5-alpha Reductase Inhibitors: Drugs that inhibit 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE. They are commonly used to reduce the production of DIHYDROTESTOSTERONE.Azasteroids: Steroidal compounds in which one or more carbon atoms in the steroid ring system have been substituted with nitrogen atoms.Finasteride: An orally active 3-OXO-5-ALPHA-STEROID 4-DEHYDROGENASE inhibitor. It is used as a surgical alternative for treatment of benign PROSTATIC HYPERPLASIA.Urinary Retention: Inability to empty the URINARY BLADDER with voiding (URINATION).Prostatic Hyperplasia: 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.3-Oxo-5-alpha-Steroid 4-Dehydrogenase: An enzyme that catalyzes the reduction of TESTOSTERONE to 5-ALPHA DIHYDROTESTOSTERONE.Cholestenone 5 alpha-Reductase: An oxidoreductase that catalyzes the conversion of 3-oxo-delta4 steroids into their corresponding 5alpha form. It plays an important role in the conversion of TESTOSTERONE into DIHYDROTESTOSTERONE and PROGESTERONE into DIHYDROPROGESTERONE.Hydroxymethylglutaryl-CoA Reductase Inhibitors: Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.Oxidoreductases Acting on CH-CH Group Donors: A subclass of enzymes which includes all dehydrogenases acting on carbon-carbon bonds. This enzyme group includes all the enzymes that introduce double bonds into substrates by direct dehydrogenation of carbon-carbon single bonds.Aldehyde Reductase: An enzyme that catalyzes reversibly the oxidation of an aldose to an alditol. It possesses broad specificity for many aldoses. EC 1.1.1.21.Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).Hydroxymethylglutaryl CoA Reductases: Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.RhodanineHeptanoic Acids: 7-carbon saturated monocarboxylic acids.Ribonucleotide ReductasesImidazolidines: Compounds based on reduced IMIDAZOLINES which contain no double bonds in the ring.Mevalonic AcidNitrate Reductases: Oxidoreductases that are specific for the reduction of NITRATES.Pyrroles: Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.Fatty Acids, Monounsaturated: Fatty acids which are unsaturated in only one position.Sorbitol: A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications.Sugar Alcohol Dehydrogenases: Reversibly catalyzes the oxidation of a hydroxyl group of sugar alcohols to form a keto sugar, aldehyde or lactone. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.; EC 1.1.2. and EC 1.1.99.Glutathione Reductase: Catalyzes the oxidation of GLUTATHIONE to GLUTATHIONE DISULFIDE in the presence of NADP+. Deficiency in the enzyme is associated with HEMOLYTIC ANEMIA. Formerly listed as EC 1.6.4.2.Cytochrome-B(5) Reductase: A FLAVOPROTEIN oxidoreductase that occurs both as a soluble enzyme and a membrane-bound enzyme due to ALTERNATIVE SPLICING of a single mRNA. The soluble form is present mainly in ERYTHROCYTES and is involved in the reduction of METHEMOGLOBIN. The membrane-bound form of the enzyme is found primarily in the ENDOPLASMIC RETICULUM and outer mitochondrial membrane, where it participates in the desaturation of FATTY ACIDS; CHOLESTEROL biosynthesis and drug metabolism. A deficiency in the enzyme can result in METHEMOGLOBINEMIA.Nitrite Reductases: A group of enzymes that oxidize diverse nitrogenous substances to yield nitrite. (Enzyme Nomenclature, 1992) EC 1.FluorobenzenesOxidoreductases: The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)FMN Reductase: An enzyme that utilizes NADH or NADPH to reduce FLAVINS. It is involved in a number of biological processes that require reduced flavin for their functions such as bacterial bioluminescence. Formerly listed as EC 1.6.8.1 and EC 1.5.1.29.Thioredoxin-Disulfide Reductase: A FLAVOPROTEIN enzyme that catalyzes the oxidation of THIOREDOXINS to thioredoxin disulfide in the presence of NADP+. It was formerly listed as EC 1.6.4.5Anticholesteremic Agents: Substances used to lower plasma CHOLESTEROL levels.NADPH-Ferrihemoprotein Reductase: A flavoprotein that catalyzes the reduction of heme-thiolate-dependent monooxygenases and is part of the microsomal hydroxylating system. EC 1.6.2.4.
(1/197) Mutagenicity tests on epristeride in vitro and in vivo.

AIM: To evaluate the genetic effects of epristeride (Epr), a new prospective drug for treating benign prostatic hyperplasia. METHODS: 1) Assaying reverse mutation in histidine nutritional deficiency strain of Salmonella typhimurium 2) detecting chromosome aberrations in Chinese hamster lung cells (CHL); 3) micronucleus assays of mouse bone marrow; 4) counting sperm shape abnormalities 35 d after first ig Epr. RESULTS: 1) The reverse mutation happened at almost the same rate of the negative control. Epr did not induce bacterial mutation. 2) In vitro, the rates of aberration were all below 3%, thus Epr did not induce chromosome damage in CHL. 3) Micronucleated polychromatic erythroblasts (PCE) were not apparently more than those of sovent control, Epr did not induce the formation of micronuclei in PCE. 4) With Epr 818, 682, and 341 mg.kg-1, the head abnormalities of sperms were 5.3% +/- 2.7%, 5.3% +/- 1.9%, and 5.2% +/- 1.2%, respectively. CONCLUSION: No genetic toxicity of Epr was detected.  (+info)

(2/197) Z-350, a novel compound with alpha 1-adrenoceptor antagonistic and steroid 5 alpha-reductase inhibitory actions: pharmacological properties in vivo.

The alpha(1)-adrenoceptor-antagonistic and steroid 5alpha-reductase-inhibitory actions of Z-350 [(S)-4-{3-{4-{1-(4-methylphenyl)-3-[4-(2-methoxyphenyl)piperazine-1-y l]propoxy}benzoyl}indole-1-yl}butyric acid hydrochloride] were investigated in rabbits and rats in vivo. Z-350 (1-30 mg/kg), administered intraduodenally, dose-dependently inhibited phenylephrine-induced increases in prostatic urethral pressure with an ED(50) value of 3.8 mg/kg in anesthetized male rabbits, whereas the effects on mean blood pressure and orthostatic hypotensive response were weaker when compared with other alpha(1)-adrenoceptor antagonists, tamsulosin and prazosin. Z-350 (1-10 mg/kg p.o.) dose-dependently inhibited the prostatic steroid 5alpha-reductase activity in rats with an ED(50) value of 2.8 mg/kg. The daily oral administration of Z-350, at >==10 mg/kg for 7 days, significantly reduced the prostatic growth induced by testosterone in castrated rats, with no effect on dihydrotestosterone-induced prostatic growth. These results indicate that Z-350 exhibited alpha(1)-adrenoceptor-antagonistic and 5alpha-reductase inhibitory actions at almost equal doses in vivo, and was expected to improve the bladder outlet obstruction associated with benign prostatic hyperplasia with smaller cardiovascular adverse effect.  (+info)

(3/197) Evaluation of the EDSTAC female pubertal assay in CD rats using 17beta-estradiol, steroid biosynthesis inhibitors, and a thyroid inhibitor.

The Endocrine Disrupter Screening and Testing Advisory Committee has recommended the female pubertal onset assay as a Tier I test to detect potential endocrine-disrupting chemicals (EDs). We evaluated this assay's ability to detect EDs acting through various mechanisms. In two similar experiments, weanling female rats were dosed for 20 days by gavage with vehicle (0.5% methocel) or the following test compounds (mg/kg/day): 17beta-estradiol (E2; 0.1, 2, or 4), ketoconazole (KETO; 24, 50, or 100), finasteride (FIN; 20), testolactone (TL; 220), fadrozole (FAD; 0.6, 1.2, or 6.0) or 6-propylthiouracil (PTU; 240). In vehicle-treated females, mean age at pubertal onset, as evidenced by vaginal opening (VO), varied interexperimentally from 32.3+/-1.6 days to 33.5+/-1.8 days. At 0.1 mg/kg E2, age at VO was reduced slightly to 31.0+/-1.6 days, but not significantly (alpha=0.05). Higher E2 doses (2.0 and 4.0) reduced age at VO to 28 days. KETO delayed VO, but this delay was significant only at 100 mg/kg (39.7+/-2.4 days). FIN and TL had no effect on age at pubertal onset; however, FAD significantly delayed VO. PTU delayed VO to 34.2+/-1.1 days and altered thyroid weight, histology, and hormone levels. With each compound, significant changes in age at VO were accompanied by decreased uterine or ovarian weights. Thus, although this assay did not detect TL or lower doses of E2 (0.1 mg/kg) or KETO (< or = 50 mg/kg), it was capable of detecting EDs operating through a variety of mechanisms.  (+info)

(4/197) Steroid 5alpha-reductase inhibitory activity and hair regrowth effects of an extract from Boehmeria nipononivea.

