Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.Abortifacient Agents, Steroidal: Steroidal compounds with abortifacient activity.Hormone Antagonists: Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.Misoprostol: A synthetic analog of natural prostaglandin E1. It produces a dose-related inhibition of gastric acid and pepsin secretion, and enhances mucosal resistance to injury. It is an effective anti-ulcer agent and also has oxytocic properties.Abortifacient Agents, Nonsteroidal: Non-steroidal chemical compounds with abortifacient activity.Contraceptives, Postcoital, Synthetic: Postcoital contraceptives which owe their effectiveness to synthetic preparations.Abortifacient Agents: Chemical substances that interrupt pregnancy after implantation.Abortion, Induced: Intentional removal of a fetus from the uterus by any of a number of techniques. (POPLINE, 1978)Contraceptives, Oral, Synthetic: Oral contraceptives which owe their effectiveness to synthetic preparations.Menstruation-Inducing Agents: Chemical compounds that induce menstruation either through direct action on the reproductive organs or through indirect action by relieving another condition of which amenorrhea is a secondary result. (From Dorland, 27th ed)Luteolytic Agents: Chemical compounds causing LUTEOLYSIS or degeneration.Levonorgestrel: A synthetic progestational hormone with actions similar to those of PROGESTERONE and about twice as potent as its racemic or (+-)-isomer (NORGESTREL). It is used for contraception, control of menstrual disorders, and treatment of endometriosis.Administration, Intravaginal: The insertion of drugs into the vagina to treat local infections, neoplasms, or to induce labor. The dosage forms may include medicated pessaries, irrigation fluids, and suppositories.Norpregnadienes: Pregnadienes which have undergone ring contractions or are lacking carbon-18 or carbon-19.Receptors, Glucocorticoid: Cytoplasmic proteins that specifically bind glucocorticoids and mediate their cellular effects. The glucocorticoid receptor-glucocorticoid complex acts in the nucleus to induce transcription of DNA. Glucocorticoids were named for their actions on blood glucose concentration, but they have equally important effects on protein and fat metabolism. Cortisol is the most important example.Endometrium: The mucous membrane lining of the uterine cavity that is hormonally responsive during the MENSTRUAL CYCLE and PREGNANCY. The endometrium undergoes cyclic changes that characterize MENSTRUATION. After successful FERTILIZATION, it serves to sustain the developing embryo.Progesterone: The major progestational steroid that is secreted primarily by the CORPUS LUTEUM and the PLACENTA. Progesterone acts on the UTERUS, the MAMMARY GLANDS and the BRAIN. It is required in EMBRYO IMPLANTATION; PREGNANCY maintenance, and the development of mammary tissue for MILK production. Progesterone, converted from PREGNENOLONE, also serves as an intermediate in the biosynthesis of GONADAL STEROID HORMONES and adrenal CORTICOSTEROIDS.Contraceptives, Postcoital: Contraceptive substances to be used after COITUS. These agents include high doses of estrogenic drugs; progesterone-receptor blockers; ANTIMETABOLITES; ALKALOIDS, and PROSTAGLANDINS.Uterine Hemorrhage: Bleeding from blood vessels in the UTERUS, sometimes manifested as vaginal bleeding.Luteal Phase: The period in the MENSTRUAL CYCLE that follows OVULATION, characterized by the development of CORPUS LUTEUM, increase in PROGESTERONE production by the OVARY and secretion by the glandular epithelium of the ENDOMETRIUM. The luteal phase begins with ovulation and ends with the onset of MENSTRUATION.Contraception, Postcoital: Means of postcoital intervention to avoid pregnancy, such as the administration of POSTCOITAL CONTRACEPTIVES to prevent FERTILIZATION of an egg or implantation of a fertilized egg (OVUM IMPLANTATION).Progestins: Compounds that interact with PROGESTERONE RECEPTORS in target tissues to bring about the effects similar to those of PROGESTERONE. Primary actions of progestins, including natural and synthetic steroids, are on the UTERUS and the MAMMARY GLAND in preparation for and in maintenance of PREGNANCY.Contraceptive Agents, Female: Chemical substances or agents with contraceptive activity in females. Use for female contraceptive agents in general or for which there is no specific heading.Gonanes: Steroids containing the fundamental tetracyclic unit with no methyl groups at C-10 and C-13 and with no side chain at C-17. The concept includes both saturated and unsaturated derivatives.Cytostatic Agents: Compounds that inhibit or prevent the proliferation of CELLS.Menstruation: The periodic shedding of the ENDOMETRIUM and associated menstrual bleeding in the MENSTRUAL CYCLE of humans and primates. Menstruation is due to the decline in circulating PROGESTERONE, and occurs at the late LUTEAL PHASE when LUTEOLYSIS of the CORPUS LUTEUM takes place.