Skip to main content

Nifedipine (Monograph)

Brand names: Adalat CC, Afeditab CR, Nifedical XL, Procardia XL, Procardia
Drug class: Dihydropyridines
- Dihydropyridine Calcium-Channel Blocking Agents
- Calcium Antagonists
VA class: CV200
CAS number: 21829-25-4

Medically reviewed by on Oct 26, 2022. Written by ASHP.


Calcium-channel blocking agent; dihydropyridine derivative.

Uses for Nifedipine


Management of Prinzmetal variant angina and chronic stable angina.

A drug of choice for the management of Prinzmetal variant angina (used alone or in combination with nitrates).

β-Blockers are recommended as the anti-ischemic drugs of choice in most patients with chronic stable angina; calcium-channel blockers may be substituted or added in patients who do not tolerate or respond adequately to β-blockers.

Also has been used in patients with unstable angina [off-label]; however, nondihydropyridine calcium-channel blockers (e.g., diltiazem, verapamil) generally recommended.

The potential risks of short-acting (conventional, immediate-release) nifedipine should be considered.


Management of hypertension, alone or in combination with other classes of antihypertensive agents.

Only extended-release formulations currently are recommended for management of hypertension. (See Cautions.)

Calcium-channel blockers are recommended as one of several preferred agents for the initial management of hypertension according to current evidence-based hypertension guidelines; other preferred options include ACE inhibitors, angiotensin II receptor antagonists, and thiazide diuretics. While there may be individual differences with respect to recommendations for initial drug selection and use in specific patient populations, current evidence indicates that these antihypertensive drug classes all generally produce comparable effects on overall mortality and cardiovascular, cerebrovascular, and renal outcomes.

Individualize choice of therapy; consider patient characteristics (e.g., age, ethnicity/race, comorbidities, cardiovascular risk) as well as drug-related factors (e.g., ease of administration, availability, adverse effects, cost).

A 2017 ACC/AHA multidisciplinary hypertension guideline classifies BP in adults into 4 categories: normal, elevated, stage 1 hypertension, and stage 2 hypertension. (See Table 1.)

Source: Whelton PK, Carey RM, Aronow WS et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71:e13-115.

Individuals with SBP and DBP in 2 different categories (e.g., elevated SBP and normal DBP) should be designated as being in the higher BP category (i.e., elevated BP).

Table 1. ACC/AHA BP Classification in Adults1200


SBP (mm Hg)

DBP (mm Hg)









Hypertension, Stage 1




Hypertension, Stage 2




The goal of hypertension management and prevention is to achieve and maintain optimal control of BP. However, the BP thresholds used to define hypertension, the optimum BP threshold at which to initiate antihypertensive drug therapy, and the ideal target BP values remain controversial.

The 2017 ACC/AHA hypertension guideline generally recommends a target BP goal (i.e., BP to achieve with drug therapy and/or nonpharmacologic intervention) <130/80 mm Hg in all adults regardless of comorbidities or level of atherosclerotic cardiovascular disease (ASCVD) risk. In addition, an SBP goal of <130 mm Hg generally is recommended for noninstitutionalized ambulatory patients ≥65 years of age with an average SBP of ≥130 mm Hg. These BP goals are based upon clinical studies demonstrating continuing reduction of cardiovascular risk at progressively lower levels of SBP.

Previous hypertension guidelines generally have based target BP goals on age and comorbidities. Guidelines such as those issued by the JNC 8 expert panel generally have targeted a BP goal of <140/90 mm Hg regardless of cardiovascular risk, and have used higher BP thresholds and target BPs in elderly patients compared with those recommended by the 2017 ACC/AHA hypertension guideline.

Some clinicians continue to support previous target BPs recommended by JNC 8 due to concerns about the lack of generalizability of data from some clinical trials (e.g., SPRINT study) used to support the 2017 ACC/AHA hypertension guideline and potential harms (e.g., adverse drug effects, costs of therapy) versus benefits of BP lowering in patients at lower risk of cardiovascular disease.

Consider potential benefits of hypertension management and drug cost, adverse effects, and risks associated with the use of multiple antihypertensive drugs when deciding a patient’s BP treatment goal.

For decisions regarding when to initiate drug therapy (BP threshold), the 2017 ACC/AHA hypertension guideline incorporates underlying cardiovascular risk factors. ASCVD risk assessment recommended by ACC/AHA for all adults with hypertension.

ACC/AHA currently recommend initiation of antihypertensive drug therapy in addition to lifestyle/behavioral modifications at an SBP ≥140 mm Hg or DBP ≥90 mm Hg in adults who have no history of cardiovascular disease (i.e., primary prevention) and a low ASCVD risk (10-year risk <10%).

For secondary prevention in adults with known cardiovascular disease or for primary prevention in those at higher risk for ASCVD (10-year risk ≥10%), ACC/AHA recommend initiation of antihypertensive drug therapy at an average SBP ≥130 mm Hg or an average DBP ≥80 mm Hg.

Adults with hypertension and diabetes mellitus, chronic kidney disease (CKD), or age ≥65 years of age are assumed to be at high risk for cardiovascular disease; ACC/AHA state that such patients should have antihypertensive drug therapy initiated at a BP ≥130/80 mm Hg. Individualize drug therapy in patients with hypertension and underlying cardiovascular or other risk factors.

In stage 1 hypertension, experts state that it is reasonable to initiate drug therapy using the stepped-care approach in which one drug is initiated and titrated and other drugs are added sequentially to achieve the target BP. Initiation of antihypertensive therapy with 2 first-line agents from different pharmacologic classes recommended in adults with stage 2 hypertension and average BP >20/10 mm Hg above BP goal.

Calcium-channel blockers may be preferred in hypertensive patients with certain coexisting conditions (e.g., ischemic heart disease) and in geriatