akt-bad

1. Glaucocalyxin A (Leukamenin F)-SBE-β-CD could be useful with a better solubility and sustained function in drug delivery. 2. Glaucocalyxin A activates caspase-3, decreases BAD phosphorylation, and reduces the expression of X-linked inhibitor of apoptosis protein. 3. Glaucocalyxin A inhibits Akt phosphorylation, suppresses proliferation, and promotes apoptosis in a dose-dependent manner, but not in normal glial cells. 4. Glaucocalyxin A inhibits collagen-stimulated tyrosine phosphorylation of Syk, LAT, and phospholipase Cγ2, the signaling events in collagen receptor GPⅥ pathway. 5. Glaucocalyxin A could potentially be developed as an antiplatelet and antithrombotic agent, can inhibit platelet p-selectin secretion and integrin activation by convulxin, is a GPVI selective ligand.

Kazinol A shows strong inhibition of arachidonic acid (AA)-induced platelet aggregation. It also exhibits potent inhibition with IC50 values ranging 0.6-164 M against XOD. Kazinol A may be a candidate for the development of effective anti-cancer drug on h

Chamaejasmine could be a candidate drug for osteosarcoma and breast cancer chemoprevention, induces apoptosis in MG63 and HEp-2 cells by Akt inactivation and dephosphorylation of BAD. It inhibits Bcl-2 expression and induces Bax expression to desintegrate