Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents

Publisher: Bentham Science Publishers

Journal description

Current Medicinal Chemistry-Anti-Inflammatory & Anti-Allergy Agents aims to cover all the latest and outstanding developments in medicinal chemistry and rational drug design for the discovery of new Anti-Inflammatory & Anti-Allergy Agents. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of current topics in Anti-Inflammatory & Anti-Allergy medicinal chemistry. Current Medicinal Chemistry-Anti-Inflammatory & Anti-Allergy Agents is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments in Anti-Inflammatory & Anti-Allergy Agents drug discovery. Discontinued. Continued by Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry (1871-5230).

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Website Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents website
Other titles Anti-inflammatory & anti-allergy agents, Anti-inflammatory and anti-allergy agents
ISSN 1568-0142
OCLC 52852761
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Bentham Science Publishers

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Author's pre-print on author's personal website, institutional repository and open access repository
    • Author's post-print on author's personal website, institutional repository, open access repository, PubMed Central and arXiv
    • Non-Commercial
    • Published source must be acknowledged
    • Must link to journal homepage with DOI
    • Publisher's version/PDF cannot be used
  • Classification
    ​ yellow

Publications in this journal

  • Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 01/2012; 11(1):3751.
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    ABSTRACT: In the last ten years, blockade of the cytokine TNF-alpha has emerged as a powerful new treatment for Rheumatoid Arthritis and related inflammatory disorders. However, differences in efficacy and side effect profiles amongst TNF antagonists have revealed important differences in their mechanisms of action. In addition, TNF is only one of more than nineteen related cytokines in the TNF superfamily, each of which plays a distinct role in immune system homeostasis and function. Blocking agents against other members of the TNF family are in development and hold promise in the treatment of Rheumatoid Arthritis and other autoimmune disorders. Recent progress in the understanding of the biology and effects of antagonizing therapeutically relevant TNF family members will be reviewed.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 12/2005; 4(6):587-596. DOI:10.2174/156801405774933133
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    ABSTRACT: Tumor necrosis factor (TNF) is the prototype member of a large family of cytokines that plays a crucial role in metazoan biology. Recent advances have identified TNF-like cytokines and their cognate receptors as critical mediators of many inflammatory diseases. The field of TNF biology is ever-expanding, with over 60,000 citations listed in the Pubmed, highlighting the progress of the field and its significance to human health in general. In this issue, we have attempted to provide a synopsis of recent advances in TNF biology, with a special emphasis on how TNF and its related cytokines contribute to the control of inflammatory processes. The reviews by Bixby et al. and Pham et al. summarize how two molecular events regulated by TNF, the control of cell death and NF kappa B activation, modulate the inflammatory process. The role of TNF in controlling inflammation is highlighted by human patients with genetic mutations in TNF receptor, a subject that is reviewed by Todd et al. Nikolov and Siegel reviewed the use of targeted therapies against TNF-mediated inflammatory diseases. Finally, Sedger provided a comprehensive review on how viruses have developed strategies to subvert TNF signaling and inflammation as a means to facilitate their survival and propagation within the infected host. It is our hope that these reviews will help the readers navigate through this rapidly expanding field of research.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 12/2005; 4(6):555-555. DOI:10.2174/156801405774933179
  • Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 12/2005; 4(6):617-617. DOI:10.2174/156801405774933142
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    ABSTRACT: The nervous system and the immune system regulate a variety of essential, co-ordinated responses. Multiple anatomical and physiological connections exist between the CNS and the immune system and communication between these systems is relayed by multiple chemical messengers, ranging from small molecules such as nitric oxide to neuroendocrine peptides such as alpha melanocyte stimulating hormone to large proteins including cytokines and growth factors and their receptors. In the last few years, our knowledge about the interactions of the brain and immune system and the molecular framework that underpins these physiological interactions has advanced considerably.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 12/2005; 4(6):625-629. DOI:10.2174/156801405774933223
