Immunology, endocrine & metabolic agents in medicinal chemistry最新文献

{"title":"Anti-Phospholipase A₂ Receptor Autoantibody: A New Biomarker for Primary Membranous Nephropathy.","authors":"Quansheng Zhu","doi":"10.2174/1871522215666150910205702","DOIUrl":"https://doi.org/10.2174/1871522215666150910205702","url":null,"abstract":"<p><p>Primary membranous nephropathy (also known as idiopathic membranous nephropathy, IMN) is an organ specific autoimmune kidney disease characterized by the development of immune complex deposits in the sub-epithelial spaces, podocyte effacement and glomerular capillary wall thickening in the later stages. Clinical studies have demonstrated that over 70% of patients with IMN possess circulating autoimmune antibodies specifically targeting the phospholipase A₂ receptor (PLA₂R) on the surface of podocytes. The autoantibodies only bind to the extracellular portion of PLA₂R under the non-reducing condition, indicating that the epitope in PLA₂R is conformational requiring specific disulfide bonds to maintain its structure. We recently have successfully located the dominant epitope in PLA₂R to the extreme N-terminus of the receptor. This finding has opened a new direction for understanding the pathogenesis of anti-PLA₂R autoantibody induced IMN and offered a strong basis for developing sensitive clinical assays for IMN diagnosis and prognosis, and potentially, new therapeutic approaches for IMN treatment.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"16 1","pages":"4-17"},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1871522215666150910205702","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35059390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Actin and Keratin are Binding Partners of the 1,25D₃-MARRS Receptor/PDIA3/ERp57.","authors":"Tremaine LeBlanc,&nbsp;Lka Nemere","doi":"10.2174/1871522214666140704171342","DOIUrl":"https://doi.org/10.2174/1871522214666140704171342","url":null,"abstract":"<p><p>We have shown that the 1,25D₃-MARRS receptor is necessary for the rapid, pre-genomic effects of 1,25(OH)₂D₃ on phosphate and/or calcium absorption in chick intestines. However, a clear understanding of the proteins involved in the signaling mechanisms by which the 1,25D₃-MARRS receptor facilitates 1,25(OH)₂D₃-mediated phosphate or calcium uptake, as well as other cellular effects, is still under investigation. We used co-immunoprecipitation studies and mass spectroscopy to identify actin and keratin as proteins that interact with the 1,25D₃-MARRS receptor. Using confocal microscopy, we visualized 1,25(OH)₂D₃- MARRS receptor localizations relative to actin and/or keratin distribution in chick enterocytes. Cells cultured in media containing phenol red had the 1,25D₃-MARRS receptor and actin localized largely in the nucleus, which was dispersed upon addition of (OH)₂ 1,25(OH)₂D₃. In the absence of phenol red, staining was cytoplasmic. Addition of steroid caused diminished staining at 10 s and 30 s, with a return of intensity between 1 and 5 min. Nuclear staining was observed after 1 min. We found that F-actin concentrations are maximal when 1,25D₃-MARRS receptor localizations within enterocytes are low suggesting that cyclical conversions of F-actin to G-actin are involved in the 1,25(OH)₂D₃-mediated redistribution of the 1,25D₃-MARRS receptor within the cell. We also found that keratin distribution remains constant with 1,25(OH)₂D₃ exposure when Factin depolymerizes into G-actin, which suggests that actin and keratin work in concert to facilitate hormonemediated redistribution of the 1,25D₃-MARRS receptor. We subsequently investigated whether the cyclical redistribution was related to either 1,25(OH)₂D₃-stimulated phosphate or calcium uptake, but no congruent pattern was found.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"14 2","pages":"55-66"},"PeriodicalIF":0.0,"publicationDate":"2014-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1871522214666140704171342","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33349690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Angiogenesis by Gene Therapy for Critical Limb Ischemia: Choice of Biological Agent.","authors":"Fumihiro Sanada, Yoshiaki Taniyama, Junya Azuma, Ikeda-Iwabe Yuka, Yasuhiro Kanbara, Masaaki Iwabayashi, Hiromi Rakugi, Ryuichi Morishita","doi":"10.2174/1871522213999131231105139","DOIUrl":"10.2174/1871522213999131231105139","url":null,"abstract":"<p><p>Peripheral artery disease (PAD) is caused by atherosclerosis, hardening and narrowing arteries over time due to buildup of fatty deposit in vascular bed called plaque. Severe blockage of an artery of the lower extremity markedly reduce blood flow, resulting in critical limb ischemia (CLI) manifested by a variety of clinical syndromes including rest pain in the feet or toes, ulcer and gangrene with infection. Despite significant advances in clinical care and interventions for revascularization, patients with CLI remain at high risk for amputation and cardiovascular death. To overcome this unmet need, therapeutic angiogenesis using angiogenic growth factors has evolved in an attempt to increase blood flow in ischemic limb. Initial animal studies and phase I clinical trials with vascular endothelial growth factor (VEGF) or fibroblast growth factor (FGF) demonstrated promising results, inspiring scientists to progress forward. However, more rigorous phase II and III clinical trials have failed to demonstrate beneficial effects of these angiogenic growth factors to date. Recently, two multicenter, double-blind, placebo-controlled clinical trials in Japan (phase III) and US (phase II) demonstrated that hepatocyte growth factor (HGF) gene therapy for CLI significant improved primary end points and tissue oxygenation up to two years in comparison to placebo. These clinical results implicate a distinct action of HGF on cellular processes involved in vascular remodeling under pathological condition. This review presents data from phase I-III clinical trials of therapeutic angiogenesis by gene therapy in patients with PAD. Further, we discuss the potential explanation for the success or failure of clinical trials in the context of the biological mechanisms underlying angiogenesis and vascular remodeling, including cellular senescence, inflammation, and tissue fibrosis.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"14 1","pages":"32-39"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/50/a4/IEMAMC-14-32.PMC4435566.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33330603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Oral L-Citrulline Supplementation on Lipoprotein Oxidation and Endothelial Dysfunction in Humans with Vasospastic Angina.","authors":"Masahiko Morita,&nbsp;Masami Sakurada,&nbsp;Fumiko Watanabe,&nbsp;Tetsuo Yamasaki,&nbsp;Hiroshi Doi,&nbsp;Hirotaka Ezaki,&nbsp;Koji Morishita,&nbsp;Takayuki Miyakex","doi":"10.2174/18715222113139990008","DOIUrl":"https://doi.org/10.2174/18715222113139990008","url":null,"abstract":"<p><strong>Background: </strong>Decreased nitric oxide (NO) bioavailability and increased lipid oxidation are associated with progressive endothelial dysfunction. L-Citrulline, the effective precursor of L-arginine which is essential as a substrate for endothelial NO synthase (eNOS), is effective in enhancing NO-dependent signaling. However, little is known about the efficacy of L-citrulline supplementation on lipoprotein oxidation and endothelial dysfunction.</p><p><strong>Methods: </strong>Twenty-two patients (aged 41 - 64 years old) diagnosed with vasospastic angina with flow-mediated dilation (FMD) of the brachial artery (< 5.5 %) received 800 mg/day of L-citrulline for 8 weeks. FMD (%), blood NOx, asymmetric dimethylarginine (ADMA), small dense LDL, oxidized lipids, amino acids concentrations were measured before and after supplementation.</p><p><strong>Results: </strong>Compared with baseline values, FMD (%) was significantly improved at 4 and 8 weeks as well as at 4 weeks after the end of intake. L-Citrulline supplementation caused a significant lowering of plasma ADMA levels. Plasma L-arginine/ADMA ratio and NOx levels rose markedly throughout the study period. Moreover, significant reductions of serum oxidized LDL and lectin-like oxidized LDL receptor 1 (LOX-1) ligand containing ApoB (LAB), an indicator of the biological activity of oxidized lipoprotein binding to LOX-1, were observed after L-citrulline intake.</p><p><strong>Conclusions: </strong>L-Citrulline supplementation improves endothelial dysfunction, probably due to potentiating NO-dependent reactions and decreasing the state of lipoprotein oxidation in humans.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"13 3","pages":"214-220"},"PeriodicalIF":0.0,"publicationDate":"2013-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/18715222113139990008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33331164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review: Evidence-based Clinical Research of Anti-obesity Supplements in Japan.","authors":"Asuka Yasueda,&nbsp;Toshinori Ito,&nbsp;Kazuhisa Maeda","doi":"10.2174/1871522213666131118221347","DOIUrl":"https://doi.org/10.2174/1871522213666131118221347","url":null,"abstract":"<p><strong>Background: </strong>The prevalence of obesity has increased dramatically throughout the world, and weight reduction through lifestyle management is urgently warranted. At present, numerous supplements advertised for their anti-overweight property are available in the Japanese market, but most of these lack proper evidence. Thus, we investigated dietary supplements that have been tested in clinical trials.</p><p><strong>Search strategy: </strong>We researched anti-obesity supplements in the Japanese market using the google search engine in Japanese with the key terms \"anti-obesity supplements,\" \"diet supplements,\" and \"weight reduction supplements.\"</p><p><strong>Results: </strong>We listed 49 companies that supply anti-obesity supplements. Of these, 11 had published clinical evidence of the anti-obesity efficacy of their supplements. These products contain the following active ingredients: <i>Angelica keiskei</i>, bofu-tsusho-san, capsaishin, DHA/EPA, forskohlii, garcinia cambogia, lactoferrin, L-carnitine, oligonol, tea catechin, and yeast hydrolysate.</p><p><strong>Conclusion: </strong>We obtained 11 supplements for which clinical evidence was published in medical journals in English. We also found 10 products for which clinical or animal evidence was published in Japanese. We expect that many companies will produce evidence of the efficacy of their products in the near future, thereby validating the use of dietary anti-obesity supplements in Japan.