Anti-Mouse TNFR2 (TR75-54.7) In Vivo Antibody - Low Endotoxin (ICH1137-100mg)

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This is a purified Armenian hamster IgG monoclonal antibody, clone TR75-54.7, raised against mouse TNFR2 (tumour necrosis factor receptor 2, CD120b; UniProt P25119). The Armenian hamster host and hamster IgG isotype pairing is a common and well-tolerated format for in-vivo mouse studies, since hamster constant regions limit the anti-isotype reactivity that can complicate repeated dosing with rat or mouse antibodies. The clone recognises the extracellular region of mouse TNFR2 and has been characterised for immunoprecipitation, western blot, flow cytometry, ELISA and functional blocking applications, making it suitable both for phenotyping TNFR2-expressing populations and for perturbing TNFR2 signalling in functional and in-vivo experiments. This preparation is produced at low endotoxin (research-grade <1 EU/mg; ultra-low <0.5 EU/mg) and supplied in bulk milligram-to-gram quantities to support animal dosing regimens where endotoxin load and lot consistency matter. For research use only (RUO); not for diagnostic or therapeutic use. TNFR2 (TNF receptor superfamily member 1B, CD120b; gene Tnfrsf1b) is one of the two receptors for tumour necrosis factor. Unlike the broadly expressed TNFR1, TNFR2 has a restricted expression pattern, found mainly on immune cells including regulatory T cells (Tregs), activated effector T cells, myeloid-derived suppressor cells, endothelial cells and some neuronal and stromal populations. TNFR2 preferentially responds to the membrane-bound form of TNF and lacks a death domain; instead it signals through TRAF2/TRAF3 adaptors to activate NF-kB and pro-survival pathways. In the immune system TNFR2 signalling supports the proliferation, stability and suppressive function of Tregs, and contributes to tissue protection and repair. Because of this role, TNFR2 has attracted interest as a target for modulating Treg activity in cancer immunotherapy and autoimmunity, where blocking or agonising the receptor can shift the balance between immune suppression and activation.