Anti-Mouse CD40L (MR1) In Vivo Antibody - Low Endotoxin (ICH1263-5mg)

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

Clone MR1 is a widely used monoclonal antibody directed against mouse CD40 ligand (CD40L/CD154), historically raised in Armenian hamster and best known as a functional blocking reagent. It is validated for ELISA, flow cytometry, neutralization, and functional assays, and is a long-standing tool for interrupting CD40-CD40L costimulation in vivo. This preparation is manufactured to in-vivo standards: low endotoxin (research grade less than 1 EU/mg; ultra-low grade less than 0.5 EU/mg), supplied in bulk milligram-to-gram quantities suitable for repeat dosing across animal cohorts, and provided for research use only. The low-endotoxin, aggregate-controlled format makes it well suited to functional immunology, transplantation, autoimmunity, and tumour-immunology studies where nonspecific inflammatory confounders from contaminating endotoxin must be minimised. Because MR1 blocks a central costimulatory checkpoint rather than depleting a cell population, it is typically used to test the contribution of CD40L-dependent T-cell help, germinal-centre formation, and antibody responses. Researchers commonly search for this reagent by clone name (MR1) when reproducing published costimulation-blockade protocols. CD40L (CD154), the target of clone MR1, is a type II transmembrane member of the TNF superfamily expressed predominantly on activated CD4+ T cells, and also on activated platelets, mast cells, and other cells. It binds CD40 on B cells, dendritic cells, macrophages, and endothelium. The CD40L-CD40 axis delivers a key costimulatory "second signal" that drives B-cell activation, immunoglobulin class-switch recombination, germinal-centre formation, and generation of high-affinity antibody and memory responses. On antigen-presenting cells, CD40 engagement licenses dendritic cells, upregulates MHC and costimulatory molecules, and promotes proinflammatory cytokine production, thereby amplifying T-cell priming. Loss-of-function mutations in CD40L cause X-linked hyper-IgM syndrome, underscoring its non-redundant role in humoral immunity. Because this pathway is central to T-dependent immune responses, transplant rejection, and multiple autoimmune processes, blockade of CD40L is a well-established strategy for inducing immune tolerance and dampening pathogenic antibody responses in preclinical models.