Medicinal Research Reviews (Med Res Rev)

Publisher: Wiley

Journal description

The journal publishes timely critical reviews of topics related to medicinal research broadly defined to which the authors have made significant contributions. Appropriate topics include but are not limited to the underlying pathophysiology of important diseases and disease vectors; therapeutic approaches to the treatment of various diseases; the properties of molecular targets for therapeutic agents; important new methodologies facilitating the search for therapies; genomics and proteomics; structure-activity correlations of drug series; the development of new imaging and diagnostic tools; drug metabolism; drug delivery; chemical pharmacological pharmacokinetic pharmacodynamic and clinical characteristics of importance. Reviews are mainly solicited by the editors; however voluntary contributions are also encouraged. In the latter case potential authors are asked to contact either co-editor with an outline before beginning to write in order to avoid duplication of effort and to ensure suitability of the topic and its level of coverage.

Current impact factor: 8.13

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 8.131
2012 Impact Factor 9.583
2011 Impact Factor 10.7
2010 Impact Factor 10.228
2009 Impact Factor 8.656
2008 Impact Factor 8.907

Impact factor over time

Impact factor
Year

Additional details

5-year impact 9.98
Cited half-life 7.20
Immediacy index 1.81
Eigenfactor 0.01
Article influence 2.73
Website Medicinal Research Reviews website
Other titles Medicinal research reviews (Online), Medicinal research reviews
ISSN 1098-1128
OCLC 38745824
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Wiley