The acetone extract of Boehmeria nipononivea showed both potent 5alpha-reductase inhibitory activity and hair regrowth promotion effects on mice. 5alpha-Reductase inhibitory activity-guided fractionation led to six active fatty acids: alpha-linolenic, linoleic, palmitic, elaidic, oleic and stearic acids. The extract of B. nipononivea, and alphalinolenic, elaidic and stearic acids exhibited a hair regrowth effect.  (+info)

(5/197) Anti-tumour effects and pharmacokinetic profile of 17-(5'-isoxazolyl)androsta-4,16-dien-3-one (L-39) in mice: an inhibitor of androgen synthesis.

17-(5'-Isoxazolyl)androsta-4,16-dien-3-one (L-39), a novel androstene derivative, was synthesized and evaluated in vitro and in vivo. L-39 showed potent and non-competitive inhibition of human testicular microsomal 17alpha-hydroxylase/C(17,20)-lyase with an IC50 value of 59 nM and Ki of 22 nM. L-39 also showed potent and competitive inhibition of 5alpha-reductase in human prostatic microsomes with IC50 and Ki values of 33 and 28 nM respectively. L-39 (5 microM) has also been shown to manifest anti-androgenic activity in cultures of human prostate cancer cell lines (LNCaP) by preventing the labelled synthetic androgen R1881 (5 nM) from binding to the androgen receptors. Androgen-dependent human prostate cancer xenografts (PC-82) were grown in nude mice and the effects of L-39 (50 mg kg(-1) day(-1)) on tumour growth and prostate-specific antigen (PSA) levels were determined after 28 days. L-39 significantly (P < 0.01) diminished tumour growth and wet weights to a similar extent as castration or flutamide treatment. L-39 also significantly (P < 0.01) reduced serum PSA levels by more than 80% in the mice bearing human prostate cancer xenografts. Pharmacokinetic studies were also conducted in male Balb/c mice. After subcutaneous administration of a single bolus dose, L-39 was rapidly absorbed into the systemic circulation. Peak plasma levels occurred at 0.75 h and then declined with a t(1/2) of 1.51 h. The bioavailability of L-39 after subcutaneous administration was 28.5%. These results demonstrate that L-39 is a potent inhibitor of androgen synthesis and is effective in reducing the growth of human prostate cancer xenografts in nude mice. Although improvements in the bioavailability are necessary, L-39 is a potential lead compound with this profile as an inhibitor of prostate cancer growth.  (+info)

(6/197) Effects of a new steroidal aromatase inhibitor, TZA-2237, and/or chlormadinone acetate on hormone-induced and spontaneous canine benign prostatic hyperplasia.

OBJECTIVE: It has been known for many years that human benign prostatic hyperplasia (BPH) is composed predominantly of hyperplastic stromal cells rather than epithelial cells. In the present study the effects of a new steroidal aromatase inhibitor on hormone-induced and spontaneous canine BPH were investigated. METHODS: (1) Effects of TZA-2237 on hormone-induced canine BPH. Ten castrated beagles were administered testosterone and androstenedione 6 days/week for 8 months, and divided randomly into three groups after 2 months of treatment as follows. Group I served as controls, Group II was given 0.5 and Group III was given 2.5 mg/kg/day TZA-2237 5 days/week for 6 months. (2) Effects of TZA-2237 on spontaneous canine BPH. Twenty aged beagles with BPH were divided into five groups, Group IV was untreated, Group V was treated with 1 and Group VI with 5mg/kg/day TZA-2237 5 days/week for 31 weeks. Group VII was treated with 5mg/kg/day Atamestane and Group VIII was treated with 0.3 mg/kg/day chlormadinone acetate (CMA) 5 days/week. (3) Effects of TZA-2237 combined with CMA on spontaneous canine BPH. Three aged beagles with BPH were treated with 1mg/kg/day TZA-2237 and 0.03 mg/kg/day CMA 5 days/week for 20 weeks (Group IX) and a further three aged beagles with BPH were treated with 0.3 mg/kg/day CMA alone 5 days/week (Group X). RESULTS: Hormone-induced prostatic growth was significantly suppressed in group III compared with that in other groups. In Group III, the intraprostatic aromatase activity, estradiol level and androgen receptor content decreased significantly in comparison with the values in Group I. The prostatic weights in Groups V, VI and VII increased significantly in comparison with the weight in Group IV. Serum LH and testosterone levels in Groups V, VI, and VII increased significantly in comparison with the level in Group IV. The prostatic weight in Group IX was decreased only slightly, but the smooth muscle component was decreased significantly. CONCLUSIONS: TZA-2237 is a new, unique and effective aromatase inhibitor that causes inhibition of both epithelial and stromal compartments in hormone-induced canine BPH. Dual inhibition of androgen and estrogen resulted in inhibition of smooth muscle growth, and should prove effective as a new method of treatment given the atrophic effects on not only the epithelium but also the stroma in human BPH.  (+info)

(7/197) Increased levels of clusterin (SGP-2) mRNA and protein accompany rat ventral prostate involution following finasteride treatment.

Finasteride is a well-known inhibitor of the prostatic enzyme 5 alpha-reductase type 2 which prevents conversion of testosterone into 5 alpha-dihydrotestosterone, the active intraprostatic androgen, which causes prostate involution through a combination of cell atrophy and cell death. The drug is widely used to improve symptoms of benign prostatic hyperplasia in man. Clusterin, a glycoprotein which is generally up-regulated under conditions inducing cell atrophy or organ involution, is produced at a high level in the regressing rat ventral prostate following androgen ablation. According to several authors, clusterin does not respond to finasteride treatment, suggesting a different action of testosterone and 5 alpha-dihydrotestosterone. We show here that, under our conditions, finasteride was capable of inducing production of both clusterin mRNA and protein in the rat ventral prostate. In fact, by using different and converging techniques, such as Northern hybridization, in situ hybridization histochemistry and immunohistochemistry, we were able to show a strong induction of the clusterin gene in the epithelial cell population of the gland. The response to finasteride, which was similar to that seen with castration, occurred with a delay of a few days. In situ and immunohistochemistry experiments indicated that both orchidectomy and finasteride administration resulted in increased transition of the epithelial cells from the columnar to the cuboidal (atrophic) shape, and this was accompanied by an increased intensity of the signal for clusterin. Thus, it appears that induction of clusterin is part of the molecular process leading to prostate involution caused by either orchidectomy or finasteride administration.  (+info)

(8/197) Antiandrogenic effects of novel androgen synthesis inhibitors on hormone-dependent prostate cancer.

We have found that in addition to being potent inhibitors of 17alpha-hydroxylase/C17,20-lyase and/or 5alpha-reductase, some of our novel androgen synthesis inhibitors also interact with the mutated androgen receptor (AR) expressed in LNCaP prostate cancer cells and the wild-type AR expressed in hormone-dependent prostatic carcinomas. The effects of these compounds on the proliferation of hormone-dependent human prostatic cancer cells were determined in vitro and in vivo. L-2 and L-10 are delta4-3-one-pregnane derivatives. L-35 and L-37 are delta5-3beta-ol-androstane derivatives, and L-36 and L-39 are delta4-3-one-androstane-derived compounds. L-2, L-10, and L-36 (L-36 at low concentrations) stimulated the growth of LNCaP cells, indicating that they were interacting agonistically with the mutated AR expressed in LNCaP cells. L-35, L-37, and L-39 acted as LNCaP AR antagonists. To determine whether the growth modulatory effects of our novel compounds were specific for the mutated LNCaP AR, competitive binding studies were performed with LNCaP cells and PC-3 cells stably transfected with the wild-type AR (designated PC-3AR). Regardless of AR receptor type, all of our novel compounds were effective at preventing binding of the synthetic androgen methyl-trienolone[17alpha-methyl-(3H)-R1881 to both the LNCaP AR and the wildtype AR. L-36, L-37, and L-39 (5.0 microM) prevented binding by >90%, whereas L-35 inhibited binding by 30%. To determine whether the compounds were acting as agonists or antagonists, LNCaP cells and PC-3AR cells were transfected with the pMAMneoLUC reporter gene. When luciferase activity was induced by dihydrotestosterone, all of the compounds were found to be potent inhibitors of transcriptional activity, and the pattern of inhibition was similar for both receptor types. However, L-2, L-10, and L-36 were determined to be AR agonists, and L-35, L-37, and L-39 were wild-type AR antagonists. When tested in vivo, L-39 was the only AR antagonist that proved to be effective at inhibiting the growth of LNCaP prostate tumor growth. L-39 slowed tumor growth rate in LNCaP tumors grown in male SCID mice to the same level as orchidectomy, significantly reduced tumor weights (P < 0.05), significantly lowered serum levels of prostate-specific antigen (P < 0.02), and significanty lowered serum levels of testosterone (P < 0.05). L-39 also proved to be effective when tested against the PC-82 prostate cancer xenograft that expresses wild-type AR. These results show that some of our compounds initially developed to be inhibitors of androgen synthesis also interact with the human AR and modulate the proliferation of hormone-dependent prostatic cancer cells. Therefore, compounds such as L-39, which have multifunctional activities, hold promise for the treatment of androgen-dependent prostate tumors.  (+info)

