Steroidal compounds in which one or more carbon atoms in the steroid ring system have been substituted with nitrogen atoms.
The transference of a part of or an entire liver from one human or animal to another.
The transference of a kidney from one human or animal to another.
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Severe inability of the LIVER to perform its normal metabolic functions, as evidenced by severe JAUNDICE and abnormal serum levels of AMMONIA; BILIRUBIN; ALKALINE PHOSPHATASE; ASPARTATE AMINOTRANSFERASE; LACTATE DEHYDROGENASES; and albumin/globulin ratio. (Blakiston's Gould Medical Dictionary, 4th ed)
The survival of a graft in a host, the factors responsible for the survival and the changes occurring within the graft during growth in the host.
Surgical treatments used to change the physiological sexual characteristics of an individual.
Severe gender dysphoria, coupled with a persistent desire for the physical characteristics and social roles that connote the opposite biological sex. (APA, DSM-IV, 1994)
A surgical specialty concerned with the study, diagnosis, and treatment of diseases of the urinary tract in both sexes, and the genital tract in the male. Common urological problems include urinary obstruction, URINARY INCONTINENCE, infections, and UROGENITAL NEOPLASMS.
A scientific or medical discipline concerning the study of male reproductive biology, diseases of the male genital organs, and male infertility. Major areas of interest include ENDOCRINOLOGY; SPERMATOGENESIS; semen analysis; FERTILIZATION; CONTRACEPTION; and CRYOPRESERVATION.
Individual's rights to obtain and use information collected or generated by others.
Tumors or cancer of the URINARY TRACT in either the male or the female.
A publication issued at stated, more or less regular, intervals.
A bis-quaternary steroid that is a competitive nicotinic antagonist. As a neuromuscular blocking agent it is more potent than CURARE but has less effect on the circulatory system and on histamine release.
Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc.
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)
A heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358)
Pregnane derivatives containing three double bonds in the ring structures.
Monoquaternary homolog of PANCURONIUM. A non-depolarizing neuromuscular blocking agent with shorter duration of action than pancuronium. Its lack of significant cardiovascular effects and lack of dependence on good kidney function for elimination as well as its short duration of action and easy reversibility provide advantages over, or alternatives to, other established neuromuscular blocking agents.
A procedure involving placement of a tube into the trachea through the mouth or nose in order to provide a patient with oxygen and anesthesia.
Absence of hair from areas where it is normally present.
Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.
A potent direct-acting peripheral vasodilator (VASODILATOR AGENTS) that reduces peripheral resistance and produces a fall in BLOOD PRESSURE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371)
The outer covering of the calvaria. It is composed of several layers: SKIN; subcutaneous connective tissue; the occipitofrontal muscle which includes the tendinous galea aponeurotica; loose connective tissue; and the pericranium (the PERIOSTEUM of the SKULL).
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)
Exclusive legal rights or privileges applied to inventions, plants, etc.
Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc.
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.
Tumors or cancer of the PROSTATE.
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.
Sequential operating programs and data which instruct the functioning of a digital computer.
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.
A cell line derived from cultured tumor cells.
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.
An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.
Tumors or cancer of the UROGENITAL SYSTEM in either the male or the female.
Drugs that inhibit 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE. They are commonly used to reduce the production of DIHYDROTESTOSTERONE.
Computerized compilations of information units (text, sound, graphics, and/or video) interconnected by logical nonlinear linkages that enable users to follow optimal paths through the material and also the systems used to create and display this information. (From Thesaurus of ERIC Descriptors, 1994)
A state of harmony between internal needs and external demands and the processes used in achieving this condition. (From APA Thesaurus of Psychological Index Terms, 8th ed)

The pharmacokinetic modelling of GI198745 (dutasteride), a compound with parallel linear and nonlinear elimination. (1/97)

AIMS: To characterize the pharmacokinetics of the dual 5alpha-reductase inhibitor GI198745 (dutasteride) to allow for more accurate predictions of GI198745 concentrations after different dosing schedules. METHODS: In this randomized, single-blind, parallel group study, 32 healthy male volunteers received single oral doses of GI198745 ranging from 0.01 to 40 mg. Data were analysed by nonlinear mixed effects modelling using NONMEM where both linear and nonlinear pharmacokinetic models were examined. RESULTS: The time course of GI198745 serum concentrations indicated concentration dependent elimination, with the apparent half-life increasing with dose. Data were best described by a two-compartment model with first order absorption and parallel linear and nonlinear elimination pathways. Drug absorption was rapid, and was followed by a short distribution phase. A high volume of distribution (511 l) and a low linear clearance (0.58 l h(-1)) combined to give a half-life of up to 5 (1-7) weeks at high concentrations. As concentrations declined towards Km (0.96 ng ml(-1)), the proportion eliminated by the relatively rapid saturable elimination pathway, with a maximum clearance of 6.2 l h(-1), increased and the half-life reduced to about 3 days. The estimated inter individual variability for the linear clearance was high (CV = 70%). CONCLUSIONS: G1198745 pharmacokinetics are well described by a pharmacokinetic model with parallel linear and nonlinear elimination. Simulations using this model show that at daily doses of 0.1 mg the steady state drug concentrations, and the rate at which these are achieved, are mainly influenced by the nonlinear pathway, while at daily doses above 1 mg they are almost entirely influenced by the linear pathway.  (+info)

