Aminoglutethimide: An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.Drug Overdose: Accidental or deliberate use of a medication or street drug in excess of normal dosage.Alcohol Drinking: Behaviors associated with the ingesting of alcoholic beverages, including social drinking.Aromatase Inhibitors: Compounds that inhibit AROMATASE in order to reduce production of estrogenic steroid hormones.18-Hydroxydesoxycorticosterone: An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Menopause: The last menstrual period. Permanent cessation of menses (MENSTRUATION) is usually defined after 6 to 12 months of AMENORRHEA in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age.Androstenedione: A delta-4 C19 steroid that is produced not only in the TESTIS, but also in the OVARY and the ADRENAL CORTEX. Depending on the tissue type, androstenedione can serve as a precursor to TESTOSTERONE as well as ESTRONE and ESTRADIOL.Tamoxifen: One of the SELECTIVE ESTROGEN RECEPTOR MODULATORS with tissue-specific activities. Tamoxifen acts as an anti-estrogen (inhibiting agent) in the mammary tissue, but as an estrogen (stimulating agent) in cholesterol metabolism, bone density, and cell proliferation in the ENDOMETRIUM.Hydrocortisone: The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.Adrenalectomy: Excision of one or both adrenal glands. (From Dorland, 28th ed)Research Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.Research Support, Non-U.S. Gov'tResearch Support, U.S. GovernmentResearch Support, American Recovery and Reinvestment ActResearch Support, N.I.H., ExtramuralResearch Support, N.I.H., IntramuralAdrenal Cortex: The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.Adrenal Glands: A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.Steroids: A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)Sleep Stages: Periods of sleep manifested by changes in EEG activity and certain behavioral correlates; includes Stage 1: sleep onset, drowsy sleep; Stage 2: light sleep; Stages 3 and 4: delta sleep, light sleep, deep sleep, telencephalic sleep.Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.Adrenergic Agents: Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.Nonprescription Drugs: Medicines that can be sold legally without a DRUG PRESCRIPTION.Drug Information Services: Services providing pharmaceutic and therapeutic drug information and consultation.Self Medication: The self administration of medication not prescribed by a physician or in a manner not directed by a physician.Directories as Topic: Lists of persons or organizations, systematically arranged, usually in alphabetic or classed order, giving address, affiliations, etc., for individuals, and giving address, officers, functions, and similar data for organizations. (ALA Glossary of Library and Information Science, 1983)Syringes: Instruments used for injecting or withdrawing fluids. (Stedman, 25th ed)BooksPrescription Drugs: Drugs that cannot be sold legally without a prescription.Community Pharmacy Services: Total pharmaceutical services provided to the public through community pharmacies.Drug Prescriptions: Directions written for the obtaining and use of DRUGS.Medical Waste Disposal: Management, removal, and elimination of biologic, infectious, pathologic, and dental waste. The concept includes blood, mucus, tissue removed at surgery or autopsy, soiled surgical dressings, and other materials requiring special control and handling. Disposal may take place where the waste is generated or elsewhere.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Pruritus: An intense itching sensation that produces the urge to rub or scratch the skin to obtain relief.Crowdsourcing: Social media model for enabling public involvement and recruitment in participation. Use of social media to collect feedback and recruit volunteer subjects.EncyclopediasTerminology as Topic: The terms, expressions, designations, or symbols used in a particular science, discipline, or specialized subject area.Relief Work: Assistance, such as money, food, or shelter, given to the needy, aged, or victims of disaster. It is usually granted on a temporary basis. (From The American Heritage Dictionary, 2d college ed)Sensation: The process in which specialized SENSORY RECEPTOR CELLS transduce peripheral stimuli (physical or chemical) into NERVE IMPULSES which are then transmitted to the various sensory centers in the CENTRAL NERVOUS SYSTEM.Vocabulary, Controlled: A specified list of terms with a fixed and unalterable meaning, and from which a selection is made when CATALOGING; ABSTRACTING AND INDEXING; or searching BOOKS; JOURNALS AS TOPIC; and other documents. The control is intended to avoid the scattering of related subjects under different headings (SUBJECT HEADINGS). The list may be altered or extended only by the publisher or issuing agency. (From Harrod's Librarians' Glossary, 7th ed, p163)Skin: The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.Unified Medical Language System: A research and development program initiated by the NATIONAL LIBRARY OF MEDICINE to build knowledge sources for the purpose of aiding the development of systems that help health professionals retrieve and integrate biomedical information. The knowledge sources can be used to link disparate information systems to overcome retrieval problems caused by differences in terminology and the scattering of relevant information across many databases. The three knowledge sources are the Metathesaurus, the Semantic Network, and the Specialist Lexicon.

A proposed sequence of hormones controlling the induction of luteal 20alpha-hydroxy steroid dehydrogenase and progesterone withdrawal in the late-pregnant rat. (1/183)

1. The previously reported induction of luteal 20alpha-hydroxy steroid dehydrogenase by administration of aminoglutethimide to late-pregnant rats was shown to be unaffected by prior removal of the foetuses. Aminoglutethimide therefore does not act via the foetuses in this context. 2. The ability of injected oestrogen to prevent the above induction was lost by delaying the injection for 12h after aminoglutethimide, although the increase in enzyme activity begins only after 24h. 3. Induction of 20alpha-hydroxy steroid dehydrogenase by foetoplacental removal on day 18 of pregnancy was inhibited by human choriogonadotropin, lutropin (luteinizing hormone) and pregnant-mare serum gonadotropin, but not by somatotropin (growth hormone), thyrotropin or follitropin (follicle-stimulating hormone) 4. Indomethacin blocked the normal induction of 20alpha-hydroxy steroid dehydrogenase in late pregnancy and that caused by aminoglutethimide. It partially blocked that caused by human choriogonadotropin given on days 19-20 and that caused by 2-bromo-alpha-ergocryptine on days 5-6, but failed to block that caused by human choriogonadotropin on days 15-16 or by foetoplacental removal on day 18 of pregnancy. 5. These findings, and the control of progesterone synthesis in late pregnancy, are interpreted in terms of a sequence of hormonal or enzymic syntheses, each of which is inhibited by the product of the preceding synthesis.  (+info)

Product of side-chain cleavage of cholesterol, isocaproaldehyde, is an endogenous specific substrate of mouse vas deferens protein, an aldose reductase-like protein in adrenocortical cells. (2/183)

Mouse vas deferens protein (MVDP) is an aldose reductase-like protein that is highly expressed in the vas deferens and adrenal glands and whose physiological functions were unknown. We hereby describe the enzymatic characteristics of MVDP and its role in murine adrenocortical Y1 cells. The murine aldose reductase (AR) and MVDP cDNAs were expressed in bacteria to obtain recombinant proteins and to compare their enzymatic activities. Recombinant MVDP was functional and displayed kinetic properties distinct from those of murine AR toward various substrates, a preference for NADH, and insensitivity to AR inhibitors. For MVDP, isocaproaldehyde, a product of side-chain cleavage of cholesterol generated during steroidogenesis, is the best natural substrate identified so far. In Y1 cells, we found that NADH-linked isocaproaldehyde reductase (ICR) activity was much higher than NADPH-linked ICR activity and was not abolished by AR inhibitors. We demonstrate that in Y1 cells, forskolin-induced MVDP expression enhanced NADH-linked ICR activity by 5-6-fold, whereas no variation in ICR-linked NADPH activity was observed in the same experiment. In cells stably transfected with MVDP antisense cDNA, NADH-linked ICR activity was abolished even in the presence of forskolin, and the isocaproaldehyde toxicity was increased compared with that of intact Y1 cells, as measured by isocaproaldehyde LD(50). In Y1 cells transfected with MVDP antisense cDNA, forskolin-induced toxicity was abolished by aminoglutethimide. These results indicate that in adrenocortical cells, MVDP is responsible for detoxifying isocaproaldehyde generated by steroidogenesis.  (+info)

