Etarfion Mechanism of Action

Pharmacology: Etarfion binds specifically to the TNF and blocks its interaction with cell surface TNFRs. TNF is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. It plays an important role in the inflammatory processes of rheumatoid arthritis (RA) and the resulting joint pathology. Elevated levels of TNF are found in the involved tissue and fluids of patients with RA.
Etanercept inhibits binding of both TNF-α and TNF-β (lymphotoxin-α [LT-α]) to cell surface TNFRs, rendering TNF biologically inactive. Etanercept can modulate biological responses that are induced or regulated by TNF, including expression of adhesion molecules responsible for leukocyte migration (ie, E-selectin and, to a lesser extent, intracellular adhesion molecule-1 [ICAM-1]), serum levels of cytokines (e.g. IL-6), and serum levels of matrix metalloproteinase-3 [MMP-3] or stromelysin.
In a randomized, double-blind, Methotrexate controlled multicenter clinical trial conducted in 238 patients with severe active rheumatoid arthritis, the patients in the study drug group received 25 mg Etarfion by subcutaneous injection twice weekly for 24 weeks and the patients in the control group received MTX orally for 24 weeks. ACR 20/50/70 criteria were used for efficacy assessment. The study results demonstrated the rate of patients achieving ACR 20 in Etarfion group was 35.59% at 2 weeks after the treatment and significantly higher than that in the MTX control group (P<0.05). At 12 weeks after the treatment, the rate of patients achieving ACR 20 in the Etarfion group was 66.10% and also significantly superior to MTX control group (P<0.05). At 24 weeks after treatment, the rate of achieving ACR 20 in Etarfion group was 80.39% and ACR70 also superior to MTX control group (P<0.05). The main observed adverse reactions were injection site reactions, rash, elevated transaminases, and infections. There was no significant difference between the two groups in incidence of infections.