Rosmantuzumab Biosimilar - Research Grade (ICH5836-10mg)

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

ICH5836 is a research-grade biosimilar of rosmantuzumab, supplied as an unconjugated, non-therapeutic analog of the originator antibody for research use only. It is built around the target R-spondin 3 (RSPO3), reproducing the binding specificity of the originator molecule while being manufactured for laboratory applications rather than clinical use. The product is a human IgG1, kappa immunoglobulin and is offered at research-grade low endotoxin (<1 EU/mg), with bulk milligram-to-gram quantities available to support antigen-binding studies, pathway-neutralisation assays, and use as a reference or control reagent in comparative work. Because it is an analog of a therapeutic that targets a human antigen, it is intended for in-vitro and functional characterisation such as ligand-binding, competition, and neutralisation experiments rather than as a clinical therapeutic. Rosmantuzumab (originator development code OMP-131R10) was developed as an anti-RSPO3 agent in the context of Wnt-pathway-driven cancers, making an RSPO3-directed biosimilar a useful tool for investigators studying Wnt/R-spondin signalling, tumour biology, and antibody-mediated ligand blockade in a research setting. RSPO3 (R-spondin 3, UniProt Q9BXY4) is one of four secreted R-spondin glycoproteins that act as potent amplifiers of Wnt/beta-catenin signalling. R-spondins bind the leucine-rich repeat-containing G-protein-coupled receptors LGR4/5/6 and the transmembrane E3 ubiquitin ligases ZNRF3 and RNF43. By engaging this complex, RSPO3 neutralises ZNRF3/RNF43-mediated turnover of Frizzled and LRP Wnt receptors, thereby stabilising receptor levels at the cell surface and sensitising cells to Wnt ligands. This activity is central to stem-cell maintenance, tissue homeostasis, and developmental patterning. Dysregulated R-spondin signalling, including RSPO3 gene fusions and overexpression, drives constitutive Wnt-pathway activation in a subset of colorectal and other cancers, which is why RSPO3 became a therapeutic target. Antibodies directed against RSPO3, such as the rosmantuzumab originator, are designed to block RSPO3 engagement of its receptors and dampen downstream Wnt signalling in RSPO3-dependent tumours.