Call 1-866-335-8064 for pricing
| Medication |
Strength |
Quantity |
| Viagra (sildenafil) |
100mg |
4 |
| Viagra (sildenafil) |
50mg |
4 |
Viagra
Sildenafil Citrate
Viagra - Viagra Side Effects - Viagra Information
Pharmacology: Sildenafil is a cGMP-specific phosphodiesterase type 5 (PDE5) inhibitor, used for the treatment of male erectile dysfunction.
The physiological mechanism responsible for erection of the penis involves the release of nitric oxide (NO) in the corpus cavernosum in response to sexual stimulation. Nitric oxide then activates the enzyme guanylate cyclase, which results in increased levels of cyclic guanosine monophosphate (cGMP), producing smooth muscle relaxation in the corpus cavernosum and allowing inflow of blood.
Sildenafil has no direct relaxant effect on isolated human corpus cavernosum, but enhances the effect of NO by inhibiting PDE5, which is responsible for the biodegradation of cGMP in the corpus cavernosum. When sexual stimulation causes local release of NO, inhibition of PDE5 by sildenafil produces increased levels of cGMP in the corpus cavernosum, resulting in smooth muscle relaxation and increased inflow of blood to the corpus cavernosum. Sildenafil, at recommended doses, has no effect in the absence of sexual stimulation.
Studies in vitro have shown that sildenafil has between 10 and 10 000-fold greater selectivity for PDE5 than for other phosphodiesterase isoforms (PDEs 1, 2, 3, 4, and 6). In particular, sildenafil has greater than 4 000-fold selectivity for PDE5 over PDE3, the cAMP-specific phosphodiesterase isoform involved in the control of cardiac contractility. Sildenafil is about 10-fold as potent for PDE5 compared to PDE6, an isoenzyme found in the retina; this lower selectivity is thought to be the basis for color vision abnormalities observed with higher doses or plasma levels of sildenafil (see Precautions).
PDE5 is also found in lower concentrations in platelets, vascular and visceral smooth muscles, and skeletal muscle. The sildenafil-induced inhibition of PDE5 in these tissues appears to be the basis for the enhanced platelet antiaggregatory activity of nitric oxide observed in vitro, and inhibition of platelet thrombus formation in vivo, and peripheral arterial-venous dilation in vivo (see Precautions).
Pharmacokinetics: Absorption: Sildenafil is rapidly absorbed. Maximum observed plasma concentrations are reached within 30 to 120 minutes (median 60 minutes) of oral dosing in the fasted state. The mean absolute bioavailability is 41% (range 25 to 63%). The oral pharmacokinetics of sildenafil is proportional over the recommended dose range studied (25 to 100 mg).
When sildenafil was administered with a high-fat meal, the rate of absorption was significantly decreased, with a 29% reduction in C max and a 60-minute delay in T max. The extent of sildenafil absorption was significantly reduced by 11% in the presence of food. The relative bioavailability fed/fasted was 89% (90% CI; 84 to 94%) (see Precautions).
Distribution: The mean steady-state volume of distribution (V ss) for sildenafil is 105 L, indicating distribution into the tissues. Sildenafil and its major circulating N-desmethyl metabolite are both approximately 96% bound to plasma proteins. Protein binding is independent of total drug concentrations.
Based upon measurements of sildenafil in the semen of healthy volunteers, less than 0.001% of the ingested dose may appear in the semen of patients 90 minutes after drug intake.
Metabolism: Sildenafil is cleared predominantly by the CYP3A4 (major route) and CYP2C9 (minor route) hepatic microsomal isoenzymes. The major circulating metabolite results from N-demethylation of sildenafil at the N-methyl piperazine moiety. This metabolite has a PDE selectivity profile similar to sildenafil and an in vitro potency against PDE5 approximately 50% that of the parent drug. Plasma concentrations of this metabolite are approximately 40% of those seen for sildenafil. The N-desmethyl metabolite is further metabolized, with a terminal half-life of approximately 4 hours.
