Atrosimab

Atrosimab (serial dilutions; 4-128 nM) binds purified human TNFR1-Fc with high affinity, and lacks binding to human complement protein C1q and human Fcγ receptors Ia, IIb, IIIa^[1].
Atrosimab (100 nM; 1, 3, 7 days) exhibits good stability in human plasma for at least 7 days and has an aggregation temperature of 64°C^[1].
Atrosimab (serial dilutions; 16-20 h, 24 h) potently inhibits TNF-mediated TNFR1 activation in HeLa, HT1080, and Kym-1 cells, with IC₅₀ values of 54.5 nM, 24.2 nM, and 16.2 nM, respectively^[1].
Atrosimab (serial dilutions; 16-20 h) does not exhibit TNFR1 agonistic activity in HT1080 cells even when cross-linked by three different goat anti-human IgG sera^[1].
Atrosimab (24 h) does not affect spontaneous or glutamate-induced altered firing rates of huTNFR1-k/i mouse embryonic day 14 primary cortical neurons after 24 h incubation^[2].
Atrosimab (100 μg; heated from 35°C to 80°C with 2 min equilibration per 1°C interval; 2-500 nM; up to 9 months) is highly thermally and long-term stable, binds selectively and with high affinity to human, rhesus, and cynomolgus TNFR1 (but not mouse/rat TNFR1 or any TNFR2), and recognizes an epitope on human TNFR1 that includes residues P23, L67, R68, H69, and Q24^[3].
Atrosimab (up to 1000 nM; 16-20 h at 37°C, 5% CO₂; 1-7 days at 37°C in 50% human serum) potently and dose-dependently inhibits TNF-induced IL-8 release in HT1080 cells with IC₅₀ values of 21.9-34.9 nM, does not exhibit agonistic activity in these cells, and maintains functional stability after incubation in human serum at 37°C for up to 7 days^[3].
Atrosimab (100 μg/mL; 24 h) inhibits TNF-induced VCAM-1 and ICAM-1 expression in hCMEC/D3 human brain microvascular endothelial cells^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.