Decreased progesterone levels and progesterone receptor antagonists promote apoptotic cell death in bovine luteal cells. (3/183)

We tested the hypothesis that progesterone (P(4)) acts at a local level to inhibit luteal apoptosis. Initial experiments employed aminoglutethimide, a P450 cholesterol side-chain cleavage inhibitor, to inhibit steroid synthesis. Cultured bovine luteal cells were treated with aminoglutethimide (0.15 mM) +/- P(4) (500 ng/ml) for 48 h. Luteal cells were recovered and snap frozen for isolation and analysis of oligonucleosomal DNA fragmentation or fixed for morphological analysis. Medium was collected for analysis of P(4) levels by RIA. Aminoglutethimide inhibited P(4) synthesis by > 95% and increased the level of apoptosis as evidenced by (32)P-labeled oligonucleosomal DNA fragmentation (> 40%). P(4) supplementation inhibited the onset of apoptosis that was induced by aminoglutethimide. These data were further supported by morphological assessment of apoptotic cells utilizing a Hoechst staining technique and together strongly suggest that P(4) has anti-apoptotic capacity. Using reverse transcription-polymerase chain reaction, we were able to isolate a 380-base pair cDNA from the bovine corpus luteum (CL) that was 100% homologous to the progesterone receptor (PR) previously found in bovine oviductal tissue. Furthermore, PR transcripts were present in large and small luteal cells. Immunohistochemistry also revealed that PR protein was present in both large and small luteal cells. To determine whether the anti-apoptotic effect of P(4) was regulated at the receptor level, luteal cells were cultured in the presence of PR antagonists, RU-486 and onapristone, for 48 h. Both antagonists caused approximately a 40% increase in (32)P-labeled oligonucleosomal DNA fragmentation. Interestingly, there was no difference (P >/= 0.05) in P(4) levels after treatment with PR antagonists. These observations support the concept that P(4) represses the onset of apoptosis in the CL by a PR-dependent mechanism.  (+info)

Status of aromatase inhibitors in relation to other breast cancer treatment modalities. (4/183)

Aromatase is one of the key enzymes possibly linked with the perpetuation or even initiation of breast cancer. Modulation of its activity by the new generation inhibitors has resulted in increased responses and improved therapeutic ratio compared with those of parent aromatase inhibitors. More recent trials have shown promising results with regard to improved therapeutic ratio compared with what is seen with presently accepted second-line hormonal approaches. Present data and laboratory research indicate that new aromatase inhibitors have the potential to play an important role as adjuvants, and possibly in the prevention of human breast cancer. It is probable that it may be as adjuvants that their real therapeutic strength in terms of a beneficial impact on survival may be realized. The absence of estrogen agonist activity of new aromatase inhibitors on lipid and bone metabolism calls for more clinical studies having late mortality in breast cancer survivors as the ultimate outcome objective; in this regard, interaction of new aromatase inhibitors with new selective estrogen receptor modulators looks promising. Achievement of these outcomes, and understanding of interactions with other therapies, await the termination of present trials and the start of new initiatives.  (+info)

Use of aromatase inhibitors in breast carcinoma. (5/183)

Aromatase, a cytochrome P-450 enzyme that catalyzes the conversion of androgens to estrogens, is the major mechanism of estrogen synthesis in the post-menopausal woman. We review some of the recent scientific advances which shed light on the biologic significance, physiology, expression and regulation of aromatase in breast tissue. Inhibition of aromatase, the terminal step in estrogen biosynthesis, provides a way of treating hormone-dependent breast cancer in older patients. Aminoglutethimide was the first widely used aromatase inhibitor but had several clinical drawbacks. Newer agents are considerably more selective, more potent, less toxic and easier to use in the clinical setting. This article reviews the clinical data supporting the use of the potent, oral competitive aromatase inhibitors anastrozole, letrozole and vorozole and the irreversible inhibitors 4-OH androstenedione and exemestane. The more potent compounds inhibit both peripheral and intra-tumoral aromatase. We discuss the evidence supporting the notion that aromatase inhibitors lack cross-resistance with antiestrogens and suggest that the newer, more potent compounds may have a particular application in breast cancer treatment in a setting of adaptive hypersensitivity to estrogens. Currently available aromatase inhibitors are safe and effective in the management of hormone-dependent breast cancer in post-menopausal women failing antiestrogen therapy and should now be used before progestational agents. There is abundant evidence to support testing these compounds as first-line hormonal therapy for metastatic breast cancer as well as part of adjuvant regimens in older patients and quite possibly in chemoprevention trials of breast cancer.  (+info)

Lipoproteins regulate expression of the steroidogenic acute regulatory protein (StAR) in mouse adrenocortical cells. (6/183)

The steroidogenic acute regulatory protein (StAR) is required for the movement of cholesterol from the outer to the inner mitochondrial membrane, the site of cholesterol side chain cleavage. Here we describe a novel form of regulation of StAR gene expression in steroidogenic cells. Treatment of Y-1 BS1 adrenocortical cells with either low density lipoprotein (LDL) or high density lipoprotein (HDL) increases expression of endogenous StAR mRNA and protein in a dose-dependent manner. Induction of StAR mRNA by lipoprotein requires basal cAMP-dependent protein kinase, since the inhibitor, R(p)-8-Br-cAMP, inhibited induction of StAR protein by LDL. Likewise, basal StAR expression or LDL induction of StAR protein was not detectable in Y-1 kin-8 cells which are deficient in cAMP-dependent protein kinase. Aminoglutethimide and ketoconazole were used to determine if side chain cleavage of lipoprotein-derived cholesterol is required for induction of StAR mRNA. Treatment with either drug alone induced StAR mRNA expression 1.5-3-fold, while induction of StAR in cells treated with either drug plus LDL, was equal to, or greater than, induction seen with either agent alone, suggesting that lipoprotein does not regulate StAR via generation of an oxysterol intermediate. Both LDL and HDL increased expression of a mouse -966 StAR promoter-reporter construct 1.5-2.5-fold, indicating that regulation occurs at the level of transcription. In contrast, neither lipoprotein was able to induce transcription from a -966 StAR promoter in which the steroidogenic factor-1 site at -135 was abolished, indicating that regulation of StAR transcription by lipoproteins requires steroidogenic factor-1. The regulation of StAR gene expression by lipoproteins may represent a positive feedback circuit which links cholesterol availability with steroidogenic output.  (+info)

