proadifen

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| ImageFile=Proadifen.png

| ImageSize=

| PIN=2-(Diethylamino)ethyl 2,2-diphenylpentanoate

| OtherNames=SKF 525-A

|Section1={{Chembox Identifiers

| CASNo=302-33-0

| PubChem=4910

| ChemSpiderID = 4741

| ChEMBL = 282567

| SMILES = O=C(OCCN(CC)CC)C(c1ccccc1)(c2ccccc2)CCC

| StdInChI = 1S/C23H31NO2/c1-4-17-23(20-13-9-7-10-14-20,21-15-11-8-12-16-21)22(25)26-19-18-24(5-2)6-3/h7-16H,4-6,17-19H2,1-3H3

| UNII_Ref = {{fdacite|correct|FDA}}

| UNII = A510CA4CBT

}}

|Section2={{Chembox Properties

| C=23 | H=31 | N=1 | O=2

| Appearance=

| Density=

| MeltingPt=

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|Section3={{Chembox Hazards

| MainHazards=

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| AutoignitionPt =

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Proadifen (SKF-525A) is a non-selective inhibitor of cytochrome P450 enzymes, preventing some types of drug metabolism.{{cite journal | pmid = 14161153 | year = 1964 | last1 = Marshall | first1 = FN | last2 = Williamson | first2 = HE | title = Natruretic Response During Infusion of Beta-Diethylaminoethyl-Diphenylpropyl Acetate Hydrocloride (Skf 525-A) | volume = 143 | pages = 395–400 | journal = The Journal of Pharmacology and Experimental Therapeutics| doi = 10.1016/S0022-3565(25)26743-X }} 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.{{cite web|url=http://www.scbt.com/datasheet-200492-skf-525a-hcl-proadifen.html|author= |title = Proadifen hydrochloride (CAS 62-68-0) |website=Santa Cruz Biotech}}

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.{{cite journal | vauthors = Jendželovský R, Koval J, Mikeš J, Papčová Z, Plšíková J, Fedoročko P | title = Inhibition of GSK-3β reverses the pro-apoptotic effect of proadifen (SKF-525A) in HT-29 colon adenocarcinoma cells | journal = Toxicol in Vitro | volume = 26 | issue = 6 | pages = 775–82 | date = September 2012 | pmid = 22683934 | doi = 10.1016/j.tiv.2012.05.014 | bibcode = 2012ToxVi..26..775J }}

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