Nivolumab is a monoclonal antibody and is a humanized PD-1 antibody. Nivolumab has anti-tumor activity and is used in the treatment of melanoma, non-small cell lung cancer, renal cell carcinoma, etc.

PD-1 (CHO cells):1.66 nM (EC50), PD1-PDL1:2.52 nM, interaction between PD-1 and PD-L2:2.59 nM, PD-1 (activated T cells):0.64 nM (EC50)

METHODS: CD4+ T cells were co-cultured with DC cells for 6 days, treated with Nivolumab (0-1000 nmol/L), and the supernatant was collected on day 5 to measure IFNγ production by ELISA.
RESULTS: In allogeneic MLR, blockade of PD-1 with Nivolumab systematically resulted in titratable enhancement of IFNγ release. [1]
METHODS: Human colon cancer cells HT29, HCT116 and LoVo were treated with Nivolumab (1 µM) and different chemotherapeutic regimens for 72 h. Cell viability was measured by SRB assay.
RESULTS: Nivolumab decreased the efficacy of chemotherapy and increased the IC50 of 5-FU (3.1-fold, 2.2-fold, and 1.9-fold), OXA (2.8-fold, 4.8-fold, and 15.8-fold), and IRI (2.2-fold, 1.7-fold, and 2.9-fold) in HT29, HCT116, and LoVo, respectively. Nivolumab increased the IC50 for CDDP, DOXO, and TAX.[2]

METHODS: To assay antitumor activity in vivo, Nivolumab (200 µg) was injected intraperitoneally into huNOG or huNOG FcγR-/- mice harboring HSC4, RKO, HCC827, or NCI-H1975 tumors once a week for four weeks.
RESULTS: In huNOG mice, Nivolumab did not inhibit any xenogeneic human tumors, whereas the growth of HSC4, HCC827, and NCI-H1975 (but not RKO) tumors in huNOG FcγR-/- mice was strongly inhibited or even rejected after Nivolumab treatment. In some experiments, tumor growth was enhanced in Nivolumab-treated huNOG mice, such as HCC827.[3]

Human

Monoclonal

Unconjugated