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Receptors, Progesterone: Specific proteins found in or on cells of progesterone target tissues that specifically combine with progesterone. The cytosol progesterone-receptor complex then associates with the nucleic acids to initiate protein synthesis. There are two kinds of progesterone receptors, A and B. Both are induced by estrogen and have short half-lives.Labor Stage, First: Period from the onset of true OBSTETRIC LABOR to the complete dilatation of the CERVIX UTERI.Pregnancy Trimester, First: The beginning third of a human PREGNANCY, from the first day of the last normal menstrual period (MENSTRUATION) through the completion of 14 weeks (98 days) of gestation.Administration, Sublingual: Administration of a soluble dosage form by placement under the tongue.Pregnanediol: An inactive metabolite of PROGESTERONE by reduction at C5, C3, and C20 position. Pregnanediol has two hydroxyl groups, at 3-alpha and 20-alpha. It is detectable in URINE after OVULATION and is found in great quantities in the pregnancy urine.Ovulation Inhibition: Blocking the process leading to OVULATION. Various factors are known to inhibit ovulation, such as neuroendocrine, psychological, and pharmacological agents.Menstrual Cycle: The period from onset of one menstrual bleeding (MENSTRUATION) to the next in an ovulating woman or female primate. The menstrual cycle is regulated by endocrine interactions of the HYPOTHALAMUS; the PITUITARY GLAND; the ovaries; and the genital tract. The menstrual cycle is divided by OVULATION into two phases. Based on the endocrine status of the OVARY, there is a FOLLICULAR PHASE and a LUTEAL PHASE. Based on the response in the ENDOMETRIUM, the menstrual cycle is divided into a proliferative and a secretory phase.Danazol: A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders.Megestrol: 17-Hydroxy-6-methylpregna-3,6-diene-3,20-dione. A progestational hormone used most commonly as the acetate ester. As the acetate, it is more potent than progesterone both as a progestagen and as an ovulation inhibitor. It has also been used in the palliative treatment of breast cancer.Alcohol-Induced Disorders, Nervous System: Acute and chronic neurologic disorders associated with the various neurologic effects of ETHANOL. Primary sites of injury include the brain and peripheral nerves.Vacuum Curettage: Aspiration of the contents of the uterus with a vacuum curette.Embryo Implantation: Endometrial implantation of EMBRYO, MAMMALIAN at the BLASTOCYST stage.Metrorrhagia: Abnormal uterine bleeding that is not related to MENSTRUATION, usually in females without regular MENSTRUAL CYCLE. The irregular and unpredictable bleeding usually comes from a dysfunctional ENDOMETRIUM.Contraceptives, Postcoital, Hormonal: Postcoital contraceptives which owe their effectiveness to hormonal preparations.Fallopian Tubes: A pair of highly specialized muscular canals extending from the UTERUS to its corresponding OVARY. They provide the means for OVUM collection, and the site for the final maturation of gametes and FERTILIZATION. The fallopian tube consists of an interstitium, an isthmus, an ampulla, an infundibulum, and fimbriae. Its wall consists of three histologic layers: serous, muscular, and an internal mucosal layer lined with both ciliated and secretory cells.Algestone: A synthetic progestational dihydroxy derivative of PROGESTERONE. Its acetonide possesses anti-inflammatory properties.Glucocorticoids: A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.Norgestrel: A synthetic progestational agent with actions similar to those of PROGESTERONE. This racemic or (+-)-form has about half the potency of the levo form (LEVONORGESTREL). Norgestrel is used as a contraceptive, ovulation inhibitor, and for the control of menstrual disorders and endometriosis.Oxytocics: Drugs that stimulate contraction of the myometrium. They are used to induce LABOR, OBSTETRIC at term, to prevent or control postpartum or postabortion hemorrhage, and to assess fetal status in high risk pregnancies. They may also be used alone or with other drugs to induce abortions (ABORTIFACIENTS). Oxytocics used clinically include the neurohypophyseal hormone OXYTOCIN and certain prostaglandins and ergot alkaloids. (From AMA Drug Evaluations, 1994, p1157)Abortion, Legal: Termination of pregnancy under conditions allowed under local laws. (POPLINE Thesaurus, 1991)Menorrhagia: Excessive uterine bleeding during MENSTRUATION.Corticosterone: An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1437)Pessaries: Devices worn in the vagina to provide support to displaced uterus or rectum. Pessaries are used in conditions such as UTERINE PROLAPSE; CYSTOCELE; or RECTOCELE.Clostridium sordellii: A species of gram-positive bacteria in the family Clostridiaceae, found in INTESTINES and SOIL.Dexamethasone: An anti-inflammatory 9-fluoro-glucocorticoid.Ethinyl Estradiol: A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.Leiomyoma: A benign tumor derived from smooth muscle tissue, also known as a fibroid tumor. They rarely occur outside of the UTERUS and the GASTROINTESTINAL TRACT but can occur in the SKIN and SUBCUTANEOUS TISSUE, probably arising from the smooth muscle of small blood vessels in these tissues.Receptors, Mineralocorticoid: Cytoplasmic proteins that specifically bind MINERALOCORTICOIDS and mediate their cellular effects. The receptor with its bound ligand acts in the nucleus to induce transcription of specific segments of DNA.