Evaluation and characterization of micronuclei induced by the antitumour agent ASE [3beta-hydroxy-13alpha-amino-13, 17-seco-5alpha-androstan-17-oic-13, 17-lactam-p-bis(2-chloroethyl)amino phenylacetate] in human lymphocyte cultures. (2/97)

3beta - Hydroxy - 13alpha - amino - 13, 17 - seco - 5alpha - androstan - 17 -oic-13,17-lactam-p-bis(2-chloroethyl)amino phenylacetate (ASE) is a homo-aza-steroidal ester of p-bis(2-chloroethyl) amino phenyl acetic acid and has been shown to display antineoplastic, mutagenic and genotoxic activity. In the present study an effort has been made to evaluate the ability of ASE to induce micronuclei (MN) in human lymphocytes treated in vitro using the cytokinesis-block assay. Lympocytes were treated with different concentrations of ASE (0.1, 0.25, 0.5, 1, 2.5, 5, 10 and 20 microg/ml) at two different cell culture times, 21 and 41 h after culture initiation. ASE treatment lasted until cell harvest, for 51 and 31 h, respectively. Two types of cultures were used, whole blood and isolated lymphocyte cultures. The content of induced MN was identified by FISH analysis, using an alpha-satellite DNA probe, in binucleate cells. Our results suggest that ASE is capable of increasing MN frequencies in human lymphocytes under both culture conditions. This increase is related to the concentration in a linear dose-dependent manner and is also dependent on the duration of treatment. FISH analysis has shown that the induced MN resulted mainly from breakage events. Additionally, a weak aneugenic effect was found at the higher concentrations in whole blood cultures as well as in isolated lymphocyte cultures. Cytotoxic effects of ASE were observed under both cell culture conditions with a linear dose-dependent relationship according to CBPI evaluation and were more pronounced in isolated lymphocyte cultures.  (+info)

Linear relationships between the ligand binding energy and the activation energy of time-dependent inhibition of steroid 5alpha-reductase by delta 1-4-azasteroids. (3/97)

The inhibition of steroid 5alpha-reductase (5AR) by Delta(1)-4-azasteroids is characterized by a two-step time-dependent kinetic mechanism where inhibitor combines with enzyme in a fast equilibrium, defined by the inhibition constant K(i), to form an initial reversible enzyme-inhibitor complex, which subsequently undergoes a time-dependent chemical rearrangement, defined by the rate constant k(3), leading to the formation of an apparently irreversible, tight-binding enzyme-inhibitor complex (Tian, G., Mook, R. A., Jr., Moss, M. L., and Frye, S. V. (1995) Biochemistry 34, 13453-13459). A detailed kinetic analysis of this process with a series of Delta(1)-4-azasteroids having different C-17 substituents was performed to understand the relationships between the rate of time-dependent inhibition and the affinity of the time-dependent inhibitors for the enzyme. A linear correlation was observed between ln(1/K(i)), which is proportional to the ligand binding energy for the formation of the enzyme-inhibitor complex, and ln(1/(k(3)/K(i))), which is proportional to the activation energy for the inhibition reaction under the second order reaction condition, which leads to the formation of the irreversible, tight-binding enzyme-inhibitor complex. The coefficient of the correlation was -0.88 +/- 0.07 for type 1 5AR and -1.0 +/- 0.2 for type 2 5AR. In comparison, there was no obvious correlation between ln(1/K(i)) and ln(1/k(3)), which is proportional to the activation energy of the second, time-dependent step of the inhibition reaction. These data are consistent with a model where ligand binding energies provided at C-17 of Delta(1)-4-azasteroids is fully expressed to lower the activation energy of k(3)/K(i) with little perturbation of the energy barrier of the second, time-dependent step.  (+info)

Mass spectral fragmentation reactions of a therapeutic 4-azasteroid and related compounds. (4/97)

Mass spectra were acquired for a therapeutic 4-azasteroid (dutasteride), and some related compounds, using various ionization conditions (EI, CI, APCI and ESI) in both positive and negative ion modes. The ionization and fragmentation behavior of the compound dutasteride, its precursors and several analogs is reported. Positive atmospheric pressure chemical ionization (APCI+) and positive electrospray ionization (ESI+) produced distinctive collision-induced dissociation (CID) spectra for the respective [MH]+ ions of dutasteride. The spectral differences are attributed to ion populations having either different structures or different internal energy distributions (as a consequence of the method of ionization). Irrespective of their origin, the protonated molecules undergo interesting fragmentation reactions when collisionally activated. The identity of the major fragmentation products was confirmed by accurate mass measurement. The negative APCI mass spectrum of dutasteride displays extensive dehydrohalogenation, apparently due to the thermal component of the APCI process. Some of the resulting radical anions display remarkable stability toward collisional decomposition. Details of the fragmentation behavior for the negative ion species and their relationship to the positive ion results are discussed.  (+info)