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    ABSTRACT: The white adipose tissue (WAT) represents the most important structure of the organism able to provide energy stores and heat insulation. Recently, its has been postulated that the adipose tissue can be considered as a complex, essential, and highly active metabolic and endocrine organ. Indeed, it is able to respond to different signals from the endocrine organs and from the nervous the immune systems. More recently, the adipose tissue has also been hypothesised to represent an "extension" of the immune system, for its capacity to contain immune cells, lymph nodes, thymus, but above all, for its ability to produce a series of cytokines and chemokines typical of the immune system (generally named adipokines). A better understanding of the immune and endocrine function of the adipose tissue will lead to the development of innovative therapeutic strategies in inflammatory disorders.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 12/2005; 4(6):619-624. DOI:10.2174/156801405774933205
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    ABSTRACT: Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors with key metabolic roles in adipose tissue, liver and skeletal muscle. They are also expressed at significant levels in polymorphonuclear cells, monocyte/ macrophages, dendritic cells, T cells and B cells, suggesting that they may have a role in modulating the immune response. To date, evidence for such a role comes from numerous studies describing changes in gene expression within immunoregulatory cells in response to pharmacological PPAR ligands, reports of beneficial effects of PPAR agonists in auto-immune disease in rodents, and accelerated auto-immune disease in genetically modified rodents with reduced PPAR expression. Coupled with the knowledge that the PPARs may act as "lipid sensors", these data have added to the growing scientific awareness of links between nutritional status and immune function.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 11/2005; 4(6):631-635. DOI:10.2174/156801405774933115
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    ABSTRACT: Vitamin D receptor (VDR) agonists are well-known for their capacity to control calcium metabolism and to regulate growth and differentiation of many cell types. More recently, it has become clear that VDR agonists possess exquisite immunoregulatory properties, mostly by targeting dendritic cells and T cells. These properties have been exploited in the treatment of several Th1-mediated experimental autoimmune diseases, and a considerable body of work documents their beneficial effects in inhibiting the development of type 1 diabetes (T1D), a chronic-progressive autoimmune disease leading to the destruction of insulin-producing pancreatic β cells. This review analyzes the capacity of different VDR agonists to inhibit spontaneous T1D development in the non-obese diabetic (NOD) mouse, and shows that 1α,25-(OH)2-16,23Z-diene-26,27-hexafluoro-19-nor D3 (compound 6) is the most effective analog, among those tested, in delaying and reducing disease progression. Identified mechanisms of action underlying the efficacy of this VDR agonist in inhibiting T1D development in the NOD mouse are also reviewed.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 11/2005; 4(6):645-651. DOI:10.2174/156801405774933197
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    ABSTRACT: Histamine is a biogenic amine with a broad spectrum of activities in various physiological and pathological situations. Besides its well-characterised effects in allergic responses and in acute inflammation, histamine modulates the cytokine network, influencing T helper 1 and T helper 2 balance, and antibody isotype. In multiple sclerosis (MS), and its animal model of experimental autoimmune encephalomyelitis (EAE), there are several steps in the autoimmune attack against myelin of the central nervous system where histamine might play an important role. Indeed, blockade of specific histamine receptors has been proven to prevent early acute EAE by reducing encephalitogenic T helper 1 response and altering antigen presentation. A deeper understanding of the mechanisms by which histamine regulates the development and progression of EAE and MS might open new strategies for immune intervention.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 11/2005; 4(6):637-643. DOI:10.2174/156801405774933151
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    ABSTRACT: Tumor necrosis factor receptor associated periodic syndrome (TRAPS) is a hereditary auto-inflammatory periodic fever syndrome associated with autosomal dominant ectodomain mutations in the 55kDa tumor necrosis factor receptor (TNFRSF1A). Over forty mutations in TNFRSF1A are associated with TRAPS. Plasma levels of soluble TNFRSF1A (sTNFRSF1A) are abnormally low in TRAPS patients, as is shedding of TNFRSF1A by some patients' leucocytes. It was hypothesised that a deficit in neutralisation of TNF by sTNFRSF1A in TRAPS might result in an increased sensitivity to the inflammatory effects of TNF. However, not all TRAPS-related TNFRSF1A mutations result in defective receptor shedding by leucocytes. We found that dermal fibroblasts, but not leucocytes, from TRAPS patients with C33Y mutation demonstrated