Adalat XL (Nifedipine)

General Information

Brand Name:



Scientific Name:

Antianginal – Antihypertensive

System Components and Performance

Adalat XL extended release tablets, while similar in appearance to a conventional tablet, nonetheless consist of a semipermeable membrane surrounding an osmotically active drug core. The core itself is divided into 2 layers: an “active” layer containing the drug, and a “push” layer containing pharmacologically inert, but osmotically active components. As water from the gastrointestinal tract enters the tablet, pressure increases in the osmotic layer and “pushes” against the drug layer, forcing drug through the orifice in the active layer. Drug delivery is essentially constant as long as the osmotic gradient remains constant, and then gradually falls to zero as drug is exhausted from the tablet. Upon swallowing, the biologically inert components of the tablet remain intact during gastrointestinal transit and are eliminated in the feces as an insoluble shell.


Nifedipine is a calcium ion influx inhibitor (calcium channel blocker or calcium ion antagonist). The antianginal and antihypertensive actions of nifedipine are believed to be related to a specific cellular action of selectively inhibiting transmembrane influx of calcium ions into cardiac muscle and vascular smooth muscle. The contractile processes of these tissues are dependent upon the movement of extracellular calcium into the cells through specific ion channels. Nifedipine selectively inhibits the transmembrane influx of calcium through the slow channel without affecting, to any significant degree, the transmembrane influx of sodium through the fast channel. This results in a reduction of free calcium ions available within the muscle cells and an inhibition of the contractile processes. Nifedipine does not alter total serum calcium. The specific mechanisms by which nifedipine relieves angina and reduces blood pressure have not been fully determined but are believed to be brought about largely by its vasodilatory action. Nifedipine dilates the main coronary arteries and coronary arterioles both in normal and ischemic regions resulting in an increase in blood flow and hence in myocardial oxygen delivery. Nifedipine by its vasodilatory action on peripheral arterioles, reduces the total peripheral vascular resistance. This reduces the workload of the heart and thus reduces myocardial energy consumption and oxygen requirements which probably accounts for the effectiveness of nifedipine in chronic stable angina. The mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilation and subsequent reduction in peripheral vascular resistance. The increased peripheral vascular resistance that is an underlying cause of hypertension results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium. The negative inotropic effect of nifedipine is usually not of major clinical significance because at therapeutic doses, nifedipine’s vasodilatory property evokes a baroreceptor mediated reflex tachycardia which tends to counterbalance this negative inotropic effect. Continued administration of nifedipine to hypertensive patients has shown no significant increase in heart rate. Although nifedipine causes a slight depression of sinoatrial node function and AV conduction in isolated myocardial preparations, such effects have not been seen in studies in intact animals or in man. In formal electrophysiologic studies, predominantly in patients with normal conduction systems, nifedipine has had no tendency to prolong AV conduction or sinus node recovery time, or to slow sinus rate.

