Immunoglobulin G (exogenous human polyclonal pool) (IVIG)

Immunoglobulin G (exogenous human polyclonal pool) refers to a therapeutic preparation of highly purified IgG antibodies concentrated from the plasma of thousands of healthy donors. It contains a broad spectrum of antibody specificities against various infectious agents and self-antigens, reflecting the cumulative immunity of the donor population. Biologically, these molecules perform critical functions such as neutralizing toxins, opsonizing pathogens for phagocytosis, and activating the classical complement pathway. In clinical practice, it is used as replacement therapy for patients with primary or secondary immunodeficiencies and as an immunomodulatory agent in various autoimmune and inflammatory disorders. As a molecular target, exogenous IgG is central to the mechanism of neonatal Fc receptor (FcRn) blockers, which compete with IgG for binding to FcRn to accelerate its clearance and reduce the half-life of both therapeutic and pathogenic antibodies. It is also the substrate for IgG-degrading enzymes like Imlifidase, which are used to rapidly deplete IgG before organ transplantation or in severe autoimmune crises. The therapeutic efficacy of the IgG pool is often monitored via serum trough levels, while safety considerations include the risk of systemic inflammatory reactions, renal toxicity, and potential pro-thrombotic effects due to increased blood viscosity.

Other names

Intravenous immunoglobulinSubcutaneous immunoglobulinPooled human IgGPolyvalent immunoglobulin GSCIGNormal human immunoglobulin

Exogenous IgG acts as a therapeutic agent by providing passive immunity and modulating the immune system through Fc receptor saturation, neutralization of autoantibodies, and inhibition of complement deposition. When considered as a target, it is bound by the neonatal Fc receptor (FcRn) to prevent lysosomal degradation, a process inhibited by FcRn blockers to reduce pathogenic IgG levels. Additionally, it can be enzymatically cleaved by Imlifidase to rapidly eliminate IgG-mediated pathology.