度他雄胺
度他雄胺软胶囊fda说明书
HIGHLIGHTS OF PRESCRIBING INFORMATIONThese highlights do not include all the information needed to use AVODART safely and effectively. See full prescribing information for AVODART.AVODART (dutasteride) Soft Gelatin CapsulesInitial U.S. Approval: 2001---------------------------RECENT MAJOR CHANGES--------------------Warnings and Precautions, Evaluation for Other Urological 03/2012 Diseases (5.3)----------------------------INDICATIONS AND USAGE---------------------AVODART is a 5 alpha-reductase inhibitor indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to: (1.1)x improve symptoms,x reduce the risk of acute urinary retention, andx reduce the risk of the need for BPH-related surgery.AVODART in combination with the alpha adrenergic antagonist, tamsulosin, is indicated for the treatment of symptomatic BPH in men with an enlarged prostate. (1.2)Limitations of Use: AVODART is not approved for the prevention of prostate cancer. (1.3)-----------------------DOSAGE AND ADMINISTRATION ----------------Monotherapy: 0.5 mg once daily. (2.1)Combination with tamsulosin: 0.5 mg once daily and tamsulosin 0.4 mg once daily. (2.2)Dosing considerations: Swallow whole. May take with or without food. (2)---------------------DOSAGE FORMS AND STRENGTHS --------------0.5-mg soft gelatin capsules (3)-------------------------------CONTRAINDICATIONS------------------------x Pregnancy and women of childbearing potential. (4, 5.4, 8.1)x Pediatric patients. (4)FULL PRESCRIBING INFORMATION: CONTENTS*1INDICATIONS AND USAGE1.1Monotherapy1.2Combination With Alpha AdrenergicAntagonist1.3Limitations of Use2DOSAGE AND ADMINISTRATION2.1Monotherapy2.2Combination With Alpha AdrenergicAntagonist3DOSAGE FORMS AND STRENGTHS4 CO NTRAINDICATIO NS5WARNINGS AND PRECAUTIONS5.1Effects on Prostate-Specific Antigen (PSA)and the Use of PSA in Prostate CancerDetection5.2Increased Risk of High-Grade Prostate Cancer5.3Evaluation for Other Urological Diseases5.4Exposure of Women—Risk to Male Fetus5.5B lood Donation5.6Effect on Semen Characteristics6ADVERSE REACTIONS6.1Clinical Trials Experience6.2Postmarketing Experience7DRUG INTERACTIONS7.1Cytochrome P450 3A Inhibitors7.2Alpha Adrenergic Antagonists7.3Calcium Channel Antagonists7.4Cholestyramine7.5Digoxin7.6Warfarin x Patients with previously demonstrated, clinically significant hypersensitivity (e.g., serious skin reactions, angioedema) toAVODART or other 5 alpha-reductase inhibitors. (4)-----------------------WARNINGS AND PRECAUTIONS ----------------x AVODART reduces serum prostate-specific antigen (PSA) concentration by approximately 50%. However, any confirmed increase in PSA while on AVODART may signal the presence of prostate cancer and should be evaluated, even if those values are still within the normal range foruntreated men. (5.1)x AVODART may increase the risk of high-grade prostate cancer. (5.2, 6.1) x Prior to initiating treatment with AVODART, consideration should be given to other urological conditions that may cause similar symptoms.(5.3)x Women who are pregnant or could become pregnant should not handle AVODART Capsules due to potential risk to a male fetus. (5.4, 8.1)x Patients should not donate blood until 6 months after their last dose of AVODART. (5.5)------------------------------ADVERSE REACTIONS -----------------------The most common adverse reactions, reported in t1% of subjects treated with AVODART and more commonly than in subjects treated with placebo, are impotence, decreased libido, ejaculation disorders, and breast disorders. (6.1)To report SUSPECTED ADVERSE REACTIONS, contact GlaxoSmithKline at 1-888-825-5249 or FDA at 1-800-FDA-1088 or /medwatch.-------------------------------DRUG INTERACTIONS------------------------Use with caution in patients taking potent, chronic CYP3A4 enzyme inhibitors (e.g., ritonavir). (7)See 17 for PATIENT COUNSELING INFORMATION and FDA-approved patient labeling.Revised: 10/20128USE IN SPECIFIC POPULATIONS8.1Pregnancy8.3Nursing Mothers8.4Pediatric Use8.5Geriatric Use8.6Renal Impairment8.7Hepatic Impairment10OVERDOSAGE11DESCRIPTION12CLINICAL PHARMACOLOGY12.1Mechanism of Action12.2Pharmacodynamics12.3Pharmacokinetics13NONCLINICAL TOXICOLOGY13.1Carcinogenesis, Mutagenesis, Impairment ofFertility13.2Animal Toxicology and/or Pharmacology14CLINICAL STUDIES14.1Monotherapy14.2Combination With Alpha-Blocker Therapy(CombAT)16HOW SUPPLIED/STORAGE AND HANDLING17PATIENT COUNSELING INFORMATION17.1PSA Monitoring17.2Increased Risk of High-Grade Prostate Cancer17.3Exposure of Women—Risk to Male Fetus17.4Blood Donation*Sections or subsections omitted from the full prescribing information are not listed.