Tamsulosin

408.51

408.51

1533716-785-6

G3P28OML5I

DTXSID3023631

G04CA02|G - Genito urinary system and sex hormones

2935009090

108

2.7

Solid

1.191±0.06 g/cm3(Predicted)

228-230 °C

595.5±60.0 °C(Predicted)

313.9±32.9 °C

1.553

Sparingly soluble in water

Store at 25 deg C (77 deg F); excursions permitted to 15-30 deg C (59-86 deg F).

3.96X10-11 mm Hg at 25 deg C (est)

Henry's Law constant = 4.95X10-15 atm-cu m/mol at 25 °C (est)

Hydroxyl radical reaction rate constant = 1.55X10-10 cu cm/molec-sec at 25 °C (est)|MW 444.97. MP 228-230 °C; Specfic optical rotation: -4.0 deg at 24 °C/D (c = 0.35 in methanol) /Tamsulosin hydrochloride/

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl tamsulosin hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Tamsulosin hydrochloride/

In the event of overdose, patients may experience hypotension and should lie down in a supine position to maintain blood pressure and heart rate. If further measures are required intravenous fluids should be considered. If further progression is required, vasopressors may be used and renal function should be monitored. Dialysis is unlikely to assist in treating overdose because tamsulosin is extensively protein bound. The oral LD50 in rats is 650mg/kg.[MSDS] Tamsulosin is not indicated for use in women and no studies have been performed in pregnancy, though animal studies have not shown fetal harm. Tamsulosin is excreted in the milk of rats but there is no available data on what the effect of this tamsulosin exposure may be. Animal studies have shown male and female rat fertility is affected by tamsulosin due to impairment of ejaculation and fertilization. In men, tamsulosin is associated with abnormal ejaculation. Tamsulosin is not mutagenic but may be carcinogenic at levels above the maximum recommended human dose. Female rats experience a slight increase in the rates of mammary gland fibroadenomas and adenocarcinomas.

Tamsulosin has been associated with a low rate of serum aminotransferase elevations (

The effects of cimetidine at the highest recommended dose (400 mg every six hours for six days) on the pharmacokinetics of a single tamsulosin hydrochloride capsule 0.4 mg dose was investigated in ten healthy volunteers (age range 21-38 years). Treatment with cimetidine resulted in a significant decrease (26%) in the clearance of tamsulosin hydrochloride which resulted in a moderate increase in tamsulosin hydrochloride AUC (44%). Therefore, Tamsulosin hydrochloride capsules should be used with caution in combination with cimetidine, particularly at doses higher than 0.4 mg.|Results from limited in vitro and in vivo drug-drug interaction studies between tamsulosin hydrochloride and warfarin are inconclusive. Therefore, caution should be exercised with concomitant administration of warfarin and tamsulosin hydrochloride capsules.|... Interactions between the two drugs were evaluated in rats after simultaneous 1 or 15 min iv infusion or after po administration of udenafil (30 mg x kg(-1)) and/or tamsulosin (1 mg x kg(-1)). In vitro metabolism of tamsulosin with udenafil was measured to obtain the inhibition constant (K(i)) and [I]/K(i) ratio of udenafil. The total area under the plasma concentration-time curve from time zero to time infinity (AUC)s (or AUC(0-4 h)) of tamsulosin were significantly greater after 15 min of i.v. infusion or after oral administration with udenafil, compared with tamsulosin alone. The hepatic first-pass metabolism of tamsulosin was inhibited by udenafil, and the inhibition in vitro was in a non-competitive mode. The arterial systolic blood pressure was significantly lower at 5, 10 and 60 min after oral co-administration of the drugs. The significantly greater AUC of tamsulosin after i.v. and p.o. administration of both drugs may be attributable to non-competitive inhibition of cytochrome P450 3A1/2-mediated hepatic tamsulosin metabolism by udenafil. The inhibition was also observed in human liver S9 fractions, suggesting that a reassessment of the oral dosage of tamsulosin is necessary when udenafil and tamsulosin are co-administered to patients with benign prostatic hyperplasia.

