What is the mechanism of Infliximab-QBTX?

Infliximab-QBTX is a biosimilar to Infliximab, a chimeric monoclonal antibody that has been widely used in the treatment of various autoimmune diseases, including Crohn's disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and plaque psoriasis. Biosimilars like Infliximab-QBTX are designed to be highly similar to an already approved biologic, with no clinically meaningful differences in terms of safety, purity, and potency. Understanding the mechanism of action of Infliximab-QBTX is crucial for appreciating its therapeutic potential and applications.

The primary mechanism of Infliximab-QBTX involves the inhibition of tumor necrosis factor-alpha (TNF-α), a pro-inflammatory cytokine. TNF-α plays a critical role in the inflammatory process and is found in elevated levels in various autoimmune and inflammatory conditions. By targeting and neutralizing TNF-α, Infliximab-QBTX can effectively reduce inflammation and modify disease activity.

Specifically, Infliximab-QBTX binds with high affinity to both the soluble and transmembrane forms of TNF-α. This binding prevents TNF-α from interacting with its receptors on the surface of cells, thereby inhibiting the downstream signaling pathways that lead to inflammation. The blockade of TNF-α activity results in a decrease in the production of other pro-inflammatory cytokines and mediators, such as interleukin-1 (IL-1) and interleukin-6 (IL-6), which further contributes to the reduction of inflammation.

In addition to neutralizing soluble TNF-α, the interaction of Infliximab-QBTX with the transmembrane form of TNF-α can lead to reverse signaling. This reverse signaling can induce apoptosis (programmed cell death) of activated T-cells and macrophages that express transmembrane TNF-α, thereby reducing the number of inflammatory cells and contributing to the resolution of inflammation.

The clinical efficacy of Infliximab-QBTX in treating autoimmune diseases is supported by its ability to reduce inflammation, alleviate symptoms, and induce and maintain remission in various conditions. For instance, in patients with rheumatoid arthritis, Infliximab-QBTX can reduce joint pain, swelling, and stiffness, leading to improved physical function and quality of life. In inflammatory bowel diseases like Crohn's disease and ulcerative colitis, Infliximab-QBTX can help heal the intestinal lining, reduce gastrointestinal symptoms, and improve overall patient well-being.

In conclusion, the mechanism of Infliximab-QBTX centers around its capacity to inhibit TNF-α, a key cytokine in the inflammatory process. By binding to both soluble and transmembrane TNF-α, Infliximab-QBTX effectively neutralizes its activity, reduces the production of other pro-inflammatory mediators, and induces apoptosis of activated inflammatory cells. These actions collectively contribute to its therapeutic efficacy in managing a range of autoimmune and inflammatory diseases.