Pharmacokinetics: Nifedipine is completely absorbed after oral administration. Plasma drug concentrations rise at a gradual, controlled rate exhibiting zero-order absorption kinetics after nifedipine administration and reach a plateau at approximately 6 hours after the first dose. For subsequent doses, relatively constant plasma concentrations at this plateau are maintained with minimal fluctuations over the 24-hour dosing interval. About a 4-fold higher fluctuation index (ratio of peak to trough plasma concentration) was observed with the conventional immediate release Adalat capsule at t.i.d. dosing than with once daily Adalat XL tablets. At steady state the bioavailability of the Adalat XL tablet is 86% relative to Adalat capsules. Administration of the Adalat XL tablet in the presence of food slightly alters the early rate of drug absorption, but does not influence the extent of drug bioavailability. Markedly reduced gastrointestinal retention time over prolonged periods (i.e., short bowel syndrome), however, may influence the pharmacokinetic profile of the drug which could potentially result in lower plasma concentrations. Pharmacokinetics of Adalat XL tablets are linear over the dose range of 30 to 180 mg in that plasma drug concentrations are proportional to dose administered. There was no evidence of dose dumping either in the presence or absence of food. Nifedipine is extensively metabolized to highly water-soluble, inactive metabolites accounting for 60 to 80% of the dose excreted in the urine. The remainder is excreted in the feces in metabolized form, most likely as a result of biliary excretion. The main metabolite (95%) is the hydroxycarbolic acid derivative, the remaining 5% is the corresponding lactone. Only traces (less that 0.1% of the dose) of unchanged nifedipine can be detected in the urine. Thus, the pharmacokinetics of nifedipine are not significantly influenced by the degree of renal impairment. Patients in hemodialysis or chronic ambulatory peritoneal dialysis have not reported significantly altered pharmacokinetics of nifedipine. Since hepatic biotransformation is the predominant route for the disposition of nifedipine, the pharmacokinetics may be altered in patients with chronic liver disease. Pharmacokinetic studies in patients with hepatic cirrhosis showed a clinically significant prolongation of elimination half-life and a decrease in total clearance of nifedipine. The degree of serum protein binding of nifedipine is high (92 to 98%). Protein binding may be greatly reduced in patients with renal or hepatic impairment (see Precautions). Nifedipine is metabolized by the cytochrome P450 enzyme system, predominantly via CYP3A4, but also by CYP1A2 and CYP2A6 isoenzymes. Compounds found in grapefruit juice inhibit the cytochrome P450 system, especially CYP3A4. In a grapefruit juice-nifedipine interaction study in healthy male volunteers pharmacokinetics of nifedipine showed significant alteration. Following administration of a single dose of nifedipine 10 mg with 250 mL of grapefruit juice, the mean value of nifedipine AUC increased by 34% and the tmax increased from 0.8 to 1.2 hours, as compared to water (see Precautions, Interaction With Grapefruit Juice).


  • Chronic Stable Angina: In the management of chronic stable angina (effort-associated angina) without evidence of vasospasm in patients who remain symptomatic despite adequate doses of beta-blockers and/or nitrates, or who cannot tolerate these agents. May be used in combination with beta-blocking drugs in patients with chronic stable angina. However, available information is not sufficient to predict with confidence the effects of concurrent treatment, especially in patients with compromised left ventricular function or cardiac conduction abnormalities. When introducing such concomitant therapy, care must be taken to monitor blood pressure closely, since severe hypotension can occur from the combined effects of the drugs (see Warnings);
  • Hypertension: In the management of mild to moderate essential hypertension. Should normally be used in those patients in whom treatment with diuretics or beta-blockers has been ineffective, or has been associated with unacceptable adverse effects. It can be tried as an initial agent in those patients in whom the use of diuretics and/or beta-blockers is contraindicated, or in patients with medical conditions in which these drugs frequently cause serious adverse effects. Combination of Adalat XL with a diuretic has been found compatible and has shown added antihypertensive effect. Safety of concurrent use of Adalat XL with other antihypertensive agents has not been established.


  • Pregnancy and Lactation: Nifedipine is contraindicated in pregnancy, during lactation, and in women of childbearing potential. Fetal malformations and adverse effects on pregnancy have been reported in animals;
  • An increase in the number of fetal mortalities and resorptions occurred after the administration of 30 and 100 mg/kg of nifedipine to pregnant mice, rats and rabbits. Fetal malformations occurred after the administration of 30 and 100 mg/kg nifedipine to pregnant mice and 100 mg/kg to pregnant rats;
  • In patients with hypersensitivity to nifedipine;
  • In patients with severe hypotension.


