Evidence map›Paper›PMID 20590565›Full record

ArticleBritish journal of pharmacology2010

Biochanin A, a naturally occurring inhibitor of fatty acid amide hydrolase.

L Thors, J J Burston, B J Alter, M K McKinney, B F Cravatt, R A Ross, R G Pertwee, R W Gereau, J L Wiley, C J Fowler

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

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  19. Contributions of nonhematopoietic cells and mediators to immune responses: implications for immunotoxicology.Toxicological sciences : an official journal of the Society of Toxicology · 2015
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 3 countries.

L ThorsDepartment of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.
J J Burston
B J Alter
M K McKinney
B F Cravatt
R A Ross
R G Pertwee
R W Gereau
J L Wiley
C J Fowler
Scripps Research Institute · USUmeå University · SEUniversity of Aberdeen · GBVirginia Commonwealth University · USWashington University in St. Louis · US

Funding

SYNTHESIS OF SR141716A AND ANANDAMIDE ANALOGSP01DA009789 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI CRAVATT, BENJAMIN F · 1995 to 2013
$11.6M
THC RECEPTORSR01DA003672 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI WILEY, JENNY L. · 1985 to 2018
$4.9M
THC RECEPTORSR37DA003672 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI MARTIN, BILLY R · 1997 to 2006
$2.8M
NIDA NIH HHS DA-03672NIDA NIH HHS DA-09789NIDA NIH HHS P01 DA009789NIDA NIH HHS R01 DA003672NIDA NIH HHS R37 DA003672
6 · The paper itself

Abstract

background and purposeInhibitors of fatty acid amide hydrolase (FAAH), the enzyme responsible for the metabolism of the endogenous cannabinoid (CB) receptor ligand anandamide (AEA), are effective in a number of animal models of pain. Here, we investigated a series of isoflavones with respect to their abilities to inhibit FAAH. EXPERIMENTAL APPROACH: In vitro assays of FAAH activity and affinity for CB receptors were used to characterize key compounds. In vivo assays used were biochemical responses to formalin in anaesthetized mice and the 'tetrad' test for central CB receptor activation. KEY

resultsOf the compounds tested, biochanin A was adjudged to be the most promising. Biochanin A inhibited the hydrolysis of 0.5 microM AEA by mouse, rat and human FAAH with IC(50) values of 1.8, 1.4 and 2.4 microM respectively. The compound did not interact to any major extent with CB(1) or CB(2) receptors, nor with FAAH-2. In anaesthetized mice, URB597 (30 microg i.pl.) and biochanin A (100 microg i.pl.) both inhibited the spinal phosphorylation of extracellular signal-regulated kinase produced by the intraplantar injection of formalin. The effects of both compounds were significantly reduced by the CB(1) receptor antagonist/inverse agonist AM251 (30 microg i.pl.). Biochanin A (15 mg.kg(-1) i.v.) did not increase brain AEA concentrations, but produced a modest potentiation of the effects of 10 mg.kg(-1) i.v. AEA in the tetrad test. CONCLUSIONS AND IMPLICATIONS: It is concluded that biochanin A, in addition to its other biochemical properties, inhibits FAAH both in vitro and peripherally in vivo.

Indexed as

AmidohydrolasesAnimalsArachidonic AcidsBehavior, AnimalBenzamidesBrainCannabinoid Receptor AntagonistsCarbamatesCell Line, TransformedChlorocebus aethiopsCOS CellsDrug InteractionsEndocannabinoidsExtracellular Signal-Regulated MAP KinasesFatty Acid Amide HydrolasesFormaldehydeAM 251AmidohydrolasesanandamideArachidonic AcidsBenzamidesbiochanin ACannabinoid Receptor AntagonistsCarbamatescyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl esterEndocannabinoidsExtracellular Signal-Regulated MAP KinasesFatty Acid Amide HydrolasesFormaldehydeGenisteinIsoflavonesPiperidinesPolyunsaturated AlkamidesPyrazoles

Identifiers

PMID20590565
PMCPMC2931556
OpenAlexW1504913331

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.