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DRUGS & SUPPLEMENTS
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What are the side effects you encounter while taking this medicine? |
For those patients who fail to respond to the 0.4 mg dose after 2 to 4 weeks of dosing, the dose of Tamsulosine LP capsules can be increased to 0.8 mg once daily. Tamsulosine LP capsules 0.4 mg should not be used in combination with strong inhibitors of CYP3A4 (e.g., ketoconazole) [ see Warnings and Precautions (5.2) ].
If Tamsulosine LP capsules administration is discontinued or interrupted for several days at either the 0.4 mg or 0.8 mg dose, therapy should be started again with the 0.4 mg once-daily dose.
Tamsulosine LP capsules should be used with caution in combination with cimetidine, particularly at a dose higher than 0.4 mg (e.g., 0.8 mg) [ see Drug Interactions (7.1) and Clinical Pharmacology (12.3) ].
Tamsulosine LP capsules should not be used in combination with other alpha adrenergic blocking agents [ see Drug Interactions (7.2) and Clinical Pharmacology (12.3) ].
Caution is advised when alpha adrenergic blocking agents including Tamsulosine LP are co-administered with PDE5 inhibitors. Alpha-adrenergic blockers and PDE5 inhibitors are both vasodilators that can lower blood pressure. Concomitant use of these two drug classes can potentially cause symptomatic hypotension [ see Drug Interactions (7.3) and Clinical Pharmacology (12.3) ].
Caution should be exercised with concomitant administration of warfarin and Tamsulosine LP capsules [ see Drug Interactions (7.4) and Clinical Pharmacology (12.3) ].
Most reports were in patients taking the alpha1 blocker when IFIS occurred, but in some cases, the alpha1 blocker had been stopped prior to surgery. In most of these cases, the alpha1 blocker had been stopped recently prior to surgery (2 to 14 days), but in a few cases, IFIS was reported after the patient had been off the alpha1 blocker for a longer period (5 weeks to 9 months). IFIS is a variant of small pupil syndrome and is characterized by the combination of 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. 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.
IFIS may increase the risk of eye complications during and after the operation. The benefit of stopping alpha1 blocker therapy prior to cataract surgery has not been established. The initiation of therapy with tamsulosin in patients for whom cataract surgery is scheduled is not recommended.
The incidence of treatment-emergent adverse events has been ascertained from six short-term U.S. and European placebo-controlled clinical trials in which daily doses of 0.1 to 0.8 mg Tamsulosine LP capsules were used. These studies evaluated safety in 1783 patients treated with Tamsulosine LP capsules and 798 patients administered placebo. Table 1 summarizes the treatment-emergent adverse events that occurred in ≥2% of patients receiving either Tamsulosine LP capsules 0.4 mg or 0.8 mg and at an incidence numerically higher than that in the placebo group during two 13-week U.S. trials (US92-03A and US93-01) conducted in 1487 men.
BODY SYSTEM/ ADVERSE EVENT | Tamsulosine LP CAPSULES GROUPS | PLACEBO | |
---|---|---|---|
0.4 mg n=502 | 0.8 mg n=492 | n=493 | |
1 A treatment-emergent adverse event was defined as any event satisfying one of the following criteria:
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2 Coding preferred terms also include cold, common cold, head cold, flu, and flu-like symptoms. | |||
3 Coding preferred terms also include nasal congestion, stuffy nose, runny nose, sinus congestion, and hay fever. | |||
BODY AS WHOLE | |||
Headache | 97 (19.3%) | 104 (21.1%) | 99 (20.1%) |
Infection2 | 45 (9.0%) | 53 (10.8%) | 37 (7.5%) |
Asthenia | 39 (7.8%) | 42 (8.5%) | 27 (5.5%) |
Back pain | 35 (7.0%) | 41 (8.3%) | 27 (5.5%) |
Chest pain | 20 (4.0%) | 20 (4.1%) | 18 (3.7%) |
NERVOUS SYSTEM | |||
Dizziness | 75 (14.9%) | 84 (17.1%) | 50 (10.1%) |
Somnolence | 15 (3.0%) | 21 (4.3%) | 8 (1.6%) |
Insomnia | 12 (2.4%) | 7 (1.4%) | 3 (0.6%) |
Libido decreased | 5 (1.0%) | 10 (2.0%) | 6 (1.2%) |
RESPIRATORY SYSTEM | |||
