Compounds that specifically inhibit STEROL 14-DEMETHYLASE. A variety of azole-derived ANTIFUNGAL AGENTS act through this mechanism.
An NADPH-dependent P450 enzyme that plays an essential role in the sterol biosynthetic pathway by catalyzing the demethylation of 14-methyl sterols such as lanosterol. The enzyme acts via the repeated hydroxylation of the 14-methyl group, resulting in its stepwise conversion into an alcohol, an aldehyde and then a carboxylate, which is removed as formic acid. Sterol 14-demethylase is an unusual cytochrome P450 enzyme in that it is found in a broad variety of organisms including ANIMALS; PLANTS; FUNGI; and protozoa.
A triterpene that derives from the chair-boat-chair-boat folding of 2,3-oxidosqualene. It is metabolized to CHOLESTEROL and CUCURBITACINS.
Enzymes that catalyse the removal of methyl groups from LYSINE or ARGININE residues found on HISTONES. Many histone demethylases generally function through an oxidoreductive mechanism.
A family of histone demethylases that share a conserved Jumonji C domain. The enzymes function via an iron-dependent dioxygenase mechanism that couples the conversion of 2-oxoglutarate to succinate to the hydroxylation of N-methyl groups.

Tumor necrosis factor alpha increases P-glycoprotein expression in a BME-UV in vitro model of mammary epithelial cells. (1/31)

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Comparison of the inhibitory profiles of itraconazole and cimetidine in cytochrome P450 3A4 genetic variants. (2/31)

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Brain P450 epoxygenase activity is required for the antinociceptive effects of improgan, a nonopioid analgesic. (3/31)

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In vivo investigation in pigs of intestinal absorption, hepatobiliary disposition, and metabolism of the 5alpha-reductase inhibitor finasteride and the effects of coadministered ketoconazole. (4/31)

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Effects of strong CYP2D6 and 3A4 inhibitors, paroxetine and ketoconazole, on the pharmacokinetics and cardiovascular safety of tamsulosin. (5/31)

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Overexpression of CYP3A4, but not of CYP2D6, promotes hypoxic response and cell growth of Hep3B cells. (6/31)

Cytochrome P450s (P450s) contribute to carcinogenesis by activating procarcinogens and also metabolize anti-cancer drugs. The activity and protein levels of P450s are important in cancer risk and in cancer therapy. In this study, we found that overexpression of CYP3A4 induced growth of a human hepatoma cell line, Hep3B. Overexpression of CYP2D6, by comparison, decreased cell growth. An inhibitor of CYP3A4, ketoconazole, significantly suppressed the growth of Hep3B cells overexpressing CYP3A4, but an inhibitor of CYP2D6, quinidine, did not restore Hep3B cell growth to baseline levels. Overexpression of CYP3A4 increased the production of reactive oxygen species, but this was not the cause of the CYP3A4-induced growth. Previously, we showed that CYP3A4 can produce epoxyeicosatrienoic acids (EETs) from arachidonic acid. The CYP3A4-enhanced cell growth was attenuated by a putative EET receptor antagonist, 14,15-EEZE. CYP3A4 promoted progression of the cell cycle from the G1 to the S phase. CYP3A4 also induced a hypoxic response of Hep3B cells, detected as enhanced erythropoietin gene expression (a typical hypoxic response). The cell growth promoted by CYP3A4 was inhibited by PI3K inhibitor LY294002. These results suggest that CYP3A4 plays an important role in tumor progression, independent of the activation of carcinogens and metabolism of anti-cancer drugs.  (+info)

Substrate preferences and catalytic parameters determined by structural characteristics of sterol 14alpha-demethylase (CYP51) from Leishmania infantum. (7/31)

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Effectiveness of chronic treatment with ketoconazole in a patient with diabetic Cushing's disease resistant to surgery. (8/31)

