoid arthritis patients with at least six months of follow-up. In addition, there were no relapses and no requirement for new immunomodulatory agents, as per data to be presented across five abstracts at the AlloNK cell therapy EULAR 2026 Congress in London this June.
The data come from a pooled interim analysis of Artiva's company-sponsored Phase IIa basket trial and a parallel investigator-initiated basket trial, together enrolling 31 patients with rheumatologic diseases including refractory RA and severe Sjögren's disease. Both trials evaluate AB-101 in combination with anti-CD20 monoclonal antibodies across B-cell driven autoimmune diseases.
Key readouts from EULAR
The headline figure — 71% ACR50 in refractory RA at six-plus months — is notable in a population that has, by definition, exhausted multiple prior targeted therapies. No patients in that cohort relapsed or required new immunomodulatory agents during follow-up, suggesting durability of response, though the small sample size and absence of a control arm limit interpretation. Poster data further describe deep B-cell depletion that the company characterizes as comparable to CD19 CAR T-cell therapies, and a favorable safety profile across immune-mediated disease indications. A separate oral presentation will detail the first patient with severe Sjögren's disease treated with the combination, an indication for which no targeted therapy is currently approved.
The full data package spans a late-breaking oral presentation (abstract LB0003), one additional oral, two poster sessions, and one publication-only abstract. A post-meeting webcast is scheduled for June 8, featuring Paul Emery, Arthritis UK professor of rheumatology at the University of Leeds.
Mechanism and competitive positioning
AB-101 is an off-the-shelf, non-genetically modified, cryopreserved NK cell therapy derived from cord blood. Its proposed mechanism centers on augmenting the antibody-dependent cellular cytotoxicity effect of anti-CD20 antibodies — specifically Genentech/Roche's Rituxan (rituximab) — to drive deeper B-cell depletion than rituximab alone can achieve. Where rituximab depletes peripheral B cells through complement-dependent cytotoxicity and ADCC, the addition of allogeneic NK cells is intended to extend cytotoxic activity to rituximab-resistant or tissue-resident B-cell populations that are thought to underpin incomplete responses and relapse in autoimmune disease.