Informa Healthcare – one of the world’s leading medical and scientific publishers – has released its latest Journal Impact Factor* results, with outstanding performances across the division’s diverse selection of peer-reviewed journals.
Highlights included Critical Reviews in Biochemistry and Molecular Biology, which registered a staggering 10.216 Impact Factor, up 23% from 8.306 last year; The World Journal of Biological Psychiatry, increased more than 55% to 5.564; and Chronobiology International jumped up to 3.987.
Impact Factors are a method of measuring the influence which a journal has on the scientific community. They are calculated by Thomson Reuters and are designed to indicate how many times the published articles of a journal are cited during the course of a year, providing an insight to how much ‘impact’ the journal is making on the scientific community.
“The Impact Factor can help validate the importance of our journals to the medical and scientific communities we serve,” explains Phil Garner, Divisional Managing Director at Informa Healthcare.
“We are extremely proud of the high quality information which we publish for our readers and the wide range of healthcare fields covered by our titles. We are delighted that this year’s Impact Factor increases for each journal clearly reflect the quality and importance of the research and pinpoint how much it is being used throughout the year”
Informa’s Expert Opinion series – which provides in-depth analysis of the pharmaceutical R&D pipeline – has registered noteworthy performances in Expert Opinion on Investigational Drugs which increased its Impact Factor to 4.218, and Expert Opinion on Drug Delivery which impressed with a first-ever Impact Factor of 3.345.
“These results demonstrate the comprehensive, intelligent content that makes our Expert Opinion journals the definitive reference source for leading pharmaceutical scientists,” says Phil.
Four other Informa titles to enter the market with a remarkable impact include: Journal of Immunotoxicology with a first-ever impact factor of 1.218; Computer Aided Surgery with an impact factor of 1.221; Logopedics, Phoniatrics Vocology had a 1.175 Impact Factor in its first year; and Australasian Psychiatry entering the market at 0.657.
“We are justifiably proud of the performance of all of our journals,” adds Phil. “Our established journals have continued to move from strength to strength, with many titles solidifying an upward trend in their respective rankings.”
The World Journal of Biological Psychiatry moved up 22 places in the Psychiatry category, while the Amyotrophic Lateral Sclerosis Impact Factor increased 63% to 2.963, moving 37 places up within its Clinical Neurology sector. The Scandinavian Journal of Primary Health Care also moved up 13 places with a 27.9% Impact Factor increase to 2.205.
Other titles that registered impressive Impact Factor performances were: Cancer Investigation, with an increased impact factor of 2.105; Autoimmunity at 2.813; Critical Reviews in Microbiology with 3.207; Leukemia & Lymphoma at 2.397; and Nanotoxicology which registered a 72.5% increase to 5.774.
“Our overall performance – together with the outstanding individual performances of many of our titles – ensures that Informa continues to serve as a leading force in medical and scientific publishing, providing the market with the lion’s share of must-read titles,” explains Phil.
*© Thomson Reuters, Journal Citation Reports® 2010
Showing posts with label Expert Opinion on Investigational Drugs. Show all posts
Showing posts with label Expert Opinion on Investigational Drugs. Show all posts
Tuesday, 22 June 2010
Thursday, 19 March 2009
Phospholipases may not be targets of choice for medicinal chemistry, but two inhibitors are now in clinical development for atherosclerosis
By Editorial Board member Dr Keith Suckling
Phospholipases do not appear high on the list of major druggable target types. There are significant challenges in medicinal chemistry to provide specificity and in enzymology to generate data that can support chemistry for reactions that take place at a lipid-water interface at which active concentrations of compounds are difficult to define. So it is perhaps surprising that there are now two phospholipase inhibitors in clinical development for the treatment of atherosclerosis - surprising because of the chemical challenges but also because the final proof of efficacy in patients requires extended outcome studies in around 16,000 subjects.
The first of these compounds is darapladib (GSK) for which Phase 2 results were presented last year [1]. Darapladib inhibits the enzyme known as lipoprotein-associated phospholipase A2. As the name suggests, this phospholipase is found in the circulation associated with LDL and is thought to catalyse the hydrolysis of oxidised phospholipids. The products of the hydrolysis promote the expression of adhesion molecules on the artery wall and chemokines in macrophages and so promote the development of the vulnerable plaque. Inhibition of this process would therefore be expected to be of benefit and recent studies in a pig model support this concept [2] and some of the Phase 2 data are consistent with it too. This mechanism would be expected to have a similar overall effect on the pathogenesis of atherosclerosis to a chemokine receptor antagonist, for example CCR2. Importantly this approach does not reduce plasma LDL, and is not expected to.
