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FlutamideAndrogen AntagonistsAndrogensGenitalia, MaleTestosteroneDihydrotestosteroneAndrogen Receptor AntagonistsReceptors, AndrogenOrchiectomyMetestrusAnilidesMethyltestosteroneAntineoplastic Agents, HormonalProstateHyaenidaeTosyl CompoundsHyperandrogenismLinuronProstatic NeoplasmsCytochrome P-450 CYP1A2CryptorchidismProstate-Specific AntigenNeoplasm MetastasisLibrary ServicesLibraries, MedicalPolycystic Ovary SyndromeMetforminHirsutismPatient Access to RecordsOvaryElectronic MailFood Dispensers, AutomaticEditorial PoliciesAuthorshipPeriodicals as TopicPostal ServiceInternetNeoplasms, Hormone-DependentCarboxylic Ester HydrolasesCarboxylesteraseMicrosomes, LiverMicrosomesHydrolysisPharmaceutical Services, OnlineCounterfeit DrugsLegislation, PharmacyPharmaciesDrug and Narcotic ControlPrescription DrugsGynecomastiaGonadotropin-Releasing Hormone
Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species.Androgen Antagonists: Compounds which inhibit or antagonize the biosynthesis or actions of androgens.Androgens: Compounds that interact with ANDROGEN RECEPTORS in target tissues to bring about the effects similar to those of TESTOSTERONE. Depending on the target tissues, androgenic effects can be on SEX DIFFERENTIATION; male reproductive organs, SPERMATOGENESIS; secondary male SEX CHARACTERISTICS; LIBIDO; development of muscle mass, strength, and power.Genitalia, Male: The male reproductive organs. They are divided into the external organs (PENIS; SCROTUM;and URETHRA) and the internal organs (TESTIS; EPIDIDYMIS; VAS DEFERENS; SEMINAL VESICLES; EJACULATORY DUCTS; PROSTATE; and BULBOURETHRAL GLANDS).Testosterone: A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.Dihydrotestosterone: A potent androgenic metabolite of TESTOSTERONE. It is produced by the action of the enzyme 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE.Androgen Receptor Antagonists: Compounds that bind to and inhibit the activation of ANDROGEN RECEPTORS.Receptors, Androgen: Proteins, generally found in the CYTOPLASM, that specifically bind ANDROGENS and mediate their cellular actions. The complex of the androgen and receptor migrates to the CELL NUCLEUS where it induces transcription of specific segments of DNA.Orchiectomy: The surgical removal of one or both testicles.Metestrus: The period following ESTRUS during which the phenomena of estrus subside in those animals in which pregnancy or pseudopregnancy does not occur.AnilidesMethyltestosterone: A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).Antineoplastic Agents, Hormonal: Antineoplastic agents that are used to treat hormone-sensitive tumors. Hormone-sensitive tumors may be hormone-dependent, hormone-responsive, or both. A hormone-dependent tumor regresses on removal of the hormonal stimulus, by surgery or pharmacological block. Hormone-responsive tumors may regress when pharmacologic amounts of hormones are administered regardless of whether previous signs of hormone sensitivity were observed. The major hormone-responsive cancers include carcinomas of the breast, prostate, and endometrium; lymphomas; and certain leukemias. (From AMA Drug Evaluations Annual 1994, p2079)Prostate: A gland in males that surrounds the neck of the URINARY BLADDER and the URETHRA. It secretes a substance that liquefies coagulated semen. It is situated in the pelvic cavity behind the lower part of the PUBIC SYMPHYSIS, above the deep layer of the triangular ligament, and rests upon the RECTUM.Hyaenidae: A family of large terrestrial carnivores possessing long legs, coarse guard hairs and a busy tail. It is comprised of hyenas and aardwolves.Tosyl CompoundsHyperandrogenism: A condition caused by the excessive secretion of ANDROGENS from the ADRENAL CORTEX; the OVARIES; or the TESTES. The clinical significance in males is negligible. In women, the common manifestations are HIRSUTISM and VIRILISM as seen in patients with POLYCYSTIC OVARY SYNDROME and ADRENOCORTICAL HYPERFUNCTION.Linuron: A selective pre- and post-emergence herbicide. (From Merck Index, 11th ed)Prostatic Neoplasms: Tumors or cancer of the PROSTATE.Cytochrome P-450 CYP1A2: A cytochrome P450 enzyme subtype that has specificity for relatively planar heteroaromatic small molecules, such as CAFFEINE and ACETAMINOPHEN.Cryptorchidism: A developmental defect in which a TESTIS or both TESTES failed to descend from high in the ABDOMEN to the bottom of the SCROTUM. Testicular descent is essential to normal SPERMATOGENESIS which requires temperature lower than the BODY TEMPERATURE. Cryptorchidism can be subclassified by the location of the maldescended testis.Prostate-Specific Antigen: A glycoprotein that is a kallikrein-like serine proteinase and an esterase, produced by epithelial cells of both normal and malignant prostate tissue. It is an important marker for the diagnosis of prostate cancer.Neoplasm Metastasis: The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.Library Services: Services offered to the library user. They include reference and circulation.Libraries, MedicalPolycystic Ovary Syndrome: A complex disorder characterized by infertility, HIRSUTISM; OBESITY; and various menstrual disturbances such as OLIGOMENORRHEA; AMENORRHEA; ANOVULATION. Polycystic ovary syndrome is usually associated with bilateral enlarged ovaries studded with atretic follicles, not with cysts. The term, polycystic ovary, is misleading.Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)Hirsutism: A condition observed in WOMEN and CHILDREN when there is excess coarse body hair of an adult male distribution pattern, such as facial and chest areas. It is the result of elevated ANDROGENS from the OVARIES, the ADRENAL GLANDS, or exogenous sources. The concept does not include HYPERTRICHOSIS, which is an androgen-independent excessive hair growth.Patient Access to Records: The freedom of patients to review their own medical, genetic, or other health-related records.Ovary: The reproductive organ (GONADS) in female animals. In vertebrates, the ovary contains two functional parts: the OVARIAN FOLLICLE for the production of female germ cells (OOGENESIS); and the endocrine cells (GRANULOSA CELLS; THECA CELLS; and LUTEAL CELLS) for the production of ESTROGENS and PROGESTERONE.Electronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Food Dispensers, Automatic: Mechanical food dispensing machines.Editorial Policies: The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.Authorship: The profession of writing. Also the identity of the writer as the creator of a literary production.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Postal Service: The functions and activities carried out by the U.S. Postal Service, foreign postal services, and private postal services such as Federal Express.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Neoplasms, Hormone-Dependent: Certain tumors that 1, arise in organs that are normally dependent on specific hormones and 2, are stimulated or caused to regress by manipulation of the endocrine environment.Carboxylic Ester Hydrolases: Enzymes which catalyze the hydrolysis of carboxylic acid esters with the formation of an alcohol and a carboxylic acid anion.Carboxylesterase: Carboxylesterase is a serine-dependent esterase with wide substrate specificity. The enzyme is involved in the detoxification of XENOBIOTICS and the activation of ester and of amide PRODRUGS.Microsomes, Liver: Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.Microsomes: Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water.Pharmaceutical Services, Online: Pharmacy services accessed via electronic means.Counterfeit Drugs: Drugs manufactured and sold with the intent to misrepresent its origin, authenticity, chemical composition, and or efficacy. Counterfeit drugs may contain inappropriate quantities of ingredients not listed on the label or package. In order to further deceive the consumer, the packaging, container, or labeling, may be inaccurate, incorrect, or fake.Legislation, Pharmacy: Laws and regulations, pertaining to the field of pharmacy, proposed for enactment or enacted by a legislative body.Pharmacies: Facilities for the preparation and dispensing of drugs.Drug and Narcotic Control: Control of drug and narcotic use by international agreement, or by institutional systems for handling prescribed drugs. This includes regulations concerned with the manufacturing, dispensing, approval (DRUG APPROVAL), and marketing of drugs.Prescription Drugs: Drugs that cannot be sold legally without a prescription.Gynecomastia: Enlargement of the BREAST in the males, caused by an excess of ESTROGENS. Physiological gynecomastia is normally observed in NEWBORNS; ADOLESCENT; and AGING males.Gonadotropin-Releasing Hormone: A decapeptide that stimulates the synthesis and secretion of both pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE. GnRH is produced by neurons in the septum PREOPTIC AREA of the HYPOTHALAMUS and released into the pituitary portal blood, leading to stimulation of GONADOTROPHS in the ANTERIOR PITUITARY GLAND.

