HSDVHK-NH2 TFA 

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

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

834.80

C₃₂H₄₉F₃N₁₂O₁₁

HSDVHK-NH2

NCCCC[C@@H](C(N)=O)NC([C@H](CC1=CNC=N1)NC([C@H](C(C)C)NC([C@H](CC(O)=O)NC([C@H](CO)NC([C@H](CC2=CNC=N2)N)=O)=O)=O)=O)=O.O=C(O)C(F)(F)F

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• [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.  [Content Brief]

  [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.  [Content Brief]

  [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.  [Content Brief]