Proteomic changes during disturbance of cholesterol metabolism by azacoprostane treatment in Caenorhabditis elegans. (5/97)

Although nematodes like Caenorhabditis elegans are incapable of de novo cholesterol biosynthesis, they can utilize nonfunctional sterols by converting them into cholesterol and other sterols for cellular function. The results reported previously and presented here suggest that blocking of sterol conversion to cholesterol in C. elegans by 25-azacoprostane-HCl (azacoprostane) treatment causes a serious defect in germ cell development, growth, cuticle development, and motility behavior. To establish a biochemical basis for these physiological abnormalities, we performed proteomic analysis of mixed stage worms that had been treated with the drug. Our results from a differential display proteomic analysis revealed significant decreases in the levels of proteins involved in collagen and cytoskeleton organization such as protein disulfide isomerase (6.7-fold), beta-tubulin (5.41-fold), and NEX-1 protein (>30-fold). Also reduced were enzymes involved in energy production such as phosphoglycerate kinase (4.8-fold) and phosphoenolpyruvate carboxykinase (8.5-fold), a target for antifilarial drugs such as azacoprostane. In particular, reductions in the expression of lipoprotein families such as vitellogenin-2 (7.7-fold) and vitellogenin-6 (5.4-fold) were prominent in the drug-treated worms, indicating that sterol metabolism disturbance caused by azacoprostane treatment is tightly coupled with suppression of the lipid transfer-related proteins at the protein level. However, competitive quantitative reverse transcriptase polymerase chain reaction showed that the transcriptional levels of vit-2, vit-6, and their receptors (e.g. rme-2 and lrp-1) in drug-treated worms were 3- to 5-fold higher than those in the untreated group, suggesting a presence of a sterol regulatory element-binding protein (SREBP)-like pathway in these genes. In fact, multiple predicted sterol regulatory elements or related regulatory sequences responding to sterols were found to be located at the 5'-flanking regions in vit-2 and lrp-1 genes, and their transcriptional activities fluctuated highly in response to changes in sterol concentration. Thus, many physiological abnormalities caused by azacoprostane-mediated sterol metabolism disturbance appear to be exerted at least in part through SREBP pathway in C. elegans.  (+info)

Four-amino acid segment in steroid 5 alpha-reductase 1 confers sensitivity to finasteride, a competitive inhibitor. (6/97)

The 4-azasteroid 17 beta-(N-t-butyl)carbamoyl-4-aza-5 alpha-androst-1-en-3-one (finasteride) is 100-fold more potent as a competitive inhibitor of the rat NADPH:delta 4-3-oxosteroid-5-alpha- oxidoreductase (steroid 5 alpha-reductase) type 1 enzyme (Ki = 3-5 nM) than of the human type 1 enzyme (Ki greater than or equal to 300 nM). In this study, we exploit this differential sensitivity to map a major determinant of finasteride sensitivity in steroid 5 alpha-reductase. Chimeric steroid 5 alpha-reductase cDNAs composed of different combinations of rat and human exon sequences were created by genetic engineering, expressed in human embryonic kidney 293 cells, and assayed for their sensitivity to finasteride. Hybrid proteins containing sequences encoded by rat exon 1 were found to be as sensitive to finasteride as the parental enzyme. The exchange of progressively smaller protein segments encoded within exon 1 identified a tetrapeptide sequence (Val-Ser-Ile-Val) in the rat enzyme that conferred sensitivity to finasteride. The analogous sequence in the human enzyme (Ala-Val-Phe-Ala) conferred partial resistance to the drug. Finasteride was a competitive inhibitor of the native and all chimeric enzymes tested, suggesting that the tetrapeptide segments form a portion of the substrate-binding domain of steroid 5 alpha-reductase.  (+info)

Laboratory monitoring of androgenic activity in benign prostate hypertrophy treated with a 5 alpha-reductase inhibitor. (7/97)

Testosterone and androstenedione are metabolized by 5 alpha- and 5 beta-reductases to androsterone (A) and etiocholanolone (E), respectively. These are excreted in the urine as conjugates, and the A/E ratio in normal men is usually greater than or equal to 1.5 (as opposed to 1 in women) because of the high 5 alpha-reductase activity in the prostate. The A/E ratio can be determined simply by gas chromatography after acid hydrolysis of a urine sample, extraction of steroids, and formation of trimethylsilyl derivatives. A timed collection of urine is unnecessary because the ratio of A/E is used rather than absolute values. In men suffering from benign prostate hypertrophy who are treated with Finasteride (a 5 alpha-reductase inhibitor), the A/E ratio decreases to less than 0.5. The A/E ratio decrease can be detected long before there is clinical improvement.  (+info)

The effect of finasteride in men with benign prostatic hyperplasia. The Finasteride Study Group. (8/97)