Pharmacokinetics of flutamide in patients with renal insufficiency. (1/384)

AIMS: The aim of this study was to determine the pharmacokinetic parameters of flutamide, a nonsteroidal antiandrogenic compound, and its pharmacologically active metabolite, hydroxyflutamide, in renal insufficiency. Haemodialysis (HD) clearance of flutamide and hydroxyflutamide was also determined. METHODS: Pharmacokinetic parameters were assessed for flutamide and hydroxyflutamide in 26 male subjects with normal renal function (creatinine clearance by 24 h urine collection, CLcr, greater than 80 ml min(-1) 1.73 m(-2); n=6) or reduced renal function; CLcr=50-80 (n=7), 30-49 (n=3), 5-29 (n=4), and <5 ml min(-1) 1.73 m(-2)-HD (n=6), following a single, oral 250 mg flutamide dose. Subjects undergoing HD received a second 250 mg dose of flutamide 4 h prior to HD; blood and dialysate were collected during HD to determine dialysability of flutamide and hydroxyflutamide. RESULTS: Cmax, tmax, AUC, t1/2, and renal clearance of flutamide and hydroxyflutamide did not differ between groups. Less than 1% of the dose appeared in dialysate as hydroxyflutamide. No serious adverse events were observed. CONCLUSIONS: Renal function did not affect flutamide nor hydroxyflutamide disposition. HD did not alter hydroxyflutamide pharmacokinetics. Dosing adjustments for renal impairment or HD are not indicated for flutamide.  (+info)