Elimination: The total body clearance of sildenafil is 41 L/h with a resultant terminal phase half-life of 3 to 5 hours. After either oral or i.v. administration, sildenafil is excreted as metabolites predominantly in the feces (approximately 80% of administered dose) and to a lesser extent in the urine (approximately 13% of the administered dose).
Pharmacokinetics in Special Populations: Geriatrics: Healthy elderly subjects (65 years or older) had a reduced clearance of sildenafil, with free plasma concentrations approximately 40% greater than those seen in healthy younger volunteers (18-45 years).
Renal Insufficiency: In volunteers with mild (CLcr=50-80 mL/min) and moderate (CLcr=30-49 mL/min) renal impairment, the pharmacokinetics of a single oral dose of sildenafil (50 mg) were not altered. In volunteers with severe (CLcr <30 mL/min) renal impairment, sildenafil clearance was reduced, resulting in increases in AUC (100%) and C max (88%) compared to age-matched volunteers with no renal impairment.
Hepatic Insufficiency: In volunteers with hepatic cirrhosis (Child-Pugh A and B), sildenafil clearance was reduced, resulting in increases in AUC (84%) and C max (47%) compared to age-matched volunteers with no hepatic impairment.
Since sildenafil clearance is reduced in geriatric patients (65 years or older), patients with renal impairment or patients with hepatic impairment, a starting dose of 25 mg should be considered. Based on efficacy and toleration, the dose may be increased to 50 or 100 mg (see Precautions and Dosage).
Pharmacodynamics: Effects of Sildenafil on Blood Pressure (BP): Single oral doses of sildenafil (100 mg) administered to healthy volunteers produced decreases in supine blood pressure (mean maximum decrease of 8.4/5.5 mmHg). The decrease in blood pressure was most notable approximately 1-2 hours after dosing. The effects are not related to dose or plasma levels. Larger effects were recorded among patients receiving concomitant nitrates (see Contraindications).
Effects of Sildenafil on Cardiac Parameters: Single oral doses of sildenafil up to 100 mg in healthy volunteers produced no clinically relevant effects on ECG.
Indications: For the treatment of erectile dysfunction.
Contraindications: Sildenafil has been shown to potentiate the hypotensive effects of nitrates in healthy volunteers and in patients, and is therefore contraindicated in patients who are taking any type of nitrate drug therapy, or who utilize short-acting nitrate-containing medications, due to the risk of developing potentially life-threatening hypotension. The use of organic nitrates, either regularly and/or intermittently, in any form (e.g., oral, sublingual, transdermal, by inhalation) is absolutely contraindicated (see Pharmacology and Dosage).
After patients have taken sildenafil, it is unknown when nitrates, if necessary, can be safely administered. Plasma levels of sildenafil at 24 hours post-dose are much lower (2 ng/mL) than at peak concentration (440 ng/mL). In the following patients: age >65, hepatic impairment (e.g., cirrhosis), severe renal impairment (e.g., CLcr <30 mL/min), and concomitant use of potent cytochrome P450 3A4 inhibitors (erythromycin), plasma levels of sildenafil at 24 hours post-dose have been found to be 3 to 8 times higher than those seen in healthy volunteers. Although plasma levels of sildenafil at 24 hours post-dose are much lower than at peak concentration, it is unknown whether nitrates can be safely coadministered at this time point (see Pharmacology).
Treatments for erectile dysfunction should not be generally used in men for whom sexual activity is inadvisable (see also Warnings).
Sildenafil is contraindicated in patients with a known hypersensitivity to any component of the tablet (see Supplied).
Warnings: As with all treatments for erectile dysfunction, there is a potential cardiac risk of sexual activity in patients with pre-existing cardiovascular disease. Therefore, treatments for erectile dysfunction, including sildenafil, should not be generally administered in men for whom sexual activity is inadvisable because of their underlying cardiovascular status.
