This product is an unconjugated, non-therapeutic recombinant analog of satralizumab, a humanized anti-interleukin-6 receptor (IL-6R) monoclonal antibody. It is built around the IL-6R target to reproduce the binding specificity of the originator molecule for use as a research reagent only (RUO); it is not the clinical drug and is not intended for human or veterinary use. The originator is notable as a "recycling" antibody engineered for pH-dependent antigen binding (tight association at neutral plasma pH, release in the acidic endosome) plus FcRn-mediated recycling, extending half-life and IL-6R engagement; the mutation-rich IgG2 constant region on this card is consistent with that engineering. As a research-grade analog it is useful as a positive control and reference standard in IL-6R binding and neutralization assays, for benchmarking anti-IL-6R biosimilars and novel candidates, for characterizing IL-6/IL-6R signaling in cell-based systems, and as a building block for conjugate or assay development. It is supplied unconjugated at low endotoxin (research grade <1 EU/mg; ultra-low <0.5 EU/mg) and available in bulk milligram-to-gram quantities for preclinical and in-vitro workflows.
Interleukin-6 receptor (IL-6R, encoded by IL6R; UniProt P08887, also called CD126) is the ligand-binding subunit of the IL-6 signaling system. It exists in a membrane-bound form and as a soluble form (sIL-6R) generated by proteolytic shedding or alternative splicing. IL-6 binding to IL-6R does not signal directly; the IL-6/IL-6R complex recruits two copies of the signal-transducing subunit gp130 (IL6ST/CD130), triggering JAK/STAT3, SHP-2/MAPK, and PI3K/AKT signaling. Membrane IL-6R drives classic signaling in cells that express it (hepatocytes, subsets of leukocytes), while sIL-6R enables trans-signaling on gp130-bearing cells lacking membrane IL-6R, broadening IL-6 responses. IL-6 signaling regulates acute-phase responses, B- and T-cell differentiation, Th17 development, and inflammation. Dysregulated IL-6R signaling is implicated in autoimmune and inflammatory disease, motivating IL-6R blockade.