  • 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
    • On a non-profit server
    • 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
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic lymphocytic leukemia (CLL) remains the most incurable leukemia. Early chemotherapeutic treatments, including alkylating agents, purine nucleoside derivatives, and immunotherapeutic antibodies, only show limited benefits for patients but severe off-target related side effects. Recent advances in understanding of the critical molecular pathways of regulating proliferation and survival of B-CLL cells have spurred a new therapeutical strategy by selectively targeting phosphoinositide 3-kinase delta (PI3Kδ). Idelalisib, a first-in-class PI3Kδ-selective small molecule has received the FDA's fast-track approval in July of 2014 as a new treatment of CLL, indolent B-cell non-Hodgkin's lymphoma, and relapsed small lymphocytic lymphoma. Undoubtedly, the success of idelalisib has provided a solid support in the development of PI3Kδ-specific inhibitors and reformed the concept of treating CLL. However, the number of reported selective inhibitors of PI3Kδ is very limited and very few have advanced into clinical trials. The mechanism of their actions remains elusive. More profound understanding on the modes of action of new PI3Kδ inhibitors will further validate the PI3Kδ-targeting strategy, and help to identify biomarkers capable of stratifying patients who will most likely benefit from the therapy. © 2015 Wiley Periodicals, Inc.
    Medicinal Research Reviews 03/2015; DOI:10.1002/med.21341
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    ABSTRACT: Camptothecins (CPTs) are cytotoxic natural alkaloids that specifically target DNA topoisomerase I. Research on CPTs has undergone a significant evolution from the initial discovery of CPT in the late 1960s through the study of synthetic small-molecule derivatives to investigation of macromolecular constructs and formulations. Over the past years, intensive medicinal chemistry efforts have generated numerous CPT derivatives. Three derivatives, topotecan, irinotecan, and belotecan, are currently prescribed as anticancer drugs, and several related compounds are now in clinical trials. Interest in other biological effects, besides anticancer activity, of CPTs is also growing exponentially, as indicated by the large number of publications on the subject during the last decades. Therefore, the main focus of the present review is to provide an ample but condensed overview on various biological activities of CPT derivatives, in addition to continued up-to-date coverage of anticancer effects. © 2015 Wiley Periodicals, Inc.
    Medicinal Research Reviews 03/2015; DOI:10.1002/med.21342
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    ABSTRACT: Antiviral drug development has often followed a curious meandrous route, guided by serendipity rather than rationality. This will be illustrated by ten examples. The polyanionic compounds (i) polyethylene alanine (PEA) and (ii) suramin were designed as an antiviral agent (PEA) or known as an antitrypanosomal agent (suramin), before they emerged as, respectively, a depilatory agent, or reverse transcriptase inhibitor. The 2',3'-dideoxynucleosides (ddNs analogues) (iii) have been (and are still) used in the "Sanger" DNA sequencing technique, although they are now commercialized as nucleoside reverse transcriptase inhibitors (NRTIs) in the treatment of HIV infections. (E)-5-(2-Bromovinyl)-2'-deoxyuridine (iv) was discovered as a selective anti-herpes simplex virus compound and is now primarily used for the treatment of varicella-zoster virus infections. The prototype of the acyclic nucleoside phosphonates (ANPs), (S)-9-(3-hydroxy-2-phosphonylmethoxypropyl)adenine [(S)-HPMPA], (v) was never commercialized, although it gave rise to several marketed products (cidofovir, adefovir, and tenofovir). 1-[2-(Hydroxyethoxy)methyl]-6-(phenylthio)thymine (vi) and TIBO (tetrahydroimidazo[4,5,1-jk][1,4-benzodiazepin-2(1H)]-one and -thione) (vii) paved the way to a number of compounds (i.e., nevirapine, delavirdine, etravirine, and rilpivirine), which are now collectively called non-NRTIs. The bicyclam AMD3100 (viii) was originally described as an anti-HIV agent before it became later marketed as a stem cell mobilizer. The S-adenosylhomocysteine hydrolase inhibitors (ix), while active against a broad range of (-)RNA viruses and poxviruses may be particularly effective against Ebola virus, and for (x) the O-ANP derivatives, the potential application range encompasses virtually all DNA viruses. © 2015 Wiley Periodicals, Inc.
    Medicinal Research Reviews 02/2015; DOI:10.1002/med.21340
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    ABSTRACT: Chemotherapy and targeted therapy have opened new avenues in clinical oncology. However, there is a lack of response in a substantial percentage of cancer patients and diseases frequently relapse in those who even initially respond. Resistance is, at present, the major barrier to conquering cancer, the most lethal age-related pathology. Identification of mechanisms underlying resistance and development of effective strategies to circumvent treatment pitfalls thereby improving clinical outcomes remain overarching tasks for scientists and clinicians. Growing bodies of data indicate that stromal cells within the genetically stable but metabolically dynamic tumor microenvironment confer acquired resistance against anticancer therapies. Further, treatment itself activates the microenvironment by damaging a large population of benign cells, which can drastically exacerbate disease conditions in a cell nonautonomous manner, and such off-target effects should be well taken into account when establishing future therapeutic rationale. In this review, we highlight relevant biological mechanisms through which the tumor microenvironment drives development of resistance. We discuss some unsolved issues related to the preclinical and clinical trial paradigms that need to be carefully devised, and provide implications for personalized medicine. In the long run, an insightful and accurate understanding of the intricate signaling networks of the tumor microenvironment in pathological settings will guide the design of new clinical interventions particularly combinatorial therapies, and it might help overcome, or at least prevent, the onset of acquired resistance. © 2015 Wiley Periodicals, Inc.
    Medicinal Research Reviews 01/2015; 35(2). DOI:10.1002/med.21338