Contribution of progesterone, follicle stimulating hormone and glucocorticoids in survival of serum-free cultured granulosa cell explants. (7/183)

To investigate the role of progesterone (P4) as a survival factor in quail granulosa cell explants, P4 content was determined under various conditions and correlated with apoptotic indexes (AIs) evaluated by 2',6'-diamidino-2-phenylindole (DAPI)-staining. Analysis of serum-free cultures from 24 to 96 h shows decreased P4 levels in the medium paralleled by increasing AI. Inhibiting apoptosis by gonadotropic support (FSH, 100 ng/ml) stimulates a 3-fold increase of the P4 level in the medium (83.49+/-8.69 vs 26.31+/-1.61 ng/ml in serum-free controls) together with a significant decrease in AI from 8.81+/-1.06% in serum-free controls to 3.50+/-0.72%. Substantial evidence for P4 as an autocrine/paracrine survival factor can be inferred from experiments with aminoglutethimide (AG, 1 mM) and RU486 (20 microM). Blocking P4 synthesis by AG causes a 2-fold increase in apoptosis from 6.08+/-0.67% in serum-free controls to 12.53+/-1.60%. Blocking P4 receptors by RU486 causes a similar increase in AI (3.02+/-0.98% in serum-free controls to 17.07+/-3.20%) and about a 50% decrease in P4. The effect of RU486 could be attenuated by exogenous P4 but not by dexamethasone indicating selective binding of P4 to the progesterone receptor. Dexamethasone treatment promotes survival without affecting P4 levels. In further support of an autocrine/paracrine action for P4 in the granulosa cells, both the A and B form of the avian P4 receptor (PR) are identified in vivo and in vitro by Western blotting. Exogenous administration of P4 only affects survival when endogenous P4 synthesis is blocked or after 48 h of serum-free culture when endogenous P4 production is very low. Because FSH also affects survival when its stimulatory effect on P4 synthesis is blocked by AG (AI decrease from 6.08+/-0.67% in serum-free controls to 1.64+/-0.71% in FSH+AG treated) it is proposed that (1) P4 is an autocrine/paracrine survival factor in the preovulatory granulosa and (2) FSH mediates both P4-dependent and P4-independent survival pathways.  (+info)

Aromatase inhibition by an 11,13-dihydroderivative of a sesquiterpene lactone. (8/183)

Compounds that inhibit aromatase activity are used for the treatment of breast cancer. A group of sesquiterpene lactones inhibit aromatase activity and also exert cytotoxicity through their reactive alpha-methylene-gamma-lactone group. To synthesize sesquiterpene lactones with greater specificity for aromatase inhibition and lower cytotoxicity, we chemically reduced the alpha-methylene-gamma-lactone group in the active aromatase inhibitor 10-epi-8-deoxycumambrin B (compound 1), to obtain the new compound 11betaH,13-dihydro-10-epi-8-deoxycumambrin B (compound 2). Reduction of the alpha-methylene-gamma-lactone group abrogated the cytotoxic activity of compound 1 against the JEG-3, HeLa, and COS-7 cell lines. Compound 2 had higher aromatase inhibitory activity than compound 1 (IC(50) = 2 +/- 0.5 microM versus 7 +/- 0.5 microM, K(i) = 1.5 microM versus 4.0 microM) and was a more potent type II ligand to the heme iron present in the cytochrome P450(arom) active site. Compound 2 inhibited aromatase activity in JEG-3 cells in a comparable manner to the inhibitor aminoglutethimide (AG) used clinically for the treatment of breast cancer. Additionally, compound 2 inhibited androstenedione-induced uterine hypertrophy in sexually immature mice (41% of uterine weight suppression for compound 2 versus 51% for AG). We conclude that the anti-aromatase activity of sesquiterpene lactones does not depend on the presence of the highly reactive alpha-methylene-gamma-lactone group, whereas their cytotoxicity does. These findings may facilitate the development of safer agents for breast cancer therapy.  (+info)

*Aminoglutethimide

... aminoglutethimide is used by bodybuilders in a steroid cycle. Aminoglutethimide has two mechanisms of action: It blocks ... Aminoglutethimide is an anti-steroid drug marketed under the tradename Cytadren by Novartis around the world. It blocks the ... Aminoglutethimide is abused by bodybuilders and other steroid users to lower circulating levels of cortisol in the body and ... Aminoglutethimide is indicated in conjunction with other drugs for the suppression of adrenal function in patients with ...

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Cash, Ralph; Brough, A. Joseph; Margo, N.P.Cohen; Satoh, Paul S. (1967). "Aminoglutethimide as an inhibitor of adrenal ... Cohen, Margo P. (1968). "Aminoglutethimide inhibition of adrenal desmolase activity". Proc Soc Exper Biol & Med. 127: 1086-1090 ...

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Aminoglutethimide Amphenone B Metyrapone J. Larry Jameson; Leslie J. De Groot (18 May 2010). Endocrinology - E-Book: Adult and ...

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These drugs include aminoglutethimide, ketoconazole, and abiraterone acetate. Aminoglutethimide inhibits cholesterol side-chain ... The earlier androgen synthesis inhibitors aminoglutethimide and ketoconazole have only limitedly been used in the treatment of ... The androgen synthesis inhibitors aminoglutethimide and ketoconazole were first marketed in 1960 and 1977, respectively, and ... These include, to varying extents, cyproterone acetate, flutamide, nilutamide, bicalutamide, aminoglutethimide, and ...

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Abiraterone acetate Aminoglutethimide Levoketoconazole "Ketoconazole". Merriam-Webster Dictionary. "Ketoconazole". Dictionary. ...