Rhinitis3 | 66 (13.1%) | 88 (17.9%) | 41 (8.3%) |
Pharyngitis | 29 (5.8%) | 25 (5.1%) | 23 (4.7%) |
Cough increased | 17 (3.4%) | 22 (4.5%) | 12 (2.4%) |
Sinusitis | 11 (2.2%) | 18 (3.7%) | 8 (1.6%) |
DIGESTIVE SYSTEM | |||
Diarrhea | 31 (6.2%) | 21 (4.3%) | 22 (4.5%) |
Nausea | 13 (2.6%) | 19 (3.9%) | 16 (3.2%) |
Tooth disorder | 6 (1.2%) | 10 (2.0%) | 7 (1.4%) |
UROGENITAL SYSTEM | |||
Abnormal ejaculation | 42 (8.4%) | 89 (18.1%) | 1 (0.2%) |
SPECIAL SENSES | |||
Blurred vision | 1 (0.2%) | 10 (2.0%) | 2 (0.4%) |
Multiple testing for orthostatic hypotension was conducted in a number of studies. Such a test was considered positive if it met one or more of the following criteria: (1) a decrease in systolic blood pressure of ≥20 mmHg upon standing from the supine position during the orthostatic tests; (2) a decrease in diastolic blood pressure ≥10 mmHg upon standing, with the standing diastolic blood pressure <65 mmHg during the orthostatic test; (3) an increase in pulse rate of ≥20 bpm upon standing with a standing pulse rate ≥100 bpm during the orthostatic test; and (4) the presence of clinical symptoms (faintness, lightheadedness/lightheaded, dizziness, spinning sensation, vertigo, or postural hypotension) upon standing during the orthostatic test.
Following the first dose of double-blind medication in Study 1, a positive orthostatic test result at 4 hours post-dose was observed in 7% of patients (37 of 498) who received Tamsulosine LP capsules 0.4 mg once daily and in 3% of the patients (8 of 253) who received placebo. At 8 hours post-dose, a positive orthostatic test result was observed for 6% of the patients (31 of 498) who received Tamsulosine LP capsules 0.4 mg once daily and 4% (9 of 250) who received placebo (Note: patients in the 0.8 mg group received 0.4 mg once daily for the first week of Study 1).
In Studies 1 and 2, at least one positive orthostatic test result was observed during the course of these studies for 81 of the 502 patients (16%) in the Tamsulosine LP capsules 0.4 mg once-daily group, 92 of the 491 patients (19%) in the Tamsulosine LP capsules 0.8 mg once-daily group, and 54 of the 493 patients (11%) in the placebo group.
Because orthostasis was detected more frequently in Tamsulosine LP capsule-treated patients than in placebo recipients, there is a potential risk of syncope [ see Warnings and Precautions (5.1) ].
Allergic-type reactions such as skin rash, urticaria, pruritus, angioedema, and respiratory symptoms have been reported with positive rechallenge in some cases. Priapism has been reported rarely. Infrequent reports of dyspnea, palpitations, hypotension, atrial fibrillation, arrhythmia, tachycardia, skin desquamation including reports of Stevens-Johnson syndrome, constipation, and vomiting have been received during the postmarketing period.
During cataract surgery, a variant of small pupil syndrome known as Intraoperative Floppy Iris Syndrome (IFIS) has been reported in association with alpha1 blocker therapy [ see Warnings and Precautions (5.5) ].
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 [ see Warnings and Precautions (5.2) and Clinical Pharmacology (12.3) ]. The effects of concomitant administration of a moderate CYP3A4 inhibitor (e.g., erythromycin) on the pharmacokinetics of Tamsulosine LP have not been evaluated [ see Warnings and Precautions (5.2) and Clinical Pharmacology (12.3) ].
Concomitant treatment with paroxetine (a strong inhibitor of CYP2D6) resulted in an increase in the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively [ see Warnings and Precautions (5.2) and Clinical Pharmacology (12.3) ]. A similar increase in exposure is expected in CYP2D6 poor metabolizers (PM) as compared to extensive metabolizers (EM). Since CYP2D6 PMs cannot be readily identified and the potential for significant increase in tamsulosin exposure exists when Tamsulosine LP 0.4 mg is co-administered with strong CYP3A4 inhibitors in CYP2D6 PMs, Tamsulosine LP 0.4 mg capsules should not be used in combination with strong inhibitors of CYP3A4 (e.g., ketoconazole) [ see Warnings and Precautions (5.2) and Clinical Pharmacology (12.3) ].