BACKGROUND: Benign prostatic hyperplasia is a progressive, androgen-dependent disease resulting in enlargement of the prostate gland and urinary obstruction. Preventing the conversion of testosterone to its tissue-active form, dihydrotestosterone, by inhibiting the enzyme 5 alpha-reductase could decrease the action of androgens in their target tissues; in the prostate the result might be a decrease in prostatic hyperplasia and therefore in symptoms of urinary obstruction. METHODS: In a double-blind study, we evaluated the effect of two doses of finasteride (1 mg and 5 mg) and placebo, each given once daily for 12 months, in 895 men with prostatic hyperplasia. Urinary symptoms, urinary flow, prostatic volume, and serum concentrations of dihydrotestosterone and prostate-specific antigen were determined periodically during the treatment period. RESULTS: As compared with the men in the placebo group, the men treated with 5 mg of finasteride per day had a significant decrease in total urinary-symptom scores (P less than 0.001), an increase of 1.6 ml per second (22 percent, P less than 0.001) in the maximal urinary-flow rate, and a 19 percent decrease in prostatic volume (P less than 0.001). The men treated with 1 mg of finasteride per day did not have a significant decrease in total urinary-symptom scores, but had an increase of 1.4 ml per second (23 percent) in the maximal urinary-flow rate, and an 18 percent decrease in prostatic volume. The men given placebo had no changes in total urinary-symptom scores, an increase of 0.2 ml per second (8 percent) in the maximal urinary-flow rate, and a 3 percent decrease in prostatic volume. The frequency of adverse effects in the three groups was similar, except for a higher incidence of decreased libido, impotence, and ejaculatory disorders in the finasteride-treated groups. CONCLUSIONS: The treatment of benign prostatic hyperplasia with 5 mg of finasteride per day results in a significant decrease in symptoms of obstruction, an increase in urinary flow, and a decrease in prostatic volume, but at a slightly increased risk of sexual dysfunction.  (+info)