________________________________________________________________________________ FULL PRESCRIBING INFORMATION1 INDICATIONS AND USAGE1.1MonotherapyAVODART® (dutasteride) Soft Gelatin Capsules are indicated for the treatment ofsymptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to:x improve symptoms,x reduce the risk of acute urinary retention (AUR), andx reduce the risk of the need for BPH-related surgery.1.2Combination With Alpha Adrenergic AntagonistAVODART in combination with the alpha adrenergic antagonist, tamsulosin, is indicated for the treatment of symptomatic BPH in men with an enlarged prostate.1.3Limitations of UseAVODART is not approved for the prevention of prostate cancer.2 DOSAGE AND ADMINISTRATIONThe capsules should be swallowed whole and not chewed or opened, as contact with the capsule contents may result in irritation of the oropharyngeal mucosa. AVODART may beadministered with or without food.2.1MonotherapyThe recommended dose of AVODART is 1 capsule (0.5 mg) taken once daily.2.2Combination With Alpha Adrenergic AntagonistThe recommended dose of AVODART is 1 capsule (0.5 mg) taken once daily and tamsulosin 0.4 mg taken once daily.3 DOSAGE FORMS AND STRENGTHS0.5-mg, opaque, dull yellow, gelatin capsules imprinted with “GX CE2” in red ink on oneside.O NTRAINDICATIO NS4 CAVODART is contraindicated for use in:x Pregnancy. In animal reproduction and developmental toxicity studies, dutasteride inhibited development of male fetus external genitalia. Therefore, AVODART may cause fetal harmwhen administered to a pregnant woman. If AVODART is used during pregnancy or if thepatient becomes pregnant while taking AVODART, the patient should be apprised of thepotential hazard to the fetus [see Warnings and Precautions (5.4), Use in Specific Populations(8.1)].x Women of childbearing potential [see Warnings and Precautions (5.4), Use in Specific Populations (8.1)].x Pediatric patients [see Use in Specific Populations (8.4)].x Patients with previously demonstrated clinically significant hypersensitivity (e.g., serious skin reactions, angioedema) to AVODART or other 5 alpha-reductase inhibitors [see AdverseReactions (6.2)].5 WARNINGS AND PRECAUTIONS5.1Effects on Prostate-Specific Antigen (PSA) and the Use of PSA in Prostate Cancer DetectionIn clinical trials, AVODART reduced serum PSA concentration by approximately 50% within 3 to 6 months of treatment. This decrease was predictable over the entire range of PSA values in subjects with symptomatic BPH, although it may vary in individuals. AVODART may also cause decreases in serum PSA in the presence of prostate cancer. To interpret serial PSAs in men taking AVODART, a new PSA baseline should be established at least 3 months after starting treatment and PSA monitored periodically thereafter. Any confirmed increase from the lowest PSA value while on AVODART may signal the presence of prostate cancer and should be evaluated, even if PSA levels are still within the normal range for men not taking a 5 alpha-reductase inhibitor. Noncompliance with AVODART may also affect PSA test results.To interpret an isolated PSA value in a man treated with AVODART for 3 months or more, the PSA value should be doubled for comparison with normal values in untreated men. The free-to-total PSA ratio (percent free PSA) remains constant, even under the influence of AVODART. If clinicians elect to use percent free PSA as an aid in the detection of prostate cancer in men receiving AVODART, no adjustment to its value appears necessary.Coadministration of dutasteride and tamsulosin resulted in similar changes to serum PSA as dutasteride monotherapy.5.2Increased Risk of High-Grade Prostate CancerIn men aged 50 to 75 years with a prior negative biopsy for prostate cancer and a baseline PSA between 2.5 ng/mL and 10.0 ng/mL taking AVODART in the 4-year Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial, there was an increased incidence of Gleason score 8-10 prostate cancer compared with men taking placebo (AVODART 1.0% versus placebo 0.5%) [see Indications and Usage (1.3), Adverse Reactions (6.1)]. In a 7-yearplacebo-controlled clinical trial with another 5 alpha-reductase inhibitor (finasteride 5 mg, PROSCAR), similar results for Gleason score 8-10 prostate cancer were observed (finasteride 1.8% versus placebo 1.1%).5 alpha-reductase inhibitors may increase the risk of development of high-grade prostate cancer. Whether the effect of 5 alpha-reductase inhibitors to reduce prostate volume or trial-related factors impacted the results of these trials has not been established.5.3Evaluation for Other Urological DiseasesPrior to initiating treatment with AVODART, consideration should be given to other urological conditions that may cause similar symptoms. In addition, BPH and prostate cancer may coexist.5.4Exposure of Women—Risk to Male FetusAVODART Capsules should not be handled by a woman who is pregnant or who could become pregnant. Dutasteride is absorbed through