From HER2/Neu signal cascade to androgen receptor and its coactivators: a novel pathway by induction of androgen target genes through MAP kinase in prostate cancer cells. (2/384)

Overexpression of the HER2/Neu protooncogene has been linked to the progression of breast cancer. Here we demonstrate that the growth of prostate cancer LNCaP cells can also be increased by the stable transfection of HER2/Neu. Using AG879, a HER2/Neu inhibitor, and PD98059, a MAP kinase inhibitor, as well as MAP kinase phosphatase-1 (MPK-1), in the transfection assay, we found that HER2/Neu could induce prostate-specific antigen (PSA), a marker for the progression of prostate cancer, through the MAP kinase pathway at a low androgen level. Reporter assays and mammalian two-hybrid assays further suggest this HER2/Neu-induced androgen receptor (AR) transactivation may function through the promotion of interaction between AR and AR coactivators, such as ARA70. Furthermore, we found this HER2/Neu --> MAP kinase --> AR-ARAs --> PSA pathway could not be blocked completely by hydroxyflutamide, an antiandrogen used in the treatment of prostate cancer. Together, these data provide a novel pathway from HER2/Neu to AR transactivation, and they may represent one of the reasons for the PSA re-elevation and hormone resistance during androgen ablation therapy in prostate cancer patients.  (+info)

Selection for androgen receptor mutations in prostate cancers treated with androgen antagonist. (3/384)

The role of androgen receptor (AR) mutations in androgen-independent prostate cancer (PCa) was determined by examining AR transcripts and genes from a large series of bone marrow metastases. Mutations were found in 5 of 16 patients who received combined androgen blockade with the AR antagonist flutamide, and these mutant ARs were strongly stimulated by flutamide. In contrast, the single mutant AR found among 17 patients treated with androgen ablation monotherapy was not flutamide stimulated. Patients with flutamide-stimulated AR mutations responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant ARs. These findings demonstrate that AR mutations occur in response to strong selective pressure from flutamide treatment.  (+info)

Pharmacokinetics of flutamide and its metabolite 2-hydroxyflutamide in normal and hepatic injury rats. (4/384)

AIM: To develop a new HPLC assay to study the pharmacokinetics of flutamide (Flu) and its active metabolite 2-hydroxyflutamide (HF) in rats. METHODS: Normal or hepatic injury rats were given i.g. Flu 50 mg.kg-1. Reverse phase HPLC was developed with a mu-Bondapak C 18 column. Internal standard was methyltestosterone. The mobile phase was a mixture of methanol:acetonitrile:water:diethyl ether = 40:20:35:1 (vol). Absorbance was measured at lambda 234 nm. RESULTS: The pharmacokinetic parameters of Flu were as follows: in normal rats, K = 0.62 +/- 0.16 h-1, Cl = 6.0 +/- 1.0 L.kg-1.h-1, AUC = 8.6 +/- 1.3 mg.L-1.h, Cmax = 2.4 +/- 0.7 mg.L-1; in hepatic injury rats, K = 0.16 +/- 0.03 h-1, Cl = 0.63 +/- 0.29 L.kg-1.h-1, AUC = 100 +/- 44 mg.L-1.h, Cmax = 6.7 +/- 2.8 mg.L-1. The pharmacokinetic parameters of HF were as follows: in normal rats, K(m) = 0.07 +/- 0.01 h-1, AUC = 219 +/- 22 mg.L-1.h, Cmax = 8.6 +/- 0.6 mg.L-1; in hepatic injury rats, K(m) = 0.05 +/- 0.01 h-1, AUC = 170 +/- 42 mg.L-1.h, Cmax = 3.8 +/- 0.8 mg.L-1. There were significant differences between the parameters of normal and hepatic injury rats (P < 0.01) except AUC of HF (P > 0.05). CONCLUSION: This HPLC assay was sensitive and precise, and the elimination of Flu and HF was inhibited significantly due to hepatic injury.  (+info)

Androgen and epidermal growth factor down-regulate cyclin-dependent kinase inhibitor p27Kip1 and costimulate proliferation of MDA PCa 2a and MDA PCa 2b prostate cancer cells. (5/384)

