Anti-Mouse GM-CSF (MP1-22E9) In Vivo Antibody - Low Endotoxin (ICH1125-100mg)

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

This is the MP1-22E9 monoclonal antibody, a rat IgG2a raised against mouse GM-CSF (UniProt P01587). It recognizes and neutralizes mouse granulocyte-macrophage colony-stimulating factor, making it a widely used tool for blocking GM-CSF activity in mouse models. The rat IgG2a isotype and neutralizing capacity make MP1-22E9 well suited to in-vivo cytokine-blockade and functional studies, where sustained neutralization of a soluble mediator is required. Reported applications include Western blot, ELISA, ELISPOT, blocking/neutralization, immunocytochemistry, and IHC on frozen sections, so the same clone can support both in-vitro characterization and in-vivo intervention. This preparation is supplied at low endotoxin and in bulk milligram-to-gram quantities appropriate for repeated dosing in animal cohorts, and is labeled for research use only (RUO). Low endotoxin is particularly important for GM-CSF studies because endotoxin contamination independently activates myeloid cells and drives inflammatory readouts, which can confound the very phenotypes GM-CSF blockade is used to interrogate. GM-CSF (granulocyte-macrophage colony-stimulating factor, gene Csf2) is a secreted cytokine that signals through a heterodimeric receptor composed of a ligand-specific alpha chain (CSF2RA) and the shared beta common chain (CSF2RB), activating JAK2/STAT5 and downstream pathways. It is produced by activated T cells, NK cells, endothelial cells, and other stromal and immune populations, particularly under inflammatory conditions. GM-CSF promotes the survival, proliferation, and differentiation of granulocyte and macrophage progenitors and licenses inflammatory, tissue-damaging functions in monocytes, macrophages, and dendritic cells. It is a key effector of pathogenic T-cell responses and has been implicated in autoimmune and inflammatory disease models such as experimental autoimmune encephalomyelitis and arthritis, as well as in myeloid recruitment within the tumor microenvironment. Because of these roles, GM-CSF neutralization is a common strategy for dissecting myeloid-driven inflammation.