Anti-Mouse/Human CXCL12 Antibody (K15C) is an antibody targeting SDF-1/CXCL12. Anti-Mouse/Human CXCL12 Antibody (K15C) blocks the biological activity of SDF-1 secreted by cancer-associated fibroblasts. Anti-Mouse/Human CXCL12 Antibody (K15C) inhibits tumor growth, reduces tumor microvessel density, and decreases the proportion of Sca1 + CD31 + endothelial progenitor cells in tumors. Anti-Mouse/Human CXCL12 Antibody (K15C) can be used for research on aggressive human breast cancer. The recommended isotype control is Mouse IgG2a kappa, Isotype Control [1].
In Vivo, Administration of the Anti-Mouse/Human CXCL12 Antibody (K15C) (32 µg/mouse; i.p.; twice weekly; 68 days) reduces CAF-driven breast tumor growth by 53% via inhibition of angiogenesis and 36% via reduction of EPC recruitment in nude mice[1].
In Vitro, Anti-Mouse/Human CXCL12 Antibody (K15C) (10-20 μg/mL; 18 h) dose-dependently inhibits the enhanced in vitro chemotaxis of mouse Sca1+CD31+ endothelial progenitor cells (EPCs) toward human CAF1 cells, a process mediated by SDF-1/CXCL12 secreted by prostate cancer-associated fibroblasts (CAFs)[1].
References:
[1]. Orimo A, et al. Stromal fibroblasts present in invasive human breast carcinomas promote tumor growth and angiogenesis through elevated SDF-1/CXCL12 secretion. Cell. 2005 May 06;121(3):335-48.
In Vivo, Administration of the Anti-Mouse/Human CXCL12 Antibody (K15C) (32 µg/mouse; i.p.; twice weekly; 68 days) reduces CAF-driven breast tumor growth by 53% via inhibition of angiogenesis and 36% via reduction of EPC recruitment in nude mice[1].
In Vitro, Anti-Mouse/Human CXCL12 Antibody (K15C) (10-20 μg/mL; 18 h) dose-dependently inhibits the enhanced in vitro chemotaxis of mouse Sca1+CD31+ endothelial progenitor cells (EPCs) toward human CAF1 cells, a process mediated by SDF-1/CXCL12 secreted by prostate cancer-associated fibroblasts (CAFs)[1].
References:
[1]. Orimo A, et al. Stromal fibroblasts present in invasive human breast carcinomas promote tumor growth and angiogenesis through elevated SDF-1/CXCL12 secretion. Cell. 2005 May 06;121(3):335-48.