British Journal of Pharmacology (BRIT J PHARMACOL)

Publisher: British Pharmacological Society, Wiley

Journal description

All aspects of experimental pharmacology including: Cellular and molecular pharmacology Biochemical pharmacology Neuroscience All aspects of general pharmacology Special Reports for rapid publication of important new results of special pharmacological significance The British Journal of Pharmacology is the leading 'original papers' publication in the field of general pharmacology.

Current impact factor: 4.84

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 4.842
2013 Impact Factor 4.99
2012 Impact Factor 5.067
2011 Impact Factor 4.409
2010 Impact Factor 4.925
2009 Impact Factor 5.204
2008 Impact Factor 4.902
2007 Impact Factor 3.767
2006 Impact Factor 3.825
2005 Impact Factor 3.41
2004 Impact Factor 3.325
2003 Impact Factor 3.611
2002 Impact Factor 3.45
2001 Impact Factor 3.502
2000 Impact Factor 3.689
1999 Impact Factor 3.722
1998 Impact Factor 3.704
1997 Impact Factor 3.619
1996 Impact Factor 4.075
1995 Impact Factor 4.739
1994 Impact Factor 4.695
1993 Impact Factor 5.27
1992 Impact Factor 5.094

Impact factor over time

Impact factor

Additional details

5-year impact 4.96
Cited half-life 7.50
Immediacy index 1.51
Eigenfactor 0.05
Article influence 1.32
Website British Journal of Pharmacology website
Other titles British journal of pharmacology, BJP, Proceedings of the British Pharmacological Society
ISSN 0007-1188
OCLC 1240522
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • Non-Commercial
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • Publisher last contacted on 07/08/2014
    • This policy is an exception to the default policies of 'Wiley'
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Endothelin (ET) receptor antagonism reduces neointimal lesion formation in animal models. This investigation addressed the hypothesis that the selective ETA receptor antagonist sitaxentan would be more effective than mixed ETA/B antagonism at inhibiting neointimal proliferation in a mouse model of intra-luminal injury. Antagonism of ETA receptors by sitaxentan (1-100nM) was assessed in femoral arteries isolated from adult, male C57Bl6 mice (25-35g) using isometric wire myography. Neointimal lesion development was induced by intraluminal injury in mice receiving sitaxentan (ETA antagonist; 15mg/kg/day), A192621 (ETB antagonist; 30 mg/kg/day), the combination of both antagonists, or vehicle (n=6-16). Treatment began one week before, and continued for 28 days after, surgery. Femoral arteries were then harvested for analysis of lesion size and composition. Sitaxentan produced a selective, concentration-dependent parallel rightward shift of ET-1-mediated contraction (pD2 ; 8.2±0.1 Control vs 7.2±0.1 100nM sitaxentan; P<0.001) in isolated femoral arteries. Sitaxentan reduced neointimal lesion size (23±5% vs 51±4%; P<0.05), whereas ETB (A192621; 61±7%) and combined ETA/B antagonism (51±7% P>0.05) did not. Macrophage and α-smooth muscle actin content were unaltered by ET antagonism but sitaxentan reduced the amount of collagen in lesions (14±2% vs 44±6%; p<0.01). These results suggest that ETA antagonism would be more effective than combined ETA / ETB antagonism at reducing neointimal lesion formation. This article is protected by copyright. All rights reserved.
    British Journal of Pharmacology 01/2015; 172(11). DOI:10.1111/bph.13086
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    ABSTRACT: Palmitoylethanolamide (PEA) is an endogenous congener of anandamide and an enhancer of its actions at cannabinoid receptors, CB1 and CB2, and transient receptor potential vanilloid type-1 (TRPV1) channels. The other endocannabinoid, 2-arachidonoylglycerol (2-AG), was recently suggested to act as a TRPV1 agonist. We investigated if PEA enhances the levels of 2-AG in vitro or in vivo and 2-AG activity at TRPV1. Endogenous lipid levels were measured by liquid chromatography-mass spectrometry in: 1) human keratinocytes treated with PEA (10-20 μM, 40 min, 6h and 24 h, 37°C); 2) in the blood of spontaneously Ascaris suum hypersensitive Beagle dogs given a single oral dose of ultramicronized PEA (30 mg/kg, 1, 2, 4 and 8 h from administration); 3) the blood of healthy volunteers given a single oral dose of micronized PEA (300 mg, 2, 4 and 6 h from administration). The effect of 2-AG at TRPV1 was assessed by measuring intracellular Ca(2+) in HEK-293 cells over-expressing human TRPV1. PEA significantly elevated the amounts of 2-AG in keratinocytes (∼3-fold) and its plasma levels in humans and dogs (∼2 and ∼20-fold, respectively). 2-AG dose-dependently elevated intracellular Ca(2+) in HEK-293-TRPV1 cells in a TRPV1-dependent manner, and desensitized the cells to the effect of capsaicin. PEA only slightly enhanced 2-AG activation of TRPV1, but significantly increased 2-AG-induced TRPV1 desensitization to capsaicin (IC50 from 0.75±0.04 to 0.45±0.02 μM, with PEA 2 μM). These observations may explain why several effects of PEA can be attenuated by cannabinoid receptor or TRPV1 channel antagonists. This article is protected by copyright. All rights reserved.
    British Journal of Pharmacology 01/2015; DOI:10.1111/bph.13084