reduced shedding of TNFRSF1A, and that shedding of both wild-type and mutant truncated TNFRSF1A from transfected cell lines was similar. It is unlikely that a defect in TNFRSF1A shedding fully explains the clinical features of TRAPS. We investigated the behaviour of TRAPS-related TNFRSF1A mutants compared with wildtype in transfected cell lines: the mutant forms of TNFRSF1A retained signalling functions, but showed abnormalities of intra-cellular trafficking and TNF binding suggestive of protein misfolding. The severity of the abnormalities were observed with different mutants correlated with the degree of penetrance and clinical severity. We hypothesise that aggregation and ligand-independent signalling of mutant TNFRSF1A may occur. The increased understanding of the genetic basis and pathophysiology of TRAPS has facilitated therapeutic advances in the clinical management of this condition, particularly the use of the TNF-neutralising agent etanercept.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 11/2005; 4(6):577-585. DOI:10.2174/156801405774933160
  • Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 10/2005; 4(5):449-449. DOI:10.2174/156801405774330420
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    ABSTRACT: Cutaneous adverse reactions to systemic antihistamines are rare but an important finding. The reaction may vary from an eczematous eruption as the most frequent type, to rare but severe reactions such as urticaria/angioedema, erythema multiforme/Stevens-Johnson syndrome or Lyell syndrome. This is a review of the reported types of cutaneous adverse reactions due to systemically administered old and new antihistamines.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 10/2005; 4(5):521-529. DOI:10.2174/156801405774330376
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    ABSTRACT: Antihistamines can be used in various disorders of dermatology. They are the mainstay of pharmacological therapy used in the management of urticaria and angioedema. They are also important in the management of atopic dermatitis, mastocytosis, eosinophilic disorders, contact dermatitis and flushing. Pruritus associated with other conditions such as lichen planus, pityriasis rosea, lichen simplex chronicus, dermatomyositis, amyloidosis, nummular dermatitis, exfoliative dermatitis, prurigo gravidarum, herpes gestationis, pruritic urticarial papules and plaques of pregnancy, erythema annulare centrifugum and erythema gyratum repens may also be relieved by antihistamines. Sedative antihistamines may help patients to reduce pruritus in scabies, prurigo nodularis, pruritus ani, lichen sclerosus and Grover disease. In bedbug, spider, human flea, bee, wasp, hornet or mosquito bites and in autosensitization dermatitis besides topical antipruritic agents, systemic antihistamines can be used against pruritus. Also, antihistamines may relieve pruritus in infestations, sponge dermatitis or cercarial dermatitis and can be used in varicella infection. Antihistamines are often helpful for relieving pruritus in exanthematous reactions to medications. Pruritus secondary to underlying medical disorders or of an idiopathic nature may also be relieved by these antihistamines, although controlled trials do not exist.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 10/2005; 4(5):485-493. DOI:10.2174/156801405774330321
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    ABSTRACT: PPAR-γ (peroxisome proliferator activated receptor gamma) mediates ligand-dependent transcriptional activation and repression. PPAR-γ was shown to be directly activated by naturally occurring fatty acids and several synthetic compounds such as thiazolidinediones (TZDs), agonists of PPAR-γ. TZDs are used in the first place as orally active antidiabetic agents in the treatment of type 2 diabetes. Lately, it has been implicated that TZDs might also serve as regulators of inflammatory diseases. TZDs inhibit the production of monocyte inflammatory cytokines such as RANTES, TNF-α, IL-6 and IL-1β in vitro and reduce plasma concentrations of TNF-α, sICAM-1, MCP-1, CRP and PAI-1 in vivo. TZDs can also stimulate the secretion of IL-6, IL-8 and CSF-1 in a cultured human endometrial cell line (EM42), which suggested a role of PPAR-γ in the pathogenesis of endometriosis. Although TZDs are not currently in clinical use as anti-inflammatory drugs, more recent observations were done to show that TZDs act as anti-inflammatory substances in several diseases. TZDs have anti-inflammatory, antiatherogenic and anti-oxidative stress effects reducing the incidence and severity of atherosclerosis and can reduce blood pressure. TZDs may be of therapeutic benefits in patients with Alzheimer's disease (AD) based on convergent findings that insulin also plays a role in aspects of CNS function. It has been confirmed that TZDs can prevent progressive cavitation by limiting inflammation subsequent secondary damage after CNS trauma in vivo and in vitro. TZDs can also prevent experimental autoimmune encephalomyelitis. The beneficial effects of TZDs in some autoimmune or atopic diseases, such as multiple sclerosis (MS), psoriasis, atopic dermatitis and asthma, and a common chronic liver disease, nonalcoholic steatohepatitis (NASH) have been shown in several clinical trials. There are some recent data demonstrating that TZDs may have anti-inflammatory properties in animal models and in cellular systems of other diseases such as inflammatory bowel disease, arthritis, glomerulonephritis, sepsis, chronic obstructive pulmonary disease (COPD) and endometriosis. All of the above mentioned results reveal a novel potential anti-inflammatory pathway of TZDs in these diseases.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 10/2005; 4(5):531-541. DOI:10.2174/156801405774330367
  • Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 10/2005; 4(5):481-483. DOI:10.2174/156801405774330439
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    ABSTRACT: We found that compounds, which can selectively inhibit the activity of mammalian DNA polymerase (pol ) in vitro, show an anti-12-O-tetradecanoylphorbol-13-acetate (TPA)-induced inflammatory effect in mice. Originally, we screened selective inhibitors for each of the mammalian DNA polymerases, and found two novel pol -inhibitors, phenolic compounds termed petasiphenol and curcumin (diferuloylmethane). Curcumin is known as an anti-chronic inflammatory agent and structurally quite similar to petasiphenol. The IC50 values of petasiphenol and curcumin for pol were 7.8 M and 7.0 M, respectively, and neither compound influenced any other mammalian DNA polymerases. Expectedly, petasiphenol also showed an anti-TPA-induced inflammatory effect. A relationship between the pol -inhibition and the anti-inflammatory activity is suggested. Therefore, we investigated whether other anti-inflammatory compounds such as terpeno benzoic acids, triterpene acids and epolactaene derivatives could be pol -inhibitors. Although all the compounds influenced not only several different DNA polymerase species but DNA topoisomerase II, they all most efficiently inhibited the pol -activity. These results unexpectedly suggest that there is a physiological relationship between pol l inhibition and anti-TPA-induced inflammation. This finding may provide insight into the molecular mechanism of TPAinduced inflammation, or neoplastic promotion.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 09/2005; 4(5):543-553. DOI:10.2174/156801405774330330
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    ABSTRACT: Antihistamines have an important role in dermatology. In order to understand how antihistamines work, effects of histamine should be examined first. Histamine was first defined in 1920s and was shown to take part in the pathogenesis of diseases such as urticaria, anaphylaxis, asthma, and allergic rhinitis. The main goal in the treatment of urticaria and other diseases related to histamine is to keep this powerful mediator's effects under control. So many antihistamines have been presented to the market since 1942 and still, new compounds are being developed. For years, antihistamines have been categorized as first, second and third generation. In this text, a review of the action mechanism of antihistamines and the new antihistamines will be presented.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 09/2005; 4(5):465-475. DOI:10.2174/156801405774330385
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    ABSTRACT: Allergic rhinitis is a common disease worldwide and antihistamines remain the mainstay of pharmacotherapy for allergic rhinitis. Histamine is one of main mediators involved in the disease pathophysiology. The primary mechanism of antihistamine action is believed to be competitive antagonism of histamine receptors, specifically the H1-receptors. These receptors are present on nerve endings, smooth muscles, and glandular cells. However, H1- antagonism may not be their sole mechanism of action. Antihistamines have been used in two forms; oral and topical, in the management of allergic rhinitis. The use of the first-generation oral antihistamines (chlorpheniramine, diphenhydramine, promethazine, tripolidine, clemastine, and tripelennamine) is considerably limited by their sedative and anticholinergic effects. The secondgeneration antihistamines (acrivastine, astemizole, azelastine, cetirizine, ebastine, fexofenadine, loratadine, mizolastine, and terfenadine) are effective in reducing nasal symptoms, and have no sedative effects. However, terfenadine, astemizole and recently, loratadine, have been found to cause prolongation of the QT interval on electrocardiogram, and can increase the risk for development of potentially lethal ventricular tachyarrhythmias, or torsades de pointes. The next-generation antihistamines (fexofenadine, desloratadine, tecastemizole, and levocetirizine) are typically the structurally modified, active metabolites or isomers of second-generation antihistamines. These agents retain the non-sedating properties of second- generation antihistamines while eliminating or limiting the cardiac risks. Topical antihistamines (azelastine and levocabastine), delivered by nasal spray, avoid or minimize systemic adverse effects. They have a rapid onset of action (less than 15 min) at low drug dosage, but their action is limited to the treated organ.
    Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 09/2005; 4(5):477-480. DOI:10.2174/156801405774330349