Tamsulosin is an oral alpha-blocker that can be administered once-daily for the treatment of benign prostatic hyperplasia (BPH). Tamsulosin appears to cause less hypotension than other alpha-blockers due to enhanced specificity for the alpha-receptors on the prostate. As a result, tamsulosin therapy can be initiated at the optimum dose whereas other alpha-blockers require gradual upward titration to reduce the risk of an exaggerated response to the 'first-dose' effects. Additionally, because no significant interactions were noted when tamsulosin was administered with atenolol, enalapril, and nifedipine, tamsulosin may be safer to use in patients with both BPH and hypertension. Tamsulosin, however, is not indicated as a treatment for hypertension and should not be used with other alpha-blockers. In June 2008, dutasteride was approved by the FDA for use in combination with tamsulosin for the treatment of symptomatic BPH in men with an enlarged prostate. The approval followed favorable results from a 2-year interim analysis of the Combination With Alpha-Blocker Therapy (CombAT) trial in which treatment with dutasteride plus tamsulosin (n = 1,610) was compared to dutasteride alone (n = 1,623) or tamsulosin alone (n = 1,611). The symptom score, as determined by the International Prostate Symptom Score (IPSS) questionnaire, was significantly decreased in those receiving combination therapy compared to the dutasteride or tamsulosin monotherapy groups beginning at Month 3 and Month 9, respectively. The maximum urine flow rate increased significantly in the combination group compared to either monotherapy group from Months 6 to 24. The mean percent change in prostate volume from baseline was only significant between the combination group and the tamsulosin monotherapy group (-26.9% vs 0%). Results from Months 25-48 of the study are not yet available. Tamsulosin was FDA approved for BPH in April 1997.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
Route-Specific Administration
Oral Administration
-Administer approximately 30 minutes after the same meal each day.
-Per the package label, the capsules should be swallowed whole and not crushed, chewed, or opened. However, trials with pediatric patients have reported that the capsules were opened if the patient had difficulty swallowing or if the prescribed dosage required. The contents of a capsule (i.e., granules) were mixed with cool, soft food (e.g., yogurt or pudding) or with juice. If tamsulosin is administered via this method, instruct the patient not to chew, crush, or dissolve the granules as these actions may result in rapid drug release and serious side effects.
-The administration of tamsulosin through nasogastric, gastric, or jejunostomy tubes has not been formally evaluated by the manufacturer; reports suggest that the granules may adhere to the sides of the tube, which complicates administration and increases the risk of tube blockage.
The adverse reaction profile of tamsulosin is based on reports from two US 13-week, placebo-controlled trials conducted in 1487 men. The most common adverse reactions reported in >= 2% of patients receiving tamsulosin (and numerically greater than placebo) included: asthenia (7.8-8.5%), back pain (7-8.3%), blurred vision (0.2-2%), chest pain (unspecified) (4-4.1%), cough increase (3.4-4.5%), diarrhea (4.3-6.2%), drowsiness/somnolence (3-4.3%), headache (19.3-21.1%), infection (9-10.8%), insomnia (1.4-2.4%), nausea (2.6-3.9%), pharyngitis (5.1-5.8%), rhinitis (13.1-17.9%), sinusitis (2.2-3.7%), and tooth disorder (1.2-2%). Epistaxis was reported during post-marketing surveillance of tamsulosin.
Allergic-type and dermatologic reactions have been reported post-marketing; some events have occurred again on drug rechallenge. These reactions have included skin rash (unspecified), pruritus, angioedema of tongue, lips and face, urticaria, erythema multiforme, exfoliative dermatitis, and respiratory symptoms (unspecified). Infrequent reports of dyspnea and skin desquamation (including Stevens-Johnson syndrome) have been received during the post-marketing period. Published data indicate that the appearance of skin rash (unspecified) is fairly common, with a published incidence of 2-5% of patients in a pharmacovigilance study (n=12,484) , and up to 7% of patients in a phase III open-label multicenter study (n = 949) , respectively.
Even though tamsulosin causes less hypotension than other alpha-blockers, signs and symptoms of orthostasis were reported during two US short-term, placebo-controlled trials conducted in 1487 men. The most common symptoms included dizziness, syncope, symptomatic orthostatic hypotension, and vertigo. Symptomatic orthostatic hypotension was reported by 0.2% and 0.4% of patients in the 0.4-mg (n=502) and 0.8-mg (n=492) groups, respectively. Syncope was reported by 0.2%, 0.4%, and 0.6% of patients in the 0.4-mg, 0.8-mg, and placebo (n=493) groups, respectively. Vertigo was reported by 0.6% of patients in the 0.4-mg and placebo group and by 1% of patients in the 0.8-mg group. Dizziness was reported by 14.9%, 17.1%, and 10.1% of patients in the 0.4-mg, 0.8-mg, and placebo groups, respectively. Because orthostasis occurred more frequently in tamsulosin-treated patients than in placebo, patients should be monitored for signs of orthostasis. Multiple testing for orthostatic hypotension has been conducted. Positive orthostatic test results (i.e., 20 mm Hg drop in systolic blood pressure, 10 mm Hg drop in diastolic blood pressure, or 20 bpm increase in heart rate or symptoms of orthostasis when going from supine to standing position) have been reported in 6-19% of patients receiving tamsulosin. Infrequent reports of palpitations, hypotension, atrial fibrillation, arrhythmia exacerbation, and sinus tachycardia have been reported during the post-marketing period.
Ejaculation dysfunction (includes ejaculation failure, ejaculation decrease, and retrograde ejaculation) is a dose-related adverse reaction associated with tamsulosin therapy. During two U.S. short-term, placebo-controlled studies, about 42 of 502 patients (8.4%) in the 0.4-mg group experienced abnormal ejaculation whereas about 89 of 492 patients (18.1%) in the 0.8-mg group experienced abnormal ejaculation. Withdrawal from these clinical studies because of abnormal ejaculation was also dose-dependent. Eight (8) of 492 patients (1.6%) in the 0.8-mg group discontinued treatment whereas no patients in the 0.4-mg or placebo groups discontinued treatment. Also, libido decrease was seen in 5 of 502 patients (1%) in the 0.4-mg group and in 10 of 492 patients (2%) of the 0.8-mg group. Rarely (probably less than 1 in 50,000 patients), tamsulosin, like other alpha-blockers, has been associated with priapism and this adverse effect has been reported by patients during the postmarketing period.
Infrequent reports of constipation, xerostomia, and vomiting have been received during the post-marketing period.