Low levels of p27Kip1 in primary prostate cancer specimens have been shown to be associated with higher rates of disease recurrence and poor rates of disease-free survival in patients with localized disease. In this study, we provide the first direct evidence showing that dihydrotestosterone (DHT), a major proliferation regulator of prostate cancer, can down-regulate p27Kip1 and stimulate cyclin-dependent kinase-2 (CDK2) activity in established prostate cancer cell lines. We investigated the cooperative effects of DHT and epidermal growth factor (EGF) on the proliferation of androgen-responsive MDA PCa 2a and MDA PCa 2b prostate cancer cells. DHT and EGF each stimulated proliferation of these cells, but exposure of the cells to DHT and EGF together stimulated greater proliferation. Stimulation of cell proliferation by DHT and/or EGF was associated with increased CDK2 activity and a decreased level of p27Kip1. There seems to be a positive feedback stimulation loop between androgen-induced gene transcription and EGF-stimulated signal transduction, as one could stimulate the synthesis of the receptors for the other. Dual blockade of androgen receptor function with the antiandrogen hydroxyflutamide and EGF receptor superfamily-mediated signal transduction with the anti-EGF receptor monoclonal antibody C225 and the anti-HER2 receptor monoclonal antibody Herceptin significantly enhanced growth inhibition of the MDA PCa 2a cells. Our results demonstrate the importance of counteracting both androgen receptors and EGF receptors in the development of novel therapies for prostate cancer.  (+info)

Detection of the environmental antiandrogen p,p-DDE in CD and long-evans rats using a tier I screening battery and a Hershberger assay. (6/384)

In this report, p,p'-DDE, a weak androgen receptor (AR) antagonist, has been examined in a Tier I screening battery designed to detect endocrine-active compounds (EACs). The screening battery that was used to examine p,p'-DDE was an abbreviated version of a proposed Tier I screening battery (Cook et al., 1997, Regul. ToxicoL Pharmacol. 26, 60-68) that consisted of a 15-day intact male in vivo battery and an in vitro yeast transactivation system (YTS). In addition, strain sensitivity differences were evaluated using male Crl:CDIGS BR (CD) and Long-Evans (LE) rats. Finally, p,p'-DDE was examined in a Hershberger assay designed to detect AR agonists. In the in vivo male battery using CD rats, responses to p,p'-DDE included organ weight changes (increased relative liver weight and decreased absolute epididymis weight) and hormonal alterations (increased serum estradiol [E2] levels and decreased serum FSH and T4 levels). Responses to p,p'-DDE in LE rats included organ weight changes (increased relative liver weight, absolute epididymis weight, relative accessory sex gland [ASG] unit weight, as well as the individual component weights of the ASG [prostate and seminal vesicles]), and hormonal alterations (increased serum testosterone [T], E2, dihydrotestosterone [DHT], thyroid-stimulating hormone [TSH], and decreased T4 levels). These data demonstrate that there are considerable strain-sensitivity differences to p,p'-DDE exposure. The described in vivo male battery using CD rats did not identify p,p'-DDE as an EAC. In contrast, the in vivo male battery using LE rats identified p,p'-DDE as a EAC. Evaluation of the data for the LE rats demonstrate that p,p'-DDE appears to be acting as an AR antagonist whose primary effects are more potent centrally than peripherally. In the YTS for the AR, p,p'-DDE had an EC50 value of 3.5 x 10(-4) M; however, in the AR YTS competition assay, p,p'-DDE did not inhibit DHT binding to the AR. p,p'-DDE was inactive in the YTS containing the estrogen receptor or progesterone receptor at the concentrations evaluated. In the Hershberger assay, p,p'-DDE administration caused antiandrogen-like effects characterized by attenuation of the testosterone propionate-induced increases in reproductive-organ weights. In summary, these data suggest that strain selection will affect the ability to detect certain weak EACs. However, a Tier I screening battery consisting of both in vivo and in vitro endpoints would reduce the chance that weak-acting compounds such as p,p'-DDE would not be identified as potential EACs.  (+info)

Testosterone signaling through internalizable surface receptors in androgen receptor-free macrophages. (7/384)

Testosterone acts on cells through intracellular transcription-regulating androgen receptors (ARs). Here, we show that mouse IC-21 macrophages lack the classical AR yet exhibit specific nongenomic responses to testosterone. These manifest themselves as testosterone-induced rapid increase in intracellular free [Ca(2+)], which is due to release of Ca(2+) from intracellular Ca(2+) stores. This Ca(2+) mobilization is also inducible by plasma membrane-impermeable testosterone-BSA. It is not affected by the AR blockers cyproterone and flutamide, whereas it is completely inhibited by the phospholipase C inhibitor U-73122 and pertussis toxin. Binding sites for testosterone are detectable on the surface of intact IC-21 cells, which become selectively internalized independent on caveolae and clathrin-coated vesicles upon agonist stimulation. Internalization is dependent on temperature, ATP, cytoskeletal elements, phospholipase C, and G-proteins. Collectively, our data provide evidence for the existence of G-protein-coupled, agonist-sequestrable receptors for testosterone in plasma membranes, which initiate a transcription-independent signaling pathway of testosterone.  (+info)

Combined treatment with the 5 alpha-reductase inhibitor PNU 157706 and the antiandrogen flutamide on the Dunning R3327 prostatic carcinoma in rats. (8/384)