The effects of concomitant administration of a moderate CYP2D6 inhibitor (e.g., terbinafine) on the pharmacokinetics of Tamsulosine LP have not been evaluated [ see Warnings and Precautions (5.2) and Clinical Pharmacology (12.3) ].
The effects of co-administration of both a CYP3A4 and a CYP2D6 inhibitor with Tamsulosine LP capsules have not been evaluated. However, there is a potential for significant increase in tamsulosin exposure when Tamsulosine LP 0.4 mg is co-administered with a combination of both CYP3A4 and CYP2D6 inhibitors [ see Warnings and Precautions (5.2) and Clinical Pharmacology (12.3) ].
Efficacy and positive benefit/risk of Tamsulosine LP was not demonstrated in two studies conducted in patients 2 years to 16 years of age with elevated detrusor leak point pressure associated with known neurological disorder (e.g., spina bifida). Patients in both studies were treated on a weight-based mg/kg schema (0.025 mg, 0.05 mg, 0.1 mg, 0.2 mg, or 0.4 mg Tamsulosine LP) for the reduction in detrusor leak point pressure below 40 cm H2O. In a randomized, double-blind, placebo-controlled, 14-week, pharmacokinetic, safety and efficacy study in 161 patients, no statistically significant difference in the proportion of responders was observed between groups receiving Tamsulosine LP and placebo. In an open-label, 12-month safety study, 87 patients were treated with Tamsulosine LP. The most frequently reported adverse events (≥5%) from the pooled data of both studies were urinary tract infection, vomiting, pyrexia, headache, nasopharyngitis, cough, pharyngitis, influenza, diarrhea, abdominal pain, and constipation.
Tamsulosine LP is (-)-( R )-5-[2-[[2-( o -Ethoxyphenoxy) ethyl]amino]propyl]-2-methoxybenzenesulfonamide, monohydrochloride. Tamsulosine LP is a white crystalline powder that melts with decomposition at approximately 230°C. It is sparingly soluble in water and methanol, slightly soluble in glacial acetic acid and ethanol, and practically insoluble in ether.
The empirical formula of Tamsulosine LP is C20H28N2O5S - HCl. The molecular weight of Tamsulosine LP is 444.98. Its structural formula is:
Each Tamsulosine LP capsule for oral administration contains Tamsulosine LP 0.4 mg, and the following inactive ingredients: methacrylic acid copolymer dispersion, NF; microcrystalline cellulose, NF; triacetin, USP; calcium stearate, NF; talc, USP; FD&C blue No. 2; titanium dioxide; ferric oxide; gelatin, and trace amounts of black edible ink.
Tamsulosin, an alpha1 adrenoceptor blocking agent, exhibits selectivity for alpha1 receptors in the human prostate. At least three discrete alpha1 adrenoceptor subtypes have been identified: alpha1A, alpha1B, and alpha1D; their distribution differs between human organs and tissue. Approximately 70% of the alpha1 receptors in the human prostate are of the alpha1A subtype.
Tamsulosine LP capsules are not intended for use as an antihypertensive drug.
Figure 1 Mean Plasma Tamsulosine LP Concentrations Following Single-Dose Administration of Tamsulosine LP Capsules 0.4 mg Under Fasted and Fed Conditions (n=8)
The effects of food on the pharmacokinetics of Tamsulosine LP are consistent regardless of whether a Tamsulosine LP capsule is taken with a light breakfast or a high-fat breakfast (Table 2).