Tamsulosin is 94%-99% protein bound, mostly to alpha-1-acid glycoprotein.

Tamsulosin's production and use in the treatment of benign prostatic hypertrophy(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 3.0X10+4(SRC), determined from a structure estimation method(2), indicates that tamsulosin is expected to be immobile in soil(SRC). Volatilization of tamsulosin from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.9X10-15 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Tamsulosin is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 4.0X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2009).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 3.0X10+4(SRC), determined from a structure estimation method(2), indicates that tamsulosin is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 4.9X10-15 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 20(SRC), from an estimated log Kow of 2.5(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2009).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), tamsulosin, which has an estimated vapor pressure of 4.0X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase tamsulosin may be removed from the air by wet or dry deposition(SRC). Tamsulosin does not contain chromophores that absorb at wavelengths >290 nm(3) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

Tamsulosin is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Tamsulosin does not contain chromophores that absorb at wavelengths >290 nm(1) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 20 was calculated in fish for tamsulosin(SRC), using an estimated log Kow of 2.5(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of tamsulosin can be estimated to be 3.0X10+4(SRC). According to a classification scheme(2), this estimated Koc value suggests that tamsulosin is expected to be immobile in soil.

The Henry's Law constant for tamsulosin is estimated as 4.9X10-15 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that tamsulosin is expected to be essentially nonvolatile from water surfaces(2). Tamsulosin is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 4.0X10-11 mm Hg(SRC), determined from a fragment constant method(3).

While data specific to tamsulosin were not located(SRC, 2009), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2).

Occupational exposure to tamsulosin may occur through inhalation and dermal contact with this compound at workplaces where tamsulosin is produced or used. Exposure to tamsulosin among the general male population may be limited to those administered the drug Flomax, an alpha-1 adrenoreceptor blocker. (SRC)

Tamsulosin is indicated for the treatment of signs and symptoms of benign prostatic hyperplasia. Tamsulosin is also used off label for the treatment of ureteral stones, prostatitis, and female voiding dysfunction.|FDA Label

Tamsulosin is a selective alpha-1a adrenergic antagonist used in the therapy of benign prostatic hypertrophy. Tamsulosin therapy is associated with a low rate of serum aminotransferase elevations, but clinically apparent acute liver injury due to tamsulosin is very rare.

Benign Prostatic Hypertrophy Agents

Sulfonamides; Adrenergic alpha-Antagonists|Tamsulosin hydrochloride capsules are indicated for the treatment of the signs and symptoms of benign prostatic hyperplasia (BPH). /Included in US product label/|Tamsulosin hydrochloride capsules are not intended for use as an antihypertensive drug. /Included in US product label/|Tamsulosin hydrochloride capsules are not indicated for use in women. /Included in US product label/|For more Therapeutic Uses (Complete) data for Tamsulosin (6 total), please visit the HSDB record page.

Contraindications /include/ known hypersensitivity to tamsulosin or any ingredient in the formulation.|Potential for postural hypotension, dizziness, or vertigo; syncope may occur.|The signs and symptoms of orthostasis (postural hypotension, dizziness and vertigo) were detected more frequently in tamsulosin hydrochloride capsule treated patients than in placebo recipients. As with other alpha-adrenergic blocking agents there is a potential risk of syncope.|Patients beginning treatment with tamsulosin hydrochloride capsules should be cautioned to avoid situations where injury could result should syncope occur. ... Patients should be told about the possible occurrence of symptoms related to postural hypotension such as dizziness when taking tamsulosin hydrochloride capsules, and they should be cautioned about driving, operating machinery or performing hazardous tasks.|For more Drug Warnings (Complete) data for Tamsulosin (17 total), please visit the HSDB record page.