Modulation of oestrogenic effects by progesterone antagonists in the rat uterus. (1/1154)

Antiprogestins can modulate oestrogenic effects in various oestrogen-dependent tissues, dependent on species, tissue, dose and duration of treatment. Enhanced oestrogenic responses to mifepristone and onapristone occur in vitro and in vivo. However, the antiprogestins mifepristone, onapristone, and ZK 137 316 can block the ability of oestradiol to increase endometrial growth in non-human primates. Our purposes were firstly, to decide whether mifepristone and onapristone had direct oestrogenic activity in vitro and in the uterus of spayed and immature rats, and secondly, to discover whether antiprogestins exhibit inhibitory effects on oestrogen action in the uterus in spayed, oestrogen-substituted rats. In transactivation assays, mifepristone induced oestrogenic response, whereas onapristone had only marginal effects on reporter gene transcription. In immature rats, onapristone and mifepristone markedly increased uterine weights, and onapristone, but not mifepristone significantly enhanced endometrial luminal epithelial height, a sensitive oestrogen parameter. Conversely, in spayed and adrenalectomized rats, neither onapristone nor mifepristone changed uterine weights or endometrial morphology, indicating that their effects in immature rats were indirect. In spayed, oestrogen-substituted rats, antiprogestins did not block oestradiol-stimulated endometrial growth and luminal and glandular epithelium were stimulated more after antiprogestin plus oestrogen, than after oestradiol alone. All compounds induced compaction of the uterine stroma. In spayed rats, onapristone and some other 13alpha-configured (type 1) antagonists (ZK 135 569, ZK 131 535) reduced oestradiol-stimulated myometrial proliferation and induced an overall uterine weight reduction in animals treated with oestrogen and antiprogestins, in comparison with oestradiol-treated controls. 13beta- configured (type II) antagonists, including mifepristone, lilopristone and ZK 112 993, were not effective. In the uteri of spayed rats, onapristone was also found to enhance the oestradiol-stimulatory effect on expression of the oestrogen-dependent proto-oncogene, c-fos. In conclusion, antiprogestins do not inhibit, but rather enhance, oestrogen-induced uterine glandular and luminal epithelium in spayed rats, contrary to their effects in primates. The rat model is unsuitable to study endometrial antiproliferative effects of antiprogestins in primate uteri.  (+info)

Altered leucocyte trafficking and suppressed tumour necrosis factor alpha release from peripheral blood monocytes after intra-articular glucocorticoid treatment. (2/1154)