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Treating symptoms of benign prostatic hyperplasia (BPH) in men who have an enlarged prostate gland. Dutasteride/tamsulosin is a 5 alpha-reductase inhibitor and alpha-blocker combination. The 5 alpha-reductase inhibitor (dutasteride) works by lowering levels of a hormone called dihydrotestosterone (DHT), which is a major cause of prostate growth. The alpha-blocker (tamsulosin) works by relaxing muscles in the prostate and bladder. Dutasteride/tamsulosin helps to decrease the size of the prostate and reduce symptoms of BPH.. Genérico Jalyn (Dutasteride + Tamsulosin 0.5mg + 0.4mg) € 3.03 comprimido -Salud Masculina @ Mydiscountpills.com: Fildena|Cenforce|Vidalista|Tadalista-UPD:2020. Cheap price on popular Indian brand names such as: Fildena, Cenforce, Vidalista, Tadalista and more! Full satisfaction of all Your desires :)
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Absorption: Following administration of a single 0.5 mg dose of a soft gelatin capsule, time to peak serum concentrations (T max) of dutasteride occurs within 2 to 3 hours. Absolute bioavailability in 5 healthy subjects is approximately 60% (range: 40% to 94%). When the drug is administered with food, the maximum serum concentrations were reduced by 10% to 15%. This reduction is of no clinical significance. Distribution: Pharmacokinetic data following single and repeat oral doses show that dutasteride has a large volume of distribution (300 to 500 L). Dutasteride is highly bound to plasma albumin (99%) and alpha-1 acid glycoprotein (96.6%). In a trial of healthy subjects (n = 26) receiving dutasteride 0.5 mg/day for 12 months, semen dutasteride concentrations averaged 3.4 ng/mL (range, 0.4 to 14 ng/mL) at 12 months and, similar to serum, achieved steady-state concentrations at 6 months. On average, at 12 months 11.5% of serum dutasteride concentrations partitioned into semen.. Metabolism and ...
Absorption Following administration of a single 0.5-mg dose of a soft gelatin capsule, time to peak serum concentrations (Tmax) of dutasteride occurs within 2 to 3 hours. Absolute bioavailability in 5 healthy subjects is approximately 60% (range: 40% to 94%). When the drug is administered with food, the maximum serum concentrations were reduced by 10% to 15%. This reduction is of no clinical significance.. Distribution Pharmacokinetic data following single and repeat oral doses show that dutasteride has a large volume of distribution (300 to 500 L). Dutasteride is highly bound to plasma albumin (99.0%) and alpha-1 acid glycoprotein (96.6%).. In a trial of healthy subjects (n = 26) receiving dutasteride 0.5 mg/day for 12 months, semen dutasteride concentrations averaged 3.4 ng/mL (range: 0.4 to 14 ng/mL) at 12 months and, similar to serum, achieved steady-state concentrations at 6 months. On average, at 12 months 11.5% of serum dutasteride concentrations partitioned into semen.. Metabolism and ...
Dutasteride can also be prescribed to treat male pattern hair loss although the FDA has not given specific approval that dutasteride can treat male pattern hair loss. When a medication is prescribed for something else than the FDA has allowed for a companys marketing claims, this is known as off-label.. The manufacturer, GlaxoSmithKline, completed a Phase I and II study of dutasteride for hair loss, but suddenly and unexpectedly, called off the trials in 2002 and no one really knows why. However, these trials were restarted in Korea in 2006 and were completed in January of 2009. The results of this study have not been released yet. However, some early speculation is that it does offer a superior hair count in comparison to finasteride. (2,3,). The promise and hope behind dutasteride over finasteride is that it blocks or inhibits BOTH isoforms of 5-alpha reductase, while finasteride only works on one.. Whether or not dutasteride is clinically proven to be more effective than finasteride, remains ...
This study is being done to determine how much certain hormone levels in the prostate decrease when a patient takes dutasteride 0.5mg daily for 3 months prior to TURP. Male patients at least 50 years old willing to take either dutasteride or a placebo (dummy pill) once daily by mouth for 3 months prior to having a surgery to reduce the size of their prostate. During the surgery, very small pieces of the prostate that are removed will be tested to see how much dihydrotestosterone and testosterone (male hormones) are in the tissue ...
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Dutasteride belongs to a class of drugs called 5-alpha-reductase inhibitors, which block the action of the 5-alpha-reductase enzymes that convert testosterone into dihydrotestosterone (DHT). Finasteride also belongs to this group, but while dutasteride inhibits both isoforms of 5-alpha reductase, finasteride inhibits only one. Even so, a clinical study done by GlaxoSmithKline, the EPICS trial, did not find dutasteride to be more effective than finasteride in treating BPH. [Wikipedia]
Buy Dutasteride Online! Dutasteride is used alone or with another medication to treat benign prostatic hyperplasia (BPH; enlargement of the prostate gland). Dutasteride is in a class of medications called 5-alpha reductase inhibitors.
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Dutasteride prevents the conversion of testosterone to dihydrotestosterone (DHT) in the body. DHT is involved in the development of benign prostatic hyperplasia (BPH). Dutasteride is used to treat benign prostatic hyperplasia (BPH) in men with an enlarged prostate. Dutasteride helps improve urinary flow and may also...
Dutasteride is used to treat benign prostatic hyperplasia (BPH) in men with an enlarged prostate. Dutasteride helps improve urinary flow and may also reduce your need for prostate surgery later on. This medicine is for use in men only. Dutasteride may also be used for purposes not listed in this medication guide.
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Sandoz Dutasteride: Dutasteride belongs to a class of medications known as 5-alpha-reductase inhibitors. It is used to relieve symptoms of benign prostatic hyperplasia (BPH) in men with enlarged prostates. BPH is a noncancerous enlargement of the prostate gland that usually occurs in men after the age of 50.