  • Excessive Hypotension in Patients with Angina: Since nifedipine lowers peripheral vascular resistance and blood pressure, it should be used cautiously in patients with angina who are prone to develop hypotension and those with a history of cerebrovascular insufficiency. Occasional patients have had excessive and poorly tolerated hypotension. Syncope has been reported (see Adverse Effects). These responses have usually occurred during initial titration or at the time of subsequent upward dosage adjustment, and may be more likely in patients on concomitant beta-blockers. If excessive hypotension occurs, dosage should be lowered or the drug should be discontinued (see Contraindications). Severe hypotension and/or increased fluid volume requirements have been reported in patients receiving nifedipine, with a beta-blocker, who underwent coronary artery bypass surgery using high dose fentanyl anesthesia. The interaction with high dose fentanyl appears to be due to the combination of nifedipine and a beta-blocker, but the possibility that it may occur with nifedipine alone, with low doses of fentanyl in other surgical procedures, or with other narcotic analgesics cannot be ruled out. In nifedipine-treated patients where surgery using high dose fentanyl anesthesia is contemplated, the physician should be aware of these potential problems and if the patient’s condition permits, sufficient time (at least 36 hours), should be allowed for nifedipine to be washed out of the body prior to surgery. The following information should be taken into account in those patients who are being treated for hypertension as well as angina;
  • Increased Angina and/or Myocardial Infarction: Rarely, patients, particularly those who have severe obstructive coronary artery disease have developed well-documented increased frequency, duration and/or severity of angina or acute myocardial infarction on starting nifedipine or at the time of dosage increase. The mechanism of the response is not established. Since there has not been a study of Adalat XL in acute myocardial infarction reported, similar effects of Adalat XL to that of immediate-release nifedipine cannot be excluded. Immediate-release nifedipine is contraindicated in acute myocardial infarction;
  • Beta-blocker Withdrawal: Patients with angina recently withdrawn from beta-blockers may develop a withdrawal syndrome with increased angina, probably related to increased sensitivity to catecholamines. Initiation of treatment with nifedipine will not prevent this occurrence and might be expected to exacerbate it by provoking reflex catecholamine release. There have been occasional reports of increased angina in a setting of beta-blocker withdrawal and initiation of nifedipine. It is important to taper beta-blockers if possible, rather than stopping them abruptly before beginning nifedipine;
  • Patients with Heart Failure: There have been isolated reports of severe hypotension and lowering of cardiac output following administration of nifedipine to patients with severe heart failure. Thus, nifedipine should be used cautiously in patients with severe heart failure. Rarely, patients usually receiving a beta-blocker, have developed heart failure after beginning nifedipine therapy. In patients with severe aortic stenosis, nifedipine will not produce its usual afterload reducing effects and there is a possibility that an unopposed negative inotropic action of the drug may produce heart failure if the end-diastolic pressure is raised. Caution should therefore be exercised when using nifedipine in patients with these conditions;
  • Patients with Pre-existing Gastrointestinal Narrowing: Since the Adalat XL delivery system contains a nondeformable material, caution should be used when administering it in patients with pre-existing severe gastrointestinal narrowing (pathologic or iatrogenic). There have been rare reports of obstructive symptoms in patients with known strictures in association with the ingestion of Adalat XL tablets.


  • Hypotension/Heart Rate: Because nifedipine is an arterial and arteriolar vasodilator, hypotension and a compensatory increase in heart rate may occur. Thus, blood pressure and heart rate should be monitored carefully during nifedipine therapy. Close monitoring is especially recommended for patients who are prone to develop hypotension, those with a history of cerebrovascular insufficiency, and those who are taking medications that are known to lower blood pressure (see Warnings);
  • Peripheral Edema: Mild to moderate peripheral edema, typically associated with arterial vasodilation and not due to left ventricular dysfunction, has been reported to occur in patients treated with nifedipine (see Adverse Effects). This edema occurs primarily in the lower extremities and may respond to diuretic therapy. With patients whose angina or hypertension is complicated by congestive heart failure, care should be taken to differentiate this peripheral edema from the effects of increasing left ventricular dysfunction. Geriatrics: Nifedipine should be administered cautiously to elderly patients, especially to those with a history of hypotension or cerebral vascular insufficiency. Diabetic Patients: The use of nifedipine in diabetic patients may require adjustment for their control;
  • Patients With Impaired Liver Function: Nifedipine should be used with caution in patients with impaired liver function (see Pharmacology). A dose reduction, particularly in severe cases, may be required. Close monitoring of response and metabolic effect should apply.

