Drug News & Perspectives Journal Impact Factor & Information

Publisher: Thomson Reuters

Journal description

A highly diversified and fully illustrated drug newsmagazine for scientists and managers in pharmaceutical research and development.

Current impact factor: 3.13

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2012 Impact Factor 3.132
2011 Impact Factor 2.208
2010 Impact Factor 2.598
2009 Impact Factor 2.101
2008 Impact Factor 1.989
2007 Impact Factor 2.721
2006 Impact Factor 2.489
2005 Impact Factor 2.159
2004 Impact Factor 1.254
2003 Impact Factor 0.412
2002 Impact Factor 0.524
2001 Impact Factor 0.629
2000 Impact Factor 0.835
1999 Impact Factor 0.462
1998 Impact Factor 0.381

Impact factor over time

Impact factor

Additional details

5-year impact 2.49
Cited half-life 5.80
Immediacy index 0.26
Eigenfactor 0.00
Article influence 0.79
Website Drug News and Perspectives website
Other titles Drug news & perspectives, Drug news and perspectives
ISSN 0214-0934
OCLC 17985509
Material type Periodical
Document type Journal / Magazine / Newspaper

Publisher details

Thomson Reuters

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Published source must be acknowledged
    • On a non-profit server
    • Embargo until published
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: For the last two decades, we have seen remarkable growth in the pharmaceutical industry. This growth has mainly been due to the approximately 100 new blockbuster drugs, such as Lipitor® (atorvastatin) and Plavix® (clopidogrel). More than half of the revenue of major pharmaceutical companies and above one-third of the total pharmaceutical revenues came from the sales of these blockbuster drugs. Questions concerning the fate of these blockbuster drugs are beginning to surface as they are approaching their patent expiration dates, and as they are expected to face significant competition from generic versions. Branded drugs with more than USD 120 billion in sales (as of 2008) are expected to lose their patent protection in the next 3 to 4 years, while the less expensive generic versions are ready to enter the market. It is plausible that a major paradigm shift in our thinking is needed to stay innovative, competitive and economically feasible in this new era of drug development. A new wave of innovations is expected to boost the blockbuster regime. Herein, we discuss the different threats facing the branded monopoly, as well as some of the hopeful expectations for the blockbuster drug.
    Drug News & Perspectives 12/2010; 23(10):670-84. DOI:10.1358/dnp.2010.23.10.1506088
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    ABSTRACT: MicroRNAs (miRNAs) are a class of short noncoding RNAs that participate in mastering the balance of gene-regulating networks. By targeting and controlling expression of messenger RNA, miRNAs can control highly complex signal transduction pathways and other biological pathways. Unique aberrant expression of miRNA at each stage of cancer development suggests that miRNA could play a novel role in cancer diagnosis and therapeutic strategies. Accumulated information on epigenetic modification of miRNA suggests a promising platform for miRNA in cancer therapy. Clinical applications exploiting the understanding of miRNA's function will be the next great challenge in cancer research.
    Drug News & Perspectives 12/2010; 23(10):655-61. DOI:10.1358/dnp.2010.23.10.1560143
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    ABSTRACT: Fifty years ago, the issue of conflict of interest in biomedical research appeared in the national spotlight and has remained in a state of constant evolution. Government legislation caused a boom in collaborations between physicians, researchers, academic institutions and industry. These relationships continue to advance medical science and make meaningful progress, yet they may threaten the integrity of physicians and researchers and the public's trust in medicine. This article will highlight the evolution of industry relationships and conflict of interest over time, discuss methods by which industry can potentially exert effects and propose new directions for the future.
    Drug News & Perspectives 11/2010; 23(9):607-12. DOI:10.1358/dnp.2010.23.9.1521763
