[{"id":"captivate-incat-relapse","name":"Time to INCAT Relapse During Randomized Withdrawal","type":"PRIMARY","unit":"time-to-event","results":[],"timepoint":"Variable (randomized withdrawal period)","description":"INCAT (Inflammatory Neuropathy Cause and Treatment) disability score measures arm and leg disability on a 0-10 scale. Relapse = ≥1-point worsening from randomization baseline. Same endpoint as Vyvgart's ADHERE trial, enabling cross-trial comparison (though different mechanisms)."}]

OPEN QUESTIONS: 1. What is the exact dosing regimen (mg, frequency) for claseprubart in CAPTIVATE? 2. What proportion of patients will respond during the open-label run-in? 3. How will relapse rates compare to ADHERE (Vyvgart)? 4. Will DNTH pursue additional endpoints like I-RODS for sensitivity? INVESTMENT IMPLICATIONS: - POSITIVE: Validates C1s mechanism in CIDP, establishes DNTH as first C1s in CIDP, may define complement-driven CIDP subpopulation - NEGATIVE: Failure would raise questions about complement's role in broad CIDP and hurt the entire C1s class (including riliprubart) - Same design as ADHERE enables (imperfect) cross-trial efficacy comparison KEY COMPETITIVE DYNAMIC: - Readout ~Sep 2026, same timeframe as MOBILIZE - If both succeed: validates C1s class, market segments by mechanism - If CAPTIVATE succeeds but MOBILIZE fails: DNTH gains massive advantage (different design, may be population issue) - If both fail: C1s class in CIDP questioned Source: ClinicalTrials.gov NCT06176690, DNTH corporate presentations

CIDP pathology involves complement-mediated demyelination in a subset of patients. C1s inhibition blocks the classical complement pathway (antibody-triggered) while preserving the alternative pathway (immune defense). Claseprubart targets only active C1s, avoiding TMDD from the abundant zymogen pool.