Absorption, Distribution and Excretion
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.

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Metabolism / Metabolites
Tamsulosin is mostly metabolized in the liver by cytochrome P450 (CYP) 3A4 and 2D6, with some metabolism by other CYPs. CYP3A4 is responsible for the deethylation of tamsulosin to the M-1 metabolite and the oxidative deamination to the AM-1 metabolite, while CYP2D6 is responsible for the hydroxylation of tamsulosin to the M-3 metabolite and the demethylation of tamsulosin to the M-4 metabolite. In addition, tamsulosin can be hydroxylated at a different position by an unknown enzyme to form the M-2 metabolite. The M-1, M-2, M-3, and M-4 metabolites can be glucuronidated, and 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-ethoxy-5-hydroxyphenoxy)ethylamino]propyl]-2-methoxybenzenesulfonamide, 5-[2-[2-(2-Ethoxyphenoxy)ethylamino]propyl]-2-hydroxybenzenesulfonamide, and 5-[2-[2-(2-hydroxyphenoxy)ethylamino]propyl]-2-methoxybenzenesulfonamide.

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Biological Half-Life
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. ...

Hepatotoxicity
Tamsulosin has been associated with a low rate of serum aminotransferase elevations (
Likelihood score: D (possible rare cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Although tamsulosin is not FDA approved for use in women, it is used off-label in women with kidney stones. No information is available on the use of tamsulosin during breastfeeding. Because it is 94 to 99% bound to plasma proteins, amounts in milk are likely to be small. If tamsulosin is required by the mother, it is not a reason to discontinue breastfeeding. However, the breastfed infant should be carefully monitored.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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

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Interactions
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.

[1]. Tamsulosin: an overview. World J Urol. 2002 Apr;19(6):397-404.

[2]. Tamsulosin Attenuates Abdominal Aortic Aneurysm Growth. Surgery. 2018 Nov; 164(5): 1087–1092.

Therapeutic Uses
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.

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Drug Warnings
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.

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Pharmacodynamics
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.

C20H28N2O5S

408.5117

408.171

106133-20-4

Tamsulosin hydrochloride;106463-17-6

129211

White to off-white solid powder

1.2±0.1 g/cm3

595.5±60.0 °C at 760 mmHg

226-228ºC

313.9±32.9 °C

0.0±1.7 mmHg at 25°C

1.553

2.24

2

7

11

28

539

1

CCOC1=CC=CC=C1OCCN[C@H](C)CC2=CC(=C(C=C2)OC)S(=O)(=O)N

DRHKJLXJIQTDTD-OAHLLOKOSA-N

InChI=1S/C20H28N2O5S/c1-4-26-17-7-5-6-8-18(17)27-12-11-22-15(2)13-16-9-10-19(25-3)20(14-16)28(21,23)24/h5-10,14-15,22H,4,11-13H2,1-3H3,(H2,21,23,24)/t15-/m1/s1

5-[(2R)-2-[2-(2-ethoxyphenoxy)ethylamino]propyl]-2-methoxybenzenesulfonamide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~244.79 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.12 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.12 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.12 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)