the skin and could result in unintended fetal exposure. If a woman who is pregnant or who could become pregnant comes in contact with leaking dutasteride capsules, the contact area should be washed immediately with soap and water [see Use in Specific Populations (8.1)].5.5Blood DonationMen being treated with AVODART should not donate blood until at least 6 months have passed following their last dose. The purpose of this deferred period is to prevent administration of dutasteride to a pregnant female transfusion recipient.5.6Effect on Semen CharacteristicsThe effects of dutasteride 0.5 mg/day on semen characteristics were evaluated in normal volunteers aged 18 to 52 (n = 27 dutasteride, n = 23 placebo) throughout 52 weeks of treatment and 24 weeks of post-treatment follow-up. At 52 weeks, the mean percent reductions from baseline in total sperm count, semen volume, and sperm motility were 23%, 26%, and 18%, respectively, in the dutasteride group when adjusted for changes from baseline in the placebo group. Sperm concentration and sperm morphology were unaffected. After 24 weeks of follow-up, the mean percent change in total sperm count in the dutasteride group remained 23% lower than baseline. While mean values for all semen parameters at all time-points remained within the normal ranges and did not meet predefined criteria for a clinically significant change (30%), 2 subjects in the dutasteride group had decreases in sperm count of greater than 90% from baseline at 52 weeks, with partial recovery at the 24-week follow-up. The clinical significance of dutasteride’s effect on semen characteristics for an individual patient’s fertility is not known.REACTIO NS6 ADVERSE6.1Clinical Trials ExperienceBecause clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared with rates in the clinical trial of another drug and may not reflect the rates observed in practice.From clinical trials with AVODART as monotherapy or in combination with tamsulosin:x The most common adverse reactions reported in subjects receiving AVODART were impotence, decreased libido, breast disorders (including breast enlargement and tenderness), and ejaculation disorders. The most common adverse reactions reported in subjects receiving combination therapy (AVODART plus tamsulosin) were impotence, decreased libido, breast disorders (including breast enlargement and tenderness), ejaculation disorders, and dizziness.Ejaculation disorders occurred significantly more in subjects receiving combination therapy (11%) compared with those receiving AVODART (2%) or tamsulosin (4%) as monotherapy.x Trial withdrawal due to adverse reactions occurred in 4% of subjects receiving AVODART and 3% of subjects receiving placebo in placebo-controlled trials with AVODART. The mostcommon adverse reaction leading to trial withdrawal was impotence (1%).x In the clinical trial evaluating the combination therapy, trial withdrawal due to adverse reactions occurred in 6% of subjects receiving combination therapy (AVODART plus tamsulosin) and 4% of subjects receiving AVODART or tamsulosin as monotherapy. The most commonadverse reaction in all treatment arms leading to trial withdrawal was erectile dysfunction (1% to 1.5%).Monotherapy: Over 4,300 male subjects with BPH were randomly assigned to receive placebo or 0.5-mg daily doses of AVODART in 3 identical 2-year, placebo-controlled,double-blind, Phase 3 treatment trials, each followed by a 2-year open-label extension. During the double-blind treatment period, 2,167 male subjects were exposed to AVODART, including 1,772 exposed for 1 year and 1,510 exposed for 2 years. When including the open-label extensions,1,009 male subjects were exposed to AVODART for 3 years and 812 were exposed for 4 years. The population was aged 47 to 94 years (mean age: 66 years) and greater than 90% were Caucasian. Table 1 summarizes clinical adverse reactions reported in at least 1% of subjects receiving AVODART and at a higher incidence than subjects receiving placebo.Table 1. Adverse Reactions Reported in t1% of Subjects Over a 24-Month Period andMore Frequently in the Group Receiving AVODART Than the Placebo Group (Randomized, Double-Blind, Placebo-Controlled Trials Pooled) by Time of OnsetAdverse Reaction AVODART (n)Placebo (n)Adverse Reaction Time of OnsetMonths 0-6(n = 2,167)(n = 2,158)Months 7-12(n = 1,901)(n = 1,922)Months 13-18(n = 1,725)(n = 1,714)Months 19-24(n = 1,605)(n = 1,555)Impotence aAVODART Placebo 4.7%1.7%1.4%1.5%1.0%0.5%0.8%0.9%Decreased libido aAVODART Placebo 3.0%1.4%0.7%0.6%0.3%0.2%0.3%0.1%Ejaculation disorders aAVODART Placebo 1.4%0.5%0.5%0.3%0.5%0.1%0.1%0.0%Breast disorders bAVODART Placebo 0.5%0.2%0.8%0.3%1.1%0.3%0.6%0.1%a These sexual adverse reactions are associated with dutasteride treatment (includingmonotherapy and combination with