What is the mechanism of Infliximab-ABDA?

Infliximab-ABDA is a specific biosimilar to the monoclonal antibody Infliximab, which targets and inhibits tumor necrosis factor-alpha (TNF-α). Understanding the mechanism of action of Infliximab-ABDA requires a detailed look into the biological processes it affects and how it exerts its therapeutic effects.

Tumor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine central to the inflammatory response in several autoimmune diseases, including rheumatoid arthritis, Crohn's disease, ulcerative colitis, ankylosing spondylitis, and psoriasis. TNF-α is predominantly produced by activated macrophages, T-cells, and other immune cells and is a key mediator in the pathogenesis of these conditions.

Infliximab-ABDA is designed to mimic the structure and function of the original Infliximab. It is a chimeric monoclonal antibody composed of human constant and murine variable regions. This structure allows Infliximab-ABDA to specifically bind to TNF-α with high affinity. Once bound, Infliximab-ABDA neutralizes the biological activity of TNF-α, preventing it from interacting with its receptors (TNFR1 and TNFR2) on the surface of cells.

The binding of Infliximab-ABDA to TNF-α initiates several downstream effects:

1. Neutralization of Soluble and Transmembrane TNF-α: Infliximab-ABDA binds to both the soluble form and the transmembrane form of TNF-α. This binding prevents TNF-α from interacting with its receptors, TNFR1 and TNFR2, which are involved in the promotion of inflammatory responses. This inhibition reduces the recruitment and activation of other immune cells, thereby decreasing inflammation.

2. Complement-Dependent Cytotoxicity (CDC): Through its Fc region, Infliximab-ABDA can initiate the complement cascade, leading to the formation of the membrane attack complex (MAC) and subsequent lysis of cells presenting transmembrane TNF-α. This effect is particularly significant in the depletion of activated immune cells involved in the inflammatory process.

3. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC): Infliximab-ABDA can also mediate ADCC, wherein immune effector cells such as natural killer (NK) cells recognize and bind to the Fc region of Infliximab-ABDA that is attached to TNF-α-expressing cells. This binding triggers the release of cytotoxic granules from NK cells, leading to the destruction of the target cells.

4. Induction of Apoptosis: Infliximab-ABDA has been shown to induce apoptosis in cells expressing membrane-bound TNF-α. This occurs through the activation of apoptotic pathways within these cells, further contributing to the reduction of inflammation and tissue damage.

The collective effect of these mechanisms is the suppression of the inflammatory cascade that characterizes autoimmune diseases. By neutralizing TNF-α, Infliximab-ABDA effectively reduces the signs and symptoms of inflammation, leading to clinical improvement in patients with conditions driven by excessive TNF-α activity.

In clinical practice, the use of Infliximab-ABDA has shown to be beneficial in reducing disease activity and improving quality of life for patients suffering from chronic inflammatory diseases. Its efficacy and safety profile make it a valuable therapeutic option in the management of these complex conditions.

In conclusion, Infliximab-ABDA's mechanism of action revolves around its ability to specifically target and neutralize TNF-α, thereby mitigating the inflammatory response that underpins many autoimmune diseases. Its role in complement activation, cell-mediated cytotoxicity, and apoptosis induction further enhances its therapeutic effects, making it a crucial agent in the treatment arsenal for chronic inflammatory disorders.

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