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proadifen

Structure via PubChem · Public domain (PubChem)

EntityQ7246819· pop 6· linked from 321 articles

Proadifen (SKF-525A) is a non-selective inhibitor of cytochrome P450 enzymes, preventing some types of 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.

In the Vinony graph

Vinony's link graph records 321 inbound references to proadifen, and connects out to valproic acid, conotoxin and Hypericum perforatum.

It sits within the topics Carboxylate esters, Cytochrome P450 inhibitors and Diethylamino compounds.

Vinony links it to 5 Wikipedia language editions.

Chemical data

Formula
C23H31NO2
Molecular weight
353.5 g/mol
IUPAC name
2-(diethylamino)ethyl 2,2-diphenylpentanoate

via PubChem

Drug data · ChEMBL

Max clinical phase
Phase 2
Molecule type
Small molecule

via ChEMBL · EBI

Research

1,586 papers

via PubMed

Wikidata facts

Mass
353.235
Show 3 more facts
chemical formula
C₂₃H₃₁NO₂
canonical SMILES
CCCC(C1=CC=CC=C1)(C2=CC=CC=C2)C(=O)OCCN(CC)CC
Commons category
Proadifen
Sources (2)

via Wikidata · CC0

~1 min read

Encyclopedic overview

2 sections
Contents
  • References
  • External links

Proadifen (SKF-525A) is a non-selective inhibitor of cytochrome P450 enzymes, preventing some types of 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/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.

Excerpted from Wikipedia’s “proadifen” article, available under the CC BY-SA 4.0 licence.

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