In vitro activity: Forskolin increases cAMP levels in preparations of membranes, cells, or tissues. Forskolin not only activates AC but also interacts with certain other proteins, including glucose transporters and ion channels. Forskolin is able to promote activation of nine different transmembrane iso-forms of AC, albeit with somewhat less efficacy for AC9, which could be used to provides a means to identify and quantify high-affinity binding sites, i.e., G-proteins (Gs)–AC complexes. Activation of by GPCRs contributes to Forskolin-stimulated cAMP generation in cells because of Forskolin potentiation of AC activity. Forskolin stimulates adenylate cyclase activity without interacting with cell surface receptors. Forskolin's potentiation of cAMP in turn inhibits basophil and mast cell degranulation and histamine release, lowers blood pressure and intraocular pressure, inhibits platelet aggregation, promotes vasodilation, bronchodilation, and thyroid hormone secretion, and stimulates lipolysis in fat cells. Forskolin inhibits the binding of platelet-activating factor (PAF), independently of cAMP formation, which may be a result of Forskolin's direct effect on PAF or via interference with PAF binding to receptor sites. Forskolin also appears to have an effect on several membrane transport proteins, and inhibits glucose transport in erythrocytes, adipocytes, platelets, and other cells. Forskolin is used to treat with glaucoma.

Cell Assay: Forskolin concentration-dependently decreased human mesenchymal stem cells proliferation after 4 days. Moreover, Forskolin increased alkaline phosphatase (ALP) expression of human mesenchymal stem cells in a dose-dependent manner. Additionally, Forskolin (10 μM) significantly stimulated both vasopressin and oxytocin release from the rat hypothalamo-neurohypophysial (H-NH) system.

Cell Mol Neurobiol. 2003 Jun;23(3):305-14; J Postgrad Med. 2012 Jul-Sep;58(3):199-202; Endokrynol Pol. 2014;65(2):125-31