Absorption, Distribution and Excretion
The absorption rate of tamsulosin after oral administration in fasting patients is 90%. The area under the curve (AUC) for the 0.4 mg oral dose is 151-199 ng/mLhr, and for the 0.8 mg oral dose, it is 440-557 ng/mLhr. The peak plasma concentration (PPC) for the 0.4 mg oral dose is 3.1-5.3 ng/mL, and for the 0.8 mg oral dose, it is 2.5-3.6 ng/mL. Co-administration with food prolongs the time to peak concentration from 4-5 hours to 6-7 hours, but increases bioavailability by 30% and peak plasma concentration by 40-70%. Studies have shown that 97% of the drug is recovered 168 hours after oral administration, with 76% excreted in the urine and 21% in the feces. 8.7% of the dose is excreted as unmetabolized tamsulosin. The blood flow rate after intravenous administration is 16 liters.
Blood flow velocity was 2.88 L/h.
Patients with moderate hepatic impairment experienced altered protein binding, leading to changes in total plasma concentration; however, intrinsic clearance and free drug concentration remained largely unchanged.
Patients with renal impairment experienced altered protein binding, leading to changes in total plasma concentration; however, intrinsic clearance and free drug concentration remained largely unchanged.
After oral administration of tamsulosin hydrochloride on an empty stomach, absorption was essentially complete (>90%). Tamsulosin hydrochloride exhibited linear pharmacokinetics after both single and multiple doses, reaching steady-state concentrations by day 5 after once-daily administration.
After oral administration on an empty stomach, absorption was essentially complete; peak plasma concentrations were reached within 4–5 hours.
For more complete data on absorption, distribution, and excretion of tamsulosin (14 parameters), please visit the HSDB record page.
Metabolism/Metabolites
Tamsulosin is primarily metabolized in the liver by cytochrome P450 (CYP) 3A4 and 2D6, with some metabolism accomplished by other CYP enzymes. CYP3A4 is responsible for deethylating tamsulosin to the M-1 metabolite and oxidatively deaminated to generate the AM-1 metabolite; CYP2D6 is responsible for hydroxylating tamsulosin to the M-3 metabolite and demethylating it to generate the M-4 metabolite. In addition, tamsulosin can be hydroxylated at different positions by an unknown enzyme to generate the M-2 metabolite. The M-1, M-2, M-3, and M-4 metabolites can undergo glucuronidation, with the M-1 and M-3 metabolites undergoing sulfate conjugation before excretion to form other metabolites.
In the liver, it is mainly metabolized by CYP enzymes (specific isoenzymes have not yet been determined). Metabolites undergo further conjugation reactions before excretion. In the human body, tamsulosin hydrochloride [R(-) isomer] does not undergo enantiomeric biotransformation to the S(+) isomer. Tamsulosin hydrochloride is primarily metabolized in the liver by cytochrome P450 enzymes, with less than 10% of the dose excreted unchanged in the urine. However, the pharmacokinetic characteristics of its metabolites in the human body have not been determined. In vitro studies have shown that CYP3A4 and CYP2D6 are involved in the metabolism of tamsulosin, with other CYP isoenzymes also involved in small amounts. Inhibition of hepatic drug-metabolizing enzymes may lead to increased tamsulosin exposure. Tamsulosin hydrochloride metabolites are extensively bound to glucuronic acid or sulfate before renal excretion. …Four healthy male subjects underwent a single oral administration of 0.2 mg 14C-tamsulosin… Quantitative analysis of unchanged tamsulosin (TMS) and 11 metabolites in urinary samples from 0–24 hours was performed. TMS accounted for 8.7% of the administered dose. Significant excretion of the O-deethyl metabolite sulfate (M-1-Sul) and o-ethoxyphenoxyacetic acid (AM-1) was observed, accounting for 15.7% and 7.5% of the administered dose, respectively. This study investigated the metabolism of the potent α1-adrenergic receptor blocker tamsulosin hydrochloride (TMS) in rats and dogs following a single oral administration. Eleven metabolites (1, 2, 3, 4 and their glucuronides, sulfates of 1 and 3, and A-1) were identified from the urine and bile of rats and dogs administered TMS. Unmetabolized drug and its metabolites in the urine and bile of rats and dogs administered 14C-TMS (1 mg/kg) were quantitatively analyzed. In rats, the main metabolic pathways included deethylation of the o-ethoxyphenoxy moiety, demethylation of the methoxybenzenesulfonamide moiety, and conjugation of the resulting metabolites with glucuronic acid and sulfate. In dogs, the main metabolic pathways include deethylation of the ethoxyphenoxy moiety, conjugation of the deethylated product with sulfuric acid, and oxidative deamination of the side chain. Organs responsible for TMS metabolism in rats were evaluated using homogenates of liver, kidney, small intestine, and large intestine after centrifugation at 9000g, as well as plasma supernatant. The drug is rapidly metabolized in the liver but is hardly metabolized in other organs or plasma. For more complete data on the metabolism/metabolites of tamsulosin (6 metabolites), please visit the HSDB record page. Known human metabolites of tamsulosin 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.
Biological Half-Life
The half-life in fasting patients is 14.9 ± 3.9 hours. The elimination half-life in healthy subjects is 5–7 hours, and the apparent half-life is 9–13 hours. For patients requiring tamsulosin, the apparent half-life is 14–15 hours.