Tamsulosin is an alpha adrenoceptor blocker with specificity for the alpha-1A and alpha-1D subtypes, which are more common in the prostate and submaxillary tissue. The final subtype, alpha-1B, are most common in the aorta and spleen. Tamsulosin binds to alpha-1A receptors 3.9-38 times more selectively than alpha-1B and 3-20 times more selectively than alpha-1D. This selectivity allows for a significant effect on urinary flow with a reduced incidence of adverse reactions like orthostatic hypotension.

Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS. (See all compounds classified as Adrenergic alpha-1 Receptor Antagonists.)|Drugs used in the treatment of urogenital conditions and diseases such as URINARY INCONTINENCE; PROSTATIC HYPERPLASIA; and ERECTILE DYSFUNCTION. (See all compounds classified as Urological Agents.)

Oral tamsulosin is 90% absorbed in fasted patients. The area under the curve is 151-199ng/mL\*hr for a 0.4mg oral dose and 440-557ng/mL*hr for a 0.8mg oral dose. The maximum plasma concentration is 3.1-5.3ng/mL for a 0.4mg oral dose and 2.5-3.6ng/mL for a 0.8mg oral dose. Taking tamsulosin with food increases the time to maximum concentration from 4-5 hours to 6-7 hours but increases bioavailability by 30% and maximum plasma concentration by 40-70%.|97% of an orally administered does is recovered in studies, which 76% in the urine and 21% in the feces after 168 hours. 8.7% of the dose is excreted as unmetabolized tamsulosin.|16L after intravenous administration.|2.88L/h.|In patients with moderate hepatic impairment, protein binding is altered, resulting in changes in overall plasma concentrations; however, no substantial alterations in intrinsic clearance and concentrations of unbound drug.|In patients with renal impairment, protein binding is altered, resulting in changes in overall plasma concentrations, however, no substantial alterations in intrinsic clearance and concentrations of unbound drug.|Absorption of tamsulosin hydrochloride ... is essentially complete (>90%) following oral administration under fasting conditions. Tamsulosin hydrochloride exhibits linear kinetics following single and multiple dosing, with achievement of steady-state concentrations by the fifth day of once-a-day dosing.|Essentially completely absorbed following oral administration under fasting conditions; peak plasma concentrations attained within 4-5 hours.|For more Absorption, Distribution and Excretion (Complete) data for Tamsulosin (14 total), please visit the HSDB record page.