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"13 3","pages":"185-195"},"PeriodicalIF":0.0,"publicationDate":"2013-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1871522213666131118221347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33331161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Review of the Diagnostic Scope of Biomarker Techniques, Genetic Screening and Virtual Scanning.","authors":"Graham Wilfred Ewing","doi":"10.2174/1871522211313010004","DOIUrl":"https://doi.org/10.2174/1871522211313010004","url":null,"abstract":"<p><p>The purpose of this article is to compare and evaluate the advantages and benefits of the cognitive screening technique Virtual Scanning with contemporary diagnostic and screening techniques, in particular genetic screening and biomarkers. In the last 50 years biomarker techniques and more recently genetic screening have been developed to characterise the onset, progression and regression of pathologies. Nevertheless the scientific picture is not yet complete. It does not yet include an understanding of relationship between genotype and phenotype; the regulatory function of the autonomic nervous system; or the rate or level of the expressed protein, protein conformation, the rate at which proteins react, and the reaction conditions such as pH, levels of minerals and cofactors, and temperature. By contrast, Virtual Scanning is based upon the light absorbing and emitting properties of proteins and how this bioluminescence influences colour perception. It provides a measure of the level of expressed protein and the rate at which such expressed protein subsequently reacts with its reactive substrate. The article highlights the limitations of genetic screening and biomarkers and the perceived advantages which Virtual Scanning may have for routine mass screening <i>e.g.</i> of diabetes, cardiovascular disease, cancers, depression, migraine, etc.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"13 1","pages":"35-45"},"PeriodicalIF":0.0,"publicationDate":"2013-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1871522211313010004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33331160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MODULATING CO-STIMULATION DURING ANTIGEN PRESENTATION TO ENHANCE CANCER IMMUNOTHERAPY.","authors":"Therese Liechtenstein, Ines Dufait, Alessio Lanna, Karine Breckpot, David Escors","doi":"10.2174/187152212802001875","DOIUrl":"10.2174/187152212802001875","url":null,"abstract":"<p><p>One of the key roles of the immune system is the identification of potentially dangerous pathogens or tumour cells, and raising a wide range of mechanisms to eliminate them from the organism. One of these mechanisms is activation and expansion of antigen-specific cytotoxic T cells, after recognition of antigenic peptides on the surface of antigen presenting cells such as dendritic cells (DCs). However, DCs also process and present autoantigens. Therefore, antigen presentation has to occur in the appropriate context to either trigger immune responses or establishing immunological tolerance. This is achieved by co-stimulation of T cells during antigen presentation. Co-stimulation consists on the simultaneous binding of ligand-receptor molecules at the immunological synapse which will determine the type and extent of T cell responses. In addition, the type of cytokines/chemokines present during antigen presentation will influence the polarisation of T cell responses, whether they lead to tolerance, antibody responses or cytotoxicity. In this review, we will focus on approaches manipulating co-stimulation during antigen presentation, and the role of cytokine stimulation on effective T cell responses. More specifically, we will address the experimental strategies to interfere with negative co-stimulation such as that mediated by PD-L1 (Programmed cell death 1 ligand 1)/PD-1 (Programmed death 1) to enhance anti-tumour immunity.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"12 3","pages":"224-235"},"PeriodicalIF":0.0,"publicationDate":"2012-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428911/pdf/ukmss-49320.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30879047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPR30 FORMS AN INTEGRAL PART OF E2-PROTECTIVE PATHWAY IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS.","authors":"Sheetal Bodhankar, Halina Offner","doi":"10.2174/1871522211108040262","DOIUrl":"10.2174/1871522211108040262","url":null,"abstract":"<p><p>A major focus of our laboratory has been an in-depth evaluation as to how estrogens exert a pronounced protective effect on clinical and histological disease in the animal model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE). An important issue regarding their therapeutic application has been the undesirable estrogenic side effects thought to be mediated primarily through 17β-estradiol (E2) binding to intracellular estrogen receptor alpha (ERα). With the discovery and characterization of GPR30 as the putative membrane estrogen receptor, we sought to study whether signaling through GPR30 was sufficient to mediate