Patients considering cataract or glaucoma surgery should be advised to tell their ophthalmologist that they have taken tamsulosin. Tamsulosin has been associated with an ocular condition known as intraoperative floppy iris syndrome. Tamsulosin selectively blocks alpha-1A receptor subtypes whereas other selective alpha-1 receptor blockers do not distinguish between alpha-1 receptor subtypes 1A, 1B, or 1D; it is not known if other selective alpha-1 receptor blockers are associated with this condition. Intraoperative floppy iris syndrome has been reported during cataract and glaucoma surgery in some patients treated with tamsulosin and is a variant of small pupil syndrome. The syndrome is characterized by a triad of features that distinguish it: 1) a flaccid iris that billows in response to intraoperative irrigation currents, 2) progressive intraoperative miosis despite preoperative dilation with standard mydriatic drugs, and 3) potential prolapse of the iris toward the phacoemulsification incisions. Most reports were in patients taking tamsulosin when IFIS occurred, but in some cases, the alpha-1 blocker had been stopped prior to surgery. In most cases, tamsulosin had been discontinued within 2 to 14 days, but in a few cases, IFIS was reported after tamsulosin therapy was stopped for a longer period (5 weeks to 9 months). The mechanism of this syndrome is thought to be inhibition of alpha-1A receptors in the iris. Based on animal data in rabbits, which are purported to have similar iris alpha-1 receptor subtypes to human, tamsulosin selectively blocks the alpha-1A receptors in iris dilator smooth muscle. Since tamsulosin has a long half-life, this alpha-1A receptor blockade in the iris can cause a form of disuse atrophy of the iris dilator smooth muscle. Patients receiving tamsulosin often have poor pupil dilation; amblyopia is reported frequently. The patient's ophthalmologist should be prepared for possible modifications to their surgical technique, such as the utilization of iris hooks, iris dilator rings, or viscoelastic substances. The benefit of stopping alpha-1 blocker therapy prior to cataract or glaucoma surgery has not been established. During post-marketing surveillance of tamsulosin, visual impairment was also reported.
Tamsulosin is a non-arylamine sulfonamide derivative. In patients with sulfonamide hypersensitivity, allergic reaction to tamsulosin has been rarely reported. If a patient reports a serious or life threatening sulfonamide allergy, the manufacturer advises caution when administering tamsulosin. However, tamsulosin is not contraindicated for use in patients with sulfonamide allergy. Based on clinical trials and post-marketing experience with tamsulosin, the potential for cross-reactivity in patients with sulfonamide allergy has not been established. In post-marketing experience, allergic-type reactions (such as skin rash, pruritus, urticaria, and angioedema of the tongue, lips, and face) have been reported in some cases, and, in very rare cases, in patients who had a history of sulfa allergy (manufacturer data on file). According to the manufacturer, clinical trials with tamsulosin did not screen for or exclude patients with a history of sulfonamide allergy; therefore, the actual potential for sulfonamide cross-reactivity with tamsulosin is unknown. Non-arylamine sulfonamide derivatives (e.g., tamsulosin) have been reported to be proposed to have a lower risk of allergic reactions in patients with sulfonamide allergy, presumably due to the lack of one of the proposed structural sites of action for sulfonamide allergy (arylamine group in the N4 position). One large retrospective cohort study has reported that in patients with the presence of an allergic reaction after exposure to a sulfonamide antibiotic, 9.9% had an allergic reaction after receiving a non-antibiotic sulfonamide derivative, and 1.6% of patients who lacked an allergic reaction after sulfonamide antibiotic exposure had an allergic reaction after administration of a non-antibiotic sulfonamide derivative (adjusted odds ratio 2.8; 95% CI, 2.1-3.7). A causal relationship between sulfonamide hypersensitivity and allergic reactions with non-arylamine sulfonamide derivatives has not been definitively established and remains controversial. In general, patients with a documented sulfonamide allergy are considered to be predisposed for development of allergic drug reactions. Until further data are available, caution is prudent when administering sulfonamide derivatives to patients with a documented sulfonamide hypersensitivity.
Tamsulosin should be used cautiously in patients with orthostatic hypotension, vertigo, or syncope. The signs and symptoms of orthostasis (postural hypotension, dizziness, and vertigo) were more frequently reported in tamsulosin-treated patients than those receiving placebo. As with other alpha-adrenergic blocking agents, there is a potential risk of syncope and patients should be cautioned to avoid situations where injury could result should syncope occur. Elderly patients and patients with renal impairment or renal failure should be monitored carefully for exaggerated hypotensive effects (e.g., first dose effect).
Prostate cancer and benign prostatic hyperplasia (BPH) cause many of the same symptoms and frequently they coexist. Patients should be evaluated prior to starting tamsulosin therapy to rule out the presence of prostate cancer.
Tamsulosin has not been studied in patients with severe hepatic impairment. Since tamsulosin is extensively metabolized, cautious dosage initiation at a lower dosage is prudent in patients with severe hepatic disease.
Tamsulosin is only approved by the FDA to treat benign prostatic hyperplasia in men. Tamsulosin is not indicated for use in women and there are no adequate data on the developmental risks associated with the use of tamsulosin during human pregnancy. Animals studies have not revealed adverse developmental effects; however, animal studies are not always predictive of human response.
Tamsulosin is only approved by the FDA to treat benign prostatic hyperplasia in men. Tamsulosin is not indicated in women, and there are no data on the use of tamsulosin in breast-feeding women. There are no data regarding the presence or absence of tamsulosin in human milk, the effects of tamsulosin on the breastfed infant, or the effects on milk production.
Tamsulosin is only FDA-approved to treat benign prostatic hyperplasia in men; the drug is not FDA-approved for use in children. There are limited clinical data regarding use in pediatric patients for off-label purposes; use with caution. There are no data describing tamsulosin use in infants.
Patients receiving or who have previously received treatment with tamsulosin or other alpha-1 blockers may be at risk for intraoperative floppy iris syndrome (IFIS) during surgery for cataracts (ocular surgery). Intraoperative floppy iris syndrome is a small pupil syndrome variant that is characterized by a flaccid iris that billows in response to intraoperative irrigation currents, progressive intraoperative miosis despite preoperative dilation with standard mydriatic drugs, and potential prolapse of the iris toward the phacoemulsification incisions. IFIS may increase the risk of eye complications during and after surgery. Ophthalmologists should be notified of a patient's use of tamsulosin or other alpha-1 blockers prior to cataract surgery and should be prepared for possible modifications to their surgical technique such as the use of iris hooks, iris dilator rings, or viscoelastic substances. The benefit of stopping alpha-1 blocker therapy prior to cataract surgery has not been established. However, it is recommended to avoid initiation of new therapy with tamsulosin in patients scheduled for cataract surgery.
Rarely (probably less than 1 in 50,000), tamsulosin, like other alpha adrenergic antagonists, has been associated with priapism (persistent painful penile erection unrelated to sexual activity). Priapism, if not treated promptly, can result in irreversible damage to the erectile tissue. Patients who have an erection lasting greater than 4 hours, whether painful or not, should seek emergency medical attention.