tamsulosin). These adverse reactions may persist after treatment discontinuation. The role of dutasteride in this persistence is unknown.b Includes breast tenderness and breast enlargement.Long-Term Treatment (Up to 4 Years):High-Grade Prostate Cancer: The REDUCE trial was a randomized, double-blind, placebo-controlled trial that enrolled 8,231 men aged 50 to 75 years with a serum PSA of2.5 ng/mL to 10 ng/mL and a negative prostate biopsy within the previous 6 months. Subjects were randomized to receive placebo (N = 4,126) or 0.5-mg daily doses of AVODART (N = 4,105) for up to 4 years. The mean age was 63 years and 91% were Caucasian. Subjects underwent protocol-mandated scheduled prostate biopsies at 2 and 4 years of treatment or had “for-cause biopsies” at non-scheduled times if clinically indicated. There was a higher incidence of Gleason score 8-10 prostate cancer in men receiving AVODART (1.0%) compared with men on placebo (0.5%) [see Indications and Usage (1.3), Warnings and Precautions (5.2)]. In a 7-year placebo-controlled clinical trial with another 5 alpha-reductase inhibitor (finasteride 5 mg, PROSCAR), similar results for Gleason score 8-10 prostate cancer were observed (finasteride 1.8% versus placebo 1.1%).No clinical benefit has been demonstrated in patients with prostate cancer treated with AVODART.Reproductive and Breast Disorders: In the 3 pivotal placebo-controlled BPH trials with AVODART, each 4 years in duration, there was no evidence of increased sexual adverse reactions (impotence, decreased libido, and ejaculation disorder) or breast disorders with increased duration of treatment. Among these 3 trials, there was 1 case of breast cancer in the dutasteride group and1 case in the placebo group. No cases of breast cancer were reported in any treatment group in the 4-year CombAT trial or the 4-year REDUCE trial.The relationship between long-term use of dutasteride and male breast neoplasia is currently unknown.Combination With Alpha-Blocker Therapy (CombAT): Over 4,800 male subjects with BPH were randomly assigned to receive 0.5-mg AVODART, 0.4-mg tamsulosin, or combination therapy (0.5-mg AVODART plus 0.4-mg tamsulosin) administered once daily in a 4-yeardouble-blind trial. Overall, 1,623 subjects received monotherapy with AVODART; 1,611 subjects received monotherapy with tamsulosin; and 1,610 subjects received combination therapy. The population was aged 49 to 88 years (mean age: 66 years) and 88% were Caucasian. Table 2 summarizes adverse reactions reported in at least 1% of subjects in the combination group and at a higher incidence than subjects receiving monotherapy with AVODART or tamsulosin.Table 2. Adverse Reactions Reported Over a 48-Month Period in t1% of Subjects and More Frequently in the Coadministration Therapy Group Than the Groups Receiving Monotherapy With AVODART or Tamsulosin (CombAT) by Time of OnsetAdverse ReactionAdverse Reaction Time of OnsetYear 1Year 2 Year 3 Year 4 Months 0-6 Months 7-12Combination a AVODART Tamsulosin (n = 1,610)(n = 1,623)(n = 1,611)(n = 1,527)(n = 1,548)(n = 1,545)(n = 1,428)(n = 1,464)(n = 1,468)(n = 1,283)(n = 1,325)(n = 1,281)(n = 1,200)(n = 1,200)(n = 1,112)Ejaculationdisorders b,cCombination 7.8% 1.6% 1.0% 0.5% <0.1% AVODART 1.0% 0.5% 0.5% 0.2% 0.3% Tamsulosin 2.2% 0.5% 0.5% 0.2% 0.3% Impotence c,dCombination 5.4% 1.1% 1.8% 0.9% 0.4%AVODART 4.0% 1.1% 1.6% 0.6% 0.3% Tamsulosin 2.6% 0.8% 1.0% 0.6% 1.1% Decreased libido c,eCombination 4.5% 0.9% 0.8% 0.2% 0.0% AVODART 3.1% 0.7% 1.0% 0.2% 0.0% Tamsulosin 2.0% 0.6% 0.7% 0.2% <0.1% Breast disorders fCombination 1.1% 1.1% 0.8% 0.9% 0.6%AVODART 0.9% 0.9% 1.2% 0.5% 0.7% Tamsulosin 0.4% 0.4% 0.4% 0.2% 0.0% DizzinessCombination 1.1% 0.4% 0.1% <0.1% 0.2%AVODART 0.5% 0.3% 0.1% <0.1%<0.1% Tamsulosin 0.9% 0.5% 0.4% <0.1% 0.0%a Combination = AVODART 0.5 mg once daily plus tamsulosin 0.4 mg once daily.b Includes anorgasmia, retrograde ejaculation, semen volume decreased, orgasmic sensationdecreased, orgasm abnormal, ejaculation delayed, ejaculation disorder, ejaculation failure, andpremature ejaculation.c These sexual adverse reactions are associated with dutasteride treatment (includingmonotherapy and combination with tamsulosin). These adverse reactions may persist aftertreatment discontinuation. The role of dutasteride in this persistence is unknown.d Includes erectile dysfunction and disturbance in sexual arousal.e Includes libido decreased, libido disorder, loss of libido, sexual dysfunction, and male sexualdysfunction.f Includes breast enlargement, gynecomastia, breast swelling, breast pain, breast tenderness,nipple pain, and nipple swelling.Cardiac Failure: In CombAT, after 4 years of treatment, the incidence of the composite term cardiac failure in the combination therapy group (12/1,610; 0.7%) was higher than in either