Names | |
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Preferred IUPAC name
2-(Diethylamino)ethyl 2,2-diphenylpentanoate | |
Other names
SKF 525-A
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Identifiers | |
3D model (JSmol)
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ChEMBL | |
ChemSpider | |
PubChem CID
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UNII | |
CompTox Dashboard (EPA)
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Properties | |
C23H31NO2 | |
Molar mass | 353.506 g·mol−1 |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Proadifen (SKF-525A) is a non-selective inhibitor of cytochrome P450 enzymes, preventing some types of drug metabolism.[1] It is also an inhibitor of neuronal nitric oxide synthase (NOS), CYP-dependent (cytochrome P450-dependent) arachidonate metabolism, transmembrane calcium influx, and platelet thromboxane synthesis. Further documented effects include the blockade of ATP-sensitive inward rectifier potassium channel 8 (KIR6.1), and stimulation of endothelial cell prostacyclin production.[2]
Proadifen exerts apoptotic/anti-proliferate (tumour suppressing) effects in certain forms of cancer (HT-29 colon adenocarcinoma), believed to be caused by mediation of glycogen synthase kinase 3 β (GSK-3β). In the same study administration of proadifen was demonstrated to produce time- and dose-dependent phosphatidylserine externalization, caspase-3 activation and PARP cleavage. Intense upregulation of NAG-1 and ATF3 and downregulation of Mcl-1 and Egr-1 were also observed.[3]
Proadifen has been demonstrated to normally inhibit the nicotinic acetylcholine receptor (NAChR) and muscarinic acetylcholine receptor (MAChR) in rats.[2]