Tamsulosin can cause orthostatic hypotension with accompanying dizziness or vertigo. Geriatric adults should be monitored carefully for exaggerated hypotensive effects (e.g., first dose effect).
For the treatment of benign prostatic hyperplasia (BPH):
Oral dosage:
Adults: 0.4 mg PO once daily, initially. May increase the dose to 0.8 mg PO once daily after 2 to 4 weeks based on clinical response. If therapy is interrupted for several days, restart at 0.4 mg PO once daily.
For medical expulsive treatment (MET) as an adjunct to conservative management of distal uretal nephrolithiasis*:
Oral dosage:
Adults: Adults with radiopaque lower ureteral stones of 10 mm or smaller have received tamsulosin 0.4 mg PO at bedtime for 28 days or until definite stone passage (i.e., evidence of stone on urine straining) in addition to standard analgesia (e.g., NSAID, etc.) in clinical studies. Data suggest that patients receiving tamsulosin for medical expulsive therapy (MET) with stones of 5 to 10 mm pass the stones earlier and with less pain than if no tamsulosin is received; thus, MET may be considered in these patients. Tamsulosin may offer little benefit over placebo for patients with stones of less than 5 mm.
Children and Adolescents: Pediatric patients with radiopaque lower ureteral stones of 10 or 12 mm or smaller have received the following doses: tamsulosin 0.4 mg PO at bedtime for children older than 4 years and 0.2 mg PO at bedtime for children 4 years or younger, given for 28 days or until definite stone passage (i.e., evidence of stone on urine straining). Tamsulosin is given in addition to standard analgesia (e.g., ibuprofen). Most patients receiving tamsulosin pass stones earlier and with less pain than if no tamsulosin is received. Mild somnolence is common. In children, if pain is controlled with oral analgesia, clear liquids are tolerated, and there is no evidence of infection, they are closely monitored for spontaneous passage for 3 to 4 weeks prior to definitive therapy, since most data demonstrate safe lower uretal stone expulsion in the first 10 days of conservative medical management.
Maximum Dosage Limits:
-Adults
0.8 mg/day PO.
-Elderly
0.8 mg/day PO.
-Adolescents
Safety and efficacy have not been established.
-Children
Safety and efficacy have not been established.
Patients with Hepatic Impairment Dosing
Mild to moderate hepatic impairment (Child Pugh Class A or B): No dosage adjustment is needed.
Severe hepatic impairment (Child Pugh Class C): No dosage recommendations are available. Tamsulosin has not been studied in patients with severe hepatic impairment.
Patients with Renal Impairment Dosing
No dosage adjustment is needed. Patients with renal impairment should be monitored carefully for exaggerated hypotensive effects (e.g., first dose effect). Patients with end-stage renal disease (CrCl less than 10 mL/minute/1.73 m2) have not been specifically studied.
Intermittent hemodialysis:
No dosage adjustment appears to be needed. Patients with renal impairment should be monitored carefully for exaggerated hypotensive effects (e.g., first dose effect). Tamsulosin is highly protein bound and is not likely to be significantly removed during hemodialysis. Patients with end-stage renal disease (CrCl less than 10 mL/minute/1.73 m2) have not been specifically studied.
*non-FDA-approved indication
Abiraterone: (Moderate) Monitor for an increase in tamsulosin-related adverse reactions if coadministration with abiraterone is necessary. Tamsulosin is a CYP2D6 substrate and abiraterone is a moderate CYP2D6 inhibitor. The effects of coadministration with a moderate CYP2D6 on the pharmacokinetics of tamsulosin have not been evaluated; however, the manufacturer of tamsulosin recommends caution with use.
Acebutolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Acetaminophen; Aspirin; Diphenhydramine: (Moderate) Use caution if coadministration of diphenhydramine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and diphenhydramine is a moderate CYP2D6 inhibitor.
Acetaminophen; Chlorpheniramine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Acetaminophen; Chlorpheniramine; Dextromethorphan: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Acetaminophen; Chlorpheniramine; Dextromethorphan; Phenylephrine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Acetaminophen; Chlorpheniramine; Dextromethorphan; Pseudoephedrine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Acetaminophen; Chlorpheniramine; Phenylephrine : (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Acetaminophen; Diphenhydramine: (Moderate) Use caution if coadministration of diphenhydramine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and diphenhydramine is a moderate CYP2D6 inhibitor.
Adagrasib: (Major) Concurrent use of tamsulosin and adagrasib is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A and CYP2D6 substrate and adagrasib is a strong CYP3A and moderate CYP2D6 inhibitor. Concomitant treatment with another strong CYP3A inhibitor increased the AUC of tamsulosin by 2.8-fold.
Alpha-blockers: (Major) Tamsulosin should not be administered in combination with other alpha-blockers. The pharmacokinetic and pharmacodynamic interactions between tamsulosin and other alpha-blockers (used for high blood pressure or for benign prostatic hyperplasia) have not been determined. However, interactions or side effects (dizziness, hypotension, syncope, etc.) may be expected from the duplication of pharmacologic effects.
Ambrisentan: (Minor) Because symptoms of orthostasis (e.g., postural hypotension, dizziness, vertigo) are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Amiodarone: (Moderate) Use caution if coadministration of amiodarone with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A4 and CYP2D6 substrate and amiodarone is a moderate CYP3A4 and CYP2D6 inhibitor. The effects of concomitant administration of a moderate CYP3A4 and CYP2D6 inhibitor on the pharmacokinetics of tamsulosin have not been evaluated, but tamsulosin exposure may increase based on the effects of strong CYP3A4 and CYP2D6 inhibition.
Amlodipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Amlodipine; Atorvastatin: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Amlodipine; Benazepril: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Amlodipine; Celecoxib: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Amlodipine; Olmesartan: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Amlodipine; Valsartan: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Amlodipine; Valsartan; Hydrochlorothiazide, HCTZ: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Amobarbital: (Moderate) Concurrent use of amobarbital with antihypertensive agents may lead to hypotension. Monitor for decreases in blood pressure during times of coadministration.
Amoxicillin; Clarithromycin; Omeprazole: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of clarithromycin. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use with a strong CYP3A4 inhibitor, such as clarithromycin, should be avoided.
