Chronic inflammatory demyelinating polyneuropathy (CIDP)
CIDP is an acquired chronic immune-mediated demyelinating polyneuropathy of the peripheral nerves — symmetric proximal and distal weakness, sensory loss, areflexia, and characteristic cytoalbuminologic dissociation on CSF testing. Nerve conduction studies show demyelinating features (conduction block, temporal dispersion, prolonged distal latencies, reduced conduction velocities). Diagnostic frameworks: EFNS/PNS 2010 and 2021 + EAN/PNS 2021 revised criteria + INCAT and ONLS scores for disability tracking. Standard of care multi-tiered: IVIG (intravenous immunoglobulin, ICE trial 2008 Lancet Neurology), SCIg (subcutaneous immunoglobulin, PATH trial 2018 Lancet Neurology, Hizentra FDA-approved for CIDP maintenance 2018), corticosteroids, and plasmapheresis remain first-line; efgartigimod (Vyvgart Hytrulo for CIDP, FDA-approved June 2024 via ADHERE Phase 3 trial) is the first FcRn antagonist approved for CIDP and is changing the maintenance landscape, with nipocalimab and rozanolixizumab in trials. Rituximab off-label for refractory CIDP and nodal/paranodal antibody subtypes (anti-NF155, anti-NF186, anti-Contactin-1, anti-CASPR1 — these subtypes often respond preferentially to rituximab over IVIG). AAN 2024 + EFNS/PNS 2021 + EAN/PNS 2021 + GBS/CIDP Foundation International. No peptide in the Juno library has a defensible CIDP discovery-card case. Twenty-seventh deliberate non-elevation.
What changes during this transition
CIDP sits at the intersection of two patterns that make peptide marketing especially seductive: it is a chronic disease that responds incompletely or unpredictably to standard treatment in a meaningful minority of patients, and 'nerve' is a category that the peptide community has built a parallel vocabulary around — nerve regeneration, neurotrophic support, neuroprotection, axonal repair. The editorial work this page has to do is to draw the line between those two categories cleanly, because the marketing erases it. The first thing to be clear about: CIDP is not a single disease. It is a clinical syndrome with multiple variants — typical CIDP, MADSAM (Lewis-Sumner syndrome), DADS (distal acquired demyelinating sensory), focal CIDP, sensory-predominant CIDP — and, increasingly important, a set of antibody-defined subtypes (anti-Neurofascin-155, anti-Neurofascin-186, anti-Contactin-1, anti-CASPR1) that behave differently from antibody-negative CIDP. The nodal/paranodal-antibody subtypes often respond poorly to IVIG and respond better to rituximab; identifying them changes treatment. CIDP also needs to be distinguished from its mimics — POEMS syndrome (VEGF elevation plus M-protein plus osteosclerotic myeloma, a very different disease), anti-MAG IgM neuropathy, MMN (multifocal motor neuropathy, which is IVIG-responsive but specifically does NOT respond to corticosteroids and can be worsened by them), and chronicity itself distinguishes CIDP from GBS by the >8-week criterion. The differential matters because the treatment decision tree branches on it. A peptide clinic offering 'CIDP support' has, almost without exception, not engaged with any of this. The second thing to be clear about: the standard-of-care toolset in 2026 is broader and better than it was even three years ago. The first-line options (IVIG, SCIg, corticosteroids, plasmapheresis) have decades of evidence; SCIg for maintenance, validated in the PATH trial and FDA-approved in the Hizentra formulation in 2018, has shifted many patients out of hospital-infusion-center IVIG schedules and into home subcutaneous regimens. Efgartigimod (Vyvgart Hytrulo for CIDP, approved June 2024 via the ADHERE Phase 3 trial) is the first FcRn antagonist approved for CIDP — a paradigm shift because it depletes pathogenic IgG by accelerating its turnover at the FcRn receptor, mechanistically distinct from immunoglobulin replacement or general immunosuppression. Nipocalimab and rozanolixizumab are in trials behind it. Rituximab, while off-label, has an established role in the nodal/paranodal antibody-defined subtypes and in IVIG-refractory disease. The treatment landscape is moving in the direction of more options, better-targeted immunology, and clearer subtyping. Peptide alternatives offered as a hedge against the standard of care are being offered against a moving target that is improving, not against a stagnant or failed standard. The third thing to be clear about: 'nerve' is not one biological category. BPC-157's rat-sciatic-crush regeneration data — taken at face value — speaks to mechanical injury repair via Schwann-cell-mediated axonal regrowth in a healthy rodent nervous system. That is not CIDP. Semax's Russian-jurisdiction stroke and cognitive-decline registration — which is legitimate evidence within that jurisdiction, respected here, not dismissed — speaks to central ischemic injury and chronic CNS conditions. That is not CIDP. Cerebrolysin's multi-jurisdictional