Interaction With Grapefruit Juice: Published data indicate that through inhibition of cytochrome P450, flavonoids present in the grapefruit juice can increase plasma levels and augment pharmacodynamic effects of some dihydropyridine calcium channel blockers, including nifedipine (see Pharmacology). Therefore, the administration of nifedipine with grapefruit juice should be avoided.

Drug Interactions: As with all drugs, care should be exercised when treating patients with multiple medications. Dihydrophyridine calcium channel blockers undergo biotransformation by the cytochrome P450 system, mainly via the CYP3A4 isoenzyme. Coadministration of nifedipine with other drugs which follow the same route of biotransformation may result in alter bioavailability. Dosages of similarly metabolized drugs, particularly those of low therapeutic ratio, and especially in patients with renal and/or hepatic impairment, may require adjustment when starting or stopping concomitantly administered nifedipine to maintain optimum therapeutic blood levels.

  • Drugs known to be inhibitors of the cytochrome P450 system include: azole antifungals, cimetidine, cyclosporine, erythromycin, quinidine, terfenadine and warfarin. Drugs known to be inducers of the cytochrome P450 system include: phenobarbital, phenytoin and rifampin. Drugs known to be biotransformed via cytochrome P450 include: benzodiazepines, flecainide, theophylline, imipramine and propafenone;
  • Beta Adrenergic Blocking Agents: Concomitant administration of nifedipine and beta-blocking agents is usually well tolerated but there have been occasional literature reports suggesting that the combination may increase the likelihood of congestive heart failure, severe hypotension, or exacerbation of angina. Therefore, caution and careful monitoring of patients on concomitant therapy is recommended (see Indications and Warnings);
  • Long-acting Nitrates: Nifedipine may be safely coadministered with nitrates, but there have been no controlled studies to evaluate the antianginal effectiveness of this combination. Digoxin: Administration of nifedipine with digoxin may lead to reduced digoxin clearance, and therefore, an increase in the plasma digoxin level. It is recommended that digoxin levels be monitored when initiating, adjusting and discontinuing nifedipine to avoid possible “under-” or “over-” dosing with digitalis;
  • Coumarin Anticoagulants: There have been rare reports of increased prothrombin time in patients taking coumarin anticoagulants to whom nifedipine was administered. However, the relationship to nifedipine therapy is uncertain;
  • Quinidine: The addition of nifedipine to a stable quinidine regimen may reduce the quinidine by 50%, an enhanced response to nifedipine may also occur. The addition of quinidine to a stable nifedipine regimen may result in elevated nifedipine concentrations and a reduced response to quinidine. Some patients have experienced elevated quinidine levels when nifedipine was discontinued. Therefore, patients receiving concomitant therapy of nifedipine and quinidine, or those who had their nifedipine discontinued while still receiving quinidine, should be closely monitored, including determination of plasma levels of quinidine. Consideration should be given to dosage adjustment;
  • Cimetidine and Ranitidine: Pharmacokinetic studies have shown that concurrent administration of cimetidine or ranitidine with nifedipine results in significant increases in nifedipine plasma levels (ca. 80% with cimetidine, and 70% with ranitidine). Patients receiving either of these drugs concomitantly with nifedipine should be monitored carefully for the possible exacerbation of effects of nifedipine, such as hypotension. Adjustment of nifedipine dosage may be necessary.