Other forms of phospholipase have been implicated in atherogenesis in recent years and in particular those known as secretory phospholipases [3], of which the Group V enzymes have been of particular interest. Animal data also supports a role for these enzymes in atherogenesis [4], but the mechanism is different. In this case the phospholipase modifies HDL and LDL particles making the former less able to support reverse cholesterol transport and the latter more susceptible to oxidation. Very recently Phase 2 data have been reported of the effects of an sPLA2 inhibitor, varespladib (A-002, Anthera Pharmaceuticals) [5]. This compound inhibits a range of sPLA2 s (sPLA2-IIa>sPLA2-X>sPLA2-V) and, in contrast to darapladib, does have an effect on plasma LDL concentration and also on hsCRP. Recent animal data are consistent with an effect of varespladib on atherogenesis in the mouse [6]
It is important to recognize that the effects of these two phospholipase inhibitors on the process of atherogenesis are quite different and as a result, at least in Phase 2, they require different end points to be studied. If this is not borne clearly in mind there is a danger of serious confusion amongst non-experts. In this respect we should no more talk about phospholipase inhibitors as a class than we might about PPAR agonists: there are so many differences. Nevertheless, for both mechanisms, it is necessary to show that they improve outcomes in patients, and at this point the differences are not important. A large outcome study is beginning for darapladib (STABILITY) with around 15,000 patients [7].
By Keith Suckling, PhD, Editorial Board member of Expert Opinion on Investigational Drugs
Reference List
1. Serruys P.W., Garcia-Garcia H.M., Buszman P., Erne P., Verheye S., Aschermann M., Duckers H., Bleie O., Dudek D., Botker H.E. et al. (2008). Effects of the direct lipoprotein-associated phospholipase A(2) inhibitor darapladib on human coronary atherosclerotic plaque. Circulation 118: 1172-1182.
2. Wilensky R.L., Shi Y., Mohler E.R., III, Hamamdzic D., Burgert M.E., Li J., Postle A., Fenning R.S., Bollinger J.G., Hoffman B.E. et al. (2008). Inhibition of lipoprotein-associated phospholipase A2 reduces complex coronary atherosclerotic plaque development. Nat Med 14: 1059-1066.
3. Kimura-Matsumoto M., Ishikawa Y., Komiyama K., Tsuruta T., Murakami M., Masuda S., Akasaka Y., Ito K., Ishiguro S., Morita H. et al. (2008). Expression of secretory phospholipase A2s in human atherosclerosis development. Atherosclerosis 196: 81-91.
4. Boyanovsky B., Zack M., Forrest K., and Webb N.R. (2009). The Capacity of Group V sPLA2 to Increase Atherogenicity of ApoE-/- and LDLR-/- Mouse LDL In Vitro Predicts its Atherogenic Role In Vivo. Arterioscler Thromb Vasc Biol ATVBAHA.
5. Rosenson RS, Hislop C, McConnell D, Elliot, M, Stasiv U, et al. (2009). Effects of 1-H-indole-3-glyoxamide (A-002) on concentration of secretory phospholipase A2 (PLASMA study): a phase II double-blind, randomised, placebo-controlled trial. Lancet 373: 649-658.
6. Fraser H., Hislop C., Christie R.M., Rick H.L., Reidy C.A., Chouinard M.L., Eacho P.I., Gould K.E., and Trias J. (2009). Varespladib (A-002), a Secretory Phospholipase A2 Inhibitor, Reduces Atherosclerosis and Aneurysm Formation in ApoE-/- Mice. J Cardiovasc Pharmacol.53, 60-65
7. GSK Press release: http://www.gsk.com/media/pressreleases/2008/2008_pressrelease_10144.htm
Phospholipases do not appear high on the list of major druggable target types. There are significant challenges in medicinal chemistry to provide specificity and in enzymology to generate data that can support chemistry for reactions that take place at a lipid-water interface at which active concentrations of compounds are difficult to define. So it is perhaps surprising that there are now two phospholipase inhibitors in clinical development for the treatment of atherosclerosis - surprising because of the chemical challenges but also because the final proof of efficacy in patients requires extended outcome studies in around 16,000 subjects.
