Postulated mechanisms of action for Privigen

Intravenous immunoglobulin (IVIg) therapy supplies a broad spectrum of opsonizing and neutralizing IgG antibodies against a wide variety of bacterial and viral agents. The mechanism of action of IVIg has not been fully elucidated, but is believed to include immunomodulatory effects.^1,2

Two widely studied and accepted mechanisms of IVIg action are:

Replacement of essential antibodies^1,2
Immunomodulatory effects^1,2

Choose a condition below to learn more about how Privigen works specifically in that disorder.

CIDP

Chronic ITP

Privigen provides patients with a broad spectrum of opsonizing and neutralizing IgG antibodies against a variety of bacterial and viral agents.

Privigen is manufactured from large pools of human plasma from healthy donors and therefore includes a broad variety of antibody specificities against common pathogens to which the donor population has been exposed¹
The antibodies in Privigen are structurally and functionally intact, and their effector functions are preserved³

The mechanism of action for IgG therapy in CIDP is complex and not fully understood. However, its function in treating CIDP—an inflammatory neuropathy with an underlying autoimmune basis is believed to be attributed to immunomodulatory effects.³

A more precise mechanism of action regarding just how IgG therapy exerts its immunomodulatory effects is still being explored, but mechanisms that may play a role include^3-5:

Modulating B-cells and regulating T-cell activity potentially involved in the development of CIDP
Mediating Fc receptor blockade on macrophages, which may inhibit demyelination
Binding to and neutralizing autoantibodies
Reducing pro-inflammatory cytokines & adhesion molecules
Saturation of FcRn, resulting in accelerated catabolism of autoantibodies
Binds complement proteins, which may limit MAC (membrane attack complex) formation and cell lysis

The mechanism of action of IgG in chronic immune thrombocytopenic purpura (ITP) is complex and not fully understood. Further research will be needed to better understand how IVIg works in chronic ITP.¹ However, the success of treating chronic ITP with IgG has been attributed to the competitive inhibition of Fc receptors on phagocytic cells.^2,3

Continuing research indicates that other mechanisms may also contribute to thrombocytopenia, including¹:

Induction of FcγIIb inhibitory receptors, which may result in decreased release of proinflammatory cytokines and activation of B cell inhibitory pathways
The presence of natural anti-idiotypic antibodies in IVIg, which have been shown to bind pathogenic autoantibodies in vitro
Long-term effects of downregulation on pathogenic autoantibodies

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References: 1. Simon HU, Späth PJ. IVIG mechanisms of action. Allergy. 2003;58(7):543-552. 2. Maddur MS, Lacroix-Desmazes S, Bayry J, Kaveri SV. Intravenous polyclonal immunoglobulin in autoimmune diseases: clinical indications and mechanisms of action. Drug Discov Today Ther Strateg Autoimmun. 2009;6(1):5-11. 3. Jacob S, Rajabally Y. Current proposed mechanism of action of intravenous immunoglobulins in inflammatory neuropathies. Curr Neuropharmacol. 2009;7(4):337-342. 4. Querol L, Hartung H, et al. The role of the complement system in chronic inflammatory demyelinating polyneuropathy: implications for complement-targeted therapies. Neurotherapeutics. 2022 April 12;19:864-873. doi: 10.1007/s13311-022-01221-y. 5. Bayry J, Ahmed EA, et al. Intravenous Immunoglobulin: Mechanism of Action in Autoimmune and Inflammatory Conditions. J Allergy Clin Immunol Pract. 2023;11(6):1688-1697.