FigitumumabFigitumumab
MedChemExpress (MCE)
HY-P99197
943453-46-1
CP-751871
96.89%
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Figitumumab (CP-751871) is a potent and fully human monoclonal anti–insulin-like growth factor 1 receptor (IGF1R) antibody. Figitumumab prevents IGF1 from binding to IGF1R with an IC50 of 1.8 nM.
Figitumumab (CP-751871) (152 pM-10 μM
3 days) inhibits cancer cell proliferation[1]. Figitumumab (1 μg/mL
1 min or 24 h) induces the down-regulation of IGF-1R[2]. Figitumumab inhibits IGF1-induced autophosphorylation of IGF1R with an IC50 of 0.42 nM, and indirectly inhibits AKT activation[2]. Figitumumab recognizes the IGF-1R/IR heterodimer complex[2].
Figitumumab (CP-751871) (31-125 μg/mouse
i.p.
once) induces the down-regulation of tumor associated IGF-1R in mice[2]. Figitumumab (62.5-500 μg/mouse
i.p.
once) inhibits the growth of s.c. xenografts derived from colon (Colo-205), breast (MCF7), and lung (H460) cancer cell lines in mice[2].
IC50: 1.8 nM (IGF1R)[1] In Vitro Figitumumab (CP-751871) (152 pM-10 μM
3 days) inhibits cancer cell proliferation[1]. Figitumumab (1 μg/mL
1 min or 24 h) induces the down-regulation of IGF-1R[2]. Figitumumab inhibits IGF1-induced autophosphorylation of IGF1R with an IC50 of 0.42 nM, and indirectly inhibits AKT activation[2]. Figitumumab recognizes the IGF-1R/IR heterodimer complex[2]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Figitumumab Related Antibodies Cell Proliferation Assay[1] Cell Line: Breast, colon, lung small cell, and non–small cell cancer lines
Human
Human IgG2 kappa
Human IgG2 kappa, Isotype Control
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[1]. Pavlicek A, et al. Molecular predictors of sensitivity to the insulin-like growth factor 1 receptor inhibitor Figitumumab (CP-751,871). Mol Cancer Ther. 2013 Dec
12(12):2929-39. [Content Brief]
[2]. Cohen BD, et al. Combination therapy enhances the inhibition of tumor growth with the fully human anti-type 1 insulin-like growth factor receptor monoclonal antibody CP-751,871. Clin Cancer Res. 2005 Mar 1
11(5):2063-73. [Content Brief]