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1. A 52-year-old man with treatment-naïve CIDP responds to IVIg but requires infusions every 3 weeks to maintain strength. Which statement best reflects the current understanding of CIDP pathophysiology and an unmet need in its management?
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All first-line therapies (corticosteroids, IVIg, plasma exchange) produce a durable cure without need for ongoing maintenance therapy
The classical complement pathway, culminating in membrane attack complex formation, is increasingly recognized as a driver of demyelination and axonal injury in CIDP, but no complement-targeted agent is currently FDA-approved for this indication
Neurofascin-155 autoantibodies are present in the majority of CIDP patients and reliably predict IVIg non-response
Subcutaneous immunoglobulin (SCIg) is approved for induction therapy in newly diagnosed CIDP, replacing IVIg as first-line treatment
2. In the phase 2 study of riliprubart, a humanized monoclonal antibody that selectively inhibits activated C1s in the classical complement pathway, which finding best supports its potential for long-term disease control across varied CIDP populations?
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Riliprubart produced benefit only in treatment-naïve participants, with no meaningful response observed in SOC-refractory participants
Across all three cohorts (SOC-treated, SOC-refractory, and SOC-naïve), riliprubart was associated with improvement or stable disease in the majority of participants at 24 weeks, sustained responses through approximately one year, and a ~35% reduction in neurofilament light chain (NfL), a biomarker of axonal damage
Riliprubart demonstrated efficacy only when combined with high-dose IVIg and was not studied as monotherapy
The phase 2 data showed no reduction in disease-related biomarkers, prompting discontinuation of further development
3. A patient with CIDP has an inadequate response to IVIg despite dose optimization. Based on best practices for individualizing emerging complement-targeted therapy, which approach is most appropriate?
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Discontinue IVIg abruptly and start a complement inhibitor with no additional monitoring, since biomarkers add no value in treatment selection
Characterize the patient's prior treatment response (e.g., SOC-refractory phenotype), assess for evidence of classical complement pathway–driven disease activity, and use biomarkers such as NfL alongside clinical outcome measures to individualize and monitor complement inhibitor therapy
Increase IVIg dosing indefinitely, since complement inhibitors have no defined role in SOC-refractory patients until formal FDA approval
Reserve complement inhibitor therapy exclusively for patients with normal complement activity, since elevated complement activation is a contraindication to use
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