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Atrosimab is a next-generation, monovalent antagonistic antibody derivative that selectively targets and blocks tumor necrosis factor receptor 1 (TNFR1), while sparing TNFR2 signaling. This selectivity is designed to inhibit pro-inflammatory and tissue-degenerative effects mediated by TNFR1 without interfering with the immune-modulatory and regenerative functions of TNFR2. Atrosimab was developed as an affinity-matured follow-on product to the full-length antibody Atrosab, featuring a monovalent format lacking the hinge region and CH1 domain for improved stability and pharmacokinetics. Preclinical studies have demonstrated its efficacy in reducing neuroinflammation, neuronal cell death, cognitive impairment, glial activation, memory deficits in models of neurodegeneration, as well as therapeutic potential in mouse models of acute and chronic inflammation such as experimental arthritis, non-alcoholic steatohepatitis (NASH), hepatic fibrosis, and experimental autoimmune encephalomyelitis (EAE). Atrosimab has shown stronger inhibition of TNF-R1 activation compared to its predecessor Atrosab[1][2][3][4].
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