S1397 Long-Term Efficacy and Safety of Intravenous (IV) Tulisokibart in Patients With Crohn’s Disease (CD): Results from the Open-Label Extension Period of the Phase 2 APOLLO-CD Study

Introduction: Tumor necrosis factor–like cytokine 1A (TL1A) is a mediator of inflammation and fibrosis in CD. Tulisokibart, an anti-TL1A monoclonal antibody, demonstrated robust efficacy without adverse safety signals during the 12-week induction period in adults with moderately to severely active CD in the multicenter, open-label, phase 2a APOLLO-CD study. We report long-term efficacy and safety data for tulisokibart at week 50 from the APOLLO-CD open-label extension (OLE). Methods: During the 12-week induction period, participants received IV tulisokibart 100 mg on day 1 and 500 mg at weeks 2, 6, and 10. Responders to tulisokibart induction at 12-weeks (defined as a decrease from baseline in CD activity index [CDAI] of ≥100 points or CDAI < 150 at week 12) were given the opportunity to enter the OLE study; 12-week non-responders discontinued the study. At week 14, responders were randomized to receive IV tulisokibart 100 or 250 mg every 4 weeks until week 170. Efficacy outcomes through week 50 in the intention-to-treat population are reported. Safety was evaluated in all participants who received ≥1 dose of tulisokibart. Descriptive statistics were used to summarize observed data. Results: Overall, 53 of 55 participants completed the 12-week induction period; 37 were considered induction responders and were randomized to receive tulisokibart 250 mg (n=18) or 100 mg (n=19). A greater proportion of participants who were biologic-naive entered the OLE in the tulisokibart 250 vs 100 mg group (44% vs 21%). Improvements in clinical, endoscopic, and biomarker outcomes observed with tulisokibart were generally maintained through week 50 in both dose groups. At week 50, a greater proportion of participants achieved clinical and endoscopic outcomes with tulisokibart 250 mg vs 100 mg (Table 1). Normalization of high-sensitivity C-reactive protein favored the 250 vs the 100 mg dose. At week 50, AEs were reported in 83% and 84% of participants receiving tulisokibart 250 and 100 mg, respectively, and were mostly mild-to-moderate in severity. Serious AEs occurred in 1 (6%) and 2 (11%) participants receiving tulisokibart 250 and 100 mg, respectively. Conclusion: At week 50, maintenance of treatment efficacy was generally observed with tulisokibart in induction responders. A trend for higher maintenance efficacy was observed with tulisokibart 250 vs 100 mg. Tulisokibart was well tolerated with no safety signals identified through 50 weeks of treatment. Larger trials are needed to confirm these findings. Table 1. - Clinical, endoscopic and biomarker outcomes at week 12 and among 12-week induction responders at week 50 Week 12Tulisokibarta (n=55) Week 50 Tulisokibart100 mg (n=19) Week 50 Tulisokibart250 mg (n=18) Endoscopic responseb 13 (24) 3 (16) 5 (28) Clinical remissionc 27 (49) 8 (42) 10 (56) Clinical responsed 37 (67) 11 (58) 12 (67) Composite endoscopic and clinical responsee 9 (16) 3 (16) 4 (22) Composite biomarker and clinical responsef n = 4917 (35) n = 164 (25) n = 176 (35) Normalization of hsCRPg n = 365 (14) n = 90 n = 165 (31) Normalization of fecal calprotectinh n = 446 (14) n = 142 (14) n = 162 (13) All data are n (%).hsCRP, high-sensitivity C-reactive protein; SES-CD, simple endoscopic score-Crohn’s disease.aAll patients treated with tulisokibart with baseline CDAI and SES-CD scores were included in the full analysis set population.bEndoscopic response was defined as a decrease in SES-CD total score ≥50% from baseline.cClinical remission was defined as CDAI score < 150.dClinical response was defined as either a decrease of ≥100 points in CDAI from baseline or CDAI score < 150.eComposite endoscopic and clinical response was defined as a decrease in SES-CD score ≥50% from baseline and either a decrease of ≥100 points in CDAI from baseline or CDAI score < 150.fComposite biomarker and clinical response was defined as a decrease in hsCRP or fecal calprotectin ≥50% from baseline and either a decrease of ≥100 points in CDAI from baseline or CDAI score < 150 (evaluated in patients with ≥1 elevated biomarker at baseline).gNormalization of hsCRP was defined as a concentration of < 5 mg/L among patients with elevated levels at baseline.hNormalization of fecal calprotectin was defined as a concentration of < 250 µg/g among patients with elevated levels at baseline.

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