monotherapy group: AVODART, 2/1,623 (0.1%) and tamsulosin, 9/1,611 (0.6%). Composite cardiac failure was also examined in a separate 4-year placebo-controlled trial evaluating AVODART in men at risk for development of prostate cancer. The incidence of cardiac failure in subjects taking AVODART was 0.6% (26/4,105) compared with 0.4% (15/4,126) in subjects on placebo. A majority of subjects with cardiac failure in both trials had comorbidities associated with an increased risk of cardiac failure. Therefore, the clinical significance of the numerical imbalances in cardiac failure is unknown. No causal relationship between AVODART alone or in combination with tamsulosin and cardiac failure has been established. No imbalance was observed in the incidence of overall cardiovascular adverse events in either trial.6.2Postmarketing ExperienceThe following adverse reactions have been identified during post-approval use of AVODART. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. These reactions have been chosen for inclusion due to a combination of their seriousness, frequency of reporting, or potential causal connection to AVODART.Immune System Disorders: Hypersensitivity reactions, including rash, pruritus, urticaria, localized edema, serious skin reactions, and angioedema.Neoplasms:Male breast cancer.Disorders: Depressed mood.PsychiatricReproductive System and Breast Disorders: Testicular pain and testicular swelling.7 DRUGO NSINTERACTI7.1Cytochrome P450 3A Inhibitorsmetabolized in humans by the CYP3A4 and CYP3A5extensivelyDutasterideisisoenzymes. The effect of potent CYP3A4 inhibitors on dutasteride has not been studied. Because of the potential for drug-drug interactions, use caution when prescribing AVODART to patients taking potent, chronic CYP3A4 enzyme inhibitors (e.g., ritonavir) [see Clinical Pharmacology (12.3)].7.2Alpha Adrenergic AntagonistsThe administration of AVODART in combination with tamsulosin or terazosin has no effect on the steady-state pharmacokinetics of either alpha adrenergic antagonist. The effect of administration of tamsulosin or terazosin on dutasteride pharmacokinetic parameters has not beenevaluated.7.3Calcium Channel AntagonistsCoadministration of verapamil or diltiazem decreases dutasteride clearance and leads to increased exposure to dutasteride. The change in dutasteride exposure is not considered to be clinically significant. No dose adjustment is recommended [see Clinical Pharmacology (12.3)]. 7.4CholestyramineAdministration of a single 5-mg dose of AVODART followed 1 hour later by 12 g of cholestyramine does not affect the relative bioavailability of dutasteride [see Clinical Pharmacology (12.3)].7.5DigoxinAVODART does not alter the steady-state pharmacokinetics of digoxin when administered concomitantly at a dose of 0.5 mg/day for 3 weeks [see Clinical Pharmacology (12.3)].7.6WarfarinConcomitant administration of AVODART 0.5 mg/day for 3 weeks with warfarin does not alter the steady-state pharmacokinetics of the S- or R-warfarin isomers or alter the effect of warfarin on prothrombin time [see Clinical Pharmacology (12.3)].8 USE IN SPECIFIC POPULATIONS8.1PregnancyPregnancy Category X. AVODART is contraindicated for use in women of childbearing potential and during pregnancy. AVODART is a 5 alpha-reductase inhibitor that prevents conversion of testosterone to dihydrotestosterone (DHT), a hormone necessary for normal development of male genitalia. In animal reproduction and developmental toxicity studies, dutasteride inhibited normal development of external genitalia in male fetuses. Therefore, AVODART may cause fetal harm when administered to a pregnant woman. If AVODART is used during pregnancy or if the patient becomes pregnant while taking AVODART, the patient should be apprised of the potential hazard to the fetus.Abnormalities in the genitalia of male fetuses is an expected physiological consequence of inhibition of the conversion of testosterone to DHT by 5 alpha-reductase inhibitors. These results are similar to observations in male infants with genetic 5 alpha-reductase deficiency. Dutasteride is absorbed through the skin. To avoid potential fetal exposure, women who are pregnant or could become pregnant should not handle AVODART Soft Gelatin Capsules. If contact is made with leaking capsules, the contact area should be washed immediately with soap and water [see Warnings and Precautions (5.4)]. Dutasteride is secreted into semen. The highest measured semen concentration of dutasteride in treated men was 14 ng/mL. Assuming exposure of a 50-kg woman to 5 mL of semen and 100% absorption, the woman’s dutasteride concentration would be about 0.0175 ng/mL. This concentration is more than 100 times less than concentrations producing abnormalities of male genitalia in animal studies. Dutasteride