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    ABSTRACT: Many researchers have attempted to pharmacologically modulate the adrenergic system to control locomotion, pain, and spasms after central nervous system (CNS) trauma, although such efforts have led to conflicting results. Despite this, multiple studies highlight that α-adrenoceptors (α-ARs) are promising therapeutic targets because in the CNS, they are involved in reactivity to stressors and regulation of locomotion, pain, and spasms. These functions can be activated by direct modulation of these receptors on neuronal networks in the brain and the spinal cord. In addition, these multifunctional receptors are also broadly expressed on immune cells. This suggests that they might play a key role in modulating immunological responses, which may be crucial in treating spinal cord injury and traumatic brain injury as both diseases are characterized by a strong inflammatory component. Reducing the proinflammatory response will create a more permissive environment for axon regeneration and may support neuromodulation in combination therapies. However, pharmacological interventions are hindered by adrenergic system complexity and the even more complicated anatomical and physiological changes in the CNS after trauma. This review is the first concise overview of the pros and cons of α-AR modulation in the context of CNS trauma.
    Medicinal Research Reviews 12/2014; DOI:10.1002/med.21337
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    ABSTRACT: The ongoing search for effective antiplasmodial agents remains essential in the fight against malaria worldwide. Emerging parasitic drug resistance places an urgent need to explore chemotherapies with novel structures and mechanisms of action. Natural products have historically provided effective antimalarial drug scaffolds. In an effort to search nature's chemical potential for antiplasmodial agents, unconventionally sourced organisms coupled with innovative cultivation techniques were utilized. Approximately 60,000 niche microbes from various habitats (slow-growing terrestrial fungi, Antarctic microbes, and mangrove endophytes) were cultivated on a small-scale, extracted, and used in high-throughput screening to determine antimalarial activity. About 1% of crude extracts were considered active and 6% partially active (≥67% inhibition at 5 and 50 μg/mL, respectively). Active extracts (685) were cultivated on a large-scale, fractionated, and screened for both antimalarial activity and cytotoxicity. High interest fractions (397) with an IC50 < 1.11 μg/mL were identified and subjected to chromatographic separation for compound characterization and dereplication. Identifying active compounds with nanomolar antimalarial activity coupled with a selectivity index tenfold higher was accomplished with two of the 52 compounds isolated. This microscale, high-throughput screening project for antiplasmodial agents is discussed in the context of current natural product drug discovery efforts.
    Medicinal Research Reviews 12/2014; DOI:10.1002/med.21335
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    ABSTRACT: The serendipitous demonstration that the nonselective β-adrenergic receptor (β-AR) antagonist propranolol promotes the regression of infantile hemangiomas (IHs) aroused interest around the involvement of the β-adrenergic system in angiogenic processes. The efficacy of propranolol was related to the β2-AR blockade and the consequent inhibition of the production of vascular endothelial growth factor (VEGF), suggesting the hypothesis that propranolol could also be effective in treating retinopathy of prematurity (ROP), a retinal pathology characterized by VEGF-induced neoangiogenesis. Consequent to the encouraging animal studies, a pilot clinical trial showed that oral propranolol protects newborns from ROP progression, even though this treatment is not sufficiently safe. Further, animal studies clarified the role of β3-ARs in the development of ROP and, together with several preclinical studies demonstrating the key role of the β-adrenergic system in tumor progression, vascularization, and metastasis, prompted us to also investigate the participation of β3-ARs in tumor growth. The aim of this review is to gather the recent findings on the role of the β-adrenergic system in IHs, ROP, and cancer, highlighting the fact that these different pathologies, triggered by different pathogenic noxae, share common pathogenic mechanisms characterized by the presence of hypoxia-induced angiogenesis, which may be contrasted by targeting the β-adrenergic system. The mechanisms characterizing the pathogenesis of IHs, ROP, and cancer may also be active during the fetal–neonatal development, and a great contribution to the knowledge on the role of β-ARs in diseases characterized by chronic hypoxia may come from research focusing on the fetal and neonatal period.
    Medicinal Research Reviews 12/2014; DOI:10.1002/med.21336
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    ABSTRACT: NSAIDs are among the most widely prescribed medications across the world, but the gastrointestinal (GI) toxicity still remains the biggest problem and the challenge for current NSAIDs-based therapeutics. The development of selective COX-2 inhibitors was driven by the assumption that selective inhibition of COX-2 would reduce the GI side effects. However, the initial enthusiasm for selective COX-2 inhibitors has faded away due to the emergence of serious side effects associated with the long-term use of these NSAIDs. In the recent years, a number of novel approaches to develop gastrosparing NSAIDs have been explored with the promising results. This review deals with such approaches and strategies that have been employed in the last two decades and are being used currently in the design and development of safer NSAIDs.
    Medicinal Research Reviews 10/2014; 35(2). DOI:10.1002/med.21331
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    ABSTRACT: The biomechanical properties of cells and tissues may be instrumental in increasing our understanding of cellular behavior and cellular manifestations of diseases such as cancer. Nanomechanical properties can offer clinical translation of therapies beyond what are currently employed. Nanomechanical properties, often measured by nanoindentation methods using atomic force microscopy, may identify morphological variations, cellular binding forces, and surface adhesion behaviors that efficiently differentiate normal cells and cancer cells. The aim of this review is to examine current research involving the general use of atomic force microscopy/nanoindentation in measuring cellular nanomechanics; various factors and instrumental conditions that influence the nanomechanical properties of cells; and implementation of nanoindentation methods to distinguish cancer cells from normal cells or tissues. Applying these fundamental nanomechanical properties to current discoveries in clinical treatment may result in greater efficiency in diagnosis, treatment, and prevention of cancer, which ultimately can change the lives of patients.