Aprepitant, Fosaprepitant: (Moderate) Use caution if tamsulosin and aprepitant, fosaprepitant are used concurrently and monitor for an increase in tamsulosin-related adverse effects for several days after administration of a multi-day aprepitant regimen. Tamsulosin is a CYP3A4 substrate. Aprepitant, when administered as a 3-day oral regimen (125 mg/80 mg/80 mg), is a moderate CYP3A4 inhibitor and inducer and may increase plasma concentrations of tamsulosin. For example, a 5-day oral aprepitant regimen increased the AUC of another CYP3A4 substrate, midazolam (single dose), by 2.3-fold on day 1 and by 3.3-fold on day 5. After a 3-day oral aprepitant regimen, the AUC of midazolam (given on days 1, 4, 8, and 15) increased by 25% on day 4, and then decreased by 19% and 4% on days 8 and 15, respectively. As a single 125 mg or 40 mg oral dose, the inhibitory effect of aprepitant on CYP3A4 is weak, with the AUC of midazolam increased by 1.5-fold and 1.2-fold, respectively. After administration, fosaprepitant is rapidly converted to aprepitant and shares many of the same drug interactions. However, as a single 150 mg intravenous dose, fosaprepitant only weakly inhibits CYP3A4 for a duration of 2 days; there is no evidence of CYP3A4 induction. Fosaprepitant 150 mg IV as a single dose increased the AUC of midazolam (given on days 1 and 4) by approximately 1.8-fold on day 1; there was no effect on day 4. Less than a 2-fold increase in the midazolam AUC is not considered clinically important.
Artemether; Lumefantrine: (Moderate) Use caution when administering tamsulosin with a strong CYP2D6 inhibitor such as artemether; lumefantrine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure. If concomitant use in necessary, monitor patient closely for increased side effects.
Atazanavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Atazanavir; Cobicistat: (Major) Concurrent use of tamsulosin and cobicistat is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is metabolized by CYP3A4 and CYP2D6 hepatic enzymes. Cobicistat is a strong inhibitor of CYP3A4 and a CYP2D6 inhibitor. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively. (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Atenolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Atenolol; Chlorthalidone: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Avanafil: (Moderate) Due to the potential for symptomatic hypotension, patients should be stable on tamsulosin therapy before initiating therapy with the lowest dose of avanafil. Conversely, patients already receiving an optimized dose of avanafil should be started on the lowest dose of tamsulosin; increases in the alpha-blocker dose should be done in a stepwise fashion. Other variables, such as intravascular volume depletion, concurrent antihypertensive therapy, or evidence of hemodynamic instability with alpha-blocker monotherapy, may affect the safety of concomitant use of avanafil and tamsulosin.
Berotralstat: (Moderate) Use caution if coadministration of berotralstat with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg. The systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A4 and CYP2D6 substrate and berotralstat is a moderate CYP3A4 and CYP2D6 inhibitor. The effects of concomitant administration of a moderate CYP3A4/CYP2D6 inhibitor on the pharmacokinetics of tamsulosin have not been evaluated, but tamsulosin exposure may increase based on the effects of strong CYP3A4 inhibition.
Beta-blockers: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Betaxolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Bisoprolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Bisoprolol; Hydrochlorothiazide, HCTZ: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Brimonidine; Timolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Bupropion: (Moderate) Use caution if coadministration of bupropion with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and bupropion is a strong CYP2D6 inhibitor. Concomitant treatment with another strong CYP2D6 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively.
Bupropion; Naltrexone: (Moderate) Use caution if coadministration of bupropion with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and bupropion is a strong CYP2D6 inhibitor. Concomitant treatment with another strong CYP2D6 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively.
Calcium-channel blockers: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Capivasertib: (Moderate) Use caution if coadministration of capivasertib with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and capivasertib is a moderate CYP2D6 inhibitor.
Carteolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Carvedilol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Ceritinib: (Major) Concurrent use of tamsulosin and ceritinib is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes, and strong inhibitors of CYP3A4 like ceritinib are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Chloramphenicol: (Moderate) Use caution when administering tamsulosin with a moderate CYP3A4 inhibitor such as chloramphenicol. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure; interactions with moderate CYP3A4 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Codeine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Dextromethorphan: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Dextromethorphan; Phenylephrine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Dextromethorphan; Pseudoephedrine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Hydrocodone: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Ibuprofen; Pseudoephedrine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Phenylephrine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpheniramine; Pseudoephedrine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpheniramine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Chlorpromazine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as chlorpromazine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Cimetidine: (Moderate) Use caution if coadministration of cimetidine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Treatment with cimetidine 400 mg every 6 hours for 6 days in healthy volunteers (n = 10) resulted in a 26% decrease in the clearance of tamsulosin, which resulted in a 44% increase in tamsulosin AUC. Tamsulosin is a CYP2D6 and CYP3A substrate and cimetidine is a weak CYP2D6 and CYP3A inhibitor.
Cinacalcet: (Moderate) Use caution if coadministration of cinacalcet with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and cinacalcet is a moderate CYP2D6 inhibitor.
Clarithromycin: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of clarithromycin. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use with a strong CYP3A4 inhibitor, such as clarithromycin, should be avoided.
Clevidipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Cobicistat: (Major) Concurrent use of tamsulosin and cobicistat is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is metabolized by CYP3A4 and CYP2D6 hepatic enzymes. Cobicistat is a strong inhibitor of CYP3A4 and a CYP2D6 inhibitor. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Conivaptan: (Moderate) Use caution if coadministration of conivaptan with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A substrate and conivaptan is a moderate CYP3A inhibitor.
Crizotinib: (Moderate) Use caution if coadministration of crizotinib with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A4 substrate and crizotinib is a moderate CYP3A4 inhibitor. The effects of concomitant administration of a moderate CYP3A4 inhibitor on the pharmacokinetics of tamsulosin have not been evaluated, but tamsulosin exposure may increase based on the effects of strong CYP3A4 inhibition.
Cyclosporine: (Moderate) Use caution when administering tamsulosin with a moderate CYP3A4 inhibitor such as cyclosporine. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure; interactions with moderate CYP3A4 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Dacomitinib: (Moderate) Use caution if coadministration of dacomitinib with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and dacomitinib is a strong CYP2D6 inhibitor. Concomitant treatment with another strong CYP2D6 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively.
Danazol: (Moderate) Use caution when administering tamsulosin with a moderate CYP3A4 inhibitor such as danazol. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure; interactions with moderate CYP3A4 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Darifenacin: (Moderate) Use caution if coadministration of darifenacin with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and darifenacin is a moderate CYP2D6 inhibitor. The effects of concomitant administration of a moderate CYP2D6 inhibitor on the pharmacokinetics of tamsulosin have not been evaluated, but tamsulosin exposure may increase based on the effects of strong CYP2D6 inhibition.
Darunavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Darunavir; Cobicistat: (Major) Concurrent use of tamsulosin and cobicistat is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is metabolized by CYP3A4 and CYP2D6 hepatic enzymes. Cobicistat is a strong inhibitor of CYP3A4 and a CYP2D6 inhibitor. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively. (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Darunavir; Cobicistat; Emtricitabine; Tenofovir alafenamide: (Major) Concurrent use of tamsulosin and cobicistat is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is metabolized by CYP3A4 and CYP2D6 hepatic enzymes. Cobicistat is a strong inhibitor of CYP3A4 and a CYP2D6 inhibitor. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively. (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Delavirdine: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of delavirdine. Tamsulosin is extensively metabolized by CYP2D6 and CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Therefore, concomitant use with drugs that inhibit both CYP2D6 and CYP3A4, such as delavirdine, should be avoided.
Dextromethorphan; Bupropion: (Moderate) Use caution if coadministration of bupropion with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and bupropion is a strong CYP2D6 inhibitor. Concomitant treatment with another strong CYP2D6 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively.
Dextromethorphan; Diphenhydramine; Phenylephrine: (Moderate) Use caution if coadministration of diphenhydramine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and diphenhydramine is a moderate CYP2D6 inhibitor.
Dextromethorphan; Quinidine: (Moderate) Use caution when administering tamsulosin with a strong CYP2D6 inhibitor such as quinidine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure. If concomitant use in necessary, monitor patient closely for increased side effects.
Diltiazem: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Diphenhydramine: (Moderate) Use caution if coadministration of diphenhydramine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and diphenhydramine is a moderate CYP2D6 inhibitor.
Diphenhydramine; Ibuprofen: (Moderate) Use caution if coadministration of diphenhydramine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and diphenhydramine is a moderate CYP2D6 inhibitor.
Diphenhydramine; Naproxen: (Moderate) Use caution if coadministration of diphenhydramine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and diphenhydramine is a moderate CYP2D6 inhibitor.
Diphenhydramine; Phenylephrine: (Moderate) Use caution if coadministration of diphenhydramine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and diphenhydramine is a moderate CYP2D6 inhibitor.
Dorzolamide; Timolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Doxazosin: (Major) Tamsulosin should not be administered in combination with other alpha-blockers. The pharmacokinetic and pharmacodynamic interactions between tamsulosin and other alpha-blockers (used for high blood pressure or for benign prostatic hyperplasia) have not been determined. However, interactions or side effects (dizziness, hypotension, syncope, etc.) may be expected from the duplication of pharmacologic effects.
Dronedarone: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of dronedarone. Tamsulosin is extensively metabolized by CYP2D6 and CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Therefore, concomitant use with drugs that inhibit both CYP2D6 and CYP3A4, such as dronedarone, should be avoided.
Duloxetine: (Moderate) Use caution if coadministration of duloxetine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and duloxetine is a moderate CYP2D6 inhibitor.
Elbasvir; Grazoprevir: (Moderate) Administering tamsulosin with elbasvir; grazoprevir may result in elevated tamsulosin plasma concentrations. Tamsulosin is a substrate of CYP3A; grazoprevir is a weak CYP3A inhibitor. If these drugs are used together, closely monitor for signs of adverse events.
Eliglustat: (Moderate) Coadministration of tamsulosin and eliglustat may result in increased concentrations of tamsulosin. Use tamsulosin with caution in patients receiving eliglustat, particularly if the tamsulosin dose is greater than 0.4 mg, and monitor closely for tamsulosin-related adverse effects including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 and CYP3A4 substrate; eliglustat is a CYP2D6 inhibitor.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide: (Major) Concurrent use of tamsulosin and cobicistat is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is metabolized by CYP3A4 and CYP2D6 hepatic enzymes. Cobicistat is a strong inhibitor of CYP3A4 and a CYP2D6 inhibitor. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate: (Major) Concurrent use of tamsulosin and cobicistat is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is metabolized by CYP3A4 and CYP2D6 hepatic enzymes. Cobicistat is a strong inhibitor of CYP3A4 and a CYP2D6 inhibitor. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Erythromycin: (Moderate) Use caution if coadministration of erythromycin with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A substrate and erythromycin is a moderate CYP3A inhibitor.
Escitalopram: (Moderate) Use caution if coadministration of escitalopram with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and escitalopram is a moderate CYP2D6 inhibitor.
Esmolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Everolimus: (Moderate) Monitor for an increase in tamsulosin-related adverse reactions if coadministration with everolimus is necessary. Tamsulosin is a CYP3A4 and CYP2D6 substrate. Everolimus is a weak CYP3A4 inhibitor and a CYP2D6 inhibitor. The effects of coadministration of both a CYP3A4 and CYP2D6 inhibitor with tamsulosin have not been evaluated; however, there is a potential for significantly increased plasma concentrations of tamsulosin.
Fedratinib: (Moderate) Use caution if coadministration of fedratinib with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A4 and CYP2D6 substrate and fedratinib is a moderate CYP3A4 and CYP2D6 inhibitor. The effects of concomitant administration of moderate CYP3A4 and moderate CYP2D6 inhibitors on the pharmacokinetics of tamsulosin have not been evaluated, but tamsulosin exposure may increase based on the effects of strong CYP3A4 and CYP2D6 inhibition.
Felodipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Finasteride; Tadalafil: (Moderate) Due to the potential for symptomatic hypotension, patients should be stable on tamsulosin therapy before initiating therapy with the lowest recommended dose of tadalafil. Conversely, patients already receiving an optimized dose of tadalafil should be started on the lowest dose of tamsulosin; increases in the alpha-blocker dose should be done in a stepwise fashion. When tadalafil is used for benign prostatic hypertrophy (BPH), discontinue tamsulosin therapy at least 1 day prior to initiating tadalafil therapy. Other variables, such as intravascular volume depletion, concurrent antihypertensive therapy, or evidence of hemodynamic instability with alpha-blocker monotherapy, may affect the safety of concomitant use of tadalafil and tamsulosin.
Fluconazole: (Moderate) Use caution if coadministration of fluconazole with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A substrate and fluconazole is a moderate CYP3A inhibitor.
Fluoxetine: (Moderate) Use caution if coadministration of fluoxetine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and fluoxetine is a strong CYP2D6 inhibitor. Concomitant treatment with another strong CYP2D6 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively.
Fluvoxamine: (Moderate) Tamsulosin should be used with caution in combination with moderate inhibitors of CYP3A4 such as fluvoxamine. The cytochrome P450 enzymes CYP3A4 and CYP2D6 are responsible for the extensive metabolism of tamsulosin. Strong inhibitors of CYP3A4 are known to increase the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively. No studies have been performed with moderate CYP3A4 inhibitors. As with other alpha adrenergic blocking agents there is a potential risk of syncope with tamsulosin, particularly if serum concentrations are elevated. Monitor blood pressure and observe for symptoms of orthostasis.
Fosamprenavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Grapefruit juice: (Moderate) Hepatic cytochrome P450 enzymes 2D6 and 3A4 are responsible for the extensive metabolism of tamsulosin. Although no clinical studies have been done, tamsulosin should be used with caution with inhibitors of CYP3A4 isoenzymes (e.g., grapefruit juice).
Haloperidol: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as haloperidol. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Idelalisib: (Major) Avoid concomitant use of idelalisib, a strong CYP3A inhibitor, with tamsulosin, a CYP3A substrate, as tamsulosin toxicities may be significantly increased. The AUC of a sensitive CYP3A substrate was increased 5.4-fold when coadministered with idelalisib.
Iloprost: (Minor) Iloprost can have additive effects when administered with other antihypertensive agents, including alpha-blockers. These effects can be used to therapeutic advantage, but dosage adjustments may be necessary.
Imatinib: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of imatinib, STI-571. Tamsulosin is extensively metabolized by CYP2D6 and CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Therefore, concomitant use with drugs that inhibit both CYP2D6 and CYP3A4, such as imatinib, STI-571, should be avoided.
Indinavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Isavuconazonium: (Moderate) The plasma concentrations of tamsulosin may be elevated when administered concurrently with isavuconazonium. Clinical monitoring for adverse effects, such as hypotension, is recommended during coadministration. Tamsulosin is a substrate of the hepatic isoenzyme CYP3A4 and drug transporter P-glycoprotein (P-gp); isavuconazole, the active moiety of isavuconazonium, is an inhibitor of CYP3A4 and P-gp.
Isradipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Itraconazole: (Major) Use of tamsulosin is not recommended during and for 2 weeks after itraconazole therapy due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes, and strong inhibitors of CYP3A4 are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A4 inhibitor resulted in an increase in the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Ketoconazole: (Major) Concurrent use of tamsulosin and ketoconazole is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations are expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4. Coadministration with ketoconazole, a strong CYP3A4 inhibitor, increased the Cmax and AUC of tamsulosin 2.2 and 2.8-fold, respectively.
Labetalol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Lansoprazole; Amoxicillin; Clarithromycin: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of clarithromycin. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use with a strong CYP3A4 inhibitor, such as clarithromycin, should be avoided.
Lefamulin: (Moderate) Use caution if coadministration of oral lefamulin with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A4 substrate and oral lefamulin is a moderate CYP3A4 inhibitor; an interaction is not expected with intravenous lefamulin. The effects of concomitant administration of a moderate CYP3A4 inhibitor on the pharmacokinetics of tamsulosin have not been evaluated, but tamsulosin exposure may increase based on the effects of strong CYP3A4 inhibition.
Lenacapavir: (Moderate) Use caution if coadministration of lenacapavir with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A substrate and lenacapavir is a moderate CYP3A inhibitor.
Letermovir: (Moderate) An increase in the plasma concentration of tamsulosin may occur when given with letermovir. Avoid this combination in patients who are also receiving treatment with cyclosporine because the magnitude of this interaction may be amplified. Tamsulosin is partially metabolized by CYP3A4. Letermovir is a moderate CYP3A4 inhibitor; however, when given with cyclosporine, the combined effect on CYP3A4 substrates is similar to a strong CYP3A4 inhibitor. In a drug interaction study, concomitant use of tamsulosin with another strong CYP3A4 inhibitor resulted in increase in the maximum plasma concentration and exposure of tamsulosin by a factor of 2.2 and 2.8, respectively. The effects of concurrent use with moderate CYP3A4 inhibitors have not been evaluated.
Levamlodipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Levobunolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Levoketoconazole: (Major) Concurrent use of tamsulosin and ketoconazole is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations are expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4. Coadministration with ketoconazole, a strong CYP3A4 inhibitor, increased the Cmax and AUC of tamsulosin 2.2 and 2.8-fold, respectively.
Lonafarnib: (Major) Avoid concurrent use of tamsulosin and lonafarnib due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4, and strong inhibitors of CYP3A4, such as lonafarnib, are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Lopinavir; Ritonavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Metoprolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Metoprolol; Hydrochlorothiazide, HCTZ: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Mifepristone: (Major) Concurrent use of tamsulosin and mifepristone is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A, and strong inhibitors of CYP3A, such as mifepristone, are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Mirabegron: (Moderate) The effect of mirabegron on tamsulosin pharmacokinetics was determined in drug interaction studies, there was a lack of pharmacokinetic interaction. However, it is recommended that mirabegron be administered with caution in patients taking other medications in the setting of risks for urinary obstruction because of the risk of urinary retention. This includes caution when used with tamsulosin. In addition, mirabegron is a moderate CYP2D6 inhibitor. Exposure of drugs metabolized by CYP2D6 isoenzymes such as tamsulosin may be increased when co-administered with mirabegron.
Mitotane: (Moderate) Use caution if mitotane and tamsulosin are used concomitantly, and monitor for decreased efficacy of tamsulosin and a possible change in dosage requirements. Mitotane is a strong CYP3A4 inducer and tamsulosin is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of tamsulosin.
Nadolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Nebivolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Nebivolol; Valsartan: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Nefazodone: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of nefazodone. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use with a strong CYP3A4 inhibitor, such as nefazodone, should be avoided.
Nelfinavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Nicardipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
NIFEdipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Nimodipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Niraparib; Abiraterone: (Moderate) Monitor for an increase in tamsulosin-related adverse reactions if coadministration with abiraterone is necessary. Tamsulosin is a CYP2D6 substrate and abiraterone is a moderate CYP2D6 inhibitor. The effects of coadministration with a moderate CYP2D6 on the pharmacokinetics of tamsulosin have not been evaluated; however, the manufacturer of tamsulosin recommends caution with use.
Nirmatrelvir; Ritonavir: (Major) Consider withholding tamsulosin, if clinically appropriate, during receipt of ritonavir-boosted nirmatrelvir. If this is not feasible, consider using an alternative COVID-19 therapy or reducing the tamsulosin dose for patients receiving a dose of 0.8 mg daily. Coadministration may increase tamsulosin exposure resulting in increased hypotension or orthostasis. Tamsulosin is a CYP3A substrate and nirmatrelvir is a CYP3A inhibitor. (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Nirogacestat: (Moderate) Use caution if coadministration of nirogacestat with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A substrate and nirogacestat is a moderate CYP3A inhibitor.
Nisoldipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Olanzapine; Fluoxetine: (Moderate) Use caution if coadministration of fluoxetine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and fluoxetine is a strong CYP2D6 inhibitor. Concomitant treatment with another strong CYP2D6 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively.