Information for Patients: Adalat XL tablets must be swallowed whole. Patients should be advised to not chew, divide or crush the tablet as this can result in a massive immediate release of the drug. In Adalat XL, the medication is packed within a nonabsorbable shell that has been specially designed to slowly release the drug so the body can absorb it. When this is completed, the empty tablet is eliminated in the stool.

Adverse Effects

Angina: In 257 chronic stable angina patients treated in controlled and long-term open studies, adverse effects were reported in 30% of patients and required discontinuation of therapy in 8.5% of patients.

The most common adverse effects were: edema (10.1%), headache (3.1%) and angina pectoris (3.1%).

The following adverse effects were also reported. Incidences greater than 1% are given in parenthesis:

  • Cardiovascular: palpitation (2.3%), tachycardia, myocardial infarction, ventricular arrhythmia, extrasystoles, dyspnea, chest pain. In patients with angina, rarely, and possibly due to tachycardia, nifedipine has been reported to have precipitated an angina pectoris attack. In addition, more serious events were occasionally observed, not readily distinguishable from the natural history of the disease in these patients. It remains possible, however, that some or many of these events were drug related. These events include myocardial infarction, congestive heart failure or pulmonary edema, and ventricular arrhythmias or conduction disturbances;
  • CNS: dizziness (2.3%), hypoesthesia (1.2%), confusion, insomnia, somnolence, nervousness, asthenia, hyperkinesia. Gastrointestinal: constipation (1.9%), dyspepsia (1.2%), abdominal pain (1.2%), diarrhea, nausea, melena;
  • Genitourinary: impotence, hematuria, polyuria, dysuria;
  • Musculoskeletal: leg cramps, paresthesia, myalgia, arthralgia;
  • Dermatologic: rash, pruritus. Other: fatigue (1.2%), pain, periorbital edema;
  • Hypertension: In 661 hypertensive patients treated in controlled trials with nifedipine, adverse effects were reported in 54% of patients and required discontinuation of therapy in 11.9% of patients.

The majority of adverse effects reported occurred within the first 3 months of therapy. The most common adverse effects reported were edema, which was dose related and ranged in frequency from approximately 10 to 30% in the 30 to 120 mg dose range, headache (16.6%), fatigue (6.2%), dizziness (4.4%), constipation (3.5%) and nausea (3.5%). The following adverse effects were also reported.

Incidences greater than 1% are given in parenthesis:

  • Cardiovascular: flushing (2.4%), palpitation (2.3%), tachycardia (1.2%), chest pain (1.1%), ventricular arrhythmia, hypotension, syncope. CNS: insomnia (1.8%), nervousness (1.8%), somnolence (1.5%), depression, tremor, decreased libido, migraine, vertigo, amnesia, anxiety, impaired concentration, twitching, ataxia, hypertonia, paresthesia, hypoesthesia;
  • Gastrointestinal: dyspepsia (1.5%), flatulence (1.5%), abdominal pain (1.4%), dry mouth (1.1%), diarrhea, vomiting, thirst, melena, eructation, weight increase;
  • Genitourinary: impotence (1.5%), polyuria (1.5%), dysuria, nocturia, oliguria, urinary incontinence, urinary frequency, menstrual disorder;
  • Musculoskeletal: arthralgia, back pain, myalgia. Special Senses: abnormal vision, abnormal lacrimation, taste disturbance, conjunctivitis, tinnitus;
  • Dermatologic: rash (2.3%), pruritus (1.1%), erythematous rash, alopecia;
  • Respiratory: dyspnea (1.7%), bronchospasm, pharyngitis, upper respiratory tract infection, epistaxis;
  • Other: leg cramps (2.7%), pain (2.7%), asthenia (2.0%), face edema, gout, allergy, fever, breast pain.

