Emerging treatments
Antibodies against the neonatal Fc receptor
CIDP is associated with pathogenic IgG autoantibodies. The neonatal Fc receptor (FcRn) extends the half-life of endogenous IgG by binding and transporting it back to the cell surface to prevent it from being degraded by lysosomes. Efgartigimod, a humanized IgG1-derived Fc fragment that competitively inhibits FcRn, is approved for the treatment of myasthenia gravis and is being investigated in CIDP.[163] The anti-human FcRn monoclonal antibody rozanolixizumab has been assessed in a phase 2 trial for CIDP.[164] No antibodies have yet been approved to treat CIDP.[165]
Serum neurofilament light chain
Serum neurofilament light chain (sNfL) levels are correlated with axonal damage, and so have the potential to be used as a serum biomarker of disease activity and treatment response in patients with CIDP. Studies have demonstrated that higher sNfL levels are associated with an active disease state (nonresponders and patients who relapse after intravenous immune globulin withdrawal), and treatment-naive patients beginning induction therapy had higher levels of sNfL than those on maintenance therapy or in long-term remission without treatment. Larger studies will be needed to determine how to potentially utilize this to guide management of CIDP.[153][166][167][168]
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