Tamsulosin is mostly metabolized in the liver by cytochrome P450 (CYP) 3A4 and 2D6, with some metabolism by other CYPs. CYP3A4 can deacetylate tamsulosin to the M-1 metabolite or perform oxidative deamination to the AM-1 metabolite. CYP2D6 can hydroxylate tamsulosin to the M-3 metabolite or demethylate tamsulosin to the M-4 metabolite. Finally, an unknown enzyme can hydroxylate tamsulosin at a different position to form the M-2 metabolite. The M-1, M-2, M-3, and M-4 metabolites can be glucuronidated or the M-1 and M-3 metabolites can undergo sulfate conjugation to form other metabolites before excretion.|Extensively metabolized by CYP enzymes (specific isoenzyme[s] not identified) in the liver. Metabolites undergo further conjugation prior to excretion.|There is no enantiomeric bioconversion from tamsulosin hydrochloride [R(-) isomer] to the S(+) isomer in humans. Tamsulosin hydrochloride is extensively metabolized by cytochrome P450 enzymes in the liver and less than 10% of the dose is excreted in urine unchanged. However, the pharmacokinetic profile of the metabolites in humans has not been established. In vitro results indicate that CYP3A4 and CYP2D6 are involved in metabolism of tamsulosin as well as some minor participation of other CYP isoenzymes. Inhibition of hepatic drug metabolizing enzymes may lead to increased exposure to tamsulosin. The metabolites of tamsulosin hydrochloride undergo extensive conjugation to glucuronide or sulfate prior to renal excretion.|... After a single oral administration of 14C-tamsulosin at a dose of 0.2 mg /to/ four healthy male subjects... unchanged tamsulosin (TMS) and 11 metabolites in 0-24-hr urine samples were quantified. TMS accounted for 8.7% of the dose. Extensive excretion of the sulphate of the O-deethylated metabolite (M-1-Sul) and o-ethoxyphenoxy acetic acid (AM-1) was seen, accounting for 15.7 and 7.5% of the dose respectively.|The metabolism of tamsulosin hydrochloride (TMS), a potent alpha 1-adrenoceptor blocking agent, was studied after a single oral administration to rat and dog. Eleven metabolites (1, 2, 3, 4 and their glucuronides, sulphates of 1 and 3, and A-1) were identified from the urine and bile of rat and dog administered TMS. Unchanged drug and metabolites in urine and bile were quantified in rat and dog dosed with 14C-TMS(1 mg/kg). In rat the main metabolic routes were de-ethylation of the o-ethoxyphenoxy moiety, demethylation of the methoxybenzenesulphonamide moiety, and conjugation of the resultant metabolites by glucuronic acid and sulphuric acid. In dog the main pathways were de-ethylation of the ethoxyphenoxy moiety, conjugation of the de-ethylated product by sulphuric acid, and oxidative deamination of the side chain. The organ responsible for the metabolism of TMS in rat was estimated using 9000g supernatants of liver, kidney, small and large intestine homogenate and plasma. The drug was rapidly metabolized in liver but hardly metabolized in the other organs or plasma.|For more Metabolism/Metabolites (Complete) data for Tamsulosin (6 total), please visit the HSDB record page.|Tamsulosin has known human metabolites that include 5-[2-[2-(2-Ethoxyphenoxy)ethylamino]propyl]-2-hydroxybenzenesulfonamide, 5-[2-[2-(2-ethoxy-5-hydroxyphenoxy)ethylamino]propyl]-2-methoxybenzenesulfonamide, and 5-[2-[2-(2-hydroxyphenoxy)ethylamino]propyl]-2-methoxybenzenesulfonamide.

The half life in fasted patients is 14.9±3.9 hours. The elimination half life is 5-7 hours and the apparent half life is 9 to 13 hours in healthy subjects. In patients who require tamsulosin, the apparent half life is 14-15 hours.|Following intravenous or oral administration of an immediate-release formulation, the elimination half-life of tamsulosin hydrochloride in plasma range from five to seven hours.|Because of absorption rate-controlled pharmacokinetics of tamsulosin capsules, apparent half-life is about 9-13 hours in healthy individuals and 14-15 hours in patients with benign prostatic hyperplasia.|The pharmacokinetics of tamsulosin hydrochloride was investigated after single iv and oral dosing to rats and dogs, and oral dosing to healthy male volunteers. After iv dosing, plasma tamsulosin concentrations declined in an apparent biexponential manner with terminal half-lives of 0.32 hr in rats and 1.13 hr in dogs. ...

