Background: Celiac disease (CeD) is a chronic T-cell mediated immune disorder driven by dietary gluten with no approved pharmacologic therapies. Although a gluten-free diet is effective for many patients, persistent disease activity and the challenges of strict dietary adherence highlight the need for alternative treatment strategies. We investigated ritlecitinib, a first-in-class irreversible JAK3/TEC kinase inhibitor, for its potential to modulate pathogenic immune responses and prevent intestinal injury in CeD.
Methods: In this phase 2, randomized, double-blind, placebo-controlled study, adults with biopsy-confirmed CeD in clinical and histologic remission underwent a standardized gluten challenge (10 g/day) and were randomized 1:1 to receive ritlecitinib 200 mg once daily or placebo for 21 days. Co-primary endpoints were changes from baseline in villous height-to-crypt depth (Vh:Cd) ratio at Day 22 and CeD patient-reported outcome (PRO) scores during gluten challenge. Secondary endpoints included changes in intraepithelial lymphocyte (IEL) counts and tissue transglutaminase IgA (tTG-IgA) concentrations.
Results: Ritlecitinib attenuated gluten-induced mucosal injury compared with placebo, as demonstrated by a significantly smaller decline in Vh:Cd ratio (least-squares mean change, -0.027 vs -0.545; p=.0040). No significant between-group differences were observed in CeDPRO scores. Ritlecitinib also prevented the increase in IEL counts seen with placebo (-20.7% vs +55.7%; p<.0001). Although not statistically significant, increases in tTG-IgA were attenuated in the ritlecitinib group compared with placebo (+19.4% vs +152.7%). Treatment-emergent adverse events were generally similar between groups and were predominantly gastrointestinal, consistent with gluten challenge.
Conclusions: Ritlecitinib attenuated gluten-induced histologic and immunologic disease activity in adults with CeD in remission undergoing gluten challenge. The absence of a significant CeDPRO effect may be attributable to enrollment of a relatively asymptomatic population and exclusion of patients with severe gluten reactions. These findings provide support for further evaluation of JAK3/TEC inhibition in larger clinical studies of CeD.
(NCT05636293, https://clinicaltrials.gov/study/NCT05636293, November 1, 2022)