Without treatment, Cushing's disease has significant morbidity and mortality. Where a surgical approach may not be feasible, or is refused by the patient, medical therapy becomes the only option. In this case report, we discuss the effects of two years of ketoconazole treatment on diabetes regulation and insulin resistance in a patient reluctant to agree to surgery. A 62 year-old female patient with uncontrolled type 2 diabetes mellitus was investigated. Cushing's disease was confirmed by the results of high urine free cortisol level and dexamethasone suppression tests. We discuss the effects of two years of 600 mg/day ketoconazole treatment on diabetes regulation and insulin resistance in a patient with Cushing's disease reluctant to agree to surgery. This case report illustrates the beneficial long-term effects of 24 months of ketoconazole treatment on the clinical and laboratory findings and also on steroid and glucose metabolism.  (+info)

BioTek Affiches scientifiques, 13-Feb-15, Phenotypic and Epigenetic Mechanism of Action Determinations of Histone Methylase and Demethylase Inhibitors using Digital Widefield Microscopy
Development of tool molecules that inhibit Jumonji demethylases allows for the investigation of cancer-associated transcription. While scaffolds such as 2,4-pyridinedicarboxylic acid (2,4-PDCA) are potent inhibitors, they exhibit limited selectivity. To discover new inhibitors for the KDM4 demethylases, enzymes overexpressed in several cancers, we docked a library of 600,000 fragments into the high-resolution structure of KDM4A. Among the most interesting chemotypes were the 5-aminosalicylates, which docked in two distinct but overlapping orientations. Docking poses informed the design of covalently linked fragment compounds, which were further derivatized. This combined approach improved affinity by ∼ 3 log-orders to yield compound 35 (Ki = 43 nM). Several hybrid inhibitors were selective for KDM4C over the related enzymes FIH, KDM2A, and KDM6B while lacking selectivity against the KDM3 and KDM5 subfamilies. Cocrystal structures corroborated the docking predictions. This study extends the use of
https://doi.org/10.18632/oncotarget.26011 Janet K. Parrish, Tyler S. McCann, Marybeth Sechler, Lays M. Sobral, Wen Hua Ren, Kenneth L. Jones, Aik Choon Tan, Paul Jedlicka
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
This talk will describe our structure-based design approach towards the identification of potent JmjC histone demethylase inhibitors based upon the pyrido[3,4-d]pyrimidin-4(3H)-one scaffold which demonstrate potent and selective biochemical affinity for the KDM4 and KDM5 subfamily demethylases over the KDM2, KDM3 and KDM6 subfamilies and describe their cell-based activity profiles. ...
PURINONE DERIVATIVE | PROCESS FOR MAKING TRICYCLIC LACTAM COMPOUNDS | Cis-tetrahydro-spiro(cyclohexane-1,1?-pyrido[3,4-b]indole)-4-amine Compounds | HISTONE DEMETHYLASE INHIBITORS | Fused Heterocyclic Compounds as Selective BMP Inhibitors |
Background Little molecule modulators of epigenetic processes are sought as fundamental probes for biochemical mechanisms, so that as beginning points for development of therapeutic agents. are amenable to advancement mainly because potent inhibitors and huge diverse collections possess yet to become exploited for the finding of demethylase inhibitors. Primary Findings High-throughput testing of the 236,000-member … [Read more…]. ...
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PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
0082] Suitable monovalent substituents on a substitutable carbon atom of an optionally substituted group are independently halogen; --(CH2)0-4R.sup.◯; --(CH2)0-4OR.sup.◯; --O(CH2)0-4R.sup.◯, --O--(CH2)0-4C(O)OR.sup.◯; --(CH2)0-4--CH(OR.sup.◯)2; --(CH2)0-4SR.sup.◯; --(CH2)0-4Ph, which may be substituted with R.sup.◯; --(CH2)0-4O(CH2)0-1Ph which may be substituted with R.sup.◯; --CH═CHPh, which may be substituted with R.sup.◯; --(CH2)0-4O(CH2)0-1-pyridyl which may be substituted with R.sup.◯; --NO2; --CN; --N3; --(CH2)0-4N(R.sup.◯)2; --(CH2)0-4N(R.sup.◯)C(O)R.sup.◯; --N(R.sup.◯)C(S)R.sup.◯; --(CH2)0-4N(R.sup.◯)C(O)NR.sup.◯2; --N(R.sup.◯)C(S)NR.sup.◯2; --(CH2)0-4N(R.sup.◯)C(O)OR.sup.◯; --N(R.sup.◯)N(R.sup.◯)C(O)R.sup.◯; --N(R.sup.◯)N(R.sup.◯)C(O)NR.sup.◯.su- b.2; --N(R.sup.◯)N(R.sup.◯)C(O)OR.sup..largecircle- .; --(CH2)0-4C(O)R.sup.◯; --C(S)R.sup.◯; --(CH2)0-4C(O)OR.sup.◯; --(CH2)0-4C(O)SR.sup.◯; --(CH2)0-4C(O)OSiR.sup.◯3; ...
In this issue of Clinical Cancer Research, Huang and colleagues, characterize the effects of novel histone demethylase inhibitors, either alone or in combination with inhibitors of DNA methyltransferases (DNMTI), on the proliferation and survival of transformed cells (1). A widely accepted view holds that the origins of cancer lie, at least in part, in the silencing of genes responsible for cell death and/or differentiation, a phenomenon that generally stems from perturbations in the transcriptional regulatory machinery. In the broadest sense, silencing of such genes occurs at three fundamentally different but closely interrelated levels. For example, silencing frequently results from DNA methylation at the site of CpG islands by DNA methyltransferases (DNMT; ref. 2). Silencing can also stem from mutations in chromatin remodeling complexes [i.e., nucleosomal remodeling factors (NURF)] such as SWI/SNF. Finally, silencing can result from multiple post-translational covalent histone modifications, ...
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This study investigated the effects of ketoconazole on the pharmacokinetics of refametinib [BAY86-9766; Bayer] in healthy male volunteers. The primary endpoints
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Ketoconazole today: a review of clinical experience , Ketoconazole today: a review of clinical experience , کتابخانه دیجیتال دانشگاه علوم پزشکی اصفهان
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Mono- and Stereopictres of 5.0 Angstrom coordination sphere of Iron atom in PDB 3g1q: Crystal Structure of Sterol 14-Alpha Demethylase (CYP51) From Trypanosoma Brucei in Ligand Free State
A novel oligoamine analog inhibitor of histone demethylases blocks colon tumor cell growth in association with histone methylation and gene re-expression. It also markedly potentiates the activity of hypomethylating agents in vitro and in vivo, suggesting that histone demethylase inhibitors may represent a valuable addition to the armamentarium of epigenetic agents. (Clin Cancer Res 2009;15(23):7111-3) ...
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Multiple myeloma is one of the common hematological malignancies that affects plasma cells. Bortezomib, proteasome inhibitor, is an anticancer agent used for the treatment of multiple myeloma while methylstat is a demethylase inhibitor having anticancer potential. In this study, we investigated antiproliferative and apoptotic effects of methylstat alone or in combination with bortezomib. We also examined the genes involved in methylstat induced apoptosis. Cytotoxic effects of bortezomib and methylstat on U266 and ARH77 cells were demonstrated by MTT cell proliferation assay. To understand the apoptotic effects of these agents, loss of mitochondrial membrane potential was investigated by JC-1 method while phosphatidylserine localization was investigated by Annexin V assay. Cell cycle analysis in response to Bortezomib and Methylstat alone or in their combination were measured by flow cytometry. Changes in expression profiles of 84 genes underlying apoptosis, cell cycle control, DNA damage repair, ...
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The ability of ketoconazole to block steroid synthesis has prompted us to use it in the treatment of advanced prostatic carcinoma. This study was designed
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