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Aminoglutethimide is an anti-steroid drug marketed under the tradename Cytadren by Novartis around the world. It blocks the production of steroids derived from cholesterol and is clinically used in the treatment of Cushings syndrome and metastatic breast cancer. It is also used by bodybuilders. Aminoglutethimide is indicated in conjunction with other drugs for the suppression of adrenal function in patients with Cushings syndrome. It is also a second or third line choice for the treatment of hormone-sensitive (estrogen and progesterone) metastatic breast cancer. Aminoglutethimide is abused by bodybuilders and other steroid users to lower circulating levels of cortisol in the body and prevent muscle loss. Cortisol is catabolic to protein in muscle and effective blockade of P450scc by aminogluthethimide at high doses prevents muscle loss.[citation needed] Its side effects are skin rash, hepatotoxicity, inhibition of cortisol in the human body, and it may also cause hypothyroidism[citation ...
Aminoglutethimide - Get up-to-date information on Aminoglutethimide side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Aminoglutethimide
To the editor: Aminoglutethimide is an adrenal and peripheral blocker of steroid metabolism that has seen increasing use as a medical alternative to adrenalectomy. It has proved effective as therapy for patients with metastatic breast and prostate carcinomas, as well as those with functioning adrenal tumors (1). Adverse effects are usually transient and mild; however, serious adverse effects including bone marrow suppression, cholestasis, and systemic lupus erythematosus have been reported (2-4). We report a case of diffuse alveolar damage and hemorrhage associated with this drug.. A 47-year-old man with a known islet-cell tumor secreting corticotropin-releasing factor was started on aminoglutethimide, ...
Brand name: Cytadren. Aminoglutethimide is the drug which acts on the adrenal cortex. Production of steroids is affected by its administration. Aminoglutethimide is prescribed...
BioAssay record AID 244329 submitted by ChEMBL: Relative potency for inhibition of aromatase binding compared to aminoglutethimide.
Aminoglutethimide prevents the production of steroid hormones in the adrenal cortex. This occurs at an early stage in the process. Aminoglutethimide may also suppress the production of oestrogens elsewhere in the body. Some types of cancer, especially breast cancer, will grow in the presence of oestrogens. Reduction of oestrogen levels will limit the growth of this type of cancer. Aminoglutethimide can be used for this purpose.As aminoglutethimide also inhibits production of cortisone, it can also be used in the treatment of Cushings syndrome.
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Guidelines for Use:. Use exactly as prescribed.. The usual dose is 250 mg four times daily, every 6 hours.. If a dose is missed, take it as soon as possible. If several hours have passed or if it is nearing time for the next dose, do not double the dose in order to "catch up" (unless advised to do so by your doctor). If more than one dose is missed or it is necessary to establish a new dosage schedule, contact your doctor or pharmacist.. May cause dizziness, lightheartedness or fainting, especially when rising quickly from a sitting or lying. If these symptoms should occur, sit or lie down and contact your doctor. Use caution while driving or performing hazardous tasks requiring alertness, coordination or physical dexterity.. If severe rash, extreme drowsiness, yellowing of skin or eyes, fainting, weakness or headache occur, contact your doctor immediately.. Nausea and loss of appetite may occur during the first 2 weeks of therapy. Contact you doctor if these do not go away.. Contraceptive ...
Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.. Using this medicine with any of the following medicines may cause an increased risk of certain side effects, but using both drugs may be the best treatment for you. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines.. ...
Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.. Using this medicine with any of the following medicines may cause an increased risk of certain side effects, but using both drugs may be the best treatment for you. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines.. ...
N Engl J Med. 1981 Sep 3;305(10):545-51. Clinical Trial; Comparative Study; Randomized Controlled Trial; Research Support, U.S. Govt, P.H.S.
The pathways outlined here are common to the adrenals, the gonads and, to some extent, to the fetoplacental unit. The first committed step is the conversion of cholesterol to pregnenolone, catalysed by the P-450scc enzyme, which is under pituitary hormone control (ACTH or LH depending on the tissue). Cholesterol side-chain removal is blocked specifically by aminoglutethimide, a steroid biosynthesis inhibitor. From pregnenolone, steroid biosynthesis can proceed either through the so-called "delta-5" pathway (17α-hydroxypregnenolone, dehydroepiandrosterone, testosterone), or through the "delta-4" pathway (progesterone onwards). Progesterone is the starting point for mineralocorticoid synthesis, whereas glucocorticoids are derived from its metabolite, 17α-hydroxyprogesterone. Estrogens are formed from androgens (androstenedione and/or testosterone). Most reactions are irreversible (as denoted by a single arrow). Reversible reactions (double arrows) depend on cofactor availability (e.g. the ...
The previously reported substrate-heme complex approach is used to study the binding of type II inhibitors of the enzyme cholesterol side chain cleavage (CSCC), a cytochrome P-450 dependent enzyme involved in the oxidative cleaveage of the C(20)-C(22) bond of cholesterol. Using the derived model, we have rationalised the inhibitory activity of a number of compounds including aminoglutethimide and pyridoglutethimide and the enantiomers of ketoconazole.. ...
DISEASE CHARACTERISTICS: Histologically proven adenocarcinoma of the prostate Stage IV (D0.5; no evidence of disease on CT or bone scan after testicular androgen ablation) PSA progression after testicular androgen ablation with or without antiandrogen therapy Progression is defined as at least 2 consecutive rising PSA levels (drawn at least 2 weeks apart) with a greater than 50% rise above the last nadir level (arbitrary PSA at least 2 ng/dL). PATIENT CHARACTERISTICS: Age: Not specified Performance status: ECOG 0-2 Life expectancy: Not specified Hematopoietic: Not specified Hepatic: Not specified Renal: Not specified Other: No other medical conditions that would increase risk Fertile patients must use effective contraception. PRIOR CONCURRENT THERAPY: Biologic therapy: Not specified Chemotherapy: Not specified Endocrine therapy: See Disease Characteristics Greater than 4 weeks since prior flutamide (6 weeks for bicalutamide or nilutamide) No prior aminoglutethimide or ketoconazole for prostate ...
Lugano-CH, Brussels-BE, 2 May 2013. A study led by prominent breast cancer experts from Europe and the US has revealed a number of potentially important prospects for targeted therapies, and brings opportunities of truly personalised therapy for breast cancer a step closer, researchers said at the 5th IMPAKT Breast Cancer Conference in Brussels, Belgium.. The IMPAKT meeting presents cutting edge, translational breast cancer research that is beginning to have an impact for patients.. This current study was led by Dr Martine Piccart, Director of Medicine at the Jules Bordet Institute in Brussels, and Dr Jose Baselga, Associate Director at Memorial Sloan-Kettering Cancer Center, New York.. The researchers used modern sequencing technology to characterise the genetic aberrations of cancer genes present in tumour samples from a well-defined cohort of advanced postmenopausal patients who were enrolled in the BOLERO-2 clinical trial.. "The results of this study generated hypotheses for developing ...
Lugano-CH, Brussels-BE, 2 May 2013. A study led by prominent breast cancer experts from Europe and the US has revealed a number of potentially important prospects for targeted therapies, and brings opportunities of truly personalised therapy for breast cancer a step closer, researchers said at the 5th IMPAKT Breast Cancer Conference in Brussels, Belgium.. The IMPAKT meeting presents cutting edge, translational breast cancer research that is beginning to have an impact for patients.. This current study was led by Dr Martine Piccart, Director of Medicine at the Jules Bordet Institute in Brussels, and Dr Jose Baselga, Associate Director at Memorial Sloan-Kettering Cancer Center, New York.. The researchers used modern sequencing technology to characterise the genetic aberrations of cancer genes present in tumour samples from a well-defined cohort of advanced postmenopausal patients who were enrolled in the BOLERO-2 clinical trial.. "The results of this study generated hypotheses for developing ...