OBJECTIVES: A generalised transient improvement may follow intra-articular administration of glucocorticoids to patients with inflammatory arthropathy. This may represent a systemic anti-inflammatory effect of glucocorticoid released from the joint, mediated through processes such as altered leucocyte trafficking or suppressed release of pro-inflammatory cytokines. Patients, who had received intra-articular injections of glucocorticoids were therefore studied for evidence of these two systemic effects. METHODS: Patients with rheumatoid arthritis were studied. Peripheral blood leucocyte counts, tumour necrosis factor alpha (TNF alpha) release by peripheral blood monocytes, blood cortisol concentrations, and blood methylprednisolone concentration were measured for 96 hours after intra-articular injection of methylprednisolone acetate. RESULTS: Measurable concentrations of methylprednisolone were present in blood for up to 96 hours after injection. Significant suppression of the hypothalamic-pituitary-adrenal axis persisted throughout this time. Altered monocyte and lymphocyte trafficking, as evidenced by peripheral blood monocytopenia and lymphopenia, was apparent by four hours after injection and resolved in concordance with the elimination of methylprednisolone. Granulocytosis was observed at 24 and 48 hours. Release of TNF alpha by endotoxin stimulated peripheral blood monocytes was suppressed at four hours and thereafter. Suppression was maximal at eight hours and was largely reversed by the glucocorticoid antagonist, mifepristone. CONCLUSIONS: After intra-articular injection of methylprednisolone, blood concentrations of glucocorticoid are sufficient to suppress monocyte TNF alpha release for at least four days and to transiently alter leucocyte trafficking. These effects help to explain the transient systemic response to intra-articular glucocorticoids. Suppression of TNF alpha is principally a direct glucocorticoid effect, rather than a consequence of other methylprednisolone induced changes to blood composition.  (+info)

Pituitary adenylate cyclase-activating polypeptide, interleukin-6 and glucocorticoids regulate the release of vascular endothelial growth factor in pituitary folliculostellate cells. (3/1154)

There is increasing evidence that hormones play an important role in the control of endothelial cell function and growth by regulating the production of vascular endothelial growth factor (VEGF). VEGF regulates vascular permeability and represents the most powerful growth factor for endothelial cells. In the normal anterior pituitary, VEGF has been detected only in folliculostellate (FS) cells. In the present study, the regulation of the release of VEGF from FS-like mouse TtT/GF cells, and from FS cells of rat pituitary monolayer cell cultures was investigated using a specific VEGF ELISA. Basal release of VEGF was demonstrated in cultures of both TtT/GF cells and rat pituitary cells. Interestingly, the VEGF secretion was stimulated by both forms of pituitary adenylate cyclase-activating polypeptide (PACAP-38 and PACAP-27), indicating that this hypothalamic peptide regulates endothelial cell function and growth within the pituitary. VEGF secretion was also stimulated by interleukin-6 (IL-6) whereas basal, IL-6- and PACAP-stimulated secretion was inhibited by the synthetic glucocorticoid dexamethasone. The inhibitory action of dexamethasone was reversed by the glucocorticoid receptor antagonist RU486, suggesting that in FS cells functional glucocorticoid receptors mediate the inhibitory action of glucocorticoids on the VEGF secretion. The endocrine and auto-/paracrine control of VEGF production in pituitary FS cells by PACAP, IL-6 and glucocorticoids may play an important role both in angiogenesis and vascular permeability regulation within the pituitary under physiological and pathophysiological conditions.  (+info)

Gestational regulation of granulocyte-colony stimulating factor receptor expression in the human placenta. (4/1154)

A number of cytokines and their receptors are abundantly expressed at the materno-fetal interface and are thought to have a function in the regulation of placentation. Granulocyte-colony stimulating factor (G-CSF) is expressed by stromal cells in both placental tissue and maternal decidua throughout placentation. In this study, we examined the expression of placental G-CSF receptor (G-CSFR) mRNA and protein throughout gestation by ribonuclease protection assays, Western blotting, and immunohistochemistry. The major placental form of G-CSFR mRNA, corresponding to a membrane-bound form of the protein, was present in first-trimester placental tissues; levels decreased in second- and were highest in third-trimester placental tissues. Two placental G-CSFR molecules, 120 kDa and 150 kDa, were detected in first- and third-, but not second-, trimester tissues. The level of the 150-kDa G-CSFR was greater in the third- than in first-trimester samples. These differences were irrespective of whether or not the patients had received prostaglandin E1 analogues, prostaglandin E1 analogues and oxytocin, oxytocin alone, or mifepristone before labor. We demonstrated by immunohistochemistry that interstitial cytotrophoblast in first- and second-trimester decidual tissue and cytotrophoblast in term fetal membranes express G-CSFR. These data demonstrate that the expression of specific forms of placental G-CSFR is strictly cell type- and developmental stage-specific, and they suggest that G-CSFR may be important in decidual invasion of cytotrophoblast and in trophoblast function during placentation.  (+info)