registration (Russia, several EU member states, China, and others) for stroke, vascular dementia, Alzheimer's, and TBI — likewise legitimate evidence within those indications — speaks to CNS neuroprotection. That is not CIDP. NMN's NAD+/mitochondrial-support narrative speaks to general-aging metabolic theory. That is not CIDP, which is not a metabolic neuropathy. LL-37's cathelicidin biology is, if anything, mechanistically pointed the wrong direction in a patient with an active autoimmune disease, given the published literature on LL-37 as an autoantigen and amplifier of innate immune activation in psoriasis and lupus. The deliberate non-elevation of this page — the empty peptide_slugs array — is the editorial choice. This page exists for /ask honesty when users encounter peptide marketing aimed at CIDP and want a grounded answer about what those peptides actually have behind them for this disease. It does not exist to surface peptides as discovery options for CIDP. The right discovery surface for someone newly diagnosed with CIDP is the GBS/CIDP Foundation International patient-resource materials, the EAN/PNS 2021 guideline, the AAN 2024 guidance, and a neuromuscular neurologist who can run the EFNS/PNS-criteria diagnostic workup and discuss the IVIG/SCIg/corticosteroid/PLEX/efgartigimod/rituximab decision tree as it applies to that patient's subtype and course.
Important caveat
CIDP is a clinician-managed disease, full stop. The treating neuromuscular neurologist running the EFNS/PNS 2010/2021 or EAN/PNS 2021 criteria diagnostic workup — clinical features, nerve conduction studies for demyelinating findings, CSF analysis for cytoalbuminologic dissociation, imaging where indicated, antibody testing for the nodal/paranodal subtypes (anti-NF155, anti-NF186, anti-Contactin-1, anti-CASPR1), workup for mimics including POEMS syndrome (VEGF, serum protein electrophoresis, immunofixation, skeletal survey), anti-MAG IgM, and MMN — is the anchor of any treatment decision. The mimic workup is load-bearing because the treatment forks: POEMS is treated through hematology-oncology with directed therapy at the plasma-cell disorder, not as CIDP; MMN responds to IVIG but is worsened by corticosteroids; nodal/paranodal-antibody subtypes often respond preferentially to rituximab over IVIG. Misclassification leads to undertreatment and progressive disability. None of this is something a peptide clinic can do or should be asked to do. If a patient has CIDP and is considering any peptide for any reason, every single one of the following needs to be true: (1) the treating neuromuscular neurologist has been told about the peptide before it is administered, not after; (2) the peptide is not being substituted for guideline-anchored standard of care (IVIG, SCIg, corticosteroids, plasmapheresis, efgartigimod where appropriate, rituximab in selected subtypes); (3) the peptide is not being used to justify deferring or skipping the diagnostic workup that distinguishes CIDP from its mimics; (4) INCAT, ONLS, grip dynamometry, sensory exam, and the nerve conduction study cadence the neurologist has established remain the disease-monitoring measures; (5) in patients on immunoglobulin maintenance (IVIG or SCIg via the PATH-trial Hizentra protocol or equivalent), the prescriber knows about any added peptide so attribution of trajectory changes is not muddied; (6) in patients on efgartigimod or other FcRn antagonists, or on rituximab, the same applies with even more force; (7) for LL-37 specifically, the published literature on cathelicidin as an autoantigen and amplifier of innate immune activation in psoriasis and lupus means a clinical immunologist should be involved in any consideration — and the editorial position of this library is that LL-37 is the wrong direction in active autoimmune demyelinating disease; (8) the GBS/CIDP Foundation International is the patient organization carrying treatment-landscape updates and is the appropriate first stop for patient-resource information, not peptide-vendor marketing material. None of the peptides discussed in this substrate have any evidence in CIDP. WADA athletes: BPC-157 (S0) prohibited at all times — no CIDP use case anyway. Pregnancy: CIDP pregnancy management is neuromuscular neurology + maternal-fetal medicine coordinated; IVIG is generally pregnancy-compatible; rituximab requires pregnancy-specific timing; efgartigimod pregnancy data limited; corticosteroids managed with attention to gestational diabetes risk; cyclophosphamide ABSOLUTELY CONTRAINDICATED in pregnancy. This substrate is editorial honesty for /ask probing; it is not a recommendation to use any of these peptides in CIDP.
Want this list to grow? The library is editorial — if there’s a peptide you think belongs on this page with documented or mechanistically-clear evidence, send us a note with the citation and we’ll review it under the same evidence-tier discipline as every other entry.