The four-year REDUCE (REduction by DUtasteride of prostate Cancer Events) clinical study evaluated prostate cancer risk reduction in men taking dutasteride, a 5-alpha-reductase inhibitor (5ARI) typically used to treat enlarged prostate. REDUCE results showed that dutasteride decreased the risk of biopsy detectable prostate cancer by 22.8 percent compared to a placebo group, but concerns remained about the drugseffectiveness.
The REDUCE trial was conducted to determine whether dutasteride reduces the risk of incident prostate cancer, as detected on biopsy, among men who are at increased risk for the disease. Dutasteride was compared with placebo for 4 years period. Results showed a relative risk reduction of 22.8 % (95% CI: 15.2 to 29.8)in prostate cancer.. For REDUCE, biopsies were defined as protocol biopsy if performed at certain timeframes, and for cause if outside these predetermined timeframes.. The investigators propose a post hoc analysis that would allow them to include biopsies that really justified a clinical indication, but were excluded from for cause analysis based on occurring at either the 2 or 4 year timeframes.. Thus the investigators propose analysis of both REDUCE groups by every yearly timeframe as:. Group 1--dutasteride group biopsied for cause using several definitions: biopsy of patients who received dutasteride whose PSA rose from nadir as defined in your own protocol,who had a PSA ...
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Dutasteride belongs to a class of drugs called 5α-reductase inhibitors, which block the action of the 5α-reductase enzymes that convert testosterone into DHT.[36] It inhibits all three forms of 5α-reductase, and can decrease DHT levels in the blood by up to 98%.[1][37][38] Specifically it is a competitive, mechanism-based (irreversible) inhibitor of all three isoforms of 5α-reductase, types I, II, and III (IC50 values are 3.9 nM for type I and 1.8 nM for type II).[1][37][39][40] This is in contrast to finasteride, which is similarly an irreversible inhibitor of 5α-reductase[40][41] but only inhibits the type II and III isoenzymes.[37] As a result of this difference, dutasteride is able to achieve a reduction in circulating DHT levels of up to 98%, whereas finasteride is able to achieve a reduction of only 65 to 70%.[38][2][36][42] In spite of the differential reduction in circulating DHT levels, the two drugs decrease levels of DHT to a similar extent of approximately 85 to 90% in the ...
Dutasteride is a prescription drug that works by affecting the male hormone DHT. Although most commonly prescribed for an enlarged prostate, the drug has also shown potential as a hair loss treatment. Learn more about using dutasteride for baldness.
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Dutasteride, along with Finasteride is a 5-alpha-Reductase inhibitor which are a group of drugs with anti-androgenic properties which inhibit the conversion of testosterone into dihydrotestosterone (DHT). This is the same chemical found in Proscar...
Purpose: : This study compared time on therapy prior to discontinuation and risk of discontinuation between Medicare-aged patients and patients of all ages who are new to prostaglandin (PG) therapy. Methods: : Data was derived from the Constella managed care database. Patients 20 years of age or older who initiated therapy with latanoprost (LAT), bimatoprost (BIM), or travoprost (TRA) between 4/01 and 6/02 were included. Patients were required to be continuously enrolled and have no previous PG therapy for the 180 days prior to the index PG fill. Follow-up continued through 6/30/02. Patients were deemed persistent until they discontinued their initial therapy. Age comparison estimates were derived from Kaplan-Meier (for unadjusted medians) and Cox regression (for relative risk of discontinuation adjusted for sex, prior ocular hypotensive therapy and index PG therapy). Results: : 4356 patients met the inclusion criteria (BIM, n=993; LAT, n=2376; TRA, n=987). 74% of patients were 65 years or ...
TY - JOUR. T1 - Modeling and analysis of gleason score 8-10 prostate cancers in the REDUCE study. AU - Andriole, Gerald L.. AU - Bostwick, David G.. AU - Gomella, Leonard G.. AU - Marberger, Michael. AU - Montorsi, Francesco. AU - Tammela, Teuvo L.. AU - Tindall, Donald J.. AU - Fowler, Ivy L.. AU - Garges, Harmony P.. AU - Wilson, Timothy H.. AU - Castro, Ramiro. PY - 2014/8. Y1 - 2014/8. N2 - Objective To explore explanations for the numerical imbalance of biopsy-detected Gleason 8-10 prostate cancers (PCa) diagnosed in years 3-4 in the dutasteride and placebo groups of the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) study. Methods REDUCE was a 4-year, randomized, double-blind, placebo-controlled trial of dutasteride (0.5 mg/d) vs placebo for PCa risk reduction. We modeled the incidence of Gleason 8-10 cancer and used logistic regression analysis to evaluate the effects of baseline predictors of PCa, as well as post-baseline prostate volume at the time of biopsy, on PCa ...
Do not chew, crush, or open a dutasteride capsule. Swallow the capsule whole. Dutas can irritate your lips, mouth, or throat if the capsule has been broken or opened before you swallow it. It may take up to 6 months of using this medicine before your symptoms improve. For best results, keep using the medication as directed. Do not stop taking dutasteride without talking to your doctor.. STORAGE. Store dutasteride at room temperature away from moisture and heat. Dutas capsules may become soft and leaky, or they may stick together if they get too hot. Do not use any capsule that is cracked or leaking. ...
INDICATIONS. Sildalis is a unique medical product which is the innovative breakthrough of the best pharmacists all over the world. This combined remedy is for the treatment of the sexual dysfunction in men. This drug includes the most known active components - Sildenafil and Tadalafil. This combination allows users achieve a powerful and stable erection and at the same time prolongs the sexual act. The medication starts to act in 20 minutes. The time of action is up to 36 hours.. INSTRUCTIONS. Before the beginning of the treatment you should ask your doctor how to take this drug, what dose should be used, how often the tablets may be taken and what recommendations to increase the efficiency of the treatment are. All these recommendations are directed to provide the maximal safety of the treatment and avoid the side effects.. - Sildalis tablets are taken directly before the sexual intercourse with a little of water.. - The drug should be taken minimum 30 minutes before the beginning of the ...