*  Minamestane
... (INN (former developmental code name FCE-24,928) is a steroidal aromatase inhibitor which was under development by ... Unlike other steroidal aromatase inhibitors such as formestane and exemestane, minamestane does not have androgenic properties ... Combs, Donald W (1995). "Review Oncologic, Endocrine & Metabolic: Recent developments in aromatase inhibitors". Expert Opinion ... June 1994). "Novel aromatase and 5 alpha-reductase inhibitors". The Journal of Steroid Biochemistry and Molecular Biology. 49 ( ...
*  Finasteride
In long-term studies finasteride but not alpha-1 inhibitors reduce the risk of acute urinary retention (−57% at 4 years) and ... Aggarwal S, Thareja S, Verma A, Bhardwaj TR, Kumar M (February 2010). "An overview on 5alpha-reductase inhibitors". Steroids. ... 402-. ISBN 978-0-323-08619-6. Robaire B, Henderson NA (May 2006). "Actions of 5alpha-reductase inhibitors on the epididymis". ... "A new look at the 5alpha-reductase inhibitor finasteride". CNS Drug Reviews. 12 (1): 53-76. doi:10.1111/j.1527-3458.2006.00053. ...
*  Dutasteride
Reductase Inhibitor". Current Topics in Medicinal Chemistry. 6 (5): 405-21. doi:10.2174/156802606776743101. PMID 16719800. ... "An overview on 5alpha-reductase inhibitors". Steroids. 75 (2): 109-53. doi:10.1016/j.steroids.2009.10.005. PMID 19879888. Wu C ... It is a competitive, mechanism-based (irreversible) inhibitor of all three isoforms of 5α-reductase, types I, II, and III (IC50 ... which is similarly an irreversible inhibitor of 5α-reductase but only inhibits the type II and III isoenzymes. As a result of ...
*  Polycystic ovary syndrome
... tumour necrosis factor alpha, and interleukin-1 in modulating progesterone and oestradiol production by human luteinized ... encoding 11β-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase ... 5-alpha reductase inhibitors (such as finasteride and dutasteride) may also be used; they work by blocking the conversion of ... In PCOS, there is a so-called "follicular arrest"; i.e., several follicles develop to a size of 5-7 mm, but not further. No ...
*  Turosteride
Zaccheo T, Giudici D, di Salle E (June 1998). "Effect of early treatment of prostate cancer with the 5alpha-reductase inhibitor ... Turosteride (FCE-26,073) is a selective inhibitor of the enzyme 5α-reductase which was under investigation by GlaxoSmithKline ... Seiffert K, Seltmann H, Fritsch M, Zouboulis CC (February 2007). "Inhibition of 5alpha-reductase activity in SZ95 sebocytes and ... a comparative study of selective inhibitors". The Journal of Steroid Biochemistry and Molecular Biology. 54 (5-6): 273-9. doi: ...
*  Antiandrogen
Flores E, Bratoeff E, Cabeza M, Ramirez E, Quiroz A, Heuze I (May 2003). "Steroid 5alpha-reductase inhibitors". Mini-Reviews in ... Dörsam J, Altwein J (2009). "5alpha-Reductase inhibitor treatment of prostatic diseases: background and practical implications ... Androgen synthesis inhibitors are enzyme inhibitors that prevent the biosynthesis of androgens. This process occurs mainly in ... Examples include the CYP17A1 inhibitors ketoconazole, abiraterone acetate, and seviteronel, the CYP11A1 (P450scc) inhibitor ...
*  Prostatic artery embolization
Reductase Inhibitors Therapy: Persistent Diminished Libido and Erectile Dysfunction and Depression in a Subset of Patients". J ... such as alpha-1 receptor blockers, 5-alpha-reductase inhibitors, or phosphodiesterase-5 enzyme inhibitors.Those with severe/ ... 74 (5): 542-550. CS1 maint: Explicit use of et al. (link) Traish, AM; Hassani, J; Guay, AT; et al. (2011). "Adverse Side ... 40 (5): 655-663. doi:10.1007/s00270-016-1539-3. Assis, AM; Rodrigues, VCP; Yoshinaga, EM; et al. (2015). "Prostatic artery ...
*  FCE-28260
... has been found to inhibit rat and human 5α-reductase with half-maximal inhibitory concentrations (IC50) of 15 and 16 ... FCE-28260 is an azasteroidal 5α-reductase inhibitor which was developed for the treatment of benign prostatic hyperplasia and ... a new 5 alpha-reductase inhibitor: In vitro and in vivo effects". The Journal of Steroid Biochemistry and Molecular Biology. 58 ... 3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide", published 1997-07-09 .. ...