Pharmacokinetic Parameter | 0.4 mg QD to healthy volunteers; n=23 (age range 18-32 years) | 0.8 mg QD to healthy volunteers; n=22 (age range 55-75 years) | |||
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Light Breakfast | Fasted | Light Breakfast | High-Fat Breakfast | Fasted | |
Cmin = observed minimum concentration | |||||
Cmax = observed maximum Tamsulosine LP plasma concentration | |||||
Tmax = median time-to-maximum concentration | |||||
T1/2 = observed half-life | |||||
AUCτ = area under the Tamsulosine LP plasma time curve over the dosing interval | |||||
Cmin (ng/mL) | 4.0 ± 2.6 | 3.8 ± 2.5 | 12.3 ± 6.7 | 13.5 ± 7.6 | 13.3 ± 13.3 |
Cmax (ng/mL) | 10.1 ± 4.8 | 17.1 ± 17.1 | 29.8 ± 10.3 | 29.1 ± 11.0 | 41.6 ± 15.6 |
Cmax/Cmin Ratio | 3.1 ± 1.0 | 5.3 ± 2.2 | 2.7 ± 0.7 | 2.5 ± 0.8 | 3.6 ± 1.1 |
Tmax (hours) | 6.0 | 4.0 | 7.0 | 6.6 | 5.0 |
T1/2 (hours) | - | - | - | - | 14.9 ± 3.9 |
AUCτ (ng-hr/mL) | 151 ± 81.5 | 199 ± 94.1 | 440 ± 195 | 449 ± 217 | 557 ± 257 |
Tamsulosine LP is extensively bound to human plasma proteins, primarily alpha1 acid glycoprotein (AAG), with linear binding over a wide concentration range (20 to 600 ng/mL). The results of two-way in vitro studies indicate that the binding of Tamsulosine LP to human plasma proteins is not affected by amitriptyline, diclofenac, glyburide, simvastatin plus simvastatin-hydroxy acid metabolite, warfarin, diazepam, propranolol, trichlormethiazide, or chlormadinone. Likewise, Tamsulosine LP had no effect on the extent of binding of these drugs.
Incubations with human liver microsomes showed no evidence of clinically significant metabolic interactions between Tamsulosine LP and amitriptyline, albuterol (beta agonist), glyburide (glibenclamide) and finasteride (5alpha-reductase inhibitor for treatment of BPH). However, results of the in vitro testing of the Tamsulosine LP interaction with diclofenac and warfarin were equivocal.
Following intravenous or oral administration of an immediate-release formulation, the elimination half-life of Tamsulosine LP in plasma ranged from 5 to 7 hours. Because of absorption rate-controlled pharmacokinetics with Tamsulosine LP capsules, the apparent half-life of Tamsulosine LP is approximately 9 to 13 hours in healthy volunteers and 14 to 15 hours in the target population.
Tamsulosine LP undergoes restrictive clearance in humans, with a relatively low systemic clearance (2.88 L/h).
The effects of ketoconazole at 400 mg once daily for 5 days on the pharmacokinetics of a single Tamsulosine LP capsule 0.4 mg dose was investigated in 24 healthy volunteers (age range 23 to 47 years). 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 [ see Warnings and Precautions (5.2) and Clinical Pharmacology (12.3) ]. The effects of concomitant administration of a moderate CYP3A4 inhibitor (e.g., erythromycin) on the pharmacokinetics of Tamsulosine LP have not been evaluated [ see Warnings and Precautions (5.2) and Drug Interactions (7.1) ].
The effects of paroxetine (a strong inhibitor of CYP2D6) at 20 mg once daily for 9 days on the pharmacokinetics of a single Tamsulosine LP capsule 0.4 mg dose was investigated in 24 healthy volunteers (age range 23 to 47 years). Concomitant treatment with paroxetine resulted in an increase in the Cmax and AUC of tamsulosin by a factor of 1.3 and 1.6, respectively [ see Warnings and Precautions (5.2) and Drug Interactions (7.1) ]. A similar increase in exposure is expected in CYP2D6 poor metabolizers (PM) as compared to extensive metabolizers (EM). A fraction of the population (about 7% of Caucasians and 2% of African Americans) are CYP2D6 PMs. Since CYP2D6 PMs cannot be readily identified and the potential for significant increase in tamsulosin exposure exists when Tamsulosine LP 0.4 mg is co-administered with strong CYP3A4 inhibitors in CYP2D6 PMs, Tamsulosine LP 0.4 mg capsules should not be used in combination with strong inhibitors of CYP3A4 (e.g., ketoconazole) [ see Warnings and Precautions (5.2) and Drug Interactions (7.1) ].
The effects of concomitant administration of a moderate CYP2D6 inhibitor (e.g., terbinafine) on the pharmacokinetics of Tamsulosine LP have not been evaluated [ see Warnings and Precautions (5.2) and Drug Interactions (7.1) ].
The effects of co-administration of both a CYP3A4 and a CYP2D6 inhibitor with Tamsulosine LP capsules have not been evaluated. However, there is a potential for significant increase in tamsulosin exposure when Tamsulosine LP 0.4 mg is co-administered with a combination of both CYP3A4 and CYP2D6 inhibitors [ see Warnings and Precautions (5.2) and Drug Interactions (7.1) ].