Breast cancer pills. Box and blister packs of Orimeten pills used in the treatment of breast cancer. Each pill contains 250 milligrams of the drug aminoglutethimide. This drug inactivates the enzyme aromatase, which is involved in the production of oestrogens (female sex hormones). Breast cancers are stimulated to grow by the presence of oestrogens in the blood, and a lack of them inhibits the growth of the tumour. Orimeten has also been used to treat prostate cancer. It has numerous side-effects, including drowsiness, nausea and insomnia, and its use has now been largely superceded by drugs such as tamoxifen. - Stock Image M625/1017
The synthesis of a series of N-alkylated 4-(4()aminobenzyl)-2-oxazolidinones is described using a synthetically useful scheme which avoids the use of phosgene-since the derivatization is undertaken with the oxazolidin-2-one ring intact. The compounds were tested for human placental aromatase (AR) inhibition in vitro, using [1beta,2beta-3H]androstenedione as substrate for the AR enzyme. The compounds were found, in general, to be more potent than the standard compound, aminoglutethimide (AG), and as such proved to be good lead compounds in the search for more specific AR inhibitors.. ...
Endometriosis is the abnormal condition that the functional endometrial tissue is located outside of uterus. According to the article published in "medical magazine of gynecological science in Unite States", among every 10 women of bearing age, there is one woman suffering from the frequent pain and risk of infertility brought by endometriosis, which makes endometriosis to be the third biggest cause of gynecological disease that needs to be treated in the hospital. Once there was a case-control study report based on the population pointing out that: endometriosis that induced by all kinds of night work is up to 48% of all cases of endometriosis. And there is also evidence indicating that the endometriosis is relative with the cyclic using of the steroid. Doing night work restrains the secretion of melatonine. Because the melatonine can suppress the activity of estrogen and decrease the activity of aminoglutethimide in the gland of breast(which can work as an inhibitor to decrease the level of ...
Kongsberg Defence Systems acting president Eirik Lie said: We are very pleased to be part of the live firing exercise performed by the RNoN. The live firing demonstrated Minesnipers unique manoeuvrability, automatic navigation modes, identification and neutralisation effectiveness.. Following the successful test, Minesniper MkIII has been approved for Nato service.. The Minesniper Mk III weapon system is a lightweight and low-cost vehicle modularly designed for rapid and efficient mine verification and neutralisation.. It also provides automatic navigation and helps minimise the operators load with its intuitive operator interface.. Norwegian Defence Materiel Agency project manager Dag Jarle Archer-Lure said: "The Royal Norwegian Navy has with the Kongsberg Minesniper MkIII a state of the art One Shot Weapon System designed to meet the MCM fleets need for an effective countermine tool.. "In addition, the system with its upgraded training vehicles provides the operators with a proven ...
The conversion of androgens to estrogens occurs in a variety of cells and tissues, such as ovarian granulosa and testicular cells, placenta, adipose tissue, and various sites of the brain. The extragonadal synthesis of estrogens has great pathophysiological importance. Estrogens produced by, for example, adipose tissue have a role in the pathogenesis of certain forms of breast cancer and endometrial adenocarcinoma. The biosynthesis of estrogens is catalyzed by the aromatase, an enzyme localized in the endoplasmic reticulum that consists of two components: a cytochrome P450 (P450 Arom, P450 19 product of theCYP 19 gene) and the NADPH cytochrome P450 reductase. The alignment of the amino acid sequences of human P450 19 with other mammalian P450s shows little sequence similarity, which indicates not only that P450 19 is a unique form of the P450 superfamily but also that the aromatase may be a good target for the development of selective P450 inhibitors.. Aminoglutethimide (AG) is the pioneer drug ...
The presence of aromatase activity, estrogen receptors, and estrogenic responsiveness in MCF-7 human breast cancer cells has allowed this cell line to be used as a unique in vitro system for investigating the biological activities of potentially therapeutic aromatase inhibitors. We now report the results of studies which have examined the cytotoxicity, antiaromatase, and intrinsic estrogenic activities of aminoglutethimide, 1,2-dehydrotestolactone (testolactone), dihydrotestosterone, 4-hydroxy-4-androstene-3,17-dione, and 10-propargylestr-4-ene-3,17-dione within MCF-7 monolayer cultures. Cell viability was determined by trypan blue exclusion, and aromatase activity was assessed by quantifying the amounts of [3H]estradiol formed from [3]testosterone. Estrogenic activity was assessed by examining the ability of each inhibitor to increase cytoplasmic progesterone receptor and deplete cytoplasmic estrogen receptor concentrations in these cells during a 5-day incubation period. Cytoplasmic ...
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agents because they may reduce the negative physical side effects of using prohibited anabolic steroids. The following classes of anti-estrogenic substances are prohibited:  Aromatase inhibitors including but not limited to, anastrozole, letrozole, aminoglutethimide, exemestane, formestane, testolactone  Selective Estrogen Receptor Modulators (SERMs) including but not limited to,  Other anti-estrogenic substances including but not limited to, clomiphene,  Agents modifying myostatin function(s) including but not limited to, myostatin The LPGA list of prohibited classes and prohibited methods is subject to change by the LPGA ...
Aminoglutethimide (AG) 500 mg was administered orally to four normal volunteers and eight patients undergoing treatment for metastatic breast cancer. In each subject the acetylator phenotype was established from the monoacetyldapsone (MADDS)/dapsone (DDS) ratio. Acetylaminoglutethimide (acetylAG) rapidly appeared in the plasma and its disposition paralleled that of AG. A close relationship (P less than 0.01) was observed between the acetyl AG/AG and MADDS/DDS ratio suggesting that AG may undergo polymorphic acetylation like DDS. AG half-life was 19.5 +/- 7.7 h in seven fast acetylators of DDS and 12.6 +/- 2.3 h in five slow acetylators and its apparent metabolic clearance was significantly (P less than 0.01) related to the acetylAG/AG ratio. Over 48 h the fast acetylators excreted 7.7 +/- 4.4% of the administered AG dose in the urine as unchanged AG as compared to 12.4 +/- 2.8% in slow acetylators. A much smaller fraction of the dose was excreted as acetylAG: 3.6 +/- 1.5% by fast and 1.9 +/- ...
Principal Investigator:AKAKURA Koichiro, Project Period (FY):1997 - 1998, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Urology
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1997-2005 Healthboard.com. Healthboard.com is a purely informational website, and should not be used as a substitute for professional legal, medical or technical advice. ...
Representative and non-limiting examples for medicines, the according to this embodiment of the invention include antineoplastic agents such as vincristine, Vinblastine, vindesine, busulfan, chlorambucil, spiroplatin, cisplatin, Carboplatin, methotrexate, adriamycin, mitomycin, bleomycin, cytosine arabinoside, Arabinosyladenine, mercaptopurine, mitotane, procarbazine, dactinomycin (Antinomycin D), daunorubicin, doxorubicin hydrochloride, taxol, plicamycin, Aminoglutethimide, estramustine, flutamide, leuprolide, megestrol acetate, Tamoxifen, testolactone, trilostane, amsacrine (m-AMSA), asparaginase (L-asparaginase), etoposide, interferon a-2a and 2b, blood products like hematoporphyrins or Derivatives of the foregoing; biological reaction modifiers such as muramyl peptides; Antifungals such as ketoconazole, nystatin, griseofulvin, Flucytosine, miconazole or amphotericin B; Hormones or hormone analogues like growth hormone, the melanophore hormone, estradiol, beclo methasone dipropionate, ...
Three patients with primary aldosteronism due to adrenocortical carcinoma were studied, two with hyperaldosteronism alone and one also with hypercortisolism; in the later stages all three had hypersecretion of glucocorticoid and androgenic hormones. Although clinical presentations were similar to those of patients with benign adenoma, all had significantly higher concentrations of deoxycorticosterone and aldosterone and more profound hypokalemia. Stimulation with adrenocorticotropin in two patients showed a good cortisol response but no aldosterone response. The circadian rhythm for Cortisol was normal but absent for aldosterone and deoxycorticosterone. Sequential 24-hour circadian studies in one patient showed that as the disease progressed, corticosterone and finally Cortisol lost their circadian rhythms. Treatment with spironolactone, mitotane, or aminoglutethimide had transient clinical effects. The patients died 2 to 13 years later. ...