Tamsulosin is a blocker of alpha-1A and alpha-1D adrenoceptors. About 70% of the alpha-1 adrenoceptors in the prostate are of the alpha-1A subtype. By blocking these adrenoceptors, smooth muscle in the prostate is relaxed and urinary flow is improved. The blocking of alpha-1D adrenoceptors relaxes the detrusor muscles of the bladder which prevents storage symptoms. The specificity of tamsulosin focuses the effects to the target area while minimizing effects in other areas.|Tamsulosin hydrochloride is a sulfamoylphenethylamine-derivative alpha1-adrenergic blocking agent. The drug is pharmacologically related to doxazosin, prazosin, and terazosin; however, unlike these drugs, tamsulosin has higher affinity and selectivity for alpha1A-adrenergic receptors, which are mainly located in nonvascular smooth muscle (eg, prostate), than for alpha1B-adrenergic receptors located in vascular smooth muscle (eg, internal iliac artery). Results of in vitro studies indicate that tamsulosin has 7-38 times greater affinity for alpha1A-adrenoceptors than for alpha1B-adrenoceptors; the drug has about 12 times greater affinity for alpha1-adrenergic receptors in the prostate than for those in the aorta. Such selectivity of tamsulosin for alpha1A-receptors may result in a reduced incidence of adverse cardiovascular effects (eg, syncope, dizziness, hypotension). On a molar basis, the alpha1-adrenergic receptor affinity of tamsulosin is about 6 times that of prazosin when tested in human prostatic tissue.|Because of the prevalence of alpha-receptors on the prostate capsule, prostate adenoma, and bladder trigone and the relative absence of these receptors on the bladder body, alpha-adrenergic blocking agents decrease urinary outflow resistance in men.|The symptoms associated with benign prostatic hyperplasia (BPH) are related to bladder outlet obstruction, which is comprised of two underlying components: static and dynamic. The static component is related to an increase in prostate size caused, in part, by a proliferation of smooth muscle cells in the prostatic stroma. However, the severity of BPH symptoms and the degree of urethral obstruction do not correlate well with the size of the prostate. The dynamic component is a function of an increase in smooth muscle tone in the prostate and bladder neck leading to constriction of the bladder outlet. Smooth muscle tone is mediated by the sympathetic nervous stimulation of alpha1 adrenoceptors, which are abundant in the prostate, prostatic capsule, prostatic urethra, and bladder neck. Blockade of these adrenoceptors can cause smooth muscles in the bladder neck and prostate to relax, resulting in an improvement in urine flow rate and a reduction in symptoms of BPH.|The influence of (+/-)-tamsulosin, a selective alpha 1A-adrenoceptor antagonist, on the positive inotropic effect and the accumulation of inositol phosphates that are induced via alpha 1-adrenoceptors was studied in comparison with that of another alpha 1A-adrenoceptor ligand oxymetazoline in the rabbit ventricular myocardium. Phenylephrine elicited a concentration-dependent positive inotropic effect via alpha 1-adrenoceptors in the presence of either (+/-)-bupranolol or S(-)-timolol. The mode of antagonism induced by (+/-)-tamsulosin on the effect of phenylephrine was dependent or the concentration applied: (+/-)-tamsulosin at 1 and 3 nM acted in a competitive manner, the slope of the regression line of the Schild plot being unity and the pA2 value being 9.12; at 10 nM, it shifted further the concentration-response curve to the right without affecting the maximal response but the slope became less than unity. At 100 nM and higher, it suppressed the maximal response to phenylephrine. (+/-)-Tamsulosin effectively antagonized the positive inotropic effect of phenylephrine even after inactivation of alpha 1B-adrenoceptors by treatment with chlorethylclonidine, which is an indication that the (+/-)-tamsulosin-sensitive subtype belongs to a class resistant to chlorethylclonidine. (+/-)-Tamsulosin, over the range of concentrations at which it antagonized the positive inotropic effect mediated by alpha 1-adrenoceptors, did not affect the accumulation of [3H]inositol phosphates that was induced by 10 microM phenylephrine. Oxymetazoline antagonized the positive inotropic effect of phenylephrine in a competitive manner without affecting the accumulation of inositol monophosphate induced by phenylephrine. These results indicate that the positive inotropic effect, mediated via (+/-)-tamsulosin- and oxymetazoline-sensitive subtype of alpha 1-adrenoceptors, is exerted by a subcellular mechanism that is independent of the accumulation of inositol phosphates.

5-[(2R)-2-[bis[2-[(2-ethoxyphenoxy)ethyl]amino]propyl]-2-methoxybenzenesulfonamide|5-[(2R)-2-aminopropyl]-2-methoxybenzenesulfonamide|2-methoxy-5-[(2R)-2-[(2-phenoxyethyl)amino]propyl[benzenesulfonamide|2-methoxy-5-[(2R)-2-[[2-(2-methoxyphenoxy)ethyl]amino]propyl]benzenesulfonamide|For more Impurities (Complete) data for Tamsulosin (9 total), please visit the HSDB record page.

