Pegcetacoplan

Pegcetacoplan is an approved, prescription-only complement C3 inhibitor. As Empaveli (US) / Aspaveli (EU), a twice-weekly subcutaneous infusion, it was FDA-approved for paroxysmal nocturnal hemoglobinuria (PNH) in May 2021 and, on July 28, 2025, for C3 glomerulopathy (C3G) and primary immune-complex membranoproliferative glomerulonephritis (IC-MPGN) in patients aged 12 and older - the first approved therapy for those kidney diseases, based on the Phase 3 VALIANT trial (NCT05067127). As Syfovre, an intravitreal injection, it was FDA-approved in February 2023 as the first treatment for geographic atrophy secondary to age-related macular degeneration. It carries a boxed warning for serious infections with encapsulated bacteria and requires meningococcal (and other) vaccination under a REMS. It is administered by or under a healthcare provider and is not sold as a legitimate self-administered 'research peptide.'

Effective: July 2026

An FDA-approved synthetic cyclic peptide and CXCR4 antagonist (brand name Aphexda; research name BL-8040) used together with G-CSF to mobilize blood-forming stem cells for autologous transplant in multiple myeloma. In 2026 it is being actively studied as part of combination immunotherapy for pancreatic cancer.

A self-administered, once-daily subcutaneous macrocyclic peptide that inhibits complement component 5 (C5), FDA- and EMA-approved for anti-AChR-positive generalized myasthenia gravis.

A first-in-class, intravenous immunomodulatory fusion peptide derived from histidyl-tRNA synthetase that selectively binds neuropilin-2 (NRP2) to dampen inflammation in the lung; in Phase 3 development for pulmonary sarcoidosis, an interstitial lung disease.

A first-in-class synthetic hepcidin-mimetic (mini-hepcidin) peptide given as a weekly subcutaneous injection to control red-blood-cell overproduction in polycythemia vera (PV). By mimicking the iron-regulating hormone hepcidin, rusfertide binds the iron exporter ferroportin and restricts iron availability, reducing the need for therapeutic phlebotomy. Developed by Protagonist Therapeutics and partnered with Takeda, it met its primary endpoint in the Phase 3 VERIFY trial and, in March 2026, received FDA acceptance of its New Drug Application with Priority Review, with a decision expected in the third quarter of 2026.

Efgartigimod (efgartigimod alfa, brand names Vyvgart intravenous and Vyvgart Hytrulo subcutaneous) is a first-in-class antagonist of the neonatal Fc receptor (FcRn) developed by argenx as ARGX-113. It is not a small synthetic peptide but an engineered fragment of the human immunoglobulin G1 (IgG1) antibody - specifically the Fc portion that normally binds FcRn - modified with argenx's ABDEG technology to bind FcRn with much higher affinity than natural IgG at both neutral and acidic pH. FcRn is the salvage receptor that rescues circulating IgG from lysosomal degradation and recycles it back into the blood, giving antibodies their long half-life. By outcompeting endogenous IgG for FcRn, efgartigimod blocks that recycling and drives rapid clearance of IgG - including the pathogenic autoantibodies that cause many autoimmune diseases - typically lowering total IgG by roughly 60-70% within weeks, without reducing IgM, IgA, or albumin. It was the first FcRn blocker ever approved: FDA-approved in December 2021 (Vyvgart IV) for acetylcholine-receptor-antibody-positive generalized myasthenia gravis (gMG) on the strength of the Phase 3 ADAPT trial, followed by a subcutaneous co-formulation with recombinant hyaluronidase (Vyvgart Hytrulo) for gMG in 2023 and for chronic inflammatory demyelinating polyneuropathy (CIDP) in 2024. In May 2026 the FDA expanded the gMG label to all serotypes - including AChR-antibody-negative (seronegative) patients - based on the Phase 3 ADAPT SERON trial, making efgartigimod the first and only therapy approved across every gMG antibody subtype. It is being studied in a broad set of other IgG-driven autoimmune diseases, including primary immune thrombocytopenia, myositis, Sjogren's disease, bullous pemphigoid, and lupus nephritis.

