A dose escalating phase I study of GLPG0187, a broad spectrum integrin receptor antagonist, in adult patients with progressive high-grade glioma and other advanced solid malignancies.

Background: Integrin signaling is an attractive target for anti-cancer treatment. GLPG0187 is a broad spectrum integrin receptor antagonist (IRA). GLPG0187 inhibited tumor growth and metastasis in mouse models.

Naftidrofuryl-driven regulation of endothelial ICAM-1 involves nitric oxide.

Naftidrofuryl is a selective inhibitor of the 5-HT2 receptor expressed on human endothelial cells. This drug has been used over the years to cope with cerebral or peripheral ischemic accidents; however, no clear mechanism of action of this molecule has been highlighted to explain its vascular effects. In the present work, we demonstrate that the involvement of nitric oxide can account for the effects of naftidrofuryl.

ICAM-1 and VCAM-1 expression induced by TNF-alpha are inhibited by a glutathione peroxidase mimic.

Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are respectively involved in the endothelial recruitment of neutrophils, and in that of lymphocytes or tumor cells, in response to specific signals. We have used the glutathione peroxidase (GPx) mimic BXT-51072 to assess the possibility that endogenous hydroperoxides play a role in the tumor necrosis factor-alpha (TNFalpha)-induced expression of ICAM-1 and VCAM-1 by monolayers of human endothelial cells. The GPx mimic BXT-51072 strongly inhibits the TNFalpha-induced and cycloheximide-sensitive expression of ICAM-1 and VCAM-1.