Ebrasodebart Biosimilar - Research Grade (ICH5497-10mg)

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

This product is an unconjugated, non-therapeutic recombinant analog of the anti-TMEM219 antibody Ebrasodebart, supplied for research use only. It is a human IgG4 (lambda) biosimilar built around the same target specificity as the originator, allowing laboratories to interrogate the IGFBP3/TMEM219 signaling axis without sourcing clinical material. As a research-grade reagent it is intended for functional and mechanistic work: as a positive control in TMEM219 binding assays, for competitive/neutralization studies against IGFBP3, for receptor-blockade experiments in cultured cells and organoids, and as a benchmarking tool during antibody or assay development. It is offered at low endotoxin (research grade under 1 EU/mg; ultra-low under 0.5 EU/mg) and can be produced in bulk from milligram to gram scale for in-vitro standards and preclinical model work. This reagent is not the clinical drug, is not formulated or released for therapeutic use, and must not be used in humans or veterinary subjects. All content here is educational guidance for ichorbio to review before publication. TMEM219 (transmembrane protein 219; also called the IGFBP-3 receptor, IGFBP-3R; UniProt Q86XT9) is a single-pass type I transmembrane protein that functions as a death receptor for insulin-like growth factor binding protein 3 (IGFBP3). It has an extracellular ligand-binding region, a transmembrane segment carrying a leucine-zipper-like heptad repeat, and a short cytoplasmic tail. Binding of IGFBP3 to TMEM219 triggers a caspase-8-dependent apoptotic program, independent of IGF sequestration. The pathway is implicated in tissue homeostasis: excessive IGFBP3/TMEM219 signaling drives apoptosis of intestinal stem cells and impairs mucosal regeneration, and contributes to pancreatic beta-cell loss, where TMEM219 is the principal IGFBP3 receptor. Elevated circulating IGFBP3 has been linked to disrupted beta-cell homeostasis, making the receptor a target of interest in inflammatory bowel disease and diabetes research.