    Medicinal Research Reviews 08/2014; 35(1). DOI:10.1002/med.21329
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    ABSTRACT: Ornithine aminotransferase (OAT) and γ-aminobutyric acid aminotransferase (GABA-AT) are classified under the same evolutionary subgroup and share a large portion of structural, functional, and mechanistic features. Therefore, it is not surprising that many molecules that bind to GABA-AT also bind well to OAT. Unlike GABA-AT, OAT had not been viewed as a potential therapeutic target until recently; consequently, the number of therapeutically viable molecules that target OAT is very limited. In this review the two enzymes are compared with respect to their active-site structures, catalytic and inactivation mechanisms, and selective inhibitors. Insight is offered that could aid in the design and development of new selective inhibitors of OAT for the treatment of cancer.
    Medicinal Research Reviews 08/2014; 35(2). DOI:10.1002/med.21328
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    ABSTRACT: Inflammation is an essential immune response characterized by pain, swelling, redness, heat, and impaired function. A controlled acute inflammatory response is necessary to fight off infection and overcome injury. However, if the inflammatory process persists and enters into the chronic state, it can lead to local and systemic deleterious effects counterproductive to healing and instead constitutes a new pathology. Typically, inflamed tissues are associated with an elevated level of reactive species (reactive oxygen species (ROS)/reactive nitrogen species (RNS)). These ROS/RNS are generated during the respiratory burst of immune cells and are important factors in defense against invading pathogens. Additionally, reactive species are now known to trigger oxidative/nitrosative modifications of biomolecules. While most of these modifications lead to irreparable damage, some are subtle and fully reversible. The reversible modifications can initiate signaling cascades known as “redox signaling.” This redox signaling tightly modulates the inflammatory response. Thus, understanding the complex role of ROS/RNS-induced redox signaling in inflammation will assist in the design of relevant therapeutic intervention strategies for inflammation-associated diseases. This review will highlight the impact of oxidative stress and redox signaling on inflammation and inflammation-associated diseases, with a focus on redox modifications of inflammation-related proteins.
    Medicinal Research Reviews 08/2014; 35(2). DOI:10.1002/med.21330
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    ABSTRACT: Ribosomes are essential components of the protein synthesis machinery. The process of ribosome biogenesis is well organized and tightly regulated. Recent studies have shown that ribosomal proteins (RPs) have extraribosomal functions that are involved in cell proliferation, differentiation, apoptosis, DNA repair, and other cellular processes. The dysfunction of RPs has been linked to the development and progression of hematological, metabolic, and cardiovascular diseases and cancer. Perturbation of ribosome biogenesis results in ribosomal stress, which triggers activation of the p53 signaling pathway through RPs–MDM2 interactions, resulting in p53-dependent cell cycle arrest and apoptosis. RPs also regulate cellular functions through p53-independent mechanisms. We herein review the recent advances in several forefronts of RP research, including the understanding of their biological features and roles in regulating cellular functions, maintaining cell homeostasis, and their involvement in the pathogenesis of human diseases. We also highlight the translational potential of this research for the identification of molecular biomarkers, and in the discovery and development of novel treatments for human diseases.
    Medicinal Research Reviews 08/2014; 35(2). DOI:10.1002/med.21327
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    ABSTRACT: Hypocretins, also named as orexins, are excitatory neuropeptides secreted by neurons specifically located in lateral hypothalamus and perifornical areas. Orexinergic fibers are extensively distributed in various brain regions and involved in a number of physiological functions, such as arousal, cognition, stress, appetite, and metabolism. Arousal is the most important function of orexin system as dysfunction of orexin signaling leads to narcolepsy. In addition to narcolepsy, orexin dysfunction is associated with serious neural disorders, including addiction, depression, and anxiety. However, some results linking orexin with these disorders are still contradictory, which may result from differences of detection methods or the precision of tools used in measurements; strategies targeted to orexin system (e.g., antagonists to orexin receptors, gene delivery, and cell transplantation) are promising new tools for treatment of neuropsychiatric disorders, though studies are still in a stage of preclinical or clinical research.
    Medicinal Research Reviews 01/2015; 35(1). DOI:10.1002/med.21326
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    ABSTRACT: Podophyllotoxin (PPT), as well as its congeners and derivatives, exhibits pronounced biological activities, especially antineoplastic effects. Its strong inhibitory effect on tumor cell growth led to the development of three of the most highly prescribed anticancer drugs in the world, etoposide, teniposide, and the water-soluble prodrug etoposide phosphate. Their clinical success as well as intriguing mechanism of action stimulated great interest in further modification of PPT for better antitumor activity. The C-4 position has been a major target for structural derivatization aimed at either producing more potent compounds or overcoming drug resistance. Accordingly, numerous PPT derivatives have been prepared via hemisynthesis and important structure–activity relationship (SAR) correlations have been identified. Several resulting compounds, including GL-331, TOP-53, and NK611, reached clinical trials. Some excellent reviews on the distribution, sources, applications, synthesis, and SAR of PPT have been published. This review focuses on a second generation of new etoposide-related drugs and provides detailed coverage of the current status and recent development of C-4-modified PPT analogs as anticancer clinical trial candidates.
    Medicinal Research Reviews 05/2014; 35(1). DOI:10.1002/med.21319