The steroid 5 alpha-reductase enzyme catalyzes the conversion of testosterone to the potent androgen 5 alpha-dihydrotestosterone (DHT). PNU 157706, a novel, potent and selective dual 5 alpha-reductase inhibitor, was reported to be effective in inhibiting the growth of established tumors in the Dunning R3327 rat prostatic carcinoma model. We have studied the efficacy of combined treatment with PNU 157706 and the antiandrogen flutamide in this prostatic tumor in rats. Rats with tumor diameters of about 1 cm were treated orally 6 days a week for 9 weeks with PNU 157706 (10 mg/kg per day) alone or in combination with flutamide (1 and 5 mg/kg per day). Animals were killed 24 h after the last treatment and ventral prostates were removed for testosterone and DHT determination. PNU 157706 reduced the growth of established tumors by 36%; flutamide showed a slight effect at 1 mg/kg per day (24% inhibition), while at the dose of 5 mg/kg per day it reduced tumor growth by 48%. The combination of PNU 157706 with the lower dose of flutamide caused an additive tumor growth inhibition (60%) and the combination with the higher dose of flutamide resulted in a better inhibition of tumor growth (68%) than did either treatment alone. Castration resulted in marked tumor growth inhibition (76%). Ventral prostate weight was more markedly reduced by PNU 157706 treatment than by flutamide; combined treatment was as effective as castration. Prostatic DHT content was markedly reduced by PNU 157706 (93%), whereas prostatic testosterone increased (137%). Concomitant treatment with flutamide partially antagonized the testosterone increase induced by PNU 157706 and did not modify the already considerable suppression of DHT. These data show that the inhibitory effects of PNU 157706 and flutamide on Dunning prostatic tumor growth are additive, thus supporting the rationale of this combination therapy in advanced prostate cancer, in order to achieve adequate androgen blockade with minimal side-effects.  (+info)