There are no controlled clinical data on the safety or efficacy of sildenafil in the following groups, if prescribed, this should be done with caution: Patients who have suffered a myocardial infarction, stroke, or life-threatening arrhythmia within the last 6 months. Patients with resting hypotension (BP <90/50 at rest) or hypertension (BP >170/110 at rest). Patients with cardiac failure or coronary artery disease causing unstable angina. Patients with retinitis pigmentosa (a minority of these patients have genetic disorders of retinal phosphodiesterases) (see Pharmacology).
Although priapism had not been reported during clinical trials, prolonged erection greater than 4 hours and priapism (painful erections greater than 6 hours in duration) have been reported infrequently during the postmarketing surveillance of sildenafil. In the event of an erection that persists longer than 4 hours, the patient should seek immediate medical assistance. If priapism is not treated immediately, penile tissue damage and permanent loss of potency could result (see Adverse Effects).
The safety and efficacy of combinations of sildenafil with other agents for the treatment of erectile dysfunction have not been studied. Therefore, the use of such combinations is not recommended.
Precautions: General: The evaluation of erectile dysfunction should include a determination of potential underlying causes and the identification of appropriate treatment following a complete medical assessment.
In clinical trials, sildenafil has been shown to have systemic vasodilatory properties that result in transient decreases in blood pressure. This is of little or no consequence in most patients. However, prior to prescribing sildenafil, physicians should carefully consider whether their patients with certain underlying conditions could be adversely affected by such vasodilatory effects, especially in combination with sexual activity. Patients with increased susceptibility to vasodilators include those with left ventricular outflow obstruction (e.g., aortic stenosis, hypertrophic obstructive cardiomyopathy), or those with the rare syndrome of multiple system atrophy manifesting as severely impaired autonomic control of blood pressure.
Agents for the treatment of erectile dysfunction should be used with caution in patients with anatomical deformation of the penis (such as angulation, cavernosal fibrosis or Peyronie's disease) or in patients who have conditions which may predispose them to priapism (such as sickle cell anemia, multiple myeloma or leukemia).
In humans, sildenafil has no effect on bleeding time when taken alone or with ASA. In vitro studies with human platelets indicate that sildenafil potentiates the antiaggregatory effect of sodium nitroprusside (a nitric oxide donor). The combination of heparin and sildenafil had an additive effect on bleeding time in the anesthetized rabbit, but this interaction has not been studied in humans (see Pharmacology).
There is no safety information on the administration of sildenafil to patients with bleeding disorders or active peptic ulceration. Therefore, sildenafil should be administered with caution to these patients.
Effect of Sildenafil on Vision: A small percentage of patients experience visual effects (e.g., impairment of color discrimination, increased perception to light, blurred vision) after taking sildenafil. If this happens, then the patient should not operate a motor vehicle or any heavy machinery until the adverse effects disappear (see Pharmacology).
Drug Interactions : Sildenafil metabolism is principally mediated by the cytochrome P450 (CYP) isoforms 3A4 (major route) and 2C9 (minor route) (see Pharmacology). Therefore inhibitors of these isoenzymes may reduce sildenafil clearance.
Pharmacokinetic data from patients in clinical trials showed no effect on sildenafil pharmacokinetics of CYP2C9 inhibitors (such as tolbutamide, warfarin), CYP2D6 inhibitors (such as selective serotonin reuptake inhibitors, tricyclic antidepressants), thiazide and related diuretics, ACE inhibitors, and calcium channel blockers. The AUC of the active metabolite, N-desmethyl sildenafil, was increased 62% by loop and potassium-sparing diuretics and 102% by nonspecific beta-blockers. These effects on the metabolite are not expected to be of clinical consequence.
In normal healthy male volunteers, there was no evidence of an effect of azithromycin (500 mg daily for 3 days) on the AUC, C max, T max, elimination rate constant, or subsequent half-life of sildenafil or its principle circulating metabolite.
The concomitant use of potent cytochrome P450 3A4 inhibitors (e.g., erythromycin, saquinavir, ritonavir, ketoconazole, itraconazole) as well as the nonspecific CYP inhibitor, cimetidine, is associated with increased plasma levels of sildenafil (see Pharmacology and Dosage).
Sildenafil is a weak inhibitor of the cytochrome P450 isoforms 1A2, 2C9, 2C19, 2D6, 2E1 and 3A4 (IC 50>150 µM). Given sildenafil peak plasma concentrations of approximately 1 µM after recommended doses, it is unlikely that sildenafil will alter the clearance of the substrates of these isoenzymes.
When a single 100 mg dose of sildenafil was administered with erythromycin, a specific CYP3A4 inhibitor, at steady state (500 mg b.i.d. for 5 days), there was a 182% increase in sildenafil systemic exposure (AUC).
In addition, coadministration of the HIV protease inhibitor saquinavir, also a CYP3A4 inhibitor, at steady state (1200 mg t.i.d.) with sildenafil (100 mg single dose) resulted in a 140% increase in sildenafil C max and a 210% increase in sildenafil AUC. Sildenafil had no effect on saquinavir pharmacokinetics. Stronger CYP3A4 inhibitors such as ketoconazole, itraconazole would be expected to have still greater effects (see Dosage).
Coadministration with the HIV protease inhibitor ritonavir, which is a highly potent P450 inhibitor, at steady state (500 mg b.i.d.) with sildenafil (100 mg single dose) resulted in a 300% (4-fold) increase in sildenafil C max and a 1000% (11-fold) increase in sildenafil plasma AUC. At 24 hours the plasma levels of sildenafil were still approximately 200 ng/mL, compared to approximately 5 ng/mL when sildenafil was dosed alone. This is consistent with the marked effects of ritonavir on a broad range of P450 substrates. Sildenafil had no effect on ritonavir pharmacokinetics (see Dosage).
It can be expected that concomitant administration of CYP3A4 inducers, such as rifampin, will decrease plasma levels of sildenafil.
Cimetidine (800 mg), a nonspecific CYP3A4 inhibitor, caused a 56% increase in plasma sildenafil concentrations when coadministered with sildenafil (50 mg) to healthy volunteers.
Population pharmacokinetic analysis of clinical trial data indicated a reduction in sildenafil clearance when coadministered with CYP3A4 inhibitors (such as ketoconazole, erythromycin, cimetidine). However, there was no increased incidence of adverse events in these patients.
No significant interactions were shown with tolbutamide (single 250 mg dose) or warfarin (single 40 mg dose), both of which are metabolized by CYP2C9, when coadministered with 50 mg sildenafil.
Sildenafil (50 mg) did not potentiate the increase in bleeding time, measured using a standard simplate method, caused by ASA (150 mg).
Sildenafil (50 mg) did not potentiate the hypotensive effect of alcohol in healthy volunteers with mean maximum blood alcohol levels of 0.08%.
When sildenafil (100 mg) was co-administered with amlodipine, 5 or 10 mg, in hypertensive patients, the mean additional reduction of supine blood pressure was 8 mmHg systolic and 7 mmHg diastolic (see Pharmacology).
Food Interactions : When sildenafil is taken with a high-fat meal, the rate of absorption is reduced with a mean delay in T max of 60 minutes and a mean reduction in C max of 29%. The patient may find that it takes longer to work if taken with a high-fat meal (see Pharmacology).
Other Concomitant Therapies: Patients on multiple antihypertensive medications were included in the pivotal clinical trials for sildenafil. Analysis of the safety database was carried out after pooling of the following classes of antihypertensive medication: diuretics, beta-blockers, ACE inhibitors, angiotensin II antagonists, antihypertensive medicinal products (vasodilator and centrally-acting), adrenergic neurone blockers, calcium channel blockers and alpha-adrenoceptor blockers. The analysis showed no differences in the adverse effect profile of patients taking sildenafil with and without antihypertensive medication.