Should overdosage of Flomax (tamsulosin hydrochloride) capsules lead to hypotension ..., support of the cardiovascular system is of first importance. Restoration of blood pressure and normalization of heart rate may be accomplished by keeping the patient in the supine position. If this measure is inadequate, then administration of intravenous fluids should be considered. If necessary, vasopressors should then be used and renal function should be monitored and supported as needed. Laboratory data indicate that tamsulosin hydrochloride is 94% to 99% protein bound; therefore, dialysis is unlikely to be of benefit.|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ To assess whether tamsulosin has any effect on semen, sperm parameters were evaluated in healthy men receiving tamsulosin, alfuzosin, and placebo. Forty-eight healthy men received 5 days of tamsulosin 0.8 mg once daily (QD), alfuzosin 10 mg QD, and placebo in a randomized, double-blind, 3-way crossover study with a 10-14-day washout period between treatments. The mean (SE) changes from baseline in semen sperm concentration, semen sperm count, semen viscosity, semen fructose, sperm motility, and sperm morphology on Day 5 of treatment were assessed. The change from baseline in semen sperm concentration was 3.1 (8.3) million/mL with tamsulosin, 15.0 (6.5) million/mL with alfuzosin, and 24.4 (6.5) million/mL with placebo. The total sperm count in semen decreased from baseline with tamsulosin [-54.6 (24.0) million] but not with placebo [81.5 (18.8) million] or alfuzosin [46.2 (19.0) million]. The percentage of men with normal semen viscosity was lower with tamsulosin (65%) than with placebo (98%) or alfuzosin (92%). The change from baseline in semen fructose was comparable for all treatments. The percentage of motile sperm decreased 13.8% from baseline to Day 5 of treatment with tamsulosin compared with decreases of 2.3% with placebo and 0.4% with alfuzosin. The percentage of abnormal sperm increased marginally with tamsulosin (0.6%) but not with placebo (-2.8%) or alfuzosin (-3.9%). The most common adverse events were dizziness (alfuzosin 11%, tamsulosin 14%, placebo 0%) and orthostatic hypotension (alfuzosin 25%, tamsulosin 11%, placebo 5%). The results suggest that tamsulosin has a negative impact on sperm in healthy men. ...|/SIGNS AND SYMPTOMS/ One patient reported an overdose of thirty 0.4 mg tamsulosin hydrochloride capsules. Following the ingestion of the capsules, the patient reported a severe headache.|/CASE REPORTS/ A 65-year-old man underwent uncomplicated cataract extraction and placement of a posterior chamber intraocular lens. The patient subsequently developed three separate episodes of choroidal detachments in the operated eye. Each episode was preceded by treatment with an alpha(1)-adrenoceptor antagonist. Tamsulosin may cause adverse ocular effects including recurrent choroidal detachments ... The mechanism for choroidal detachment in this patient could include some effect of antagonists like tamsulosin on these receptors.|/CASE REPORTS/ /Investigators/ describe the case of an 80-year-old patient who was started on alpha blocker treatment after acute urinary retention with the aim to perform a voiding test. The patient presented self-limited episodes of disorientation in time and space and abnormal behavior in coincidence with the first three administrations of the drug. Treatment was stopped. ...|For more Human Toxicity Excerpts (Complete) data for Tamsulosin (12 total), please visit the HSDB record page.

5-(2-((2-(2-ethoxyphenoxy)ethyl)amino)propyl)-2-methoxybenzenesulfonamide

Formulations: (AHFS, 2009)

Analyte: tamsulosin hydrochloride; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards /tamsulosin hydrochloride/|Analyte: tamsulosin hydrochloride; matrix: chemical purity; procedure: dissolution in anhydrous formic acid; addition of acetic anhydride and glacial acetic acid; potentiometric titration with perchloric acid /tamsulosin hydrochloride/

Analyte: tamsulosin; matrix: bile, urine, microsomal incubations; procedure: high-performance liquid chromatography with ultraviolet detection at 275 nm|Analyte: tamsulosin; matrix: blood (plasma); procedure: high-performance liquid chromatography with mass spectrometry detection; limits of quantitation: 500 pg/mL (human); 1.0 ng/mL (rat, dog)