Exploring the antiperoxidative potential of morin on cyclophosphamide and flutamide-induced lipid peroxidation and changes in...Exploring the antiperoxidative potential of morin on cyclophosphamide and flutamide-induced lipid peroxidation and changes in...
Considering drug-induced lipid peroxidation as a possible mediator of drug-induced toxicity and exploiting the free radical scavenging action of antioxidants, the present study was designed to evaluate the antiperoxidative potential of morin on cyclophosphamide/flutamide-induced lipid peroxidation and also to evaluate the effect of morin on cyclophosphamide/flutamide-induced changes in cholesterol content in rabbit blood sample. This evaluation was done by measuring the malondialdehyde (MDA), reduced glutathione (GSH), 4-hydroxy-2-nonenal (4-HNE) and nitric oxide (NO) content of blood samples as markers of lipid peroxidation. In the cholesterol profile total cholesterol and high density lipoprotein cholesterol content of rabbit blood was determined. The study reveals the lipid peroxidation induction capacity of cyclophosphamide/flutamide and the antiperoxidative potential of morin on cyclophosphamide/flutamide-induced lipid peroxidation. It was also observed that morin has protective effect on
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Flutamide, an antiandrogen drug, is widely used for the treatment of prostate cancer. The major metabolic pathways of flutamide are hydroxylation and hydrolysis. The hydrolyzed metabolite, 5-amino-2-nitrobenzotrifluoride (FLU-1), is further metabolized to N-hydroxy FLU-1, an assumed hepatotoxicant. Our previous study demonstrated that arylacetamide deacetylase (AADAC), one of the major serine esterases expressed in the human liver and gastrointestinal tract, catalyzes the flutamide hydrolysis. However, the enzyme kinetics in human tissue microsomes were not consistent with the kinetics by recombinant human AADAC. Thus, it seemed that AADAC is not the sole enzyme responsible for flutamide hydrolysis in human. In the present study, we found that recombinant carboxylesterase (CES) 2 could hydrolyze flutamide at low concentrations of flutamide. In the inhibition assay, the flutamide hydrolase activities at a flutamide concentration of 5 μM in human liver and jejunum microsomes were strongly ...
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Flutamide is an antiandrogen. It works in the body to prevent the actions of androgens (male hormones). Flutamide is used together with another hormone to treat prostate cancer. Flutamide may also be used for purposes not listed in this medication guide.
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During the follicular phase of the normal menstrual cycle, luteinizing hormone (LH) pulse frequency decreases during sleep. These decreases may be important to support follicle stimulating hormone (FSH) synthesis and secretion. Polycystic ovary syndrome (PCOS) is associated with a persistently rapid gonadotropin hormone-releasing hormone (GnRH) pulse frequency, an abnormality that may account for many of the hormonal manifestations of PCOS. Although one prior study suggests that nocturnal LH frequency decreases slightly in PCOS, methodological issues limit interpretation. Our preliminary data suggest that nocturnal LH frequency does not decrease in untreated PCOS, but that nocturnal decreases of LH frequency are restored with androgen receptor blockade (flutamide) in women with PCOS. We have two hypotheses: (1) Prior to flutamide administration, sleep-associated slowing of LH pulse frequency is less pronounced in women with PCOS compared to that of normally-cycling women in the late follicular ...
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The addition of flutamide to bilateral orchiectomy does not result in a clinically meaningful improvement in survival among patients with metastatic prostate cancer.
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Materials and methods: The model used is a xenograft originating from the Gleason-9 primary prostate cancer of a 54-years old patient (DePinieux et al, Am J Pathol, 2001). PAC120 is hormone dependent, with no AR mutation. For testing hormone deprivation efficacy, swiss Nu/nu male 8-12 week old mice received the subcutaneous transplantation of PAC120 trocar pieces. Hormonal therapies tested were: inhibitors of AR (flutamide or bicalutamide), GnRH antagonist (degarelix) alone or combined with bicalutamide or trastuzumab (antibody against HER2-ERBB2), compared with surgical castration. Flutamide and bicalutamide were administered continuously orally at 50mg/kg daily, degarelix at a dose of 10mg/kg monthly sub-cutaneously, and trastuzumab at a dose of 10 mg/kg weekly by intraperitoneal injection ...
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Six-month flutamide (antiandrogen) administration to lean women with polycystic ovary syndrome (PCOS) will improve impaired glucose tolerance by glucose tolerance testing and normalize the size of enlarged subcutaneous (SC) fat cells by fat biopsy ...
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An autopsy was not performed. The upregulation of these proteins by DHT has been blocked by the androgen receptor blocker hydroxyflutamide (McCrohon et al.
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In this case, a question has been raised about using luteinizing hormone releasing hormone (LHRH) agonists to reduce sexual behavior. LHRH agonists are typically used for the suppression of centrally mediated precocious puberty, defined as puberty occurring before 9 years of age in a male. They are administered via monthly or 3 monthly injections and are also available as a 1 year depot implant. LHRH agonists, such as leuprolide and triptorelin injections, have been used for the court-ordered treatment of adult paraphilia (off-label indication).1,2 Use of leuprolide in an adult autistic male living in a group home was reportedly successful in reducing inappropriate behaviors and allowing him to continue to live in the community.3 Treatment measures, including sexual education and the antiandrogen flutamide, had been ineffective, resulting in temporary police custody for public sexual behaviors toward other people.3 Despite these reports, it is unclear if pubertal suppression for inappropriate ...