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    ABSTRACT: This review evaluates past and present clinical trials, as well as the current preclinical drug candidates focused on treating Alzheimer's disease (AD), in order to better assess the trends in AD drug discovery in context with specific drug mechanisms. The author begins by presenting a summary of the results of over 160 clinical trials targeted at AD, of which 52% have either failed to meet clinical endpoints or stalled (defined for the purpose of this review as no clinical or publicly mentioned progress for at least 3 years). The author postulates that many of the current clinical approaches fail to sufficiently regulate the amyloid cascade that includes, but is not limited to, the production of soluble β-amyloid precursor protein, β-amyloid and/or amyloid precursor protein intracellular domain and including activation of the tau cascade, ultimately translating to no improvement in cognitive function. To support this argument, the author compares clinical results and peer-reviewed opinions to postulate that appropriately focused multifunctional or dual pathway drugs could make the optimal candidate(s) for further investigations.
    Drug News & Perspectives 11/2010; 23(9):573-84. DOI:10.1358/dnp.2010.23.9.1507297
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    ABSTRACT: DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin), a C-type lectin mainly present at the surface of immature dendritic cells, plays a relevant role activating and tailoring adaptive immune responses against different pathogens. This lectin recognizes, in a multivalent and calcium-dependent manner, highly glycosylated proteins present at the surface of pathogens. Several groups have devoted remarkable efforts to develop carbohydrate multivalent compounds targeting this lectin to modulate its role in pathogen capture and in the generation of an immune response. Most of these approaches have been based on mannosylation of immunogenic proteins such as ovalbumin but new strategies have been envisaged to achieve these goals. Although mannosylated systems cannot provide the required selectivity for a specific lectin at dendritic cells, fucosylated compounds have overcome this problem specifically targeting DC-SIGN and avoiding interferences with other lectins, such as the mannose receptor. The use of these carbohydrate multivalent compounds to target DC-SIGN can be considered a promising strategy to inhibit pathogen entry and to develop new vaccines against pathogen infection or cancer. New studies are required to provide more insights into the complex immune pathway involving DC-SIGN.
    Drug News & Perspectives 11/2010; 23(9):557-72. DOI:10.1358/dnp.2010.23.9.1437246
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    ABSTRACT: Excess activation of ionotropic glutamate receptors, primarily N-methyl-D-aspartate (NMDA) receptors and free radicals, evoke nerve cell death following hypoxic-ischemic brain injury in various animal models. However, clinical trials in stroke patients using NMDA receptor antagonists have failed to show efficacy primarily due to the limited therapeutic time window for neuroprotection and a narrow therapeutic index. In comparison, antioxidants prolonged the time window for neuroprotection in animal models of ischemic stroke and showed greater therapeutic potential in clinical trials for ischemic stroke. Excess activation of NMDA receptors and free radicals mediate the two separate pathways of nerve cell death in stroke and a safe and multifunctional drug that can block both routes in the brain will likely provide a better therapeutic outcome in patients with stroke. Derivatives of the lead structures of sulfasalazine and aspirin have led to the discovery of a new molecule, Neu2000, that has demonstrated excellent neuroprotection against NMDA- and free radical-induced cell death. Neu2000 is an NR2B-selective, moderate NMDA receptor antagonist with potent cell-permeable, spin trapping antioxidant action even at nanomolar concentrations. Nonclinical and human phase I studies demonstrated that Neu2000 can be translated to treat patients with stroke with better efficacy and therapeutic time window.
    Drug News & Perspectives 11/2010; 23(9):549-56. DOI:10.1358/dnp.2010.23.9.1513493
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    ABSTRACT: It seems likely that some infants who die from sudden infant death syndrome (SIDS) have a brainstem abnormality of the serotonergic system. Evidence suggests that infants who died from SIDS had defective respiratory and/or autonomic responses that led to death instead of recovery after an acute insult. The serotonergic neuromodulator system has roles in the control of cardiac autonomic and respiratory function, as well as now being identified as abnormal in infants with SIDS. This manuscript reviews the multiple roles of serotonin with reference to the functional aspects of the relevant brain regions. Correlations with pre- or postnatal exposure to stressors, or an underlying genetic process are also reviewed. Together, these studies indicate that perturbed function of the serotonin system will have significant physiological impact during early development. Understanding the functional importance of these systems assists understanding of the pathogenesis of SIDS. In conclusion, whether an infant inherits serotonergic defects and is therefore "inherently vulnerable", or whether postnatal stressors can induce the abnormalities, any functional abnormalities of the serotonergic system that result are likely to be subclinical in the majority of cases and not easily detected with current medical tools.
