In experimental models of melanoma, tumor growth can be transiently arrested via treatment with antibodies which block the interaction between PD-L1 and its receptor PD-1. PD-L1 overexpression results in increased resistance of tumor cells to CD8 T cell mediated lysis. Induced PD-L1 expression is common in many tumors including squamous cell carcinoma, colon adenocarcinoma, and breast adenocarcinoma. Additionally, PD-1 is known to play key roles in peripheral tolerance and prevention of autoimmune disease. Upon ligand binding, PD-1 signaling inhibits T-cell activation, leading to reduced proliferation, cytokine production, and T-cell death. PD-1 signals via binding its two ligands, PD-L1 and PD-L2 both members of the B7 family. PD-1’s structure includes a ITIM (immunoreceptor tyrosine-based inhibitory motif) suggesting that PD-1 negatively regulates TCR signals. Additionally, Pdcd1 mRNA is expressed in developing B lymphocytes during the pro-B-cell stage.
PD-1 expression declines after successful elimination of antigen. PD-1 is transiently expressed on CD4 and CD8 thymocytes as well as activated T and B lymphocytes and myeloid cells. PD-1 is a 50-55 kDa cell surface receptor encoded by the Pdcd1 gene that belongs to the CD28 family of the Ig superfamily. This Nivolumab biosimilar reacts with human PD-1 (programmed death-1) also known as CD279.
This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Nivolumab making it ideal for research use. This product is for research use only, NOT FOR THERAPEUTIC USE (RUO).Ībout InVivoSIM anti-human PD-1 (Nivolumab Biosimilar)