Effects of glucocorticoids on maturation of pig oocytes and their subsequent fertilizing capacity in vitro. (5/1154)

The aim of this study was to assess the possible role of glucocorticoids in the maturation of pig oocytes and their subsequent fertilizing capacity in vitro. Pig cumulus-enclosed oocytes collected from prepubertal gilts were cultured in Waymouth MB752/1 medium supplemented with sodium pyruvate (50 microg/ml), LH (0.5 microg/ml), FSH (0.5 microg/ml), and estradiol-17beta (1 microg/ml) in the presence or absence of cortisol or dexamethasone (DEX) for 24 h; they then were cultured without hormonal supplements in the presence or absence of cortisol or DEX for an additional 16-24 h. Treatment of cumulus-enclosed or denuded oocytes with increasing concentrations of cortisol or DEX for 48 h resulted in a dose-response inhibition of germinal vesicle breakdown (GVB). Increasing duration (12-48 h) of treatment with DEX (10 microg/ml) led to a time-dependent inhibition of GVB, which achieved statistical significance by 12 h. The addition of DEX (10 microg/ml) to maturation medium immediately after culture or at 12 h, 24 h, or 36 h after culture also decreased the percentage of oocytes with GVB. When oocytes were exposed to DEX for 48 h, the maturation rate was reduced. The degree of this reduction was dependent on DEX, and a concentration of DEX higher than 0.1 microg/ml was needed. The inhibitory effect of DEX on the maturation of oocytes was prevented by the glucocorticoid receptor antagonist RU-486. Exposure of oocytes to DEX for 40 h did not prevent sperm penetration, affect the incidence of polyspermy, or decrease the ability of oocytes to form a male pronucleus. The intracellular concentration of glutathione (GSH) in cumulus-enclosed oocytes was 4.4 mM per oocyte. Exposure of oocytes to DEX (0.01-10 microg/ml) had no effect on GSH concentration. These results demonstrate that glucocorticoids directly inhibit the meiotic but not cytoplasmic maturation of pig oocytes in vitro. This inhibitory effect is not mediated through a decrease in the level of intracellular GSH.  (+info)

Once-a-month treatment with a combination of mifepristone and the prostaglandin analogue misoprostol. (6/1154)

In this two centre study, the efficacy of 200 mg mifepristone orally followed 48 h later by 0.4 mg misoprostol orally for menstrual regulation was investigated. The dose of mifepristone was taken the day before the expected day of menstruation. Each volunteer was planned to participate for up to 6 months. A plasma beta human chorionic gonadotrophin (HCG) was measured on the day of mifepristone intake. The study was disrupted prematurely due to low efficacy. In 125 treatment cycles the overall pregnancy rate was 17.6% (22 pregnancies) and the rate of continuing pregnancies (failure) was 4.0%. Eight women discontinued the study due to bleeding irregularities which were seen in 15 cycles (12%). These effects on bleeding pattern made the timing of treatment day difficult. Late luteal phase treatment with a combination of mifepristone and misoprostol is not adequately effective for menstrual regulation.  (+info)

The negative regulation of the rat aldehyde dehydrogenase 3 gene by glucocorticoids: involvement of a single imperfect palindromic glucocorticoid responsive element. (7/1154)

Glucocorticoids repressed the polycyclic aromatic hydrocarbon-dependent induction of Class 3 aldehyde dehydrogenase (ALDH3) enzyme activity and mRNA levels in isolated rat hepatocytes by more than 50 to 80%, with a concentration-dependence consistent with the involvement of the glucocorticoid receptor (GR). No consistent effect on the low basal transcription rate was observed. This effect of glucocorticoids (GC) on polycyclic aromatic hydrocarbon induction was effectively antagonized at the mRNA and protein level by the GR antagonist RU38486. The response was cycloheximide-sensitive, because the protein synthesis inhibitor caused a GC-dependent superinduction of ALDH3 mRNA levels. This suggests that the effects of GC on this gene are complex and both positive and negative gene regulation is possible. The GC-response was recapitulated in HepG2 cells using transient transfection experiments with CAT reporter constructs containing 3.5 kb of 5'-flanking region from ALDH3. This ligand-dependent response was also observed when a chimeric GR (GR DNA-binding domain and peroxisome proliferator-activated receptor ligand-binding domain) was used in place of GR in the presence of the peroxisome proliferator, nafenopin. A putative palindromic glucocorticoid-responsive element exists between -930 and -910 base pairs relative to the transcription start site. If this element was either deleted or mutated, the negative GC-response was completely lost, which suggests that this sequence is responsible, in part, for the negative regulation of the gene. Electrophoretic mobility shift analysis demonstrated that this palindromic glucocorticoid-responsive element is capable of forming a specific DNA-protein complex with human glucocorticoid receptor. In conclusion, the negative regulation of ALDH3 in rat liver is probably mediated through direct GR binding to its canonical responsive element.  (+info)