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The purpose of this study was to examine the sensitivity of the pubertal assay to an estrogen (Methoxychlor), anti-androgen (Vinclozolin and Flutamide), and a thyroid-active agent (Phenobarbital) in intact juvenile/peripubertal male and female rats. Fifty-five time-mated female (F0) Sprague Dawley Rats were received from Charles River Laboratories and allowed to litter at TherImmune. After weaning on Postnatal Day (PND) 21, 135 F1 males and 135 F1 females were assigned to male and female cohort studies, respectively. The F1 males were dosed with corn oil (0 mg/kg), or the test articles: Phenobarbital (25, 50, and 100 mg/kg/day), Vinclozolin (10, 30, and 100 mg/kg/day), or Flutamide (25 and 50 mg/kg/day), once daily via oral gavage from PND 23-53/54. The F1 females were dosed with corn oil (0 mg/kg), or the test articles: Ethinyl Estradiol (0.0025 and 0.0050 mg/kg/day), Methoxychlor (12.5, 25, and 50 mg/kg/day), or Phenobarbital (25, 50 and 100 mg/kg/day), once daily via oral gavage from PND ...
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In this study we report the development and optimization of poly (D, L-lactide-co-glycolide) (PLGA) polymer encapsulated poorly aqueous soluble nonsteroidal antiandrogen drug bicalutamide, to develop a sustained release formulation for the treatment of prostate cancer.
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The objective of the present study was to examine the effects of neonatal exposure to either agonists or antagonists of androgen and estrogen receptors on the expression of growth and differentiation factor 9 (GDF9) and bone morphogenetic protein 15 (BMP15) and their cognate receptors (TGFBR1, BMPR1B, and BMPR2) in ovarian follicles of adult pigs. Piglets were injected subcutaneously with testosterone propionate (TP, an androgen, at 20 mg/kg bw), flutamide (FLU, an antiandrogen, at 50 mg/kg bw), 4-tert-octylphenol (OP, an estrogenic compound, 100 mg/kg bw), ICI 182,780 (ICI, an antiestrogen, 400 μg/kg bw), or corn oil (control) between postnatal Days 1 and 10 (n = 5/group). Ovarian follicles were excised from adult pigs on Days 8-11 of the estrous cycle. The expression of GDF9, BMP15, TGFBR1, BMPR1B and BMPR2 were examined in the population of preantral and small antral ovarian follicles using real-time PCR, Western blot and immunohistochemistry. In preantral follicles, the upregulation of GDF9 mRNA
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  • Considering drug-induced lipid peroxidation as a possible mediator of drug-induced toxicity and exploiting the free radical scavenging action of antioxidants, the present study was designed to evaluate the antiperoxidative potential of morin on cyclophosphamide/flutamide-induced lipid peroxidation and also to evaluate the effect of morin on cyclophosphamide/flutamide-induced changes in cholesterol content in rabbit blood sample. (semanticscholar.org)
Cases1
  • Cases of flutamide-induced methemoglobinemia ( the phenomenon where erythrocytes have a higher concentration of methemoglobin which is detrimental to the body and can be fatal ), have also been reported. (pharmacybook.net)
Study1
  • The study reveals the lipid peroxidation induction capacity of cyclophosphamide/flutamide and the antiperoxidative potential of morin on cyclophosphamide/flutamide-induced lipid peroxidation. (semanticscholar.org)
250MG4
  • Cytomid 250mg tablet is a contain Flutamide as an active component. (safegenericpharmacy.net)
  • Scheda, indicazioni terapeutiche, posologia.flutamide 250mg cytoplatin-10 20ml cisplatin 10mg cytoplatin-50 cisplatin 50mg cytotam 10. (2p2e.tk)
  • Trova prezzi di flutamide hexal 30cpr 250mg e confronta le offerte di flutamide hexal 30cpr 250mg negli ecommerce italiani sicuri e affidabili.Principio attivo FLUTAMIDE Gruppo terapeutico ANTAGONISTI ORMONALI E SOSTANZE CORRELATE Tipo prodotto FARMACO GENERICO Regime S.S.N. CONCEDIB.ESENTE. (2p2e.tk)
  • does escitalopram hard on your stomach how to shoot up 200 mg seroquel piroxicam 40 mg ampolla 800 mg.Buy Glucophage (Metformin) Online Metformin Glucophage 250 Mg. And flutamide is used for gestational diabetes max dose of metformin for pcos cochrane lactic.flutamide tev*250mg 30cpr bicalutamide tev*50mg 28cpr bicalutamide hik*150mg 28cpr a101l02ba nomafen*20mg 20 cpr riv. (2p2e.tk)
Take flutamide12
Effects of flutamide8
TABLETS5
Testosterone16
Order flutamide3
Cheap flutamide1
Dosage6
Spironolactone9
Nonsteroidal antiandrogen4
Capsule4
Metastatic prostate cancer2
Acne8
  • Flutamide has been researched and used extensively in the treatment of androgen-dependent skin and hair conditions in women including acne, seborrhea, hirsutism, and scalp hair loss, as well as in hyperandrogenism (e.g., in polycystic ovary syndrome or congenital adrenal hyperplasia), and is effective in improving the symptoms of these conditions. (wikipedia.org)
  • Oral flutamide is used in women to treat hirsutism (excess body hair) and acne and in men to treat prostate cancer. (greyhairloss.com)
  • São Paulo, Brazil - Contrary to foregoing reports of significantside effects and high cost, Denise Steiner, M.D., Ph.D., contends that theanti-androgen drug flutamide 250 mg (Euflex, Euflexin) is a safe and effectivetherapy for treating female acne and androgenetic alopecia with an overallpositive relation of cost to benefit. (dermatologytimes.com)
  • Flutamide hepatotoxicity: our experience over 176 patients.pleural and can claim any signs of Vitamin C M where to buy acne aid soap LE AW Tel The anti HIV infected with a patient becomes pregnant I. After taking flutamide. (akm-freiburg.tk)