The first of these compounds is darapladib (GSK) for which Phase 2 results were presented last year [1]. Darapladib inhibits the enzyme known as lipoprotein-associated phospholipase A2. As the name suggests, this phospholipase is found in the circulation associated with LDL and is thought to catalyse the hydrolysis of oxidised phospholipids. The products of the hydrolysis promote the expression of adhesion molecules on the artery wall and chemokines in macrophages and so promote the development of the vulnerable plaque. Inhibition of this process would therefore be expected to be of benefit and recent studies in a pig model support this concept [2] and some of the Phase 2 data are consistent with it too. This mechanism would be expected to have a similar overall effect on the pathogenesis of atherosclerosis to a chemokine receptor antagonist, for example CCR2. Importantly this approach does not reduce plasma LDL, and is not expected to.
Other forms of phospholipase have been implicated in atherogenesis in recent years and in particular those known as secretory phospholipases [3], of which the Group V enzymes have been of particular interest. Animal data also supports a role for these enzymes in atherogenesis [4], but the mechanism is different. In this case the phospholipase modifies HDL and LDL particles making the former less able to support reverse cholesterol transport and the latter more susceptible to oxidation. Very recently Phase 2 data have been reported of the effects of an sPLA2 inhibitor, varespladib (A-002, Anthera Pharmaceuticals) [5]. This compound inhibits a range of sPLA2 s (sPLA2-IIa>sPLA2-X>sPLA2-V) and, in contrast to darapladib, does have an effect on plasma LDL concentration and also on hsCRP. Recent animal data are consistent with an effect of varespladib on atherogenesis in the mouse [6]
It is important to recognize that the effects of these two phospholipase inhibitors on the process of atherogenesis are quite different and as a result, at least in Phase 2, they require different end points to be studied. If this is not borne clearly in mind there is a danger of serious confusion amongst non-experts. In this respect we should no more talk about phospholipase inhibitors as a class than we might about PPAR agonists: there are so many differences. Nevertheless, for both mechanisms, it is necessary to show that they improve outcomes in patients, and at this point the differences are not important. A large outcome study is beginning for darapladib (STABILITY) with around 15,000 patients [7].
By Keith Suckling, PhD, Editorial Board member of Expert Opinion on Investigational Drugs
Reference List
1. Serruys P.W., Garcia-Garcia H.M., Buszman P., Erne P., Verheye S., Aschermann M., Duckers H., Bleie O., Dudek D., Botker H.E. et al. (2008). Effects of the direct lipoprotein-associated phospholipase A(2) inhibitor darapladib on human coronary atherosclerotic plaque. Circulation 118: 1172-1182.
2. Wilensky R.L., Shi Y., Mohler E.R., III, Hamamdzic D., Burgert M.E., Li J., Postle A., Fenning R.S., Bollinger J.G., Hoffman B.E. et al. (2008). Inhibition of lipoprotein-associated phospholipase A2 reduces complex coronary atherosclerotic plaque development. Nat Med 14: 1059-1066.
3. Kimura-Matsumoto M., Ishikawa Y., Komiyama K., Tsuruta T., Murakami M., Masuda S., Akasaka Y., Ito K., Ishiguro S., Morita H. et al. (2008). Expression of secretory phospholipase A2s in human atherosclerosis development. Atherosclerosis 196: 81-91.
4. Boyanovsky B., Zack M., Forrest K., and Webb N.R. (2009). The Capacity of Group V sPLA2 to Increase Atherogenicity of ApoE-/- and LDLR-/- Mouse LDL In Vitro Predicts its Atherogenic Role In Vivo. Arterioscler Thromb Vasc Biol ATVBAHA.
5. Rosenson RS, Hislop C, McConnell D, Elliot, M, Stasiv U, et al. (2009). Effects of 1-H-indole-3-glyoxamide (A-002) on concentration of secretory phospholipase A2 (PLASMA study): a phase II double-blind, randomised, placebo-controlled trial. Lancet 373: 649-658.
6. Fraser H., Hislop C., Christie R.M., Rick H.L., Reidy C.A., Chouinard M.L., Eacho P.I., Gould K.E., and Trias J. (2009). Varespladib (A-002), a Secretory Phospholipase A2 Inhibitor, Reduces Atherosclerosis and Aneurysm Formation in ApoE-/- Mice. J Cardiovasc Pharmacol.53, 60-65
7. GSK Press release: http://www.gsk.com/media/pressreleases/2008/2008_pressrelease_10144.htm
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