• • CYP Inhibition: It non-competitively inhibits various CYP-dependent monooxygenases (with an IC50 of 19 μM), slowing down the liver’s metabolism of numerous therapeutic compounds.
  • Secondary Effects: Beyond CYPs, it inhibits neuronal nitric oxide synthase (NOS1), transmembrane calcium influx, and platelet thromboxane synthesis.
  • Receptor & Channel Activity: It affects acetylcholine receptors (AChRs) and blocks the ATP-sensitive inward-rectifying potassium channel (KIR6.1).

• Formula: C₂₃H₃₁NO₂ ⋅ HCl
• Molecular Weight: 389.96 g/mol
• IUPAC Name: 2-(Diethylamino)ethyl 2,2-diphenylpentanoate hydrochloride
• CAS Number: 62-68-0

Proadifen for sale(SKF-525A) is a non-selective inhibitor of cytochrome P450 enzymes, thereby preventing certain drug metabolism. 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.

Proadifen exerts apoptotic/antiproliferative (tumor-suppressing) effects in certain forms of cancer (HT-29 colon adenocarcinoma), believed to be mediated by glycogen synthase kinase 3β (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.

Proadifen has been demonstrated to normally inhibit the nicotinic acetylcholine receptor (NAChR) and muscarinic acetylcholine receptor (MAChR) in rats