is highly protein bound in human semen (greater than 96%), which may reduce the amount of dutasteride available for vaginal absorption.In an embryo-fetal development study in female rats, oral administration of dutasteride at doses 10 times less than the maximum recommended human dose (MRHD) of 0.5 mg daily resulted in abnormalities of male genitalia in the fetus (decreased anogenital distance at0.05 mg/kg/day), nipple development, hypospadias, and distended preputial glands in male offspring (at all doses of 0.05, 2.5, 12.5, and 30 mg/kg/day). An increase in stillborn pups was observed at 111 times the MRHD, and reduced fetal body weight was observed at doses of about 15 times the MRHD (animal dose of 2.5 mg/kg/day). Increased incidences of skeletal variations considered to be delays in ossification associated with reduced body weight were observed at doses about 56 times the MRHD (animal dose of 12.5 mg/kg/day).In a rabbit embryo-fetal study, doses 28- to 93-fold the MRHD (animal doses of 30, 100, and 200 mg/kg/day) were administered orally during the period of major organogenesis (gestation days 7 to 29) to encompass the late period of external genitalia development. Histological evaluation of the genital papilla of fetuses revealed evidence of feminization of the male fetus at all doses. A second embryo-fetal study in rabbits at 0.3- to 53-fold the expected clinical exposure (animal doses of 0.05, 0.4, 3.0, and 30 mg/kg/day) also produced evidence of feminization of the genitalia in male fetuses at all doses.In an oral pre- and post-natal development study in rats, dutasteride doses of 0.05, 2.5, 12.5, or 30 mg/kg/day were administered. Unequivocal evidence of feminization of the genitalia (i.e., decreased anogenital distance, increased incidence of hypospadias, nipple development) of male offspring occurred at 14- to 90-fold the MRHD (animal doses of 2.5 mg/kg/day or greater). At0.05-fold the expected clinical exposure (animal dose of 0.05 mg/kg/day), evidence of feminization was limited to a small, but statistically significant, decrease in anogenital distance. Animal doses of 2.5 to 30 mg/kg/day resulted in prolonged gestation in the parental females and a decrease in time to vaginal patency for female offspring and a decrease in prostate and seminal vesicle weights in male offspring. Effects on newborn startle response were noted at doses greater than or equal to 12.5 mg/kg/day. Increased stillbirths were noted at 30 mg/kg/day.In an embryo-fetal development study, pregnant rhesus monkeys were exposed intravenously to a dutasteride blood level comparable to the dutasteride concentration found in human semen. Dutasteride was administered on gestation days 20 to 100 at doses of 400, 780,1,325, or 2,010 ng/day (12 monkeys/group). The development of male external genitalia of monkey offspring was not adversely affected. Reduction of fetal adrenal weights, reduction in fetal prostate weights, and increases in fetal ovarian and testis weights were observed at the highest dose tested in monkeys. Based on the highest measured semen concentration of dutasteride in treated men(14 ng/mL), these doses represent 0.8 to 16 times the potential maximum exposure of a 50-kg human female to 5 mL semen daily from a dutasteride-treated man, assuming 100% absorption. (These calculations are based on blood levels of parent drug which are achieved at 32 to 186 times the daily doses administered to pregnant monkeys on a ng/kg basis). Dutasteride is highly bound to proteins in human semen (greater than 96%), potentially reducing the amount of dutasteride available for vaginal absorption. It is not known whether rabbits or rhesus monkeys produce any of the major human metabolites.。
度他雄胺FDA说明书
度他雄胺治疗良性前列腺增生症临床疗效评价
良性前列腺增生症（ Ｂ Ｐ Ｈ） 是导致 中老年男性 出现下尿路症 见表 ２ 。 状 的主要原因之一 ， 发病率随着年龄 的增 加而提高 。随着社会 的老龄化 ， 前列腺增生愈发 常见 。 目前 ， 临床对前列腺增生 的治 疗方法 主要是药物治疗和手术治疗 。 药物治疗 手段 主要包括 ５ — ０ 【 还原 酶抑 制剂 、 １ 一 受体拮抗剂 以及植物药类 。５ 一 还原酶抑 制剂可以抑制前列腺 内雄性 激素的活性转化 ， 使前列腺 的体积 减小 ， 能够改善症状 ， 并遏制 Ｂ Ｈ Ｐ的进一步发展 。 度他雄胺是一 种能 同时抑制 Ｉ型和 Ⅱ型两种 同工酶 的 ５ ａ 一 还原 酶抑制剂 ， 改
良反应 ， 说 明其具有 良好 的耐受性和安全性 。此外 ， 研究脚 证实 Ｐ Ｈ患者 Ｔ Ｕ Ｒ Ｐ术 中的出血量和术 后 １ ． ５统计学方 法 ：所有数 据 录入 Ｓ Ｐ Ｓ Ｓ １ ８ ． ０统计 学软件进 行分 了度 他雄胺 能有效减少 Ｂ 析， 定量资料用 ｔ 检验 ， 等级资料用 ｘ ｚ 检验 ， Ｐ ＜ Ｏ ． ０ ５表示差异有 血尿 的发生率 ， 从 而有效降低患者术 中及术后风险 ， 提高手术安 统计学意义。 全系数 。因此 ， 度他雄胺是治疗 良性前列腺增生症 安全 、 有效的 ２ 结 果 药物 ， 值 得临床推广 。 ２ ． １治疗前后两组 的指标 变化献 １ 】 初铭彦 ， 张良锁 ， 丁军平 ， 等． 依 立雄胺 治疗 良性前列腺增 生症 分（ Ｉ Ｐ Ｓ Ｓ ） 、 生 活质 量 评分 （ Ｑ Ｏ Ｌ ） 、 残余 尿 量 （ Ｒ Ｕ） 、 最 大 尿 流率 【 （ ＭＦ Ｒ） 、 前列腺体 积 ｖ等指标均明显 改善（ Ｐ ＜ Ｏ ． ０ １ ） ， 两组 比较差 的 疗 效评 价 『 Ｊ １ ． 广 西 医学 ， ２ ０ ０ ９ ， ３ １ （ ５ ） ： ６ ６ ４ — ６ ６ ６ ． 异 无统计学 意义 （ ０ ． ０ ５ ） ， 见表 １ 。 ［ ２ 】 何 二宝 ， 李解方． 非 那雄胺 剂量对减少经尿 道前列腺 电切 术 中 ２ ． ２疗效 比较 ： 两组总有效率 比较 ， 差异无统计学意义（ Ｐ ＞ ０ ． ０ ５ ） ， 出血 的影响［ Ｊ 】 ． 现代 泌尿 外科 杂志 ， ２ ０ １ ２ ， ３ ： ２ ８ ７ — ２ ８ ９ ．
抗前列腺增生药度他雄胺可预防前列腺癌
抗前列腺增生药度他雄胺可预防前列腺癌
佚名