Mice were administered doses up to 127 mg/kg/day in males and 158 mg/kg/day in females. There were no significant tumor findings in male mice. Female mice treated for 2 years with the two highest doses of 45 and 158 mg/kg/day had statistically significant increases in the incidence of mammary gland fibroadenomas (P<0.0001) and adenocarcinomas (P<0.0075). The highest dose levels of Tamsulosine LP evaluated in the mice carcinogenicity study produced systemic exposures (AUC) in mice 8 times the exposures in men receiving the maximum therapeutic dose of 0.8 mg/day.
The increased incidences of mammary gland neoplasms in female rats and mice were considered secondary to tamsulosin hydrochloride-induced hyperprolactinemia. It is not known if Tamsulosine LP capsules elevate prolactin in humans. The relevance for human risk of the findings of prolactin-mediated endocrine tumors in rodents is not known.
Tamsulosine LP produced no evidence of mutagenic potential in vitro in the Ames reverse mutation test, mouse lymphoma thymidine kinase assay, unscheduled DNA repair synthesis assay, and chromosomal aberration assays in Chinese hamster ovary cells or human lymphocytes. There were no mutagenic effects in the in vivo sister chromatid exchange and mouse micronucleus assay.
Studies in rats revealed significantly reduced fertility in males dosed with single or multiple daily doses of 300 mg/kg/day of Tamsulosine LP (AUC exposure in rats about 50 times the human exposure with the maximum therapeutic dose). The mechanism of decreased fertility in male rats is considered to be an effect of the compound on the vaginal plug formation possibly due to changes of semen content or impairment of ejaculation. The effects on fertility were reversible, showing improvement by 3 days after a single dose and 4 weeks after multiple dosing. Effects on fertility in males were completely reversed within nine weeks of discontinuation of multiple dosing. Multiple doses of 10 and 100 mg/kg/day Tamsulosine LP (1/5 and 16 times the anticipated human AUC exposure) did not significantly alter fertility in male rats. Effects of Tamsulosine LP on sperm counts or sperm function have not been evaluated.
Studies in female rats revealed significant reductions in fertility after single or multiple dosing with 300 mg/kg/day of the R-isomer or racemic mixture of Tamsulosine LP, respectively. In female rats, the reductions in fertility after single doses were considered to be associated with impairments in fertilization. Multiple dosing with 10 or 100 mg/kg/day of the racemic mixture did not significantly alter fertility in female rats.
In the two U.S. placebo-controlled, double-blind, 13-week, multicenter studies [Study 1 (US92-03A) and Study 2 (US93-01)], 1486 men with the signs and symptoms of BPH were enrolled. In both studies, patients were randomized to either placebo, Tamsulosine LP capsules 0.4 mg once daily, or Tamsulosine LP capsules 0.8 mg once daily. Patients in Tamsulosine LP capsules 0.8 mg once-daily treatment groups received a dose of 0.4 mg once daily for one week before increasing to the 0.8 mg once-daily dose. The primary efficacy assessments included: 1) total American Urological Association (AUA) Symptom Score questionnaire, which evaluated irritative (frequency, urgency, and nocturia), and obstructive (hesitancy, incomplete emptying, intermittency, and weak stream) symptoms, where a decrease in score is consistent with improvement in symptoms; and 2) peak urine flow rate, where an increased peak urine flow rate value over baseline is consistent with decreased urinary obstruction.
Mean changes from baseline to Week 13 in total AUA Symptom Score were significantly greater for groups treated with Tamsulosine LP capsules 0.4 mg and 0.8 mg once daily compared to placebo in both U.S. studies (Table 3, Figures 2A and 2B). The changes from baseline to Week 13 in peak urine flow rate were also significantly greater for the Tamsulosine LP capsules 0.4 mg and 0.8 mg once-daily groups compared to placebo in Study 1, and for the Tamsulosine LP capsules 0.8 mg once-daily group in Study 2 (Table 3, Figures 3A and 3B). Overall there were no significant differences in improvement observed in total AUA Symptom Scores or peak urine flow rates between the 0.4 mg and the 0.8 mg dose groups with the exception that the 0.8 mg dose in Study 1 had a significantly greater improvement in total AUA Symptom Score compared to the 0.4 mg dose.