Geriatrics: Healthy elderly volunteers (65 years or over) had a reduced clearance of sildenafil, with free plasma concentrations approximately 40% greater than those seen in younger volunteers (18 to 45 years).
Since higher plasma levels may increase both the pharmacological action and incidence of some adverse events, a starting dose of 25 mg should be considered (see Pharmacology and Dosage).
Patients with Renal Insufficiency: In volunteers with mild (CLcr=50-80 mL/min) and moderate (CLcr=30-49 mL/min) renal impairment, the pharmacokinetics of a single oral dose of sildenafil (50 mg) was not altered. In volunteers with severe (CLcr <30 mL/min) renal impairment, sildenafil clearance was reduced, resulting in increases in AUC (100%) and C max (88%) compared to age-matched volunteers with no renal impairment.
A starting dose of 25 mg should be considered in patients with severe renal impairment (see Pharmacology and Dosage).
Patients with Hepatic Insufficiency: In volunteers with hepatic cirrhosis (Child-Pugh A and B), sildenafil clearance was reduced, resulting in increases in AUC (84%) and C max (47%) compared to age-matched volunteers with no hepatic impairment.
A starting dose of 25 mg should be considered (see Pharmacology and Dosage).
Children: Sildenafil is not indicated for use in children.
Pregnancy and Lactation: Sildenafil is not indicated for use in women.
Adverse Effects: Premarketing Experience: Sildenafil was administered to over 3700 patients (aged 19 to 87 years) during clinical trials worldwide. Over 550 patients were treated for longer than 1 year.
In placebo-controlled clinical studies, the discontinuation rate due to adverse events for sildenafil (2.5%) was not significantly different from placebo (2.3%). The adverse events were generally transient and mild to moderate in nature.
In trials of all designs, adverse events reported by patients receiving sildenafil were generally similar. In fixed-dose studies, the incidence of some adverse events increased with dose. The nature of the adverse events in flexible-dose studies, which more closely reflect the recommended dosage regimen, was similar to that for fixed-dose studies.
When sildenafil was taken as recommended (on an as-needed basis) in flexible-dose, placebo-controlled clinical trials, the following adverse events were reported (see Table I).
At doses above the recommended dose range, adverse events were similar to those detailed above but generally were reported more frequently.
The following events occurred in <2% of patients in controlled clinical trials where a causal relationship is uncertain: Autonomic: sweating, dry mouth.
Cardiovascular: abnormal ECG, angina pectoris, arrhythmia, AV block, cardiac arrest, cardiomyopathy, heart failure, hypertension, hypotension, palpitation, postural hypotension, myocardial ischemia, syncope, tachycardia, varicose vein, vascular anomaly.
Central and Peripheral Nervous System: tremor, abnormal dreams, anxiety, agitation, ataxia, depression, insomnia, nervousness, somnolence, paresthesia, vertigo, speech disorder, reflexes decreased, hyperesthesia, neuropathy, migraine, myasthenia, oculogyric crisis, neuralgia, hypertonia.
Gastrointestinal: vomiting, gastritis, gastrointestinal disorder, flatulence, increased appetite, gastroenteritis, stomatitis, eructation, dysphagia, colitis, glossitis, constipation, rectal hemorrhage, mouth ulceration, esophagitis, rectal disorder, gingivitis, tooth disorder.
Hematopoietic: anemia and leukopenia.
Liver/Biliary: liver function tests abnormal, ALT increased.
Metabolic/Nutritional: edema, thirst, gout, hyperuricemia, hypoglycemic reaction, unstable diabetes, hyperglycemia, hyperlipidemia, hypernatremia.
Musculoskeletal: myalgia, bone disorder, arthrosis, arthritis, tendon rupture, tenosynovitis, bone pain, joint disorder, synovitis.
Respiratory: asthma, dyspnea, laryngitis, pharyngitis, sinusitis, bronchitis, respiratory disorder, carcinoma of lung, sputum increased, cough increased.