Do not chew, crush, or open a dutasteride capsule. Swallow the capsule whole. Dutas can irritate your lips, mouth, or throat if the capsule has been broken or opened before you swallow it. It may take up to 6 months of using this medicine before your symptoms improve. For best results, keep using the medication as directed. Do not stop taking dutasteride without talking to your doctor.. STORAGE. Store dutasteride at room temperature away from moisture and heat. Dutas capsules may become soft and leaky, or they may stick together if they get too hot. Do not use any capsule that is cracked or leaking. ...
Do not chew, crush, or open a dutasteride capsule. Swallow the capsule whole. Dutas can irritate your lips, mouth, or throat if the capsule has been broken or opened before you swallow it. It may take up to 6 months of using this medicine before your symptoms improve. For best results, keep using the medication as directed. Do not stop taking dutasteride without talking to your doctor.. STORAGE. Store dutasteride at room temperature away from moisture and heat. Dutas capsules may become soft and leaky, or they may stick together if they get too hot. Do not use any capsule that is cracked or leaking. ...
Dutasteride Dutasteride 0.5mg Mens Health Brand(s): Duprost / Veltride Manufacturer: Cipla / Intas Buy Cheap Dutasteride NOW!! use coupon code VPX10 for 10% Discount!! What is this medicine? DUTASTERIDE is used to treat benign prostatic hyperplasia (BPH) in men. This is a condition that causes you to have an enlarged... Continue reading ...
Dutasteride is an oral medication used to treat benign prostatic hyperplasia. Learn who its for, how it works, its side effects, warnings, and more.
Dutasteride - Partly from want of information, and partly to allay the anxiety of the mother, it was my misfortune to make light of the trouble, and even to hold out hopes for a cure.
Generic Name: Dutasteride. Brand Name: Avodart. Manufacturer: GlaxoSmithKline Inc.. Indications: Prostatic hyperplasia, benign. Submission Type: Initial. Project Status: Complete. Date Recommendation Issued: January 20, 2005. Recommendation Type: List in a similar manner to other drugs in class. ...
GlaxoSmithKline (GSK) announced today that it will no longer pursue global approval (marketing authorisation) for the use of Avodart (dutasteride) to reduce the risk of prostate cancer.
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Find patient medical information for Dutasteride Oral on WebMD including its uses, side effects and safety, interactions, pictures, warnings and user ratings.
Consumer Medicine Information (CMI) about Duodart (Dutasteride 500 micrograms and tamsulosin HCl 400 micrograms) intended for persons living in Australia.
Dr. Marc Garnick discusses prostate cancer chemoprevention with the use of the 5 Alpha Reductase inhibitors finasteride and dutasteride.
TY - JOUR. T1 - Combination therapy with dutasteride and tamsulosin in men with moderate-to-severe benign prostatic hyperplasia and prostate enlargement. T2 - the CombAT (Combination of Avodart® and Tamsulosin) trial rationale and study design. AU - Siami, Paul. AU - Roehrborn, Claus. AU - Barkin, Jack. AU - Damiao, Ronaldo. AU - Wyczolkowski, Marek. AU - Duggan, Annette. AU - Major-Walker, Kim. AU - Morrill, Betsy B.. PY - 2007/11. Y1 - 2007/11. N2 - Benign prostatic hyperplasia (BPH) is a highly prevalent condition in aging men, which can be progressive and lead to acute urinary retention (AUR) and the need for surgery. It is commonly treated with α-blockers and 5α-reductase inhibitors (5ARIs), both of which improve the symptoms of BPH. Long-term treatment with 5ARIs can also reduce the risk of developing AUR and the need for surgery. The landmark Medical Therapy of Prostatic Symptoms (MTOPS) trial demonstrated that over 4 years the combination of the type 2-specific 5ARI, finasteride and ...
TY - JOUR. T1 - Phase II study of androgen synthesis inhibition with ketoconazole, hydrocortisone, and dutasteride in asymptomatic castration-resistant prostate cancer. AU - Taplin, Mary Ellen. AU - Regan, Meredith M.. AU - Ko, Yoo Joung. AU - Bubley, Glenn J.. AU - Duggan, Stephen E.. AU - Werner, Lillian. AU - Beer, Tomasz M.. AU - Ryan, Christopher W.. AU - Mathew, Paul. AU - Tu, Shi Ming. AU - Denmeade, Samuel R. AU - Oh, William K.. AU - Sartor, Oliver. AU - Mantzoros, Christos S.. AU - Rittmaster, Roger. AU - Kantoff, Philip W.. AU - Balk, Steven P.. PY - 2009/11/15. Y1 - 2009/11/15. N2 - Purpose: Increasing evidence indicates that enhanced intratumoral androgen synthesis contributes to prostate cancer progression after androgen deprivation therapy. This phase II study was designed to assess responses to blocking multiple steps in androgen synthesis with inhibitors of CYP17A1 (ketoconazole) and type I and II 5α-reductases (dutasteride) in patients with castration-resistant prostate cancer ...
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ABSTRACTIntroductionBenign prostatic hyperplasia (BPH) is a common problem affecting middle-aged and elderly men. First-line medical therapy includes α 1blockers and 5α-reductase inhibitors (5ARIs), such as finasteride and dutasteride. 5ARI use has been associated with adverse sexual outcomes, inclu
Dutasteride, sold under the brand name Avodart among others, is a medication used to treat benign prostatic hyperplasia (enlarged prostate) and androgenetic alopecia (pattern hair loss). It was developed by GlaxoSmithKline and is a 5α-reductase inhibitor which prevents the conversion of the androgen sex hormone testosterone into the more potent dihydrotestosterone (DHT).The drug has been licensed for the treatment of androgenetic alopecia in South Korea since 2009, but has not been approved for this specific indication in the United States,though it is commonly used off-label.
Generic Avodart is used for treating symptoms of benign prostatic hyperplasia (BPH) or enlargement of the prostate gland. It also helps to reduce the risk of urinary blockage and the need for prostate surgery.. Generic Avodart (Dutasteride 0.5mg) $ 1.00 pill - Mens Health @ KupTania.
Anti-androgen can be used in the treatment of benign prostatic hyperplasia, acne, hirsutism, and androgenic alopecia. For the search of anti-androgenic activity through steroid 5-alpha reductase...
RATIONALE: Diagnostic procedures, such as MRI and magnetic resonance spectroscopy imaging, may help in learning how well dutasteride works in patients w