*  Cancer
"Five-alpha-reductase Inhibitors for prostate cancer prevention". The Cochrane Database of Systematic Reviews (2): CD007091. doi ... Aspirin has been found to reduce the risk of death from cancer by about 7%. COX-2 inhibitors may decrease the rate of polyp ... Angiogenesis inhibitors were once incorrectly thought to have potential as a "silver bullet" treatment applicable to many types ... Angiogenesis inhibitors and other cancer therapeutics are used in combination to reduce cancer morbidity and mortality. ...
*  Cancer prevention
"Five-alpha-reductase Inhibitors for prostate cancer prevention". Cochrane Database Syst Rev (2): CD007091. doi:10.1002/14651858 ... Aspirin has been found to reduce the risk of death from cancer by about 7%. COX-2 inhibitor may decrease the rate of polyp ... "Nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors for primary prevention of colorectal cancer: a systematic ... 132 (5): 1740-5. doi:10.1053/j.gastro.2007.03.044. PMID 17484871. Zheng W, Lee SA (2009). "Well-done meat intake, heterocyclic ...
*  MK-386
... selective inhibitor of the human type 1 5alpha-reductase". J. Steroid Biochem. Mol. Biol. 58 (4): 377-84. PMID 8903421. Bentham ... an inhibitor of 5alpha-reductase type 1, reduces dihydrotestosterone concentrations in serum and sebum without affecting ... It is a 4-azasteroid and a potent and selective inhibitor of 5α-reductase type I and shows high selectivity for inhibition of ... 67-. Machetti, Fabrizio; Guarna, Antonio (2005). "Novel inhibitors of 5α-reductase". Expert Opinion on Therapeutic Patents. 12 ...
*  Aqueous humour
5 alpha-dihydrocortisol, an enzyme inhibited by 5-alpha reductase inhibitors, may be involved in production of aqueous humour. ... "5 alpha-dihydrocortisol in human aqueous humour and metabolism of cortisol by human lenses in vitro". Investigative ...
*  Transurethral resection of the prostate
This is done through alpha antagonists such as tamsulosin or 5-alpha-reductase inhibitors such as finasteride and dutasteride. ... 50 (5): 969-79; discussion 980. doi:10.1016/j.eururo.2005.12.042. PMID 16469429. Ö L Özdal, C Özden, K Benli, S Gökkaya, S ... doi:10.1038/sj.pcan.4500818; published online 5 July 2005 pubmed 15999118 http://www.nature.com/pcan/journal/v8/n3/full/ ...
*  Pre-ejaculate
Some individuals do not produce any pre-ejaculate fluid, while others emit as much as 5 ml (0.18 imp fl oz; 0.17 US fl oz). Pre ... 28 (3): 374-5. doi:10.2164/jandrol.107.002576. PMID 17251594. Chughtai B, Sawas A, O'Malley RL, Naik RR, Ali Khan S, Pentyala S ... 28 (3): 374-5. doi:10.2164/jandrol.107.002576. PMID 17251594. "Researchers find no sperm in pre-ejaculate fluid". Contraceptive ... A few case reports have indicated satisfactory results when such individuals are treated with a 5-alpha-reductase inhibitor. ...
*  Hyperplasia
The treatment of hyperplasia would consist upon which; in the case of benign prostate hyperplasia the combination of alpha-1- ... receptor blockers and 5-alpha-reductase inhibitors are effective. List of biological development disorders "Prostate ...
*  5α-Reductase inhibitor
However, it can only decrease circulating DHT levels by about 25 to 54%. Alfatradiol (brand names Ell-Cranell Alpha, Pantostin ... Reductase Inhibitor Finasteride". CNS Drug Reviews. 12 (1): 53-76. doi:10.1111/j.1527-3458.2006.00053.x. PMID 16834758. ... "A new look at the 5alpha-reductase inhibitor finasteride". CNS drug reviews. 12 (1): 53-76. doi:10.1111/j.1527-3458.2006.00053. ... McConnell J. D.; Wilson J. D.; George F. W.; Geller J.; Pappas F.; Stoner E. (1992). "Finasteride, an inhibitor of 5α-reductase ...
*  Urinary retention
BPH may respond to alpha blocker and 5-alpha-reductase inhibitor therapy, or surgically with prostatectomy or transurethral ... 2010-02-10 Fisher, Euan; Subramonian, Kesavapillai; Omar, Muhammad Imran (2014-06-10). "The role of alpha blockers prior to ... Medications: Anticholinergics and medications with anticholinergic properties, alpha-adrenergic agonists, opiates, nonsteroidal ... resection of the prostate (TURP). Use of alpha-blockers can provide relief of urinary retention following de-catheterization ...
