Expert: Selective inhibition of active C1s, the catalytic serine protease subunit of the C1 complex in the classical complement pathway. Blocks C1s cleavage of C4 and C2, preventing formation of the C3 convertase (C4b2a) and all downstream events (C3 amplification, C5a/C3a anaphylatoxin generation, MAC/C5b-9 formation). Targets ONLY the enzymatically active form of C1s (not the abundant zymogen precursor, avoiding target-mediated drug disposition). Preserves lectin pathway (MASP-2 mediated) and alternative pathway (Factor B/D mediated) fully intact, maintaining MAC-mediated bacterial defense — no meningococcal vaccination required. More targeted than C2 inhibition (blocks only classical) or C5 inhibition (blocks terminal pathway from all three routes).

Everyday: Blocks one specific step in the immune system's "demolition cascade." When autoantibodies trigger the classical complement cascade (a chain reaction of proteins that ultimately punches holes in cells), C1s is an early enzyme that relays the demolition order. By blocking active C1s, the demolition crew never gets mobilized through this pathway. Importantly, this leaves two other immune defense pathways fully intact — the "always-on" alternative pathway can still kill bacteria normally, so patients don't need meningococcal vaccination (unlike C5 inhibitors). Think of it as disconnecting one specific alarm system (the one producing false alarms in autoimmune disease) while leaving the 24/7 security cameras running.

Targets: ["C1S"]

Primary EP: [{"id":"mobilize-irods","name":"Change in I-RODS Score","type":"PRIMARY","unit":"points","results":[],"timepoint":"Week 24","description":"I-RODS (Inflammatory Rasch-built Overall Disability Scale) is

Primary EP: [{"id":"vitalize-irods","name":"Change in I-RODS Score","type":"PRIMARY","unit":"points","results":[],"timepoint":"Week 24","description":"I-RODS score change from baseline, comparing riliprubart to I

Riliprubart - CIDP (Refractory) - Ph3 - Primary Data (MOBILIZE) May 2027 (primary completion)

Riliprubart - CIDP (vs IVIg) - Ph3 - Primary Data (VITALIZE) July 2027 (primary completion)

MOLECULE PROFILE: - Format: IgG1-LALA-PG-YTE monoclonal antibody - LALA-PG mutations (L234A, L235A, P329G): Eliminate FcγR binding and complement activation (effector-silent) - YTE mutations (M252Y, S254T, T256E): Enhance FcRn binding → extended half-life - Target: Active C1s only (not zymogen — avoids TMDD) - Half-life: ~40-50 days (double claseprubart due to YTE mutations) - Route: IV loading → SC maintenance - Loading dose: 3000 mg IV (requires infusion center + HCP) - Maintenance: 450 mg SC Q4W (MOBILIZE) or 600 mg SC Q4W (VITALIZE) — self-administered at home - Self-administration: Yes for maintenance; No for loading (IV infusion) DIFFERENTIATION vs CLASEPRUBART (DNTH): - Extended half-life (~40-50d vs ~21d) enables Q4W maintenance (less frequent) - IV loading dose = requires infusion center visit for initiation - Q4W dosing = better maintenance compliance/convenience - YTE engineering = purpose-built for longer dosing intervals CLINICAL PROGRAM (CIDP TWO-TRIAL STRATEGY): - MOBILIZE: Phase 3 CIDP, parallel-group, placebo-controlled, refractory patients, I-RODS endpoint, 450mg SC Q4W, PCD Sep 2026 → Purpose: FDA regulatory approval (placebo-controlled gold standard) - VITALIZE: Phase 3 CIDP, active-comparator vs IVIg, double-dummy, I-RODS, 600mg SC Q4W, PCD Mar 2027 → Purpose: Market access and physician adoption (head-to-head vs standard of care) → UNIQUELY POWERFUL: No other CIDP program has head-to-head IVIg data SANOFI STRATEGY RATIONALE: MOBILIZE answers "Does it work?" (vs placebo) — for regulators VITALIZE answers "Is it as good as IVIg?" (vs SOC) — for payers and doctors Running both simultaneously accelerates overall program timeline by ~1-2 years