Emerging treatments
Antibodies against the neonatal Fc receptor
CIDP is associated with pathogenic IgG auto-antibodies. 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 humanised 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 (non-responders and patients who relapse after intravenous immunoglobulin 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 utilise this to guide management of CIDP.[153][166][167][168]
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