Background:

Oxy-16 is an antagonist of hedgehog activity.

Naturally occurring oxysterols that are products of cholesterol oxidation can stimulate the hedgehog (Hh) signaling pathway related to cardiovascular disease and bone formation. Activation of Hh signaling modulates inflammatory responses to additional atherogenic factors including lesion-producing macrophages and enable osteoblast differentiation, which is dependent on the target cell.

In vitro: Oxysterols have been shown to be associated with immunosuppression, apoptosis, atherosclerosis, inflammation, and cholesterol turnover. Other studies aslo indicated that oxysterols were Hedgehog (Hh) signaling pathway activators and had potent osteoinductive properties. Oxy-16, an oxysterol, was identified as a cell permeable oxygenated derivative of cholesterol that might be the end product or intermediate of the cholesterol excretion pathways. Oxy-16 is currently used as a transport form for cholesterol across the blood brain barrier and membranes. The osteogenic differentiation caused by Oxy-16 was cinsidered to be mediated via a Wnt signaling-related, Dkk-1-inhibitable mechanism [1].

In vivo: Up to now, there is no animal in vivo data reported.

Clinical trial: So far, no clinical study has been conducted.

Reference:
[1] Amantea, C. M.,Kim, W.K.,Meliton, V., et al. Oxysterol-induced osteogenic differentiation of marrow stromal cells is regulated by Dkk-1 inhibitable and PI3-kinase mediated signaling. Journal of Cellular Biochemistry 105(2), 424-436 (2008).