An open, nonrandomized postmarketing surveillance study (EXACT), involving 1 700 mild to moderate hypertensive patients, was conducted in the offices of general practitioners across Canada. Patients were enrolled in the study if they had been previously treated with either single or dual antihypertensive therapy and the physician considered Adalat XL an appropriate monotherapy. Patients were to be started on Adalat XL 30 mg. If after 3 or 6 weeks of therapy with Adalat XL 30 mg, blood pressure was uncontrolled (i.e., sitting diastolic blood pressure was >95 mm Hg), then the patient was given 60 mg Adalat XL at the physician’s discretion. Twelve patients were started immediately on Adalat XL 60 mg. Patients were followed for 20 weeks. Adverse events were reported in 605/1 700 patients (35.6%). These adverse events were typical of those seen with the dihydropyridine class of calcium channel blockers (edema, headache, dizziness) and are related to the vasodilatory properties of this class of compounds. The following adverse events have been reported with nifedipine rarely. Rare instances of allergic hepatitis, cholestasis with, or without jaundice have been reported in patients treated with nifedipine. Gingival hyperplasia similar to that caused by phenytoin has been reported in patients treated with nifedipine. The lesions usually regressed on discontinuation of the drug. However on occasion, gingivectomy was necessary. Gynecomastia has been observed rarely in older men on long-term therapy, but has so far always regressed completely on discontinuation of the drug. Isolated cases of angioedema have been reported. Angioedema may be accompanied by breathing difficulty. Anaphylaxis has been reported rarely. In postmarketing experience, there have been rare reports of exfoliative dermatitis and Stevens-Johnson syndrome. Gastrointestinal irritation and gastrointestinal bleeding were also reported; however, the causal relationship is uncertain.

Laboratory Tests: Rare, usually transient, but occasionally significant elevations of enzymes such as CPK, AST and ALT have been noted. The relationship to drug therapy is uncertain in most cases, but probable in some. These laboratory abnormalities have rarely been associated with clinical symptoms, however, cholestasis with or without jaundice has been reported. An increase (5.4%) in mean alkaline phosphatase was noted in patients treated with nifedipine. This was an isolated finding not associated with clinical symptoms and rarely resulted in values which exceeded the upper limit of the normal range. Serum potassium was unchanged in patients receiving nifedipine in the absence of concomitant diuretic therapy, and slightly decreased in patients receiving concomitant diuretics. Nifedipine decreases platelet aggregation in vitro. Limited clinical studies have demonstrated a moderate but statistically significant decrease in platelet aggregation and increase in bleeding time in some nifedipine treated patients. This is thought to be a function of inhibition of calcium transport across the platelet membrane. No clinical significance for these findings has been demonstrated. Positive direct Coombs’ tests, with or without associated hemolytic anemia, have been reported but a causal relationship between nifedipine administration and positivity of this laboratory test, including hemolysis, could not be determined. Rare reversible elevations in BUN and serum creatinine have been reported in patients with pre-existing chronic renal insufficiency. The relationship to therapy with nifedipine is uncertain in most cases, but probable in some.


  • Symptoms: There are several well documented cases of nifedipine overdosage. The following symptoms are observed in cases of severe nifedipine intoxication: disturbance of consciousness to the point of coma, a drop in blood pressure, tachycardia/bradycardia, hyperglycemia, metabolic acidosis, hypoxia, cardiogenic shock with pulmonary edema;
  • Treatment: As far as treatment is concerned, elimination of the active substance and the restoration of stable cardiovascular conditions have priority. After oral ingestion, thorough gastric lavage is indicated, if necessary in combination with irrigation of the small intestine. Particularly in cases of intoxication with slow-release products like Adalat XL, elimination must be as complete as possible including the small intestine to prevent the otherwise inevitable subsequent absorption of the active substance. Hemodialysis serves no purpose, as nifedipine is not dialyzable, but plasmapheresis is advisable (high plasma protein binding, relatively low volume of distribution). Clinically significant hypotension calls for active cardiovascular support including monitoring of cardiac and respiratory function including elevation of extremities and attention to circulating fluid volume and urine output. Hypotension as a result of arterial vasodilation can also be treated with calcium (10 mL of 10% calcium gluconate solution administered slowly via i.v. route and repeated if necessary). As a result, the serum calcium can reach the upper normal range to slightly elevated levels. If an insufficient increase in blood pressure is achieved with calcium, vasoconstricting sympathomimetics such as dopamine or norepinephrine are additionally administered as a last resort only in patients without cardiac arrhythmia or ischemic heart disease and when other safer measures have failed. The dosage of these drugs is determined solely by the effect obtained. Additional liquid or volume must be administered with caution because of the danger of overloading the heart. Bradycardia and/or bradyarrhythmias have been observed in some cases of nifedipine overdosage. Appropriate clinical measures, according to the nature and severity of the symptoms, should be applied.