The elimination half-life of tamsulosin hydrochloride in plasma after intravenous or oral immediate-release formulations is 5 to 7 hours.
Because the absorption rate of tamsulosin capsules controls pharmacokinetics, the apparent half-life in healthy individuals is approximately 9–13 hours, and the apparent half-life in patients with benign prostatic hyperplasia is approximately 14–15 hours.
The pharmacokinetics of tamsulosin hydrochloride were studied in rats and dogs after single intravenous and oral administration, and in healthy male volunteers after oral administration. Following intravenous administration, plasma tamsulosin concentrations showed an apparent double-exponential decrease, with a terminal half-life of 0.32 hours in rats and 1.13 hours in dogs.

Hepatotoxicity
Tamsulosin is associated with a low incidence of elevated serum transaminases (Probability score: D (likely a rare cause of clinically significant liver injury)). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation While tamsulosin is not FDA approved for women, it has been used off-label to treat kidney stones in women. There is currently no information regarding the use of tamsulosin during lactation. Due to its high plasma protein binding rate of 94% to 99%, its concentration in breast milk may be very low. If the mother needs to take tamsulosin, this is not a reason to stop breastfeeding. However, breastfed infants should be closely monitored. ◉ Effects on Breastfed Infants No relevant published information was found as of the revision date. ◉ Effects on Breast Milk No relevant published information was found as of the revision date. Protein Binding Tamsulosin has a protein binding rate of 94%-99%, primarily binding to α1-acid glycoprotein. Interactions This study investigated the effect of the highest recommended dose of cimetidine (400 mg every 6 hours for 6 consecutive days) on the pharmacokinetics of a single 0.4 mg dose of tamsulosin hydrochloride capsules in 10 healthy volunteers (aged 21-38 years). Cimetidine treatment significantly reduced the clearance of tamsulosin hydrochloride (26%), leading to a moderate increase in the AUC of tamsulosin hydrochloride (44%). Therefore, caution should be exercised when tamsulosin hydrochloride capsules are used concomitantly with cimetidine, especially at doses above 0.4 mg. Drug Interactions Between Tamsulosin Hydrochloride and Warfarin: Based on limited in vitro and in vivo studies, the drug interaction results between tamsulosin hydrochloride and warfarin are inconclusive. Therefore, caution should be exercised when taking warfarin and tamsulosin hydrochloride capsules concurrently.
...The interaction between the two drugs was assessed in rats following simultaneous intravenous infusion of udenafil (30 mg/kg) and/or oral administration of tamsulosin (1 mg/kg) over 1 minute or 15 minutes. The in vitro metabolism of tamsulosin and udenafil was determined to obtain the inhibition constant (K_i) and [I]/K_i ratio of udenafil. Compared with tamsulosin alone, the area under the plasma concentration-time curve (AUC_0-∞) (or AUC_{0-4 h}) of tamsulosin was significantly increased after intravenous infusion over 15 minutes or oral administration of udenafil. First-pass metabolism of tamsulosin in the liver was inhibited by udenafil, and the in vitro inhibition was non-competitive. Arterial systolic blood pressure was significantly reduced at 5, 10, and 60 minutes after oral co-administration. The AUC of tamsulosin was significantly increased after both intravenous and oral administration, which may be attributed to the non-competitive inhibition of hepatic tamsulosin metabolism mediated by urdinavianil against cytochrome P450 3A1/2. This inhibitory effect was also observed in the human liver S9 fraction, suggesting the need to reassess the oral dosage of tamsulosin when urdinavianil and tamsulosin are used in combination to treat 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; Alpha-adrenergic antagonists. Tamsulosin Hydrochloride Capsules are indicated for the treatment of signs and symptoms of benign prostatic hyperplasia (BPH). /US Product Label Includes/ Tamsulosin Hydrochloride Capsules are not indicated as an antihypertensive medication. /US Product Label Includes/ Tamsulosin Hydrochloride Capsules are not indicated for women. /US Product Label Includes/ For more complete data on the therapeutic uses of tamsulosin (of 6 types), please visit the HSDB record page. Drug Warnings Contraindications/Including/Known hypersensitivity to tamsulosin or any component of the formulation. Orthostatic hypotension, dizziness, or vertigo may occur; syncope may occur. Patients taking tamsulosin hydrochloride capsules are more likely to experience signs and symptoms of orthostatic hypotension, dizziness, and vertigo compared to the placebo group. As with other alpha-adrenergic blockers, there is a potential risk of syncope with this product.
Patients starting tamsulosin hydrochloride capsules should take precautions to avoid situations that could lead to syncope and injury. ...Patients should be informed that symptoms associated with orthostatic hypotension, such as dizziness, may occur when taking tamsulosin hydrochloride capsules, and should avoid driving, operating machinery, or engaging in hazardous work.
For more complete data on tamsulosin (17 in total), please visit the HSDB record page.

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Pharmacodynamics
Tamsulosin is an alpha-adrenergic receptor blocker, specific for alpha-1A and alpha-1D subtypes, which are more common in the prostate and submandibular gland tissues. The alpha-1B subtype is most common in the aorta and spleen. Tamsulosin has a 3.9-38 times higher selectivity for binding to alpha-1A receptors than alpha-1B and a 3-20 times higher selectivity than alpha-1D. This selectivity allows the drug to significantly improve urine flow while reducing the incidence of adverse reactions such as 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.)