Conformational change in the human glucocorticoid receptor induced by ligand binding is altered by mutation of isoleucine 747 by a threonine. (8/1154)

Limited proteolysis experiments were performed to study conformation changes induced by ligand binding on in vitro produced wild-type and I747T mutant glucocorticoid receptors. Dexamethasone-induced conformational changes were characterized by two resistant proteolysis fragments of 30 and 27 kDa. Although dexamethasone binding affinity was only slightly altered by the I747T substitution (Roux, S., Terouanne, B., Balaguer, P., Loffreda-Jausons, N., Pons, M., Chambon, P., Gronemeyer, H., and Nicolas, J.-C. (1996) Mol. Endocrinol. 10, 1214-1226), higher dexamethasone concentrations were required to obtain the same proteolysis pattern. This difference was less marked when proteolysis experiments were conducted at 0 degrees C, indicating that a step of the conformational change after ligand binding was affected by the mutation. In contrast, RU486 binding to the wild-type receptor induced a different conformational change that was not affected by the mutation. Analysis of proteolysis fragments obtained in the presence of dexamethasone or RU486 indicated that the RU486-induced conformational change affected the C-terminal part of the ligand binding domain differently. These data suggest that the ligand-induced conformational change occurs via a multistep process. In the first step, characterized by compaction of the ligand binding domain, the mutation has no effect. The second step, which stabilizes the activated conformation and does not occur at 4 degrees C, seems to be a key element in the activation process that can be altered by the mutation. This step could involve modification of the helix H12 position, explaining why the conformation induced by RU486 is not affected by the mutation.  (+info)