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0147]In another specific embodiment, the methods of the invention encompass administration of a composition of the invention in combination with the administration of one or more prophylactic/therapeutic agents that are anti-cancer agents such as, but not limited to: acivicin, aclarubicin, acodazole hydrochloride, acronine, adozelesin, aldesleukin, altretamine, ambomycin, ametantrone acetate, aminoglutethimide, amsacrine, anastrozole, anthramycin, asparaginase, asperlin, azacitidine, azetepa, azotomycin, batimastat, benzodepa, bicalutamide, bisantrene hydrochloride, bisnafide dimesylate, bizelesin, bleomycin sulfate, brequinar sodium, bropirimine, busulfan, cactinomycin, calusterone, caracemide, carbetimer, carboplatin, carmustine, carubicin hydrochloride, carzelesin, cedefingol, chlorambucil, cirolemycin, cisplatin, cladribine, crisnatol mesylate, cyclophosphamide, cytarabine, dacarbazine, dactinomycin, daunorubicin hydrochloride, decarbazine, decitabine, dexormaplatin, dezaguanine, dezaguanine ...
0164] Additional examples of anti-cancer agents (e.g., chemotherapeutic) that can be used in conjunction with the presently disclosed subject matter, including pharmaceutical compositions and dosage forms and kits of the presently disclosed subject matter, include, but are not limited to: acivicin; aclarubicin; acodazole hydrochloride; acronine; adozelesin; aldesleukin; altretamine; ambomycin; ametantrone acetate; aminoglutethimide; amsacrine; anastrozole; anthramycin; asparaginase; asperlin; azacitidine; azetepa; azotomycin; batimastat; benzodepa; bicalutamide; bisantrene hydrochloride; bisnafide dimesylate; bizelesin; bleomycin sulfate; brequinar sodium; bropirimine; busulfan; cactinomycin; calusterone; caracemide; carbetimer; carboplatin; carmustine; carubicin hydrochloride; carzelesin; cedefingol; chlorambucil; cirolemycin; cisplatin; cladribine; crisnatol mesylate; cyclophosphamide; cytarabine; dacarbazine; dactinomycin; daunorubicin hydrochloride; decitabine; dexormaplatin; dezaguanine; ...
Learn about the potential side effects of Hydrocortisone 1% In Absorbase (hydrocortisone). Includes common and rare side effects information for consumers and healthcare professionals.
Body mass index (BMI) affects the level of estradiol and estrone sulfate suppression achieved when treating postmenopausal women with estrogen receptor (ER)-positive breast cancer with either of two aromatase inhibitors, anastrozole or letrozole.
I tend to get eczema and hydrocortisone cream is the only thing that works to relieve it. However, I have read that hydrocortisone can interfere with
Zymox Otic with hydrocortisone provides quick relief for your pets ears. It eliminates the bacteria and fungi that caused the infection.
Your doctor or pharmacist may already be aware of any possible drug interactions and may be monitoring you for them. Do not start, stop, or change the dosage of any medicine before checking with your doctor or pharmacist first. This drug should not be used with the following medication because very serious interactions may occur: febuxostat. If you are currently using the medication listed above, tell your doctor or pharmacist before starting theophylline. Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbal products you may use, especially of: adenosine, adrenaline-like drugs (e.g., ephedrine, phenylephrine, pseudoephedrine), allopurinol, aminoglutethimide, certain antiarrhythmic drugs (e.g., mexiletine, propafenone), anti-seizure drugs (e.g., carbamazepine, phenytoin, phenobarbital), benzodiazepines (e.g., diazepam, flurazepam), certain beta blockers (e.g., propranolol), birth control pills, cimetidine, digoxin, disulfiram, fluvoxamine, ...
Your doctor or pharmacist may already be aware of any possible drug interactions and may be monitoring you for them. Do not start, stop, or change the dosage of any medicine before checking with your doctor or pharmacist first. This drug should not be used with the following medication because very serious interactions may occur: febuxostat. If you are currently using the medication listed above, tell your doctor or pharmacist before starting theophylline. Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbal products you may use, especially of: adenosine, adrenaline-like drugs (e.g., ephedrine, phenylephrine, pseudoephedrine), allopurinol, aminoglutethimide, certain antiarrhythmic drugs (e.g., mexiletine, propafenone), anti-seizure drugs (e.g., carbamazepine, phenytoin, phenobarbital), benzodiazepines (e.g., diazepam, flurazepam), certain beta blockers (e.g., propranolol), birth control pills, cimetidine, digoxin, disulfiram, fluvoxamine, ...
We conducted an exploratory phase II study to assess the efficacy of treatment with ketoconazole/hydrocortisone in combination with dutasteride in men with CRPC. The largest previous study of ketoconazole (Cancer and Leukemia Group B 9583) analyzed responses to ketoconazole/hydrocortisone given concurrently or subsequent to antiandrogen withdrawal (response rates of 27% and 32%, respectively), so the current study was powered to determine whether the response was ,32% (23). Although response rates to ketoconazole in other smaller studies have ranged from 20% to 75% (22), the 56% response rate to KHAD indicates that 5α-reductase inhibition by dutasteride may enhance the response rate to ketoconazole/hydrocortisone. In contrast to the response rate, response durations in this study were markedly longer than those reported previously for ketoconazole/hydrocortisone. The median duration of response was 20 months, and 9 of the 32 responding patients had not yet progressed at the time of this ...
Learn Steroid Synthesis and CAH, FA318 facts using a simple interactive process (flashcard, matching, or multiple choice). Finally a format that helps you memorize and understand. Browse or search in thousands of pages or create your own page using a simple wizard. No signup required!
Biocidan Hydrocortisone information about active ingredients, pharmaceutical forms and doses by Sanofi-Aventis, Biocidan Hydrocortisone indications, usages and related health products lists
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The agents used for endocrine therapy in patients with breast cancer have changed markedly over the past decade. Tamoxifen remains the anti-oestrogen of choice, but could be replaced by the oestrogen receptor down-regulator ICI 182780 or by the fixed ring triphenylethylene arzoxifene (previously SERM III) soon. Whilst aminoglutethimide and 4-OH androstenedione were the aromatase inhibitors of choice, they have been replaced by non-steroidal (anastrozole and letrozole) and steroidal (exemestane) inhibitors of high potency and low side effect profile. Previously, often used treatments such as progestogens (megestrol acetate and medroxyprogesterone acetate) and androgens are now rarely used or confined to fourth or fifth line treatments. The LHRH agonist, goserelin, remains the treatment of choice for pre-menopausal patients with advanced breast cancer although recent randomised trials indicate a response, time to progression and survival advantage for the combination of goserelin and tamoxifen ...
The aim of the study is to establish the short-term efficacy and safety of aromatase inhibition in restoring and maintaining eugonadism in hypogonadotrophic hypogonadal men. Secondary aim is to detect the short-term somatic and psychological effects.. Study design: Double blind randomized placebo-controlled trial.. Treatment: 26 weeks of either letrozole or placebo. All patients will start on 1 tablet per week, dose adjustments will be performed if serum testosterone or estradiol are outside the target range. All men will be prescribed a mildly hypocaloric diet.. Endpoints: BMI, body weight, waist circumference, body composition, exercise capacity, serum levels of several hormone markers, glucose tolerance, psychological characteristics.. All patients will be measured 6 times during the study. ...
Tumor Library - Cancer Oncology - Welcome to the James O. Johnston Orthopaedic Oncology Tumor Library. This site is intended to offer the oppotunity to cancer research of Orthopaedic Oncology diagnosis slides and imagery from Dr. Johnson s personal library.
Tumor Library - Cancer Oncology - Welcome to the James O. Johnston Orthopaedic Oncology Tumor Library. This site is intended to offer the oppotunity to cancer research of Orthopaedic Oncology diagnosis slides and imagery from Dr. Johnson s personal library.
Earlier studies have indicated that CFS patients produce about 30 percent less natural hydrocortisone (cortisol) than healthy people do. Dr. Stephen Straus and his colleagues studied a group of 70 CFS patients to see if supplemental doses of hydrocortisone might not alleviate the symptoms of CFS. They found that the patients who took hydrocortisone improved slightly compared to the patients who took a placebo, but unfortunately some potentially dangerous side effects were also demonstrated ...
Learn about the potential side effects of hydrocortisone/urea topical. Includes common and rare side effects information for consumers and healthcare professionals.