  • Acne, Flutamide: Solicitud del.PCOS: PolyCystic Ovary Syndrome By Kimberly Dovin, PGY3 Swedish Family Medicine January 13, 2003 or PCOS: A Disorder for the Generalist PCOS: Goals Identify patients. (lsrfinancial.ga)
  • Se ha estimado que el PCOS afecta de 5 a 10% de las mujeres en este grupo de edad.Flutamide is a non-steroidal anti-androgenic drug, commonly used in the treatment of advanced prostate cancer, acne and hirsutism. (lsrfinancial.ga)
  • Looking for work http://www.stichting-tabitha.com/index.php/acne-gel.pptx cognomen duac acne gel price rudely Chinese emperors embraced Confucianism for centuries,.Una de las herramientas más valiosas a disposición de los urólogos es la sonda foley, denominada así en honor del inventor, un médico norteamericano, Federico Foley. (access2emma.tk)
  • like acne, psoriasis.Estos incluyen el flutamide que bloquea los receptores de andrógenos y finasteride que bloquea la conversión de la testosterona a andrógenos más activos. (access2emma.tk)
Antiandrogen drug2
Floo1
TABLET1
LHRH3
Antiandrogens6
Luteinizing hormone1
Active metabolite1
Oral4
Interactions2
20171
  • In our hospital, 55 patients were diagnosed with CRPC after CAB therapy and administered flutamide or enzalutamide between May 2014 and December 2017. (springer.com)
Response to flutamide2
  • Fujikawa K, Matsui Y, Fukuzawa S et al (2000) Prostate-specific antigen levels and clinical response to flutamide as the second hormone therapy for hormone-refractory prostate carcinoma. (springer.com)
  • price generic help determine school lunches response to flutamide Chang who take ordering. (akm-freiburg.tk)
Allergic to flutamide2
  • tell your doctor and pharmacist if you are allergic to flutamide or any other medications. (medlineplus.gov)
  • You should not use this medicine if you are allergic to flutamide. (wellspan.org)
Dose4
Androgens3
Patients26
Pill2
  • He was immediately put on the Lupron shot every 4 month and Flutamide administered by pill daily. (cancer.org)
  • They immediately stopped the Flutamide and put him on one pill of casodex daily in conjunction with the Lupron shot every 4 months. (cancer.org)
20191
  • 2019. https://peds.unboundmedicine.com/pedscentral/view/Davis-Drug-Guide/51327/all/flutamide. (unboundmedicine.com)
Medicines3
Therapeutic1
  • The aims of this study are to introduce nanoformulation of flutamide to increase its aqueous solubility thereby improves the therapeutic efficacy of the chemodrug. (amrita.edu)
Schering2
Leuprolide2
Antiandrogenic2
Flutamide (oral) - WellSpan Health Library
Flutamide (oral) - WellSpan Health Library (wellspan.org)
Contributions of Arylacetamide Deacetylase and Carboxylesterase 2 to Flutamide Hydrolysis in Human Liver | Drug Metabolism &...
Contributions of Arylacetamide Deacetylase and Carboxylesterase 2 to Flutamide Hydrolysis in Human Liver | Drug Metabolism &... (dmd.aspetjournals.org)
Prostate Cancer Medication: Antineoplastics, GnRH Agonist, Antineoplastics, Antiandrogen, Antineoplastics, Antimicrotubular,...
Prostate Cancer Medication: Antineoplastics, GnRH Agonist, Antineoplastics, Antiandrogen, Antineoplastics, Antimicrotubular,... (emedicine.medscape.com)
DailyMed - Search Results for flutamide
DailyMed - Search Results for flutamide (dailymed.nlm.nih.gov)
Flutamide | CancerQuest
Flutamide | CancerQuest (cancerquest.org)
Hirsutism, Excess Hair in Women
Hirsutism, Excess Hair in Women (advancedfertility.com)
Androgens and Acne - ProgressiveHealth.com
Androgens and Acne - ProgressiveHealth.com (progressivehealth.com)
Antiandrogen - Wikipedia
Antiandrogen - Wikipedia (en.wikipedia.org)
Effectiveness of Flutamide in Treating Women With Premenstrual Dysphoric Disorder - Full Text View - ClinicalTrials.gov
Effectiveness of Flutamide in Treating Women With Premenstrual Dysphoric Disorder - Full Text View - ClinicalTrials.gov (clinicaltrials.gov)
Female Androgenetic Alopecia: An Update
Female Androgenetic Alopecia: An Update (medscape.com)
The Pharmacological Causes of Colon Ischemia
The Pharmacological Causes of Colon Ischemia (medscape.com)
Androgen Receptor Regulation of Prostate Cancer Progression and Metastasis | SpringerLink
Androgen Receptor Regulation of Prostate Cancer Progression and Metastasis | SpringerLink (link.springer.com)
Flutamide: MedlinePlus Drug Information
Flutamide: MedlinePlus Drug Information (medlineplus.gov)
Melasma - Wikipedia
Melasma - Wikipedia (en.wikipedia.org)
Portrait of multifaceted transporter, the multidrug resistance-associated protein 1 (MRP1/ABCC1) | SpringerLink
Portrait of multifaceted transporter, the multidrug resistance-associated protein 1 (MRP1/ABCC1) | SpringerLink (link.springer.com)
Hormone therapy for prostate cancer: MedlinePlus Medical Encyclopedia
Hormone therapy for prostate cancer: MedlinePlus Medical Encyclopedia (medlineplus.gov)
The Testosterone-Derived Neurosteroid Androstanediol Is a Positive Allosteric Modulator of GABAA Receptors | Journal of...
The Testosterone-Derived Neurosteroid Androstanediol Is a Positive Allosteric Modulator of GABAA Receptors | Journal of... (jpet.aspetjournals.org)
Prostate Cancer Treatment Options-The Prostate Cancer Research Institute
Prostate Cancer Treatment Options-The Prostate Cancer Research Institute (pcri.org)
Neoadjuvant Androgen Deprivation Therapy in Prostate Cancer: Overview, Androgen Deprivation, Selection of Candidates for NADT
Neoadjuvant Androgen Deprivation Therapy in Prostate Cancer: Overview, Androgen Deprivation, Selection of Candidates for NADT (emedicine.medscape.com)
Cancer: The Problem
Cancer: The Problem (selfgrowth.com)
Polycystic Ovary Syndrome Treatment
Polycystic Ovary Syndrome Treatment (news-medical.net)
Nitrate/Nitrite Toxicity: Clinical Assessment - Evaluation | Environmental Medicine | ATSDR
Nitrate/Nitrite Toxicity: Clinical Assessment - Evaluation | Environmental Medicine | ATSDR (atsdr.cdc.gov)
FDA Approved Drugs in Endocrinology | CenterWatch
FDA Approved Drugs in Endocrinology | CenterWatch (centerwatch.com)