Olmesartan; Amlodipine; Hydrochlorothiazide, HCTZ: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Oritavancin: (Minor) Tamsulosin is metabolized by CYP3A4 and CYP2D6; oritavancin is a weak CYP3A4 and CYP2D6 inducer. Plasma concentrations and efficacy of tamsulosin may be reduced if these drugs are administered concurrently.
Paroxetine: (Moderate) Use caution if coadministration of paroxetine with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and paroxetine is a strong CYP2D6 inhibitor. Concomitant treatment with paroxetine increased the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively.
Pazopanib: (Moderate) Pazopanib is a weak inhibitor of CYP3A4. Coadministration of pazopanib and tamsulosin, a CYP3A4 substrate, may cause an increase in systemic concentrations of tamsulosin. Use caution when administering these drugs concomitantly.
Peginterferon Alfa-2b: (Minor) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as peginterferon alfa-2b. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Perindopril; Amlodipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Perphenazine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as perphenazine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Perphenazine; Amitriptyline: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as perphenazine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Phenoxybenzamine: (Major) Tamsulosin should not be administered in combination with other alpha-blockers. The pharmacokinetic and pharmacodynamic interactions between tamsulosin and other alpha-blockers (used for high blood pressure or for benign prostatic hyperplasia) have not been determined. However, interactions or side effects (dizziness, hypotension, syncope, etc.) may be expected from the duplication of pharmacologic effects.
Phentolamine: (Major) Tamsulosin should not be administered in combination with other alpha-blockers. The pharmacokinetic and pharmacodynamic interactions between tamsulosin and other alpha-blockers (used for high blood pressure or for benign prostatic hyperplasia) have not been determined. However, interactions or side effects (dizziness, hypotension, syncope, etc.) may be expected from the duplication of pharmacologic effects.
Pindolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Posaconazole: (Major) Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes, and strong inhibitors of CYP3A4 are expected to significantly raise tamsulosin concentrations. Plasma concentrations of tamsulosin are increased with concomitant use of ketoconazole, a strong inhibitor of CYP3A4. Concomitant treatment with ketoconazole resulted in an increase in the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use with a strong CYP3A4 inhibitor, such as ketoconazole, itraconazole, posaconazole, or voriconazole should be avoided.
Prazosin: (Major) Tamsulosin should not be administered in combination with other alpha-blockers. The pharmacokinetic and pharmacodynamic interactions between tamsulosin and other alpha-blockers (used for high blood pressure or for benign prostatic hyperplasia) have not been determined. However, interactions or side effects (dizziness, hypotension, syncope, etc.) may be expected from the duplication of pharmacologic effects.
Propafenone: (Moderate) Use caution if coadministration of propafenone with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP2D6 substrate and propafenone is a moderate CYP2D6 inhibitor.
Propranolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Protease inhibitors: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Quinidine: (Moderate) Use caution when administering tamsulosin with a strong CYP2D6 inhibitor such as quinidine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure. If concomitant use in necessary, monitor patient closely for increased side effects.
Quinine: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of quinine. Tamsulosin is extensively metabolized by CYP2D6 and CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Therefore, concomitant use with drugs that inhibit both CYP2D6 and CYP3A4, such as quinine, should be avoided.
Ranolazine: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of ranolazine. Tamsulosin is extensively metabolized by CYP2D6 and CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Therefore, concomitant use with drugs that inhibit both CYP2D6 and CYP3A4, such as ranolazine, should be avoided.
Ribociclib: (Major) Concurrent use of tamsulosin and ribociclib is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes, and strong inhibitors of CYP3A4 are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Ribociclib; Letrozole: (Major) Concurrent use of tamsulosin and ribociclib is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes, and strong inhibitors of CYP3A4 are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Ritlecitinib: (Moderate) Use caution if coadministration of ritlecitinib with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A substrate and ritlecitinib is a moderate CYP3A inhibitor.
Ritonavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Rolapitant: (Major) Use caution if tamsulosin and rolapitant are used concurrently, and monitor for tamsulosin-related adverse effects. Tamsulosin is a CYP2D6 substrate and rolapitant is a moderate CYP2D6 inhibitor; the inhibitory effect of rolapitant lasts for at least 7 days, and may last longer after single dose administration. The Cmax and AUC of another CYP2D6 substrate, dextromethorphan, were increased by 120% and 160%, respectively, on day 1 with rolapitant, and by 180% and 230%, respectively, on day 8 after rolapitant administration.
Saquinavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Sildenafil: (Moderate) Due to the potential for symptomatic hypotension, patients should be stable on tamsulosin therapy before initiating therapy with the lowest dose of sildenafil. Conversely, patients already receiving an optimized dose of sildenafil should be started on the lowest dose of tamsulosin; increases in the alpha-blocker dose should be done in a stepwise fashion. Other variables, such as intravascular volume depletion, concurrent antihypertensive therapy, or evidence of hemodynamic instability with alpha-blocker monotherapy, may affect the safety of concomitant use of sildenafil and tamsulosin.
Silodosin: (Major) The pharmacodynamic effects of coadministration of silodosin and other alpha-blockers has not been studied. Additive effects on blood pressure or an increased incidence of adverse reactions common to alpha-blocker treatment is possible. Therefore, combined use of silodosin and other alpha-blockers is not recommended.
Sotalol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Tadalafil: (Moderate) Due to the potential for symptomatic hypotension, patients should be stable on tamsulosin therapy before initiating therapy with the lowest recommended dose of tadalafil. Conversely, patients already receiving an optimized dose of tadalafil should be started on the lowest dose of tamsulosin; increases in the alpha-blocker dose should be done in a stepwise fashion. When tadalafil is used for benign prostatic hypertrophy (BPH), discontinue tamsulosin therapy at least 1 day prior to initiating tadalafil therapy. Other variables, such as intravascular volume depletion, concurrent antihypertensive therapy, or evidence of hemodynamic instability with alpha-blocker monotherapy, may affect the safety of concomitant use of tadalafil and tamsulosin.
Telmisartan; Amlodipine: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Terazosin: (Major) Tamsulosin should not be administered in combination with other alpha-blockers. The pharmacokinetic and pharmacodynamic interactions between tamsulosin and other alpha-blockers (used for high blood pressure or for benign prostatic hyperplasia) have not been determined. However, interactions or side effects (dizziness, hypotension, syncope, etc.) may be expected from the duplication of pharmacologic effects.
Terbinafine: (Moderate) Use caution when administering tamsulosin with a moderate CYP2D6 inhibitor such as terbinafine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Thioridazine: (Moderate) Use caution when administering tamsulosin with a CYP2D6 inhibitor such as thioridazine. Tamsulosin is extensively metabolized by CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP2D6 inhibitor resulted in increases in tamsulosin exposure; interactions with moderate CYP2D6 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Timolol: (Minor) Tamsulosin did not potentiate the hypotensive effects of atenolol. However, since the symptoms of orthostasis are reported more frequently in tamsulosin-treated vs. placebo patients, there is a potential risk of enhanced hypotensive effects when co-administered with antihypertensive agents.
