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Chemical Compound Review:

AC1NSVE1 1-methyl-2-[(Z)-tridec-8- enyl]quinolin-4-one

Synonyms: ZINC31168223, KB-212078, NP-013315, AKOS016010722, AK120365, ...

Kano, Y. et al., Kim, N.Y. et al., Yamahara, J. et al.

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High impact information on Evocarpine

In the isolated rat thoracic aorta evocarpine significantly inhibited the contraction induced by 60 mM K+ with an IC50 of 9.8 microM, and that induced by external Ca2+ in the depolarized muscle in concentrations of 10-100 microM [1].
Pharmacokinetics of evocarpine after intravenous injection was expressed in a one-compartment model, showing a linear elimination of plasma evocarpine up to a dosage of 75 mg/kg [2].
Metabolic ratio of evocarpine into EVCA after intravenous injection was 15.4%, and absorption ratio of the unaltered compound calculated from the levels of AUC after oral administration and intravenous injection was 4.7% [2].
We investigated the involvement of protein kinase A during the evocarpine-induced apoptotic cell death [3].
These findings suggest that cyclic adenosine monophosphate-dependent activation of protein kinase A plays a crucial role in protecting HL-60 cells from the evocarpine-induced apoptotic cell death [3].

Biological context of Evocarpine

Pharmacological properties of galenical preparation. XV. Pharmacokinetics study of evocarpine and its metabolite in rats [2].

Analytical, diagnostic and therapeutic context of Evocarpine

Investigation of a blood sample after oral administration of evocarpine by high performance liquid chromatography confirmed that the substance was absorbed without alteration [2].

References

The vasorelaxant effect of evocarpine in isolated aortic strips: mode of action. Yamahara, J., Kobayashi, G., Matsuda, H., Fujimura, H. Eur. J. Pharmacol. (1988) [Pubmed]
Pharmacological properties of galenical preparation. XV. Pharmacokinetics study of evocarpine and its metabolite in rats. Kano, Y., Chen, X.F., Kanemaki, S., Zong, Q., Komatsu, K. Chem. Pharm. Bull. (1991) [Pubmed]
Cyclic adenosine monophosphate inhibits quinolone alkaloid evocarpine-induced apoptosis via activation of protein kinase A in human leukaemic HL-60 cells. Kim, N.Y., Pae, H.O., Kang, T.H., Kim, Y.C., Lee, H.S., Chung, H.T. Pharmacol. Toxicol. (2000) [Pubmed]

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