Anti-Mouse CSF1 (5A1) In Vivo Antibody - Low Endotoxin (ICH1280-100mg)

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

This is clone 5A1, a rat IgG1 kappa monoclonal antibody raised against mouse CSF1 (macrophage colony-stimulating factor, M-CSF), corresponding to UniProt P07141. It is a neutralizing antibody that binds mouse CSF1 and blocks its interaction with the CSF1 receptor (CSF1R/CD115), and is widely used to interrupt CSF1-driven macrophage biology in vivo. Validated applications include ELISA capture, functional and neutralization assays, and radioimmunoassays, reflecting its utility for both detection and blocking studies. The rat-anti-mouse format is well suited to mouse disease models, where CSF1 neutralization is used to deplete or reprogram tissue macrophages and tumor-associated macrophages. This preparation is manufactured to a low-endotoxin, in-vivo-ready standard (research grade typically less than 1 EU/mg; ultra-low options below 0.5 EU/mg) and is supplied in bulk milligram-to-gram quantities to support repeat dosing and larger cohorts. It is provided for research use only (RUO). All content here is guidance for ichorbio to review before publishing. CSF1 (colony-stimulating factor 1, also called macrophage colony-stimulating factor or M-CSF) is a secreted and membrane-bound cytokine that is the principal growth, differentiation, and survival factor for the mononuclear phagocyte lineage. It signals through the receptor tyrosine kinase CSF1R (CD115), which is also engaged by the cytokine IL-34. CSF1-CSF1R signaling controls the proliferation, differentiation, recruitment, and survival of monocytes, tissue-resident macrophages, osteoclasts, and many tumor-associated macrophages, and shapes their polarization toward pro-tumoral and tissue-remodeling phenotypes. Because of this central role, the CSF1 axis is heavily studied in cancer immunology, bone biology, fibrosis, and chronic inflammation, where excess macrophage activity contributes to disease. Blocking CSF1 reduces macrophage numbers and can reprogram the remaining population, making the ligand an attractive target for altering the myeloid compartment of the tumor microenvironment and inflamed tissues.