  • Korlym is another brand of mifepristone that is not covered in this medication guide. (cigna.com)
  • KORLYM (mifepristone) is a cortisol receptor blocker for oral administration. (rxlist.com)
  • Each KORLYM tablet for oral use contains 300 mg of mifepristone. (rxlist.com)
  • KORLYM ( mifepristone ) is a cortisol receptor blocker indicated to control hyperglycemia secondary to hypercortisolism in adult patients with endogenous Cushing's syndrome who have type 2 diabetes mellitus or glucose intolerance and have failed surgery or are not candidates for surgery. (rxlist.com)
  • Many drugs have multiple uses, and mifepristone - brand name "Korlym" at Corcept - is currently marketed by the company for the treatment of Cushing's syndrome. (infowars.com)
  • Following use by 34,000 women in France from April 1988 to February 1990 of mifepristone distributed free of charge, Roussel-Uclaf began selling Mifegyne (mifepristone) to hospitals in France in February 1990 at a price (negotiated with the French government) of $48 per 600 mg dose. (wikipedia.org)
  • Mifepristone is a synthetic steroid compound used as a pharmaceutical. (bionity.com)
  • Mifepristone is a 19-nor steroid with a bulky p -(dimethylamino)phenyl substituent above the plane of the molecule at the 11β-position responsible for inducing or stabilizing an inactive receptor conformation and a hydrophobic 1-propynyl substituent above the plane of the molecule at the 17α-position that increases its progesterone receptor binding affinity . (bionity.com)
  • Mifepristone (or RU-486) is a synthetic steroid compound with both antiprogesterone and antiglucocorticoid properties. (passionchemical.com)
  • Treatment with 200 mg of mifepristone changes steroid receptor expression in the Fallopian tube, inhibits endometrial development, and effectively prevents implantation. (passionchemical.com)
  • Before and after treatment with mifepristone, the intracellular accumulation of cisplatin in cancer cells and tumors of mice receiving treatment was evaluated by HPLC, the expression of Bcl-2 gene was assessed by RT-PCR and western blotting. (biomedcentral.com)
  • In medical abortion regimens, mifepristone blockade of progesterone receptors directly causes endometrial decidual degeneration, cervical softening and dilatation, release of endogenous prostaglandins and an increase in the sensitivity of the myometrium to the contractile effects of prostaglandins. (bionity.com)
  • Schwartz, Jill L. / Mifepristone 100 mg in abortion regimens . (elsevier.com)
  • Abortion rights activists in the United States hailed the Food and Drug Administration's (FDA) September 2000 approval of mifepristone as a "momentous step," because the drug would give American women the option of a safe, early abortion where one may not have previously existed. (guttmacher.org)
  • Danco has noted that more than 460,000 prescriptions for mifepristone have been written since its approval in 2000, making the fatal sepsis rate about 1 in 100,000. (thefreelibrary.com)
  • Our results suggest that mifepristone can improve the efficacy of cisplatin in cancer cells and this anti-hormonal drug therapy may be a candidate for further evaluation in combination with antineoplastic drugs in the treatment of cancer. (biomedcentral.com)
  • A single preovulatory 10 mg dose of mifepristone delays ovulation by 3 to 4 days and is as effective an emergency contraceptive as a single 1.5 mg dose of the progestin levonorgestrel. (bionity.com)
  • METHODS: Eighty participants received mifepristone 100 mg and then were randomized to misoprostol, administered 48 hours later, at a dose of 400 μg orally (group 1) or 800 μg vaginally (group 2). (elsevier.com)
  • CHARLESTON, S.C. -- Recent deaths due to sepsis following medical abortion may be the result of an interaction between factors specific to mifepristone--one of the drugs used in the abortions--and Clostridium sordellii, the cause of infection in at least three of the five patients who died, James A. McGregor, M.D., said at the annual meeting of the Infectious Diseases Society for Obstetrics and Gynecology. (thefreelibrary.com)
  • In 2001, AGI investigated mifepristone use and policies in these countries on the basis of information from national abortion statistics, professional guidelines and interviews with experts. (guttmacher.org)
  • The first of the five deaths that prompted the warnings occurred in Canada in 2001 during a clinical trial of mifepristone. (thefreelibrary.com)
  • In addition to being an antiprogestogen, mifepristone is also an antiglucocorticoid and a weak antiandrogen . (bionity.com)
  • In humans, an antiglucocorticoid effect of mifepristone is manifested at doses greater or equal to 4.5 mg/kg by a compensatory increase in ACTH and cortisol. (bionity.com)
  • Corcept Therapeutics (Corcept.com) manufacturers and markets an abortion pill drug called mifepristone , and Christine Blasey Ford is a co-author of at least eight published scientific papers produced by the pharmaceutical giant to promote its pills. (infowars.com)
  • It is not surprising then that, among both women and the medical community, there are several challenges to mifepristone "uptake" having to do with the procedure itself, its economics and state policies for its use. (guttmacher.org)
  • Since Harrison's discovery, Davenport and Dr. George Delgado, medical director of the Culture of Life Family Services in San Diego, have published a series of case studies "demonstrating successful reversal of mifepristone effects in women who chose to reverse the medical abortion process. (occatholic.com)
  • Mifepristone is a drug that blocks cortisol. (clinicaltrials.gov)
  • Less than two years after the Food and Drug Administration approved the use of mifepristone for early nonsurgical abortion, a majority of the specialized clinics that provide surgical abortion services in the United States are now offering it. (guttmacher.org)
  • The company offers just one drug, mifepristone , which is widely known as an "abortion pill" or RU-486. (infowars.com)
  • Whole-body rate of regenerating cortisol response to mifepristone of glucose insulin sensitivity, free fatty acid clearance, cortisol metabolites, adrenal hormones. (clinicaltrials.gov)
  • Two days later, the French government ordered Roussel-Uclaf to distribute mifepristone in the interests of public health. (wikipedia.org)
  • On October 21, 1988, in response to antiabortion protests and concerns of majority (54.5%) owner Hoechst AG of Germany, Roussel-Uclaf's executives and board of directors voted 16 to 4 to stop distribution of mifepristone, which they announced on October 26, 1988. (wikipedia.org)
  • Like all FDA-approved drugs, mifepristone is frequently prescribed off-label , meaning doctors prescribe it for conditions that it has never been approved to treat. (infowars.com)
  • During the first visit, she'll take RU-486, chemically known as mifepristone, which acts against the hormone progesterone to prevent the embryo from adhering to the wall of the uterus. (nypost.com)
  • In women, mifepristone at doses greater or equal to 1 mg/kg antagonizes the endometrial and myometrial effects of progesterone. (bionity.com)