Dosage should be individualized depending on patient tolerance and response. Adalat XL tablets must be swallowed whole and should not be bitten or divided. In general, titration steps should proceed over a 7 to 14 day period so that the physician can assess the response to each dose level before proceeding to higher doses. Since steady-state plasma levels are achieved on the second day of dosing, if symptoms so warrant, titration may proceed more rapidly provided that the patient is closely monitored.

  • Angina: Therapy should normally be initiated with 30 mg once daily. Experience with doses greater than 90 mg daily in patients with angina is limited; therefore, doses greater than 90 mg daily are not recommended. Angina patients controlled on Adalat capsules alone or in combination with beta-blockers may be safely switched to Adalat XL tablets at the nearest equivalent daily dose. Subsequent titration to higher or lower doses may be necessary and should be initiated as clinically warranted;
  • Hypertension: Therapy should normally be initiated with 30 mg once daily. Some patients, such as the elderly, may benefit from initiation of therapy at 20 mg once daily. The usual maintenance dose is 30 to 60 mg once daily. Doses greater than 90 mg are not recommended. Patients switched from Adalat PA 10 or 20 to Adalat XL therapy should receive an initial dosage of Adalat XL no higher than 30 mg once daily, based on previously prescribed dosing regimen. If clinically warranted, the dosage of Adalat XL should be increased to 60 mg once daily. Blood pressure and patient symptoms should be monitored closely following the switch from Adalat PA to Adalat XL. No “rebound effect” has been observed upon discontinuation of Adalat XL. However, if discontinuation of nifedipine is necessary, sound clinical practice suggests that the dosage should be decreased gradually under close physician supervision.


  • 20 mg: Each dusty rose, extended-release tablet, imprinted with “ADALAT 20” on one side, contains: nifedipine 20 mg.  Nonmedicinal ingredients: cellulose acetate, hydroxypropylcellulose, hydroxypropyl methylcellulose, magnesium stearate, Opadry OY-S-24914, polyethylene glycol, polyethylene oxide, red ferric oxide, sodium chloride and titanium dioxide. Bottles of 100 and 500;
  • 30 mg: Each dusty rose, extended-release tablet, imprinted with “ADALAT 30” on one side, contains: nifedipine 30 mg. Nonmedicinal ingredients: cellulose acetate, hydroxypropylcellulose, hydroxypropyl methylcellulose, magnesium stearate, pharmaceutical shellac, polyethylene glycol, polyethylene oxide, red ferric oxide, sodium chloride, synthetic black iron oxide and titanium dioxide. Lactose-free. Bottles of 100 and 500;
  • 60 mg: Each dusty rose, extended-release tablet, imprinted with “ADALAT 60” on one side, contains: nifedipine 60 mg. Nonmedicinal ingredients: cellulose acetate, hydroxypropylcellulose, hydroxypropyl methylcellulose, magnesium stearate, pharmaceutical shellac, polyethylene glycol, polyethylene oxide, red ferric oxide, sodium chloride, synthetic black iron oxide and titanium dioxide. Lactose-free. Bottles of 100. Store between 15 and 30°C. Protect from light, humidity and moisture.

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