This product is an unconjugated, non-therapeutic recombinant analog of the anti-inflammatory antibody mavrilimumab, supplied strictly for research use only. It is not the clinical drug and is not intended for human or veterinary use. Mavrilimumab is a human IgG antibody that acts on granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling; the well-established originator target is the GM-CSF receptor alpha chain (GM-CSFRalpha / CSF2RA / CD116) rather than the GM-CSF cytokine itself (see flag). The analog is useful as a functional research reagent for probing GM-CSF axis biology in vitro and in preclinical settings: as a binding and neutralization tool, an isotype-matched or pathway-specific control, a benchmarking standard alongside other GM-CSF-axis antibodies, and a starting reagent for assay development, ADCC/effector characterization, and antibody-engineering or biosimilarity workflows. It is offered at research grade with low endotoxin (typically <1 EU/mg, with an ultra-low <0.5 EU/mg option), and is available in bulk milligram-to-gram quantities to support in-vitro standards and larger preclinical studies. No clone identity is implied.
Granulocyte-macrophage colony-stimulating factor (GM-CSF, gene CSF2; UniProt P04141) is a monomeric glycoprotein cytokine that drives the survival, proliferation, differentiation, and activation of myeloid cells including granulocytes, monocytes, macrophages, and dendritic cells. It signals through a heterodimeric receptor comprising a ligand-specific alpha subunit (GM-CSFRalpha / CSF2RA / CD116) and a shared beta common subunit (CSF2RB), engaging JAK2-STAT5 as the dominant pathway along with MAPK, PI3K-AKT, and NF-kB signaling. Beyond steady-state hematopoiesis, GM-CSF is a key pro-inflammatory mediator: it licenses tissue macrophages toward inflammatory phenotypes and contributes to the pathology of rheumatoid arthritis, giant-cell arteritis, and other autoimmune and inflammatory conditions, making the GM-CSF/GM-CSFRalpha axis an actively pursued therapeutic target.