protection against EAE without engagement of ERα. Treatment of EAE in WT mice with G-1, a selective GPR30 agonist, retained estradiol's ability to protect against clinical and histological EAE without estrogenic side effects. G-1 treatment deviated cytokine profiles and enhanced suppressive activity of CD4(+)Foxp3(+) Treg cells through a GPR30- and programmed death 1 (PD-1)-dependent mechanism. This novel finding was indicative of the protective effect of GPR30 activation in EAE and provides a strong foundation for the clinical application of GPR30 agonists such as G-1 in MS. However, future studies are needed to elucidate cross-signaling and evaluate possible additive effects of combined signaling through both GPR30 and ER-α. Deciphering the possible mechanism of involvement of GPR30 in estrogen-mediated protection against EAE may result in lowering treatment doses of E2 and GPR30 agonists that could minimize risks and maximize immunoregulation and therapeutic effects in MS. Alternatively, one might envision using E2 derivatives with reduced estrogenic activity alone or in combination with GPR30 agonists as therapies for both male and female MS patients.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"11 4","pages":"262-274"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255092/pdf/nihms293937.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30388273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting ErbB3: the New RTK(id) on the Prostate Cancer Block.","authors":"Maitreyee K Jathal, Liqun Chen, Maria Mudryj, Paramita M Ghosh","doi":"10.2174/187152211795495643","DOIUrl":"10.2174/187152211795495643","url":null,"abstract":"<p><p>Most prostate cancers (PCa) are critically reliant on functional androgen receptor (AR) signaling. At its onset, PCa is androgen-dependent and although temporarily halted by surgically or pharmacologically blocking the AR (androgen ablation), the disease ultimately recurs as an aggressive, fatal castration resistant prostate cancer (CRPC). FDA-approved treatments like docetaxel, a chemotherapeutic agent, and Provenge, a cancer vaccine, extend survival by a scant 3 and 4 months, respectively. It is clear that more effective drugs targeting CRPC are urgently needed. The ErbB family (EGFR/ErbB1, ErbB2/HER2/neu, ErbB3/HER3 and ErbB4/HER4) of receptor tyrosine kinases (RTKs) have long been implicated in PCa initiation and progression, but inhibitors of ErbB1 and ErbB2 (prototypic family members) fared poorly in PCa clinical trials. Recent research suggests that another family member ErbB3 abets emergence of the castration-resistant phenotype. Considerable efforts are being directed towards understanding ErbB3-mediated molecular mechanisms of castration resistance and searching for novel ways of inhibiting ErbB3 activity via rational drug design. Antibody-based therapy that prevents ligand binding to ErbB3 appears promising and fully-humanized antibodies that inhibit ligand-induced phosphorylation of ErbB3 are currently in early development. Small molecule tyrosine kinase inhibitors are also being vigorously pursued, as are siRNA-based approaches and combination treatment strategies- the simultaneous suppression of ErbB3 and its signaling partners or downstream effectors - with the primary purpose of undermining the resiliency of ErbB3-mediated signal transduction. This review summarizes the existing literature and reinforces the importance of ErbB3 as a therapeutic target in the clinical management of prostate cancer.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"11 2","pages":"131-149"},"PeriodicalIF":0.0,"publicationDate":"2011-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3095967/pdf/nihms-294747.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40101095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPER/GPR30 and Regulation of Vascular Tone and Blood Pressure.","authors":"Matthias R Meyer,&nbsp;Eric R Prossnitz,&nbsp;Matthias Barton","doi":"10.2174/1871522211108040255","DOIUrl":"https://doi.org/10.2174/1871522211108040255","url":null,"abstract":"<p><p>Natural estrogens such as 17β-estradiol are endogenous vasodilators and have been implicated in the gender differences of hypertension. These hormones activate estrogen receptors ERα and ERβ, which mediate part of estrogen-dependent vasodilation. In addition, a novel G protein-coupled estrogen-binding receptor termed GPER/GPR30 has been identified that is expressed in the cardiovascular system. Using knock-out animals or drugs selectively targeting GPER/GPR30, a significant role for this receptor as a mediator of acute estrogen-dependent vasodilation involving nitric oxide (NO) and blood pressure-lowering activity has been demonstrated. The accumulating evidence that GPER/GPR30 is responsible for control of vascular tone indicates that this receptor may represent a novel drug target for pharmacologic treatment of hypertension in postmenopausal women and possibly also men.</p>","PeriodicalId":88256,"journal":{"name":"Immunology, endocrine & metabolic agents in medicinal chemistry","volume":"11 4","pages":"255-261"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4079007/pdf/nihms-574770.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32484030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}