Nipocalimab (brand name Imaavy, development code M281) is a fully human, aglycosylated, 'effectorless' IgG1 monoclonal antibody that blocks the neonatal Fc receptor (FcRn), developed by Johnson & Johnson (Janssen). Like efgartigimod it lowers circulating immunoglobulin G (IgG) - including the pathogenic autoantibodies that drive many autoimmune diseases - by occupying FcRn and preventing it from recycling IgG back into the blood, so unrescued IgG is routed to the lysosome and degraded, typically cutting total IgG by roughly 65-75% while sparing IgM, IgA, complement, and albumin. Unlike efgartigimod's engineered Fc fragment, nipocalimab is a full-length monoclonal antibody engineered to be aglycosylated and effectorless (it does not trigger ADCC or complement-dependent cytotoxicity), and it is dosed as a maintenance intravenous infusion for continuous IgG suppression rather than in short cycles. The FDA approved Imaavy on April 30, 2025 for generalized myasthenia gravis (gMG) in anti-AChR-antibody-positive and anti-MuSK-antibody-positive patients aged 12 and older - making it the first FcRn blocker approved for adolescents and the first to explicitly cover MuSK-positive disease - on the strength of the Phase 3 Vivacity-MG3 trial. It has since generated positive data across a striking breadth of IgG-mediated conditions: Sjogren's disease (Phase 2 DAHLIAS), rheumatoid arthritis, warm autoimmune hemolytic anemia (wAIHA), and - uniquely among FcRn blockers - maternal-fetal alloimmune disease, where it is being developed to treat hemolytic disease of the fetus and newborn (HDFN) by crossing the placenta to protect the fetus. In April 2026 the FDA granted Priority Review to nipocalimab for wAIHA, positioning it as a potential first approved therapy for that condition.

Rozanolixizumab (brand name Rystiggo, development code UCB7665) is a humanized IgG4 monoclonal antibody that blocks the neonatal Fc receptor (FcRn), developed by UCB. Like efgartigimod and nipocalimab it lowers circulating immunoglobulin G (IgG) - including the pathogenic autoantibodies that drive many autoimmune diseases - by binding FcRn and preventing it from recycling IgG back into the blood, so unrescued IgG is routed to the lysosome and degraded, typically cutting total IgG by roughly 70-80% while sparing IgM, IgA, complement, and albumin. Unlike efgartigimod's engineered Fc fragment, rozanolixizumab is a full-length humanized antibody, and unlike nipocalimab's intravenous infusion it is given as a rapid subcutaneous infusion (including via an on-body delivery device), typically in weekly cycles that are repeated based on clinical response rather than continuously. The FDA approved Rystiggo on June 27, 2023 for generalized myasthenia gravis (gMG) in adults who are anti-acetylcholine-receptor (AChR) antibody-positive or anti-muscle-specific-tyrosine-kinase (MuSK) antibody-positive - making it the first therapy ever approved to treat both of those gMG subtypes - on the strength of the Phase 3 MycarinG trial. It has since been studied across other IgG-mediated diseases, including chronic inflammatory demyelinating polyneuropathy (CIDP), where it did not show meaningful benefit and was not advanced to Phase 3, and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), primary immune thrombocytopenia (ITP), and other autoantibody conditions where development continues. The European Medicines Agency approved rozanolixizumab in January 2024 and the UK MHRA in March 2024.

Batoclimab (development codes IMVT-1401, RVT-1401, HBM9161, HL161) is an investigational, fully human IgG1 monoclonal antibody that blocks the neonatal Fc receptor (FcRn), developed by Immunovant/Roivant (U.S. and Canada) and Harbour BioMed (Greater China) under license from HanAll Biopharma. It is not a small synthetic peptide but a full-length antibody given as a low-volume subcutaneous injection that patients can self-administer at home. Like the approved FcRn blockers efgartigimod, nipocalimab and rozanolixizumab, it lowers circulating IgG - including pathogenic autoantibodies - but it is best known for two things the others are not: it is the FcRn blocker that generated positive Phase 3 myasthenia gravis data yet was deliberately NOT filed for U.S. approval, and it is the one whose FcRn-mediated albumin recycling blockade produces a distinctive on-target signal of lowered serum albumin and raised LDL cholesterol - the exact liability that drove its makers to a re-engineered successor, IMVT-1402.