【期刊名称】《药学进展》
【年(卷),期】2009(33)10
【摘要】@@ 由GlaxoSmithKline(GSK)公司开发的抗良性前列腺增生(BPH)药度他雄胺(dutasteride,Avodart)目前仅被批准用于治疗BPH症状,它可抑制Ⅰ型和Ⅱ型5-α还原酶,而这两种酶能使睾酮转化为促进前列腺生长最强效的雄性激素二氢睾酮(DHT).然而,强有力的证据表明,DHT还参与了前列腺癌的发生发展.
【总页数】1页(P479)
【正文语种】中文
【中图分类】R979.1
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1.抗前列腺癌药恩杂鲁胺的研究进展 [J], 曾令康;冯菊红;葛燕丽;胡学雷
2.度他雄胺治疗前列腺增生症和前列腺癌 [J], 何家扬
3.新型抗前列腺增生药物度他雄胺的合成 [J], 梁涌涛;徐志炳;路海滨;王恩思
4.美FDA批准度他雄胺和坦洛辛复合胶囊Jalyn治疗前列腺肥大男子的中至重度良性前列腺增生症状 [J], 马培奇
5.度他雄胺和“扶正抑瘤”中药复方对人前列腺癌PC-3细胞转移抑制效应的对照研究 [J], 周仕轶;王林;邵继春;张蜀武
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度他雄胺纳米悬浮液的制备
［ Ａ ｂ ｓ ｔ ｒ ａ ｃ ｔ ］ ０ ｂ ｊ ｅ ｃ ｔ ｉ ｖ ｅ Ｔ ｏ ｐ ｒ ｅ ｐ ａ ｒ ｅ ｄ ｕ ｔ ａ ｓ ｔ ｅ ｒ ｉ ｄ ｅ ｎ ａ ｎ ｏ ｍｅ ｔ ｅ ｒ ｓ ｕ ｓ ｐ ｅ ｎ ｓ ｉ ｏ ｎ ｂ ｙ ｈ ｉ ｇ ｈ ｐ ｒ ｅ ｓ ｓ ｕ ｒ ｅ ｈ ｏ ｍ ｏ ｇ ｅ ｎ ｉ ｚ ａ ｔ ｉ ｏ ｎ （ Ｈ Ｐ Ｈ） ． Ｍｅ ｔ ｈ ｏ ｄ ｓ
质压力 、 循环次数 、 表 面 活性 剂 种 类 和 浓 度 等 因素 对 纳 米 悬 浮 液 性 质 的影 响 ， 并 考 察 度 他 雄 胺 的溶 解 度 及 药 物 溶 出 速 率 。结
果
均质压力是影响纳米粒径的主要 因素。纳米尺度 的度他雄胺 的溶解度和体外溶 出速率 比原 药明显提高 。结论 ［ 关键词 ］ 度他雄胺功用于制备度他雄胺 纳米悬 浮液 。
Ｐｒ ｅ ｐａ ｒ ａ ｉｏ ｔ ｎ ｏ ｆ ｄｕｔ ａｓ ｔ ｅ ｒ ｉ ｄ ｅ ｎａｎ ｏｍ ｅ ｔ ｅ ｒ ｓ ｕｓ ｐｅ ｎｓ ｉ ｏ ｎ
Ｚ ｈ ａ ｏ Ｘｉ ａ ｎ ｙ ｉ ｎ ｇ ， Ｌ ｉ ｕ Ｙｉ ｍｉ ｎ ， Ｚ ｈ ｏ ｕ Ｘ ｉ ａ ｏ ｘ ｉ ａ ， Ｚ ｈ ａ ｎ ｇ Ｄ ｉ ｎ ｇ ｌ ｉ ｎ ， Ｇａ ｏ Ｊ ｉ ｎ ｉ ｎ ｇ ， Ｚ ｈ ｏ ｕ Ｍｉ ａ ｎ
・
１ ２ ８ ６・
西 南 国防医药 ２ ０ １ ３年 １ ２月第 ２ ３卷 第 １ ２期
・
论著 ・
度 他 雄 胺 纳 米 悬 浮 液 的 制 备
赵 先英 ， 刘毅敏 ， 周小霞， 张定 林 ， 高继 宁 ， 周 勉
［ 摘要 ］ 目的 运用高压均质技术制备度他雄胺 纳米悬浮液。方法 以粒径 、 多分散性和 Ｚ ｅ ｔ ａ电位为考察指标 ， 研 究均
度他雄胺市场研究报告
文档从互联网中收集，已重新修正排版，word格式支持编辑，如有帮助欢迎下载支持。 1如有帮助欢迎下载支持 中国度他雄胺行业市场前景调查及投融资战略研究报告 2017-2022年 前 言 企业成功的关键就在于，能否跳出红海，开辟蓝海。那些成功的公司往往都会倾尽毕生的精力及资源搜寻产业的当前需求、潜在需求以及新的需求！随着行业竞争的不断加剧，大型企业间并购整合与资本运作日趋频繁，国内外优秀的企业愈来愈重视对行业市场的研究，特别是对企业发展环境和客户需求趋势变化的深入研究，逐渐成为行业中的翘楚！ 中商产业研究院发布《2017-2022年中国度他雄胺行业市场前景调查及投融资战略研究报告》利用中商数据库长期对度他雄胺行业市场跟踪搜集的相关数据，全面准确地为您从行业的整体高度架构分析体系。报告从行业的宏观环境出发，以度他雄胺行业的产销状况和行业的需求走向为依托，详尽分析了近年中国度他雄胺行业当前的市场容量、产销规模、发展速度和竞争态势；报告还同时分析了度他雄胺行业进出口市场、行业的上下游产业链运营情况，行业市场需求特征等，并且对度他雄胺行业市场领先企业经营状况进行分析，最后对未来几年度他雄胺行业发展趋势与投资前景做出预测。 文档从互联网中收集，已重新修正排版，word格式支持编辑，如有帮助欢迎下载支持。
2如有帮助欢迎下载支持 【出版日期】 2016年 【交付方式】 Email电子版/特快专递 【价 格】 纸介版：12800元 电子版：12500元 纸介+电子：12800元 第一章 度他雄胺行业相关概述 第一节度他雄胺行业相关概述 一、产品概述 二、产品性能 三、产品用途 第二节 度他雄胺行业经营模式分析 一、生产模式 二、采购模式 三、销售模式 第二章 度他雄胺行业发展环境分析 第一节 中国经济发展环境分析 一、中国GDP增长情况分析 二、工业经济发展形势分析 三、社会固定资产投资分析 四、全社会消费品零售总额 五、城乡居民收入增长分析 六、居民消费价格变化分析 第二节 中国度他雄胺行业政策环境分析 一、行业监管管理体制 二、行业相关政策分析 三、上下游产业政策影响 四、进出口政策影响分析 第三节 中国度他雄胺行业技术环境分析 一、行业技术发展概况 二、行业技术发展现状 第三章 2012-2022年中国度他雄胺市场供需分析 第一节 中国度他雄胺市场供给状况 一、2012-2016年中国度他雄胺产量分析 二、2017-2022年中国度他雄胺产量预测 第二节 中国度他雄胺市场需求状况 一、2012-2016年中国度他雄胺需求分析 二、2017-2022年中国度他雄胺需求预测 第三节 2015-2016年中国度他雄胺市场价格分析 文档从互联网中收集，已重新修正排版，word格式支持编辑，如有帮助欢迎下载支持。 3如有帮助欢迎下载支持 第四章 中国度他雄胺行业产业链分析 第一节 度他雄胺行业产业链概述 第二节 度他雄胺上游产业发展状况分析 一、上游原料市场发展现状 二、上游原料生产情况分析 三、上游原料价格走势分析 第三节 度他雄胺下游应用需求市场分析 一、行业发展现状分析 二、行业生产情况分析 三、行业需求状况分析 四、行业需求前景分析 第五章 2012-2016年度他雄胺进出口数据分析 第一节 2012-2016年度他雄胺进口情况分析 一、进口数量情况分析 二、进口金额变化分析 三、进口来源地区分析 四、进口价格变动分析 第二节 2012-2016年度他雄胺出口情况分析 一、出口数量情况分析 二、出口金额变化分析 三、出口国家流向分析 四、出口价格变动分析 第六章 国内度他雄胺生产厂商竞争力分析 第一节 企业A 一、企业发展基本情况 二、企业主要产品分析 三、企业经营状况分析 四、企业销售网络布局 五、企业发展战略分析 第二节 企业B 一、企业发展基本情况 二、企业主要产品分析 三、企业经营状况分析 四、企业销售网络布局 五、企业发展战略分析 第三节 企业C 文档从互联网中收集，已重新修正排版，word格式支持编辑，如有帮助欢迎下载支持。 4如有帮助欢迎下载支持 一、企业发展基本情况 二、企业主要产品分析 三、企业经营状况分析 四、企业销售网络布局 五、企业发展战略分析 第四节 企业D 一、企业发展基本情况 二、企业主要产品分析 三、企业经营状况分析 四、企业销售网络布局 五、企业发展战略分析 第五节 企业E 一、企业发展基本情况 二、企业主要产品分析 三、企业经营状况分析 四、企业销售网络布局 五、企业发展战略分析 第七章 2017-2022年中国度他雄胺行业发展前景及投资策略 第一节 2017-2022年中国度他雄胺行业投资前景分析 一、度他雄胺行业发展前景 二、度他雄胺发展趋势分析 三、度他雄胺市场前景分析 第二节 2017-2022年中国度他雄胺行业投资风险分析 一、产业政策风险 二、原料市场风险 三、市场竞争风险 四、技术风险分析 第三节 2017-2022年中国度他雄胺行业投资策略及建议 第八章 度他雄胺企业投资战略与客户策略分析 第一节 度他雄胺企业发展战略规划背景意义 一、企业转型升级的需要 二、企业做强做大的需要 三、企业可持续发展需要 第二节 度他雄胺企业战略规划制定依据 一、国家产业政策 二、行业发展规律 文档从互联网中收集，已重新修正排版，word格式支持编辑，如有帮助欢迎下载支持。 5如有帮助欢迎下载支持 三、企业资源与能力 四、可预期的战略定位 第三节 度他雄胺企业战略规划策略分析 一、战略综合规划 二、技术开发战略 三、区域战略规划 四、产业战略规划 五、营销品牌战略 六、竞争战略规划 第四节 度他雄胺企业重点客户战略实施 一、重点客户战略的必要性 二、重点客户的鉴别与确定 三、重点客户的开发与培育 四、重点客户市场营销策略 文档从互联网中收集，已重新修正排版，word格式支持编辑，如有帮助欢迎下载支持。
度他雄胺治疗大体积良性前列腺增生症中短期效果的初步研究要点
・临床研究・ＤＯＩ：１０．３７６０／ｃｍａ．ｊ．ｉｓｓｎ．１０００－６７０２．２０１６．０２．作者单位：１００７３０北京医院泌尿外科（魏东、吴鹏杰、陈鑫、张方圆、王晓明、张耀光、王建业）；北京京煤集团总医院泌尿外科（柴攀）通信作者：王建业，Ｅｍａｉｌ：ｗａｎｇｊｙ＠ｂｊｈｍｏｈ．ｃｎ度他雄胺治疗大体积良性前列腺增生症中短期效果的初步研究魏东 柴攀 吴鹏杰 陈鑫 张方圆 王晓明 张耀光 王建业【摘要】 目的 评价度他雄胺治疗体积≥４０ｍｌ的良性前列腺增生症（ＢＰＨ）患者在下尿路症状（ＬＵＴＳ）改善方面的中短期效果。
方法 ２０１３年７月至２０１４年９月符合入选标准并且不符合任一排除标准的ＢＰＨ伴中－重度ＬＵＴＳ患者１０７例。
年龄５０～８０岁，平均６８．４岁。
患者服用度他雄胺０．５ｍｇ／ｄ治疗１２周后，ＩＰＳＳ评分相对于基线值下降率≥３０％为有效，归入有效组；否则为无效，归入无效组。
将ＱＯＬ评分、最大尿流率（Ｑｍａｘ）、残余尿量作为次要观察指标。
有效组继续服用度他雄胺，第１６周末测定前列腺体积、ＰＳＡ；无效组加用坦索罗辛（０．２ｍｇ／ｄ）联合治疗，观察至第１６周末再次评估疗效，至第２０周末完成随访并测定前列腺体积、ＰＳＡ。
随访结束后比较两组的前列腺体积、ＰＳＡ相对基线的变化。
结果 与基线值比较，１０７例患者治疗１２周后ＩＰＳＳ评分平均下降５．５４分（Ｐ＜０．０１），有效率５５．１％（５９／１０７）；ＱＯＬ评分下降１．５６分（Ｐ＜０．０１），Ｑｍａｘ增加１．０７ｍｌ／ｓ（Ｐ＝０．０４９），残余尿量下降６．４６ｍｌ（Ｐ＝０．１０７）。
有效组５９例患者中４２例１６周末前列腺体积平均缩小１４．１５％，３２例１６周末血ＰＳＡ平均下降０．６８ｎｇ／ｍｌ（Ｐ＝０．００８）；无效组４８例患者中４０例接受联合治疗，联合治疗有效率６０．０％（２４／４０）。
３６例随访至２０周末前列腺体积缩小１１．８９％，３３例２０周末测定ＰＳＡ下降０．１８ｎｇ／ｍｌ（Ｐ＝０．５８９）。
5—α还原酶抑制剂(度他雄胺)对良性前列腺增生综合治疗的研究进展
5—α还原酶抑制剂（度他雄胺）对良性前列腺增生综合治疗的研究进展良性前列腺增生（BP H ）的药物治疗和手术治疗（TURP）是目前主要治疗手段之一。