Tipranavir: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of anti-retroviral protease inhibitors. Tamsulosin is extensively metabolized by CYP3A4 and CYP2D6 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use of tamsulosin with a strong CYP3A4 inhibitor, or an agent with both CYP3A4 and CYP2D6 inhibitor activity, should be avoided.
Trandolapril; Verapamil: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Tucatinib: (Major) Concurrent use of tamsulosin and tucatinib is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4, and strong inhibitors of CYP3A4, such as tucatinib, are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Vardenafil: (Moderate) Due to the potential for symptomatic hypotension, patients should be stable on tamsulosin therapy before initiating therapy with the lowest dose of vardenafil. Conversely, patients already receiving an optimized dose of vardenafil should be started on the lowest dose of tamsulosin; increases in the alpha-blocker dose should be done in a stepwise fashion. Other variables, such as intravascular volume depletion, concurrent antihypertensive therapy, or evidence of hemodynamic instability with alpha-blocker monotherapy, may affect the safety of concomitant use of vardenafil and tamsulosin.
Vemurafenib: (Moderate) Vemurafenib is an inducer of CYP3A4 and decreased plasma concentrations of drugs metabolized by this enzyme, such as tamsulosin, could be expected with concurrent use. Use caution, and monitor therapeutic effects of tamsulosin when coadministered with vemurafenib.
Verapamil: (Moderate) The concomitant administration of tamsulosin with other antihypertensive agents can cause additive hypotensive effects. In addition, diltiazem, nicardipine, and verapamil may increase tamsulosin plasma concentrations via CYP3A4 inhibition. This interaction can be therapeutically advantageous, but dosages must be adjusted accordingly.
Vonoprazan; Amoxicillin; Clarithromycin: (Major) Plasma concentrations of tamsulosin may be increased with concomitant use of clarithromycin. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension. Therefore, concomitant use with a strong CYP3A4 inhibitor, such as clarithromycin, should be avoided.
Voriconazole: (Major) Concurrent use of tamsulosin and voriconazole is not recommended due to the potential for elevated tamsulosin concentrations. Such increases in tamsulosin concentrations may be expected to produce clinically significant and potentially serious side effects, such as hypotension, dizziness, and vertigo. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes, and strong inhibitors of CYP3A4 are expected to significantly raise tamsulosin concentrations. Concomitant treatment with another strong CYP3A4 inhibitor increased the Cmax and AUC of tamsulosin by a factor of 2.2 and 2.8, respectively.
Voxelotor: (Moderate) Use caution if coadministration of voxelotor with tamsulosin is necessary, especially at a tamsulosin dose higher than 0.4 mg, as the systemic exposure of tamsulosin may be increased resulting in increased treatment-related adverse reactions including hypotension, dizziness, and vertigo. Tamsulosin is a CYP3A substrate and voxelotor is a moderate CYP3A inhibitor. The effects of concomitant administration of a moderate CYP3A inhibitor on the pharmacokinetics of tamsulosin have not been evaluated, but tamsulosin exposure may increase based on the effects of strong CYP3A inhibition.
Zafirlukast: (Moderate) Use caution when administering tamsulosin with a moderate CYP3A4 inhibitor such as zafirlukast. Tamsulosin is extensively metabolized by CYP3A4 hepatic enzymes. In clinical evaluation, concomitant treatment with a strong CYP3A4 inhibitor resulted in significant increases in tamsulosin exposure; interactions with moderate CYP3A4 inhibitors have not been evaluated. If concomitant use in necessary, monitor patient closely for increased side effects.
Tamsulosin is a selective antagonist at alpha-1-receptors. Alpha-1-receptors are involved in contraction of smooth muscle and are abundant in the prostate, prostatic capsule, prostatic urethra, and bladder neck. Three subtypes of alpha-1-receptors have been identified: Alpha-1a, alpha-1b, and alpha-1d. Alpha-1a receptors mediate human prostatic smooth muscle contraction whereas alpha-1b and alpha-1d-receptors are involved in vascular smooth muscle contraction. Both alpha-1a and alpha-1b-receptors exist in the prostate, however, approximately 70% of the alpha-receptors in the human prostate are of the alpha-1a subtype. Tamsulosin has 7-38-fold greater affinity for alpha-1a-receptors than for alpha-1b-receptors. Blockade of these receptors by tamsulosin can cause smooth muscles in the bladder neck and prostate to relax, thereby improving urine flow rate and reducing symptoms of BPH.
Tamsulosin is administered orally. In the systemic circulation, it is extensively bound to plasma proteins (94% to 99%), primarily to alpha1-acid glycoprotein (AAG). Tamsulosin is metabolized by CYP2D6 and CYP3A4. Metabolites undergo extensive conjugation to glucuronide or sulfate prior to excretion in the urine. Less than 10% of the dose is excreted unchanged in the urine. The elimination half-life of tamsulosin in normal volunteers is 14.9 +/- 3.9 hours.
Affected cytochrome P450 isoenzymes and drug transporters: CYP2D6, CYP3A4
Tamsulosin is extensively metabolized by CYP2D6 and CYP3A4 hepatic enzymes.
-Route-Specific Pharmacokinetics
Oral Route
Following oral administration, tamsulosin is almost completely (> 90%) absorbed under fasting conditions. However, taking tamsulosin in a fasted state results in a 30% increase in bioavailability and a 40-70% increase in Cmax compared to taking tamsulosin after a meal. Taking tamsulosin on an empty stomach could potentially increase the risk of some side effects (i.e., orthostasis); therefore tamsulosin should be taken with food. The time to maximum concentration is roughly 6-7 hours under fed conditions.
-Special Populations
Hepatic Impairment
Moderate hepatic impairment (Child-Pugh's classification: Grades A or B) had no significant effect on the unbound (active) concentration of tamsulosin. Tamsulosin pharmacokinetics have not been studied in patients with severe hepatic impairment.
Renal Impairment
Mild to severe renal impairment (CrCl 10-70 ml/min) had no significant effect on the unbound (active) concentration of tamsulosin. Tamsulosin pharmacokinetics have not been studied in patients with endstage renal disease (CrCl < 10 ml/min). Tamsulosin is highly protein bound and is not likely to be significantly removed during hemodialysis.
Geriatric
A cross-study comparison indicates that the AUC and half-life for tamsulosin may be slightly prolonged in older males relative to young, healthy male volunteers. Intrinsic clearance is diminished with age, resulting in a 40% overall higher AUC in subjects aged 55 to 75 years compared to subjects aged 20 to 32 years.