Total AUA Symptom Score | Peak Urine Flow Rate | |||||
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Mean Baseline Value | Mean Change | Mean Baseline Value | Mean Change | |||
* Statistically significant difference from placebo (p-value ≤0.050; Bonferroni-Holm multiple test procedure). | ||||||
** Total AUA Symptom Scores ranged from 0 to 35. | ||||||
† Peak urine flow rate measured 4 to 8 hours post dose at Week 13. | ||||||
‡ Peak urine flow rate measured 24 to 27 hours post dose at Week 13. | ||||||
Week 13: For patients not completing the 13-week study, the last observation was carried forward. | ||||||
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Tamsulosine LP capsules 0.8 mg once daily | 19.9 ± 4.9 n=247 | -9.6* ± 6.7 n=237 | 9.57 ± 2.51 n=247 | 1.78* ± 3.35 n=247 | ||
Tamsulosine LP capsules 0.4 mg once daily | 19.8 ± 5.0 n=254 | -8.3* ± 6.5 n=246 | 9.46 ± 2.49 n=254 | 1.75* ± 3.57 n=254 | ||
Placebo | 19.6 ± 4.9 n=254 | -5.5 ± 6.6 n=246 | 9.75 ± 2.54 n=254 | 0.52 ± 3.39 n=253 | ||
| ||||||
Tamsulosine LP capsules 0.8 mg once daily | 18.2 ± 5.6 n=244 | -5.8* ± 6.4 n=238 | 9.96 ± 3.16 n=244 | 1.79* ± 3.36 n=237 | ||
Tamsulosine LP capsules 0.4 mg once daily | 17.9 ± 5.8 n=248 | -5.1* ± 6.4 n=244 | 9.94 ± 3.14 n=248 | 1.52 ± 3.64 n=244 | ||
Placebo | 19.2 ± 6.0 n=239 | -3.6 ± 5.7 n=235 | 9.95 ± 3.12 n=239 | 0.93 ± 3.28 n=235 |
In Study 1, 400 patients (53% of the originally randomized group) elected to continue in their originally assigned treatment groups in a double-blind, placebo-controlled, 40-week extension trial (138 patients on 0.4 mg, 135 patients on 0.8 mg, and 127 patients on placebo). Three hundred twenty-three patients (43% of the originally randomized group) completed one year. Of these, 81% (97 patients) on 0.4 mg, 74% (75 patients) on 0.8 mg, and 56% (57 patients) on placebo had a response ≥25% above baseline in total AUA Symptom Score at one year.
Figure 2A Mean Change from Baseline in Total AUA Symptom Score (0-35) Study 1
* indicates significant difference from placebo (p-value ≤0.050).
B = Baseline determined approximately one week prior to the initial dose of double-blind medication at Week 0.
Subsequent values are observed cases.
LOCF = Last observation carried forward for patients not completing the 13-week study.
Note: Patients in the 0.8 mg treatment group received 0.4 mg for the first week.
Note: Total AUA Symptom Scores range from 0 to 35.
Figure 2B Mean Change from Baseline in Total AUA Symptom Score (0-35) Study 2
* indicates significant difference from placebo (p-value ≤0.050).
Baseline measurement was taken Week 0. Subsequent values are observed cases.
LOCF = Last observation carried forward for patients not completing the 13-week study.
Note: Patients in the 0.8 mg treatment group received 0.4 mg for the first week.
Note: Total AUA Symptom Scores range from 0 to 35.
Figure 3A Mean Increase in Peak Urine Flow Rate (mL/Sec) Study 1
* indicates significant difference from placebo (p-value ≤0.050).
B = Baseline determined approximately one week prior to the initial dose of double-blind medication at Week 0.
Subsequent values are observed cases.
LOCF = Last observation carried forward for patients not completing the 13-week study.
Note: The uroflowmetry assessments at Week 0 were recorded 4 to 8 hours after patients received the first dose of double-blind medication.
Measurements at each visit were scheduled 4 to 8 hours after dosing (approximate peak plasma tamsulosin concentration).
Note: Patients in the 0.8 mg treatment groups received 0.4 mg for the first week.
Figure 3B Mean Increase in Peak Urine Flow Rate (mL/Sec) Study 2
* indicates significant difference from placebo (p-value ≤0.050).
Baseline measurement was taken Week 0. Subsequent values are observed cases.
LOCF = Last observation carried forward for patients not completing the 13-week study.
Note: Patients in the 0.8 mg treatment group received 0.4 mg for the first week.