*  Frontal fibrosing alopecia
2012;67(5):955-61. Banka N, Mubki T, Bunagan MJ, Mcelwee K, Shapiro J. Frontal fibrosing alopecia: a retrospective clinical ... 5-alpha-reductase inhibitors. In one study, the use of anti-androgens (finasteride or dutasteride) was associated with ...
*  Pygeum (herbal remedy)
... alpha-adrenergic blockers or 5-alpha reductase inhibitors), surgical approaches, or other herbs/supplements such as saw ...
*  Late-onset hypogonadism
The epidemiology is not clear; 20% of men in their 60s and 30% of men in their 70s have low testosterone; around 5% of men ... link) Basaria, S (5 April 2014). "Male hypogonadism". Lancet. 383 (9924): 1250-63. doi:10.1016/s0140-6736(13)61126-5. PMID ... Retrieved 5 March 2015. . NEJM Perspective piece: Nguyen, CP; et al. (20 August 2015). "Testosterone and "Age-Related ... 5 (5): 190-200. doi:10.1177/2042098614548680. PMC 4212439 . PMID 25360240 - via PubMed Central. Gabrielsen, JS; Najari, BB; ...
*  Intraoperative floppy iris syndrome
Various alpha-blockers are associated with IFIS, but tamsulosin has a stronger association than the others. A joint statement ... American Society of Cataract and Refractive Surgery; American Academy of Ophthalmology (2014), Alpha-Blocker Patient Advisory: ... Tamsulosin is a selective alpha blocker that works by relaxing the bladder and prostatic smooth muscle. As such, it also ... 51 (5): 501-512. doi:10.1016/j.survophthal.2006.06.011. PMID 16950249. Pärssinen, O.; Leppänen, E.; Keski-Rahkonen, P.; ...
*  Tamsulosin
When alpha 1 receptors in the bladder neck and the prostate are blocked, this causes a relaxation in smooth muscle and ... Tamsulosin, and other medications in the class called alpha blockers, work by relaxing bladder neck muscles and muscle fibers ... Selective action of tamsulosin in alpha 1A/D receptors is controversial and over three quarters of tamsulosin registered human ... In a retrospective analysis of 388 patients with HF and benign prostatic hypertrophy receiving alpha blockers, including ...
*  Androgen replacement therapy
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"Five-alpha-reductase Inhibitors for prostate cancer prevention". Cochrane Database Syst Rev (2): CD007091. doi:10.1002/14651858 ... Also in trials for CRPC are : checkpoint inhibitor ipilimumab, CYP17 inhibitor galeterone (TOK-001), and immunotherapy PROSTVAC ... X-linked inhibitor of apoptosis (XIAP) is hypothesized to promote prostate cancer cell survival and growth and is a target of ... Watanabe SI, Miyata Y, Kanda S, Iwata T, Hayashi T, Kanetake H, Sakai H (November 2009). "Expression of X-linked inhibitor of ...
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Alpha blockers are first-line medications for BPH. Surgical referral is indicated if BPH-related complications develop, medical ... Alpha Blockers. Alpha blockers antagonize alpha1-receptors in the prostatic urethra and bladder neck, resulting in smooth ... the alpha blockers were equally effective.15 Silodosin (Rapaflo) is another alpha blocker with demonstrated effectiveness in ... Adverse effect profiles vary among selective and non-selective alpha blockers (Table 3).2,3,15,19,20,23,24 The AUA recommends ...
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Benign prostatic hyperplasia and prostate J. Sausville, M. Naslund  Benign prostatic hyperplasia and prostate J. Sausville, M. Naslund
... the 5alpha-reductase inhibitor dutasteride gave superior symptom improvement when compared with the alpha blocker tamsulosin. ... Alpha blockers tend to work quickly, usually within a matter of a few days. 5-alpha-reductase inhibitors shrink the ... Alpha blockers relax smooth muscle tone during urination and effectively increase the size of the prostatic lumen to facilitate ... Studies have shown that alpha blockers do not alter the risk of urinary retention or the need for prostate surgery, but 5-alpha ...
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BPH - Benign Prostatic Hyperplasia- Health911.com - BPH, Benign Prostatic Hyperplasia, BPH Treatment, Cause of PPH, BPH...  BPH - Benign Prostatic Hyperplasia- Health911.com - BPH, Benign Prostatic Hyperplasia, BPH Treatment, Cause of PPH, BPH...
