Anti-Mouse RANKL (IK22/5) In Vivo Antibody - Low Endotoxin (ICH1114-100mg)

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

Clone IK22/5 is a rat IgG2a kappa monoclonal antibody, raised in rat, that recognizes mouse RANKL (TNFSF11; UniProt O35235). It is a well-characterized reagent for studying RANKL-driven osteoclast biology and immune regulation in the mouse, and is widely used in flow cytometry, immunoprecipitation, Western blot, immunofluorescence, frozen-section IHC, and functional blocking applications. The IgG2a rat backbone makes it suitable for in vivo work where a defined isotype and predictable pharmacology matter. This ichor.bio preparation is supplied low endotoxin (research grade <1 EU/mg; ultra-low <0.5 EU/mg) and in bulk milligram-to-gram quantities, making it appropriate for repeated dosing in mouse models, longitudinal osteo-immunology studies, and larger cohorts where lot-to-lot consistency and low endotoxin burden are important. Because RANKL blockade affects both bone remodeling and lymphoid/tolerance pathways, IK22/5 is a common tool in bone, tumor, autoimmunity, and thymic selection studies. Provided for research use only (RUO); all content here is guidance for ichor.bio to review before publishing. RANKL (Receptor Activator of NF-kB Ligand; also TNFSF11, TRANCE, OPGL, ODF) is a type II transmembrane member of the TNF superfamily that also exists in a shed, soluble form. It signals through its receptor RANK (TNFRSF11A) on osteoclast precursors, mature osteoclasts, and dendritic cells, and is competitively neutralized by the decoy receptor osteoprotegerin (OPG). The RANKL-RANK-OPG axis is the master regulator of osteoclast differentiation, activation, and survival, and therefore of bone resorption and remodeling. Beyond bone, RANKL is expressed by activated T cells and stromal/medullary thymic epithelial cells, where it contributes to dendritic-cell survival, lymph node organogenesis, thymic medulla formation, central tolerance, and regulatory T cell development. Dysregulated RANKL signaling drives osteoporosis, inflammatory and tumor-associated bone loss, and rheumatoid joint erosion, making it a validated therapeutic and mechanistic target.