    Drug News & Perspectives 11/2010; 23(9):537-48. DOI:10.1358/dnp.2010.23.9.1453626
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    ABSTRACT: Spinal muscular atrophy (SMA) is the second most common autosomal recessive disease and is a leading cause of infantile death. This disease has a carrier frequency of 1:35, affecting 1/6,000 live births and is the result of a homozygous loss of the survival of motor neuron 1 gene (SMN1). Humans carry a nearly identical copy gene, SMN2, that codes for very low levels of the full-length protein, ∼10% when compared to SMN1. This is due to one silent nucleotide transition at the 5' end of exon 7 that disrupts a critical splicing regulatory domain. The underlying protein coding region, however, is unaffected by this and other nucleotide differences between SMN1 and SMN2. SMN2 has, therefore, been envisioned as an outstanding target for therapeutic strategies that 1) increases SMN2 expression, 2) alters the pre-messenger RNA splicing of exon 7 or 3) stabilizes the SMN2-derived protein products. In this review, we summarize numerous therapeutic approaches including nucleic acid-based and drug-oriented therapies that have progressed toward treating SMA.
    Drug News & Perspectives 10/2010; 23(8):475-82. DOI:10.1358/dnp.2010.23.8.1507295
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    ABSTRACT: Des-γ-carboxy prothrombin (DCP) is an abnormal prothrombin induced by the absence of vitamin K₂ that is increased in the serum of patients with hepatocellular carcinoma (HCC). In hepatoma cells, genetic alterations, membrane receptors, the inability to uptake labeled low-density lipoprotein, cytoskeletal changes and hepatocyte cytoplasmic transfers involved in vitamin K metabolism could play an important role in producing detectable DCP serum levels. Serum DCP was found to have a sensitivity ranging from 48% to 62%, a specificity of 81% to 98% and a diagnostic accuracy of 59% to 84% for detecting HCC. Plasma DCP does not correlate with α-fetoprotein (AFP) levels. However, when used together, the DCP and AFP assays increase the sensitivity of detecting HCC in more than 85% of patients. The specificity of the DCP assay appears to be superior to that of AFP. These biomarkers can complement ultrasound for early HCC detection, but neither DCP nor AFP is optimal. For small HCC, a high preoperative DCP level appears to be indicative of tumor recurrence. Recently, there has been attention given to DCP because of its role in detecting HCC recurrence after living donor liver transplant. More recent research has demonstrated that DCP stimulates human vascular endothelial cell growth and migration. All the data presented above demonstrate the importance of DCP in formulating a prognosis for patients with HCC.
    Drug News & Perspectives 10/2010; 23(8):498-508. DOI:10.1358/dnp.2010.23.8.1444236
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    ABSTRACT: Dimebon (latrepirdine) was developed and used in Russia as an over-the-counter oral antihistamine for allergy treatment. In the early 1990s, Dimebon was characterized as a low-affinity NMDA receptor antagonist by Dr. Sergey Bachurin and his colleagues. An initial small-scale, open-label trial of Dimebon in 14 Alzheimer's disease (AD) patients demonstrated potential efficacy. Dimebon was then patented for the treatment of neurodegenerative disorders and licensed by Medivation. Extremely promising results were obtained in a double-blind, placebo-controlled, phase II AD trial in 183 patients; however, a phase II trial of Dimebon in 91 Huntington's disease patients was much less successful. Recently, a phase III AD trial of Dimebon in 598 patients failed to result in any significant improvement in primary or secondary outcomes. The failure of Dimebon may be in large part due to insufficient understanding of its mechanism of action. The NMDA receptor blocking activity of Dimebon is too weak to be physiologically relevant, while the proposed "novel mitochondrial mechanism of action" lacks credible scientific evidence or a molecular target. Independent studies indicate that the clinical effects of Dimebon most likely result from inhibition of histamine H₁ and serotonin 5-HT₆ receptors. Careful preclinical studies of novel potential therapies are needed to minimize chances of making similar costly mistakes in the future.
