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Chemical Compound Review

proadifen     2-diethylaminoethyl 2,2-diphenylpentanoate

Synonyms: Proadifene, Proadifeno, Proadifenum, BCTB, Lopac-P-1061, ...
 
 
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Disease relevance of proadifen

 

Psychiatry related information on proadifen

 

High impact information on proadifen

  • The effect of carbon tetrachloride (CCl4) on hepatocytes was substantially reduced by prior treatment with SKF 525A, an inhibitor of cytochrome P-450, and by exposure to the reducing reagent beta-mercaptoethanol [9].
  • The LTB4 omega-hydroxylase was inhibited significantly by carbon monoxide, ferricytochrome c, SKF-525A, and Triton X-100, but was not affected by alpha-naphthoflavone, azide, cyanide, catalase, and superoxide dismutase [10].
  • ACh-induced CD increases resistant to L-NAME and indomethacin were reduced after the administration of intracoronary quinacrine, an inhibitor of phospholipase A2, or proadifen, an inhibitor of cytochrome P-450 [11].
  • During proadifen-inhibited 42K efflux, exogenous K+ augmented overflow of 3HNE, indicating that proadifen relaxed the hypoxic artery primarily by inhibiting K+-dependent exocytosis of NE [12].
  • Because the inhibitory effects of PB on GJ intercellular communication are prevented by the nonspecific cytochrome P-450 inhibitor SKF-525A (J. E. Klauning, et al., Toxicol. Appl. Pharmacol., 102: 533-563, 1990), we investigated whether alterations in Cx32 are coincident with changes in the major PB-inducible cytochrome P-450, termed b/e or IIB1/2 [13].
 

Chemical compound and disease context of proadifen

 

Biological context of proadifen

 

Anatomical context of proadifen

 

Associations of proadifen with other chemical compounds

 

Gene context of proadifen

  • Carbon monoxide, SKF-525A, metyrapone, and benzylimidazole strongly inhibited N-demethylation and 4-hydroxylation, indicating the participation of P-450 monooxygenase in these reactions [34].
  • However, SKF-525A was ineffective against the effect of LPS alone on liver and blood GPx and CAT or on hepatic GSH and GRx, suggesting that these effects were not mediated by cytochrome P450 oxidative metabolism [35].
  • In contrast, SKF-525A weakly inhibited CYP1A2-dependent activities (46% inhibition at 1200 microM) and CYP2E1-dependent activities (65% inhibition at 1000 microM) [36].
  • Daily SKF-525A pretreatment at a dose of 30 mg/kg, i.p., for 7 days 1 hour prior to KET and COC in combination effectively reversed the effects of this combination on body weight, organ/bodyweight ratios, histopathology, and serum IgM and IL-10 concentrations without affecting leukocytic counts [37].
  • In contrast, we observed that CYP450 inhibitors such as SKF-525A, 17-octadecynoic acid, 1-aminobenzotriazole, and 6-(2-propargyloxyphenyl)hexanoic acid reduced 12(S)-HETE levels, 3T6 fibroblast growth, and DNA synthesis induced by FBS [38].
 

Analytical, diagnostic and therapeutic context of proadifen

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