Skin/Appendages: skin carcinoma, skin disorder, skin hypertrophy, skin ulcer, contact dermatitis, exfoliative dermatitis, pruritus, urticaria, photosensitivity reaction, nail disorder, acne, herpes simplex, furunculosis.
Special Senses: mydriasis, conjunctivitis, photophobia, eye pain, tinnitus, deafness, ear pain, lacrimation disorder, eye disorder, eye hemorrhage, ear disorder, cataract, dry eyes.
Urogenital: penile erection, other sexual dysfunction, cystitis, nocturia, balanitis, urinary frequency, breast enlargement, prostatic disorder, testis disorder, urinary incontinence, urinary tract disorder, urine abnormality, abnormal ejaculation, genital edema and anorgasmia.
Vascular Disorders: cerebrovascular disorder, cerebral thrombosis.
General: face edema, peripheral edema, chills, allergic reaction, asthenia, pain, infection, shock, hernia, accidental fall, abdominal pain, chest pain, accidental injury, intentional overdose.
Postmarketing Experience: Reports of adverse events temporally associated with sildenafil during postmarketing surveillance that are not listed above and for which the causal relationship is unknown, include the following:
Cardiovascular: Serious cardiovascular events--including myocardial infarction, sudden cardiac death, ventricular arrhythmia, cerebrovascular hemorrhage, and transient ischemic attack--have been reported. Most of these patients had pre-existing cardiovascular risk factors. Many of these events were reported to occur during or shortly after sexual activity, and a few were reported to occur shortly after the use of sildenafil without sexual activity. Others were reported to have occurred hours to days after the use of sildenafil with sexual activity. It is not possible to determine whether these events are related directly to sildenafil, to sexual activity, to the patient's underlying cardiovascular disease, to combination of these factors, or to other factors (see Warnings).
Central and Peripheral Nervous System: seizure.
Urogenital: prolonged erection, priapism (see Warnings) and hematuria.
Special Senses: diplopia, temporary vision loss/decreased vision, ocular redness or bloodshot appearance, ocular burning, ocular swelling/pressure, increased intraocular pressure, retinal vascular disease of bleeding, vitreous detachment/traction and paramacular edema.
Overdose: Symptoms: In studies with healthy volunteers of single doses of up to 800 mg, adverse events were similar to those seen at lower doses but incidence rates were increased.
Treatment: In cases of overdose, standard supportive measures should be adopted as required. Renal dialysis is not expected to accelerate clearance as sildenafil is highly bound to plasma proteins and not eliminated in the urine.
Treatment of Priapism: Patients should be instructed to report any erections persisting for more than 4 hours to a physician. The treatment of priapism/prolonged erection should be according to established medical practice. Physicians may refer to 2 suggested protocols for detumescence presented below.
Detumescence Protocols: 1) Aspirate 40 to 60 mL blood from either left or right corpora using vacutainer and holder for drawing blood. Patient will often detumesce while aspirating. Apply ice for 20 minutes post aspiration if erection remains. If procedure 1) is unsuccessful, then try procedure 2).
2) Put patient in supine position. Dilute 10 mg phenylephrine into 20 mL distilled water for injection (0.05%). With an insulin syringe, inject 0.1 to 0.2 mL (50 to 100 µg) into the corpora every 2 to 5 minutes, until the detumescence occurs. The occasional patient may experience transient bradycardia and hypertension when given phenylephrine injections, therefore monitor patient's bIood pressure and pulse every 10 minutes. Patients at risk include those with cardiac arrhythmias and diabetes. Refer to the prescribing information for phenylephrine before use. Do not give phenylephrine to patients on MAOIs. When phenylephrine is used within the first 12 hours of erection, the majority of patients will respond.
3) If the above measures fail to detumesce the patient, a urologist should be consulted as soon as possible, especially if the erection has been present for many hours. If priapism is not treated immediateIy, penile tissue damage and/or permanent loss of potency may result.