    Drug News & Perspectives 10/2010; 23(8):518-23. DOI:10.1358/dnp.2010.23.8.1500435
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    ABSTRACT: The Royal Society of Chemistry Biotechnology Group and Chemical Biology Interface Forum held a 1-day symposium, on April 19, 2010, on Chemical and Biological Therapeutic Approaches to Neurological Disorders, at the Royal Society of Chemistry, Burlington House, London. The purpose of the meeting, organized by Colin Bedford, Irene Francois and Klaus Rumpel, was to give an update of new developments regarding the genetics, biochemistry and pathophysiology of the major neurological disorders. These developments should facilitate the discovery of better clinical biomarkers and improved medicines for the diagnosis, monitoring and treatment of patients with neurological disease. The presentations and posters covered neurological disorders including Parkinson's disease, Alzheimer's disease, multiple sclerosis, schizophrenia, autism, epilepsy and pain. The majority of these psychiatric and neurological disorders cause long-term suffering and disability and thus create an important global public health problem. This was the central issue of a participative discussion that took place at the end of the meeting.
    Drug News & Perspectives 10/2010; 23(8):524-31. DOI:10.1358/dnp.2010.23.8.1524353
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    ABSTRACT: Activation of the nuclear factor-κB (NF-κB) family of transcription factors results in the expression of numerous genes involved in the regulation of the innate and adaptive immune responses, and has been implicated as a key mechanism in chronic inflammatory diseases including rheumatoid arthritis (RA). The IκB kinases (IKKs) are key components in the signaling pathway by which proinflammatory stimuli, such as lipopolysaccharide and tumor necrosis factor-α lead to the activation of NF-κB. The most widely studied of the IKKs is IKKβ. Inhibitors of the kinase activity of IKKβ offer opportunities for intervention in RA, as well as other inflammatory disorders. Some examples for which the most extensive data are available will here be reviewed.
    Drug News & Perspectives 10/2010; 23(8):483-90. DOI:10.1358/dnp.2010.23.8.1447844
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    ABSTRACT: New anticancer agents are needed in order to overcome the resistance of cancer cells to standard chemotherapy. At present, many of the molecular events that drive the malignant transformation and progression have been identified and there is optimism that the development of agents that specifically target such events will improve treatment outcomes. Cancer cells present common alterations in components of pathways that are involved in the normal cell cycle regulation and in mechanisms of DNA damage repair. Wee1-like protein kinase is a tyrosine kinase with a key role as an inhibitory regulator of the G2/M checkpoint that precedes entry into mitosis. Abrogation of this checkpoint through Wee1 inhibition may result in increased antitumor activity of agents that cause DNA damage such as radiation therapy or some cytotoxic agents. This has been confirmed in preclinical studies and results of clinical studies evaluating a Wee1 inhibitor are awaited to establish its activity in combination with chemotherapy. Here we review the role of Wee1 tyrosine kinase in the control of the G2/M checkpoint and the effects of G2/M checkpoint abrogation through Wee1 inhibition. We present results of preclinical studies with Wee1 inhibitors and the results of the first clinical trial recently reported, evaluating MK-1775, a small-molecule inhibitor of Wee1.
    Drug News & Perspectives 09/2010; 23(7):425-9. DOI:10.1358/dnp.2010.23.7.1490760
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    ABSTRACT: Obesity has now reached pandemic proportions leading to a collection of morbidities referred to as metabolic syndrome including insulin resistance, type 2 diabetes and cardiovascular disease. The expansion of adipose tissue is a direct cause of these comorbidities due to excessive accumulation of triglycerides within adipocytes, causing disruption of normal adipose function. There are two major types of adipose tissue, white and brown. The former stores energy as triglycerides within large droplets, whereas the latter catabolizes lipids to produce heat. A strategy to combat obesity-associated disorders, therefore, includes enhancement of brown adipose tissue activity by targeting the recently identified regulators of brown adipocyte development and function, including its master regulator, PRDM16.
    Drug News & Perspectives 09/2010; 23(7):409-17. DOI:10.1358/dnp.2010.23.7.1487083