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Aminoglutethimide - DrugBankAminoglutethimide - DrugBank

Aminoglutethimide has been used in the treatment of advanced breast and prostate cancer. It was formerly used for its weak ... Aminoglutethimide. ATC Codes. L02BG01 - Aminoglutethimide*L02BG - Aromatase inhibitors. *L02B - HORMONE ANTAGONISTS AND RELATED ... Aminoglutethimide has been used in the treatment of advanced breast and prostate cancer. It was formerly used for its weak ... Aminoglutethimide. Accession Number. DB00357 (APRD00592) Type. Small Molecule. Groups. Approved, Investigational. Description. ...
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Aminoglutethimide in the Treatment of Advanced Postmenopausal Breast Cancer | Cancer ResearchAminoglutethimide in the Treatment of Advanced Postmenopausal Breast Cancer | Cancer Research

Aminoglutethimide in the Treatment of Advanced Postmenopausal Breast Cancer. Adrian L. Harris, Trevor J. Powles and Ian E. ... Aminoglutethimide in the Treatment of Advanced Postmenopausal Breast Cancer. Adrian L. Harris, Trevor J. Powles and Ian E. ... Aminoglutethimide in the Treatment of Advanced Postmenopausal Breast Cancer. Adrian L. Harris, Trevor J. Powles and Ian E. ... Aminoglutethimide in the Treatment of Advanced Postmenopausal Breast Cancer Message Subject (Your Name) has forwarded a page to ...
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... aminoglutethimide is used by bodybuilders in a steroid cycle. Aminoglutethimide has two mechanisms of action: It blocks ... Aminoglutethimide is an anti-steroid drug marketed under the tradename Cytadren by Novartis around the world. It blocks the ... Aminoglutethimide is abused by bodybuilders and other steroid users to lower circulating levels of cortisol in the body and ... Aminoglutethimide is indicated in conjunction with other drugs for the suppression of adrenal function in patients with ...
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Aminoglutethimide  - Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol | RxWikiAminoglutethimide - Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol | RxWiki

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A randomized trial comparing surgical adrenalectomy with aminoglutethimide plus hydrocortisone in women with advanced breast...A randomized trial comparing surgical adrenalectomy with aminoglutethimide plus hydrocortisone in women with advanced breast...

A randomized trial comparing surgical adrenalectomy with aminoglutethimide plus hydrocortisone in women with advanced breast ... aminoglutethimide (AG), plus replacement hydrocortisone. Before randomization, women were stratified according to disease-free ...
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Aminoglutethimide as Treatment of Postmenopausal Women with Advanced Breast Carcinoma | Annals of Internal Medicine | American...Aminoglutethimide as Treatment of Postmenopausal Women with Advanced Breast Carcinoma | Annals of Internal Medicine | American...

Aminoglutethimide as Treatment of Postmenopausal Women with Advanced Breast Carcinoma RICHARD J. SANTEN, M.D.; THOMAS J. WORGUL ... Aminoglutethimide, a known inhibitor of steroid synthesis, is also a potent blocker of the aromatase enzyme and, thus, of ... Aminoglutethimide as Treatment of Postmenopausal Women with Advanced Breast Carcinoma. Ann Intern Med. 1982;96:94-101. doi: ... We developed an effective regimen to inhibit estrogen production in postmenopausal women using aminoglutethimide and ...
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Cytadren (Aminoglutethimide) Oral: Uses, Dosage & Side EffectsCytadren (Aminoglutethimide) Oral: Uses, Dosage & Side Effects

Aminoglutethimide is the drug which acts on the adrenal cortex. Production of steroids is affected by its administration. ... Therapeutic dosage of Aminoglutethimide is 4.8 mg/kg of body weight which is administered 8 hourly in an adult to treat a ... Aminoglutethimide is prescribed to treat certain tumors that affect the adrenal cortex. This drug is also used to prevent over- ... Aminoglutethimide is the drug which acts on the adrenal cortex. Production of steroids is affected by its administration. ...
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Phenomenex HPLC Application #17667: Aminoglutethimide on Lux 5µ  Cellulose-1 250 x 4.6mm in NPPhenomenex HPLC Application #17667: Aminoglutethimide on Lux 5µ Cellulose-1 250 x 4.6mm in NP

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ISRCTN - ISRCTN44725655: Comparison of second-line hormonal agents medroxyprogesterone acetate and aminoglutethimide in...ISRCTN - ISRCTN44725655: Comparison of second-line hormonal agents medroxyprogesterone acetate and aminoglutethimide in...

2. Group B: Aminoglutethimide 250 mg twice daily plus hydrocortisone 20 mg twice daily until disease progression or failure of ... Comparison of second-line hormonal agents medroxyprogesterone acetate and aminoglutethimide in advanced breast cancer. ... Comparison of second-line hormonal agents medroxyprogesterone acetate and aminoglutethimide in advanced breast cancer ...
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aminoglutethimide | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGYaminoglutethimide | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY

aminoglutethimide ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ... Aminoglutethimide is an aromatase (CYP19A1) and steroid 11β-hydroxylase (CYP11A1) inhibitor.. ...
more infohttp://guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7054

Effect of aminoglutethimide on blood pressure and steroid secretion in patients with low renin essential hypertension<...Effect of aminoglutethimide on blood pressure and steroid secretion in patients with low renin essential hypertension<...

