P11

HSDVHK-NH2 is an antagonist of the integrin αvβ3-vitronectin interaction, with an IC50 of 1.74 pg/mL (2.414 pM)[1][2].

Research Areas >> Cancer

Signaling Pathways >> Cytoskeleton >> Integrin

αvβ3:2.74 nM (IC50)

HSDVHK significantly inhibited bFGF-induced cell migration compared to the PBS control group[1]. The Arg-Gly-Asp (RGD)-binding site recognition by HSDVHK-NH2 (P11) is site specific because the HSDVHK-NH2 (P11) is inactive for the complex formation of a denatured form of integrin–vitronectin. HSDVHK-NH2 (P11) shows a strong antagonism against avb3-GRGDSP interaction with an IC50 value of 25.72 nM[2]. HSDVHK-NH2 (P11) inhibits the HUVEC proliferation due to the induction of HUVEC cell death through caspases activations and its mechanism is related with increased p53 expression[3]. Cell Proliferation Assay[3] Cell Line: HUVEC cells. Concentration: 0.1, 1, 10, and 100 μg/mL. Incubation Time: 72 h. Result: Significantly inhibited HUVEC proliferation on denatured collagen-coated plates in a dose-dependent manner.

[1]. Yoonsuk Lee, et al. High-throughput screening of novel peptide inhibitors of an integrin receptor from the hexapeptide library by using a protein microarray chip. J Biomol Screen. 2004 Dec;9(8):687-94.

[2]. Youngjin Choi, et al. Site-specific inhibition of integrin alpha v beta 3-vitronectin association by a ser-asp-val sequence through an Arg-Gly-Asp-binding site of the integrin. Proteomics. 2010 Jan;10(1):72-80.

[3]. Ji-Young Bang, et al. Pharmacoproteomic analysis of a novel cell-permeable peptide inhibitor of tumor-induced angiogenesis. Mol Cell Proteomics. 2011 Aug;10(8):M110.005264.