Dosage: For most patients, the recommended dose is 50 mg taken, as needed, approximately 1 hour before sexual activity. However, sildenafil may be taken anywhere from 4 hours to 0.5 hour before sexual activity. Based on effectiveness and toleration, the dose may be increased to a maximum recommended dose of 100 mg or decreased to 25 mg. The maximum recommended dosing frequency is once per day.
The following factors are associated with increased plasma levels (AUC) of sildenafil: age 65 years or over (40%); hepatic impairment (e.g. cirrhosis: 84%); severe renal impairment (e.g. creatinine clearance <30 mL/min: 100%); concomitant use of potent cytochrome P4503A4 inhibitors (e.g. erythromycin: 182%; saquinavir: 210%). It can also be expected that more potent cytochrome P4503A4 inhibitors such as ketoconazole and itraconazole would result in increased levels of sildenafil.
Since higher plasma levels may increase both efficacy and the incidence of adverse events, a starting dose of 25 mg should be considered in these patients (see Pharmacology and Precautions).
The concomitant use of the potent cytochrome P4503A4 inhibitor, ritonavir is associated with a 1000% (11-fold) increase in plasma levels (AUC) of sildenafil. Given the extent of the interaction with patients receiving concomitant therapy with ritonavir, it is recommended not to exceed a maximum single dose of 25 mg of sildenafil in a 48-hour period (see Precautions).
Sildenafil has been shown to potentiate the hypotensive effects of nitrates in healthy volunteers and in patients, and is therefore contraindicated in patients who are taking any type of nitrate drug therapy, or who utilize short-acting nitrate-containing medications, due to the risk of developing potentially life-threatening hypotension. The use of organic nitrates, either regularly and/or intermittently, in any form (e.g., oral, sublingual, transdermal, by inhalation) is absolutely contraindicated (see Pharmacology and Contraindications).
Information for the Patient: See Blue Section--Information for the Patient Viagra.
Supplied: 25 mg: Each blue, round, diamond-shaped tablet marked PFIZER on one side and VGR 25 on the other side, contains: sildenafil citrate equivalent to 25 mg. Nonmedicinal ingredients: anhydrous dibasic calcium phosphate, croscarmellose sodium, FD&C Blue #2 aluminum lake, hydroxypropyl methylcellulose, lactose, magnesium stearate, microcrystalline cellulose, titanium dioxide and triacetin. Blister packs of 4 and 8.
50 mg: Each blue, round, diamond-shaped tablet marked PFIZER on one side and VGR 50 on the other side, contains: sildenafil citrate equivalent to 50 mg. Nonmedicinal ingredients: anhydrous dibasic calcium phosphate, croscarmellose sodium, FD&C Blue #2 aluminum lake, hydroxypropyl methylcellulose, lactose, magnesium stearate, microcrystalline cellulose, titanium dioxide and triacetin. Blister packs of 4 and 8.
100 mg: Each blue, round, diamond-shaped tablet marked PFIZER on one side and VGR 100 on the other side, contains: sildenafil citrate equivalent to 100 mg. Nonmedicinal ingredients: anhydrous dibasic calcium phosphate, croscarmellose sodium, FD&C Blue #2 aluminum lake, hydroxypropyl methylcellulose, lactose, magnesium stearate, microcrystalline cellulose, titanium dioxide and triacetin. Blister packs of 4 and 8.
Store at controlled room temperature between 15 and 30°C.
IMPORTANT NOTE: THE FOLLOWING INFORMATION IS INTENDED TO SUPPLEMENT, NOT SUBSTITUTE FOR, THE EXPERTISE AND JUDGMENT OF YOUR PHYSICIAN, PHARMACIST OR OTHER HEALTHCARE PROFESSIONAL. IT SHOULD NOT BE CONSTRUED TO INDICATE THAT USE OF THE DRUG IS SAFE, APPROPRIATE, OR EFFECTIVE FOR YOU. CONSULT YOUR HEALTHCARE PROFESSIONAL BEFORE USING THIS DRUG.
|
