GRGDSPK acetate shows inhibitory activity against integrin-fibronectin binding and can be used in research on integrins in bone formation and resorption.

By measuring calcium content and 70 bonehnit area of tissue in parietal bones 18 days old isolated from pregnant Sprague-Dawley rats, we know that GRGDSPK (EMD 56574; RGD; 0.1-50 μM; for 4 days) inhibits mineralization in a dose-dependent manner.[1]
Treatment with GRGDSPK (10 and 50 μM; 4-day treatment) results in significant alterations in bone morphology, characterized by disruptions in the organization of osteoblasts and the mineralized matrix.[1]
In the presence of GRGDSPK peptide (RGD; 250 μM), added to the medium, the binding between integrins and fibronectin is effectively blocked, leading to a considerable increase in the average size of cell aggregates in wild-type cells.[2]
Addition of GRGDSPK (250 μM) leads to a significant reduction in adhesion forces and work exerted by wild-type mesendodermal progenitors, indicating the involvement of integrins expressed in these progenitors and the specificity of the detachment parameters recorded for fibronectin.[2]
GRGDSPK (RGD-containing, 1.5 mM, 1.0 mM, and 0.5 mM) and RGD-modified peptides, at concentrations of 1.5 mM, 1.0 mM, and 0.5 mM, impair the fertilization ability of bovine oocytes by sperm cells, resulting in a dose-dependent reduction in cleavage rates.[3]

DMSO: 7.76 mg/mL (10 mM), Sonication is recommended.