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    ABSTRACT: Antipsychotic drugs have been shown to modulate the expression of ATP-binding cassette transporter A1 (ABCA1), a key factor in the anti-atherogenic reverse cholesterol transport process, in vitro. Here we evaluated the potential of the typical antipsychotic drug haloperidol to modulate the macrophage cholesterol efflux function in vitro and susceptibility to atherosclerosis in vivo. Thioglycollate-elicited peritoneal macrophages were used for in vitro studies. Hyperlipidemic low-density lipoprotein (LDL) receptor knockout mice were implanted with a haloperidol-containing pellet and subsequently fed a Western-type diet for 5 weeks to induce the development of atherosclerotic lesions in vivo. Haloperidol induced a 54% decrease (P=0.043) in the mRNA expression of ABCA1 in peritoneal macrophages. This coincided with a 30% (P<0.001) decrease in the capacity of macrophages to efflux cholesterol to apolipoprotein A1. Haloperidol treatment stimulated the expression of ABCA1 (+51%; P=0.021) and other genes involved in reverse cholesterol transport, i.e. CYP7A1 (+98%; P=0.004) in livers of LDL receptor knockout mice. No change in splenic ABCA1 expression was noted. However, the average atherosclerotic lesion size was significantly smaller (-31%; P=0.039) in the context of a mildly more atherogenic metabolic phenotype upon haloperidol treatment. Importantly, haloperidol markedly lowered MCP-1 expression (-70%; P<0.001) and secretion (-28%; P=0.018) by peritoneal macrophages. These studies show that haloperidol treatment lowers the susceptibility for atherosclerotic lesion development in hyperlipidemic LDL receptor knockout mice. Our findings suggest that the beneficial effect on atherosclerosis susceptibility can be attributed to a haloperidol-induced inhibition of macrophage chemotaxis. This article is protected by copyright. All rights reserved.
    British Journal of Pharmacology 01/2015; 172(9). DOI:10.1111/bph.13067
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    ABSTRACT: Background and purpose: The fungal product (+)-antroquinonol activates AMP kinase (AMPK) activity in cancer cell lines. The present study was conducted to examine whether chemically synthesized (+)-antroquinonol exhibited beneficial metabolic effects in insulin-resistant states by activating AMPK and inhibiting dipeptidyl peptidase IV (DPP IV) activity. Experimental approach: Effects of (+)-antroquinonol on DPP IV activity were measured with a DPPIV Assay Kit and effects on GLP-1-induced PKA were measured in AR42J cells. Translocation of the glucose transporter 4, GLUT4, induced either by insulin-dependent PI3K/AKT signalling or by insulin-independent AMPK activation, was assayed in differentiated myotubes. Glucose uptake and GLUT4 translocation were assayed in L6 myocytes. Mice with diet-induced obesity were used to assess effects of acute and chronic treatment with (+)-antroquinonol on glycaemic control in vivo. Key results: The results showed that of (+)-antroquinonol (100 μM ) inhibited the DPP IV activity as effectively as the clinically used inhibitor, sitagliptin. The phosphorylation of AMPK Thr(172) in differentiated myotubes was significantly increased by (+)-antroquinonol. In cells simultaneously treated with S961 (insulin receptor antagonist), insulin and (+)-antroquinonol, the combination of (+)-antroquinonol plus insulin still increased both GLUT4 translocation and glucose uptake. Further, (+)-antroquinonol and sitagliptin reduced blood glucose, when given acutely or chronically to DIO mice. Conclusions and implications: Chemically synthesized (+)-antroquinonol exhibits dual effects to ameliorate insulin resistance, by increasing AMPK activity and GLUT4 translocation, along with inhibiting DPP IV activity.
    British Journal of Pharmacology 01/2015; 172(1). DOI:10.1111/bph.12828
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and purpose: Pancreatic cancer is characterized by alterations in several key signalling proteins, including increased expression and activity of the Src tyrosine kinase and focal adhesion kinase (FAK), which have been linked to its chemoresistance. Sustained Src inhibition reactivates survival pathways regulated by the transcription factor STAT3, also leading to resistance. Therefore, simultaneously targeting Src/FAK and STAT3 signalling could provide an important strategy for treating pancreatic cancer. Recently, we described novel quinazolinediones that increased generation of reactive oxygen species (ROS) and were cytotoxic in pancreatic cancer cells. Here, we have investigated effects of our lead compound, QD232, on Src/FAK and STAT3 signalling. Experimental approach: The major signalling pathways affected by QD232 in pancreatic cancer cell lines were identified by Kinexus proteomic analysis. Changes in key signalling proteins were confirmed by Western blotting. Cell migration was assessed by Boyden chamber and wound healing assays. Direct inhibition of kinase activity in vitro was assayed with a panel of 92 oncogenic kinases. Safety and efficacy of QD232 were determined in a xenograft mouse model of pancreatic cancer. Key results: QD232 potently inhibited Src/FAK and STAT3 phosphorylation, decreasing pancreatic cancer cell viability and migration. Furthermore, QD232 arrested cell cycle progression and induced apoptosis in these cells at low micromolar concentrations. Effects of QD232 on Src/FAK and STAT3 phosphorylation were blocked by N-acetylcysteine or glutathione. Conclusions and implications: QD232 is a novel compound with a unique, ROS-dependent mechanism, effective in drug-resistant cancer cell lines. This compound shows potential as therapy for pancreatic cancer.
    British Journal of Pharmacology 01/2015; 172(1). DOI:10.1111/bph.12855

  • British Journal of Pharmacology 03/2014;