5-α还原酶抑制剂（度他雄胺）在同类药物治疗中可以更有效减小前列腺体积，改善下尿路症状[1]。
在围手术期及TURP术后应用可以减少术中出血量及术后血尿发生率，为前列腺增生的综合治疗提供了新的临床治疗思路。
标签：前列腺增生；5-α还原酶抑制剂（度他雄胺）；术后血尿发生率良性前列腺增生症（benign prostatic hyperplasia，BPH ）是导致老年男性下尿路症状（lower urinary tract symptoms，LUTS ）的主要原因之一，其发病率随着年龄的增加而提高，最初通常发生在40岁以后，到60岁时>50%，80岁时>83%[2]。
随着我国进入老龄化社会，前列腺增生成为泌尿外科的常见病。
前列腺增生症临床表现主要可概括为膀胱刺激症状和排尿梗阻症状在内的LUTS。
目前对前列腺增生的治疗手段主要是药物治疗和手术治疗。
药物治疗目前主要包括5-α还原酶抑制剂、α1-受体阻滞剂及植物药类等三大类。
近年来国内外许多学者发现5-α还原酶抑制剂（度他雄胺）在同类药物中可以更有效、抑制前列增生的进展过程，同时也能改善因前列腺增生所引起的下尿路症状，并且诸多学者已证实度他雄胺能有效减少BPH患者血尿的发生率及TURP术中的出血量[3]，有效降低患者术中及术后风险。
因此5-α还原酶抑制剂（度他雄胺）受到了许多研究人员的重视，尤其是度他雄胺在经尿道前列腺切除术（transurethral resection prostate，TURP）术后减少血尿发生率的作用。
1 5-α还原酶抑制剂（度他雄胺）与5-α还原酶（5-alpha reductase inhibitor and 5-alpha reductase）1.1 5-α还原酶的分布研究发现人体中5α还原酶有两种同工酶，即5α还原酶1和5α还原酶2。
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简介
度他雄胺为白色至淡黄色粉末，熔点为242~250℃，不溶于水，溶于乙醇（44mg/ml），甲醇（64mg/ml),聚乙二醇400(4mg/ml)。
治疗前列腺疾病
1 5α还原酶的双重抑制剂――度他雄胺睾酮在5α还原酶的作用下转变成的双氢睾酮(DHT)作用于前列腺组织，可导致前列腺组织增生。
临床上已应用5α还原酶抑制剂来阻断这个环节，以有效地治疗前列腺增生症(BPH)。
最近的研究发现，人体中5α还原酶有两种同工酶，即5α还原酶1和5α还原酶2。
5α还原酶1存在于身体任何有5α还原酶表达的部位，包括皮肤、肝脏、脂肪的腺体、大多数毛囊和前列腺。
5α还原酶2主要存在于前列腺及其他生殖组织、生殖器的皮肤、胡须和头皮毛囊，并与男性胎儿的男性化有关[1]。
在鼠的研究中发现，虽然两种同工酶对合成代谢和分解代谢都有作用，但1型酶主要对雄激素和其他类固醇激素的分解代谢起作用，而2型酶则主要对雄激素的合成代谢起作用。
在正常前列腺组织、BPH病人和前列腺癌病人的前列腺的所有区域(包括周围带、移行带和中心带)都有两种5α还原酶的mRNA，但是在前列腺癌组织中只有5α还原酶1的表达增加[2]。
非那雄胺是5α还原酶2的抑制剂，它在临床应用的剂量时只能抑制5α还原酶2。
度他雄胺(dutasteride)是一种新的5α还原酶的双重抑制剂，它既能抑制5α还原酶1，也能抑制5α还原酶2。
它比非那雄胺更能使DHT的浓度降低(94.7%对70.8%)[3]。
度他雄胺对5α还原酶1的抑制作用是非那雄胺的60倍。
服用度他雄胺后27个月，前列腺癌的发病率比安慰剂组低50%(1.2%对
2.5%)[4]。
2 度他雄胺治疗前列腺增生症
Roehrborn等进行了一个为期2年的关于度他雄胺的临床试验。
入选这项研究的标准是：年龄在50岁以上、临床诊断为BPH、经直肠B超测量前列腺体积≥30cm3、AUA症状评分≥12分、最大尿流率≤15mL/s。
排除的标准是：剩余尿>250mL、有前列腺癌病史、既往有前列腺手术史、近3个月有急性尿潴留病史、近4周用过α受体阻滞剂或应用过任何一种5α还原酶抑制剂、PSA≤1.5ng/mL 或≥10ng/mL。
他们把度他雄胺0.5mg/d同时用于三个平行的、随机的、安慰剂对照的试验：ARIA3001(只在美国)、ARIA3002(只在美国)和ARIA3003(在欧洲、北美、澳大利亚、新西兰及南非等19个国家)共400个单位参加。
其中的2项研究证明度他雄胺在4年治疗中是有效且安全的。
在服用度他雄胺2周后血清DHT 即降低90%，在1个月时尿流率增加，在3个月时症状改善，并且急性尿潴留及需要外科处理的机会减少。
治疗男性型脱发
关于Dutasteride( 度他雄胺) 和Finasteride ( 非那雄胺、波斯卡)，在雄性秃治疗效果以及副作用的比较，一直是掉发的朋友以及治疗医师关注的话题。
在此先对睾固酮(testosterone)、DHT(二氢睾酮)、以及5α还原酶作一个深入介绍：
虽然睾酮(testosterone)是人体血液里面主要的雄性荷尔蒙，但是要造成头发的毛囊凋亡，就必须要先被转化成DHT（二氢睾酮，作用是睾固酮的五倍强）才会造成此掉发。
将睾固酮变成DHT需要5α还原酶的帮助。
5α还原酶因所在部位不同分成二种：第一型的5α还原酶，在人体皮肤皮脂腺以及汗腺的细胞内；而第二型的5α还原酶，主要是位于上皮角质细胞的细胞质，以及毛囊的内毛根鞘(inner root sheath )，当内毛根鞘的DHT浓度过高，毛发便会自动凋亡造成雄性秃。
Dutasteride能够抑制第一型以及第二型的的5α还原酶，不过目前美国食品药物管理局，只通过其应用在治疗摄护腺肥大上。
之前的研究中已经得知，Dutasteride对第二型的5α还原酶的抑制效果，是Finasteride的3倍；而对第一型5α还原酶的抑制效果，是Finasteride的100倍。
Dutasteride可以导致头皮以及血清中的DHT浓度降低，以及睾固酮的浓度升高，而且和剂量有关系：当5毫克的Finasteride，降低血清中的DHT约70%时，5毫克Dutasteride可以减少血清中DHT90 %以上。
以下是使用Finasteride(市面上的Finax, Finpecia, 保康丝(非那雄胺), 保列治(波斯卡) 均含有该成份) 的测试结果:
左边照片为第五型雄性秃finasteride服用前右边照片为服用finasteride之后八个月，头顶秃明显改善
左图为另一测试者，服用finasteride前漩涡处右边为服用finasteride 之后八个月，可明显看到漩涡处毛发变正常
研究：Dutasteride（度他雄胺）和Finasteride（非那雄胺、波斯卡）在雄性秃治疗效果以及副作用的比较：
研究报告中对416个，年龄在21~45岁间雄性秃的男性，将他们分成六组，每日分别服用Dutasteride (度他雄胺的学名) 0.05毫克、0 .1毫克、0.5毫克、2.5毫克、Finasteride 5毫克(非那雄胺的5倍剂量)，以及对照组（注：这组是没有吃，或是吃一些无相关的维他命丸等），观察24个星期。
研究结果显示Dutasteride会增加雄性秃毛发的数量，而且和剂量大小有关系，剂量愈高效果愈好，如果比较Dutasteride 2.5毫克和Finasteride 5毫克，在观察12个星期及24个星期的效果发现，Dutasteride 2 .5 毫克效果比较好。
实验结果详细解说：
实验当中发现2.5毫克的Dutasteride 比5毫克的Finasteride 生发效果好。
观察地中海雄性秃，直径一英吋的圆圈范围内(约5平分公分)，半年后发量的改变如下：
1. 对照组减少3
2.3根毛发
2. Fintasteride 5毫克-------增加75.6根毛发
3. Dutasteride 0.1毫克-------增加78.5根毛发
4. Dutasteride 0.5毫克-------增加94.6根毛发
5. Dutasteride 2.5毫克-------增加109.6根毛发
Dutasteride2.5毫克以及0.5毫克的比较--生发效果2.5毫克较佳。
2.5 毫克的Dutasteride比0.5毫克的Dutasteride 生发效果好，2.5毫克的Dutasteride对头皮内DHT可以减少79%，而0.5毫克的Dutasteride 对头皮内DHT只能够减少51%，但是对血清里面的DHT的减少量两个差不多分别是96%对92%。
Finasteride5毫克与Dutasteride0 .1毫克的比较--对DHT的抑制差不多
5毫克的Finasteride对头皮内DHT的抑制，和0 .1毫克的Dutasteride 是差不多的，分别是41 %与32%。
副作用：
性欲减退：对照组(吃安慰剂)2位
0.05毫克以及0.1毫克Dutaste ride 有2位，
0.5毫克Dutasteride有1位，
2.5毫克Dutasteride有9位，
5毫克Finasteride有3位
但是，Dutasteride每天给2.5毫克，副作用发生的比例和其它剂量相比，并没有统计上的意义。
此副作用事实上是温和或中等程度的，但大部分持续服药后，这种副作用都自动消失。
在2.5毫克Dutasteride九位性欲减退的患者当中，有四位仍然继续服用药物，后来此副作用自动消失。
其中一位在三个星期内，副作用消失，有一位停药八星期后症状消失，另一位在停药以后还是有性欲减退的现象，但后来这个被诊断为和药物无关。
其它研究也指出，Dutasteride在摄护腺肥大的十年临床实验追踪发现，Dutasteride0.5毫克是普遍可以接受的剂量，而且大部分性方面的副作用发生率非常低，并会随着服用时间愈长发生率也会减少。
Dutasteride的效用期多长？
Finasteride的血清半衰期是6~8小时，而Dutasteride的血清半衰期约4个星期，因此Dutasteride即使在停药之后，血清里面的药物成分仍会存在一段时间，因此一些学者建议有在服用Dutaste ride的男性，在停药后的半年内不要捐血，以预防这些血液被使用在孕妇的身上，造成胚胎发育畸形。
（注：孕妇接受这种血液可能会造成男性胎儿生殖器发育畸形)
板主提醒：
Dutasteride (Avodart)的安全性如何呢？
1.Dutasteride 较会造成精虫数目减少，而且会持续一段相当长的时间，即使停药之后，精虫数目的减少也会持续一段长时间。
到底Dutasteride是不是会造成不孕？目前美国FDA的报告里面还没有结论。
在性能力降低方面，发生率比1毫克的Finasteride要高。
2.此外，因为人体有不少的第一型5α还原酶的接受器存在脑部里面，Dutasteride服用之后对于第一型5α还原酶的抑制到底对脑部长期会有什么影响目前也不知道。
而Finasteride就比较没有相关，因为它是专门抑制第二型的5α还原酶。
3.美国食品药物管理局FDA，目前已经允许Dutasteride 使用在有摄护腺肥大疾病的老年人，因此如果是年纪50岁以上，有掉发的问题，Dutasteride(也就是Avodart度他雄胺)的使用是可以考虑的。
4.美国FDA的报告有提到：服用Dutasteride的男性，口水或精液里面含有的量，不会影响到胚胎的发育。
但是孕妇绝对不能碰触破裂的Dutasteride 胶囊，以免藉由皮肤吸收造成胎儿畸形。
（武汉楷伦：）。