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Urinary retention  Urinary retention
BPH may respond to alpha blocker and 5-alpha-reductase inhibitor therapy, or surgically with prostatectomy or transurethral ... Medications (including anticholinergics, antidepressants, COX-2 inhibitors, amphetamines, and opioids). Diagnosis and treatment ... Zeif HJ, Subramonian K (2009). "Alpha blockers prior to removal of a catheter for acute urinary retention in adult men". ... 5-alpha-reductase inhibitor increase the chance of normal urination following catheter removal.[3] In case, if catheter can't ...
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Alpha-a drenergic Antagonists: In a single-sequence, crossover trial in healthy volunteers, the administration of tamsulosin or ... Dutasteride is a synthetic 4-azasteroid compound that is a selective inhibitor of both the type 1 and type 2 isoforms of ... Finasteride is a competitive and specific inhibitor of Type II 5α-reductase with which it slowly forms a stable enzyme complex ... angiotensin-converting ACE inhibitors, beta-adrenergic blocking agents, calcium channel blockers, corticosteroids, diuretics, ...
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Dutasteride for hair loss : Updated for 2010 - HairLossLibrary.com  Dutasteride for hair loss : Updated for 2010 - HairLossLibrary.com
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Sale Dutasteride - Dutasteride Aurogra Pharma - Dutasteride Mail Order Visa Usa  Sale Dutasteride - Dutasteride Aurogra Pharma - Dutasteride Mail Order Visa Usa
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  • 5-ARIs are sometimes used as antiandrogens in feminizing hormone therapy for transgender women to help reduce body hair growth and scalp hair loss. (wikipedia.org)
  • The dominant route of DHT synthesis in human CRPC bypasses testosterone, and instead requires 5α-reduction of androstenedione by SRD5A1 to 5α-androstanedione, which is then converted to DHT fuelling cancer growth. (wikipedia.org)
  • The following study is underway to learn more about the relationship between 5-alpha-reductase inhibitors and erectile dysfunction, other sexual dysfunction (ejaculatory and psychosexual dysfunction, low libido, Peyronie's disease), breast outcomes, and depression. (nih.gov)
  • Erectile dysfunction, or ED (the inability to achieve a full erection), occurs in 5 to 8 percent of men, decreased libido (sex drive) in 3 to 6 percent, reduced ejaculate in 1 percent, and breast enlargement or tenderness in 0.5 percent. (healthcommunities.com)
  • Saw palmetto is probably the most well-known and also controversial 5 alpha reductase inhibitor, due to the variation in results and side effects associated with high oral dosages. (syromonoed.com)
  • An extract of Serenoa repens , also known as saw palmetto extract , is a 5-ARI that is sold as an over-the-counter dietary supplement . (wikipedia.org)
  • 5\alpha -substrate}+NADP+}}} 5α-DHP is a major hormone in circulation of normal cycling and pregnant women. (wikipedia.org)
  • Five-alpha Reductase Inhibitors have been investigated predominantly for their effects on BPH associated lower urinary tract symptoms (LUTS) and for the treatment of AGA on account of abundant 5ARI activities in the prostate and skin. (scielo.br)
  • As a result, daily use of an alpha-blocker may increase urinary flow and relieve urinary frequency, urinary urgency, and frequent nighttime urination. (healthcommunities.com)
  • In long-term studies finasteride but not alpha-1 inhibitors reduce the risk of acute urinary retention (−57% at 4 years) and the need for surgery (−54% at 4 years). (wikipedia.org)
  • 5-ARIs are clinically used in the treatment of conditions that are exacerbated by DHT: Mild-to-moderate benign prostatic hyperplasia and lower urinary tract symptoms Pattern hair loss in both men and women 5-ARIs can be used in the treatment of hirsutism in women. (wikipedia.org)
  • When alpha 1 receptors in the bladder neck and the prostate are blocked, this causes a relaxation in smooth muscle and therefore less resistance to urinary flow. (wikipedia.org)