Effect of aminoglutethimide on blood pressure and steroid secretion in patients with low renin essential hypertension. Journal ... Effect of aminoglutethimide on blood pressure and steroid secretion in patients with low renin essential hypertension. / Taylor ... title = "Effect of aminoglutethimide on blood pressure and steroid secretion in patients with low renin essential hypertension ... T1 - Effect of aminoglutethimide on blood pressure and steroid secretion in patients with low renin essential hypertension ...
more infohttps://researchexperts.utmb.edu/en/publications/effect-of-aminoglutethimide-on-blood-pressure-and-steroid-secreti

A. M. ADAM, I. D. Bradbrook, H. J. Rogers: The simultaneous assay of aminoglutethimide and Its acetyl metabolite by high...A. M. ADAM, I. D. Bradbrook, H. J. Rogers: The simultaneous assay of aminoglutethimide and Its acetyl metabolite by high...

A. M. ADAM, I. D. Bradbrook, H. J. Rogers: The simultaneous assay of aminoglutethimide and Its acetyl metabolite by high ... "A. M. ADAM, I. D. Bradbrook, H. J. Rogers: The simultaneous assay of aminoglutethimide and Its acetyl metabolite by high ... A simple rapid high-performance liquid chromatographic assay for simultaneous estimation of aminoglutethimide and its ... for pharmacokinetic studies in normal subjects and patients receiving other medication in addition to aminoglutethimide ...
more infohttps://profiles.uonbi.ac.ke/mohamedadam/publications/m-adam-i-d-bradbrook-h-j-rogers-simultaneous-assay-aminoglutethimide-and-it

Decadron (Dexamethasone ): Side Effects, Interactions, Warning, Dosage & UsesDecadron (Dexamethasone ): Side Effects, Interactions, Warning, Dosage & Uses

Aminoglutethimide. Aminoglutethimide may diminish adrenal suppression by corticosteroids.. Amphotericin B Injection And ...
more infohttps://www.rxlist.com/decadron-drug.htm

Drug InformationDrug Information

Aminoglutethimide Aminoglutethimide is an adrenal steroid inhibitor, prescribed for Cushing syndrome.. * Aminohippurate Sodium ...
more infohttps://www.medindia.net/doctors/drug_information/home.asp

Cytadren - Steroid .comCytadren - Steroid .com

Cytadren (aminoglutethimide). (Aminoglutethimide). Cytadren is an extremely powerful often labeled Aromatase Inhibitor (AI). ... Cytadren, officially known as aminoglutethimide first hit the market in 1960 as an anticonvulsant and as an AI in 1967 under ... However, very few RCLs carry Cytadren or an Aminoglutethimide product, and if they do it will typically be very expensive. ...
more infohttps://www.steroid.com/Cytadren.php

Words to Know | Living Beyond Breast CancerWords to Know | Living Beyond Breast Cancer

aminoglutethimide. A nonsteroidal aromatase inhibitor used to decrease the production of estrogen in women or testosterone in ...
more infohttps://lbbc.org/learn/basics/words-to-know?name=%5Ea&items_per_page=All

Glossary of Pharmacology Stubs related terms, short phrases and..."Glossary of Pharmacology Stubs" related terms, short phrases and...

Aminoglutethimide. *Example inducers include aminoglutethimide, carbamazepine, phenobarbital, and rifampin.. *Aminoglutethimide ...
more infohttp://keywen.com/en/GLOSSARY_OF_PHARMACOLOGY_STUBS

Acolbifene - WikipediaAcolbifene - Wikipedia

InChI=1S/C29H31NO4/c1-20-26-14-11-24(32)19-27(26)34-29(28(20)21-5-9-23(31)10-6-21)22-7-12-25(13-8-22)33-18-17-30-15-3-2-4-16-30/h5-14,19,29,31-32H,2-4,15-18H2,1H3/t29-/m0/ ...
more infohttps://en.wikipedia.org/wiki/Acolbifene

Hormone replacement therapy - WikipediaHormone replacement therapy - Wikipedia

The Womens Health Initiative trials were conducted between 1991 and 2006 and were the first large, double-blind, placebo-controlled clinical trials of HRT in healthy women.[52] Their results were both positive and negative, suggesting that during the time of hormone therapy itself, there are increases in invasive breast cancer, stroke and lung clots. Other risks include increased endometrial cancer, gallbladder disease, and urinary incontinence, while benefits include decreased hip fractures, decreased incidence of diabetes, and improvement of vasomotor symptoms. There also is an increased risk of dementia with HRT in women over 65, though when given earlier it appears to be neuroprotective. After the cessation of HRT, the WHI continued observe its participants, and found that most of these risks and benefits dissipated, though some elevation in breast cancer risk did persist.[24] Other studies have also suggested an increased risk of ovarian cancer.[43] The arm of the WHI receiving combined ...
more infohttps://en.wikipedia.org/wiki/Hormone_replacement_therapy
  • Aminoglutethimide reduces the production of D5-pregnenolone and blocks several other steps in steroid synthesis, including the C-11, C-18, and C-21 hydroxylations and the hydroxylations required for the aromatization of androgens to estrogens, mediated through the binding of aminoglutethimide to cytochrome P-450 complexes. (drugbank.ca)
  • A. M. ADAM, I. D. Bradbrook, H. J. Rogers: The simultaneous assay of aminoglutethimide and Its acetyl metabolite by high performance liquid chromatography. (ac.ke)
  • A simple rapid high-performance liquid chromatographic assay for simultaneous estimation of aminoglutethimide and its acetylated metabolite acetylamidoglutethimide in plasma, saliva, and urine is described. (ac.ke)
  • In spite of an increase in TSH, aminoglutethimide has not been associated with increased prolactin secretion. (drugbank.ca)
  • Excretion rates of 16β-hydroxydehydroepiandrosterone, 16-oxo-androstenediol, 17-hydroxycorticosteroids and 17-ketosteroids, and the secretion rate of 16β-hydroxydehydroepiandrosterone were not significantly altered by aminoglutethimide treatment whereas the excretion rate of aldosterone was reduced from 3.62±0.5 (mean±SE) in the control period to 0.9±0.2 μg/24 h after 4 days and to 1.1±0.3 μg/24 h at the termination of aminoglutethimide treatment. (utmb.edu)
  • Mean arterial pressure was reduced from a pretreatment value of 117±2 (mean±SE) mm Hg to 108±3 mm Hg after 4 days of aminoglutethimide therapy and further to 99±3 mm Hg when drug administration was stopped (usually 21 days). (utmb.edu)
  • The gradual lowering of blood pressure and body weight during aminoglutethimide therapy is consistent with the view that the antihypertensive effect of the drug is mediated through a reduction in the patients' extracellular fluid volume, probably secondary to the persistent decrease in aldosterone production. (utmb.edu)
  • Take aminoglutethimide exactly as prescribed by your doctor. (rxwiki.com)
  • Aminoglutethimide should only be prescribed by a doctor and is taken orally as a pill. (healthery.com)
  • Aminoglutethimide should be taken as prescribed by the doctor, making sure to follow the instructions on the prescription packaging carefully. (healthery.com)
  • It has been shown that use of Aminoglutethimide in pregnant women caused some babies to be born with problems. (rxwiki.com)
  • Moreover, Aminoglutethimide is prescribed by the health professionals to treat some other disorders. (findatopdoc.com)
  • How likely would you be to recommend Aminoglutethimide to a friend? (rxwiki.com)
  • How was your experience with Aminoglutethimide? (rxwiki.com)