Andriole GL, Bostwick DG, Brawley OW, et al. Effect of dutasteride on the risk of prostate cancer. N Engl J Med. 2010;362(13):1192-1202. PMID: 20357281 www.ncbi.nlm.nih.gov/pubmed/20357281.. Attard G, Parker C, Eeles RA, et al. Prostate cancer. Lancet. 2016;387(10013):70-82. PMID: 26074382 www.ncbi.nlm.nih.gov/pubmed/26074382.. Barocas DA, Mallin K, Graves AJ, et al. Effect of the USPSTF Grade D recommendation against screening for prostate cancer on incident prostate cancer diagnoses in the United States. J Urol. 2015;194(6):1587-1593. PMID: 26087383 www.ncbi.nlm.nih.gov/pubmed/26087383.. Basch E, Loblaw DA, Oliver TK, et al. Systemic therapy in men with metastatic castration-resistant prostate cancer: American Society of Clinical Oncology and cancer care Ontario clinical practice guideline. JClin Oncol. PMID: 25199761 www.ncbi.nlm.nih.gov/pubmed/25199761.. Basch E, Oliver TK, Vickers A, et al. Screening for prostate cancer with prostate-specific antigen testing: American Society of Clinical ...
A comprehensive guide to side effects including common and rare side effects when taking Jalyn (Dutasteride and Tamsulosin Hydrochloride Capsules) includes uses, warnings, and drug interactions.
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Dutasteride was developed and patented for the first time in the United States of America. It was released into mass production in 2001 as part of the drug under the trade name Avodart, which is still used today. In 2015, the term of the patent for a substance ended and it was used in the production of generic drugs.. Increasing the level of the hormone dihydrotestosterone in men leads to uncontrolled proliferation of prostate tissue, followed by possible degeneration of them into a malignant form.. In addition, the increased background of dihydrotestosterone in men is the cause of alopecia (hair loss on the head) and hirsorutism (body hair in women).. Prostate hyperplasia is considered as a precancerous condition of the body, it requires increased attention and corrective therapeutic and sometimes surgical interventions. One of the substances that selectively reduces the level of dihydrotestosterone is Dutasteride.. The substance inhibits the activity of enzymes 5-alpha-reductase of the 1st and ...
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Finasteride is an FDA-approved hair loss drug that works by blocking an enzyme that would otherwise change testosterone to DHT. It has to be taken every day and may take at least three months to take effect. It can have some side effects, including sexual problems, and its worth noting that if a man stops taking finasteride, the hair he grew back will probably be lost.. Finasteride comes as a tablet to take by mouth. It is usually taken once a day with or without food. Take finasteride at around the same time every day. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take finasteride exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.. If you are taking finasteride to treat BPH, you should know that finasteride may control your condition, but will not cure it. It may take at least 6 months before your symptoms improve. Continue to take finasteride even ...
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So i have taken dut twice, once in my early 30s and once more recently 6 years later. I stopped taking it because i was worried about the side effects but to be honest i think alot of it was psychological. Mostly it was the cost as avodart is so damn pricey. The first time i took it i literally grew most of my hair back from nw4, completely filled in and even hairline improvement. You definitely experiance some sides at first, my penis was a cooked noodle for a month but you adjust. It stopped my hairloss dead in its tracks, i mean literally nothing fell out once the initial shed was done. I ended up stopping after about 2 years just because you start to read so much online you become your own worst enemy and end up creating so many fears. I really regret it because once i stopped it didnt take my hairloss long to return and quick. So eventually after a few years of regret i restarted. Now this time while i did have some regrowth, it didnt grow nowhere near as much hair as the last time, which ...
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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 ...
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Before taking finasteride, tell your doctor if you have ever had an allergic reaction to this medication, or to a similar medicine called dutasteride (Avodart). Finasteride should never be taken by a woman or a child. Finasteride can be absorbed through the skin, and women or children should not be permitted to handle finasteride tablets. Although finasteride is not for women, this medication can cause birth defects if a woman is exposed to it during pregnancy. Finasteride tablets should not be handled by a woman who is pregnant or who may become pregnant. If a woman accidentally comes into contact with this medication from a broken or crushed tablet, wash the area with soap and water right away. Call your doctor at once if you notice any breast lumps, pain, nipple discharge, or other breast changes. These may be signs of male breast cancer ...
Before taking finasteride, tell your doctor if you have ever had an allergic reaction to this medication, or to a similar medicine called dutasteride (Avodart). Finasteride should never be taken by a woman or a child. Finasteride can be absorbed through the skin, and women or children should not be permitted to handle finasteride tablets. Although finasteride is not for use by women, this medication can cause birth defects if a woman is exposed to it during pregnancy. Finasteride tablets should not be handled by a woman who is pregnant or who may become pregnant. If a woman accidentally comes into contact with this medication from a broken or crushed tablet, wash the area with soap and water right away. Call your doctor at once if you notice any breast lumps, pain, nipple discharge, or other breast changes. These may be signs of male breast cancer ...
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The overall goal of this research project is to develop Oriental herbal compound 1,2,3,4,6-penta-O-galloyl- beta-D-glucose (PGG) for the chemoprevention of pros...
Investigators say they have found no association between the use of 5-alpha-reductase inhibitors (5ARIs) and the risk of developing high-grade or lethal prostate cancer.
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