Note: Week 1 and Week 2 measurements were scheduled 4 to 8 hours after dosing (approximate peak plasma tamsulosin concentration).
All other visits were scheduled 24 to 27 hours after dosing (approximate trough tamsulosin concentration).
Tamsulosine LP capsules 0.4 mg, 100 capsules (NDC 0597-0058-01)
Store at 25°C (77°F); excursions permitted to 15°C–30°C (59°F–86°F).
Keep Tamsulosine LP capsules and all medicines out of reach of children.
Patient labeling is provided as a tear-off leaflet at the end of this prescribing information.
Distributed by:
Boehringer Ingelheim Pharmaceuticals, Inc.
Ridgefield, CT 06877 USA
Tamsulosine LP is a registered trademark of, and licensed from:
Astellas Pharma Inc.
Tokyo 103-8411, JAPAN
Copyright 2012, ALL RIGHTS RESERVED
IT8004TE082012
PRT97
PATIENT INFORMATION
Flomax® (Flō-max)
(tamsulosin hydrochloride)
Capsules, 0.4 mg
Read the Patient Information that comes with Tamsulosine LP capsules before you start taking it and each time you refill your prescription. The information may have changed. This leaflet does not take the place of discussions with your doctor about your medical condition or your treatment.
What is Tamsulosine LP?
Tamsulosine LP is a prescription alpha-blocker medicine used to treat the signs and symptoms of benign prostatic hyperplasia (BPH), a condition your doctor may refer to as an enlarged prostate.
Do not take Tamsulosine LP capsules if you are allergic to any of its ingredients. See the end of this leaflet for a complete list of ingredients in Tamsulosine LP capsules.
What should I tell my doctor before using Tamsulosine LP?
Before taking Tamsulosine LP capsules, tell your doctor about all your medical conditions, including:
Know the medicines you take. Keep a list of them and show it to your doctor and pharmacist when you get a new medicine.
How should I take Tamsulosine LP?
Possible side effects of Tamsulosine LP may include:
Symptoms may include:
Allergic reactions may include:
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088, or by visiting www.fda.gov/medwatch.
What should I avoid while taking Tamsulosine LP capsules?
Avoid driving, operating machinery, or other dangerous activities, until you know how Tamsulosine LP affects you. Tamsulosine LP capsules may cause a sudden drop in blood pressure upon standing, especially after the first dose or when changing doses. See " What are the possible side effects of Tamsulosine LP capsules? "
How do I store Tamsulosine LP capsules?
Store Tamsulosine LP capsules at Room Temperature [77°F (25°C)]. Short-term exposure to higher or lower temperatures [from 59°F (15°C) to 86°F (30°C)] is acceptable. Ask your doctor or pharmacist if you have any questions about storing your capsules.
Keep Tamsulosine LP capsules and all medicines out of the reach of children.
General information
This medicine was prescribed for you by your doctor for your condition. Do not use it for another condition. Do not give Tamsulosine LP to other people, even if they have the same symptoms that you have. It may harm them.
While taking Tamsulosine LP, you must have regular checkups. Follow your doctor's advice about when to have these checkups.
BPH can occur with other more serious conditions, including prostate cancer. Therefore, ask your doctor about screening for prostate cancer prior to treatment with Tamsulosine LP capsules and at regular intervals afterwards.
This patient information leaflet summarizes the most important information about Tamsulosine LP. If you would like more information, talk with your doctor. You can ask your pharmacist or doctor for information about Tamsulosine LP that is written for health professionals. For more information call Boehringer Ingelheim Pharmaceuticals, Inc. at 1-800-542-6257, or (TTY) 1-800-459-9906.
What are the ingredients in Tamsulosine LP capsules?
Boehringer Ingelheim Pharmaceuticals, Inc.
Ridgefield, CT 06877 USA
Tamsulosine LP is a registered trademark of, and licensed from:
Astellas Pharma Inc.
Tokyo 103-8411, JAPAN
Copyright 2012, ALL RIGHTS RESERVED
IT8004TE082012
PRT97
Revised: May 2012
Tamsulosine LP Structure Figure 1 Figure 2a Figure 2b Figure 3a Figure 3b
Depending on the reaction of the Tamsulosine LP after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Tamsulosine LP not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.
Is Tamsulosine LP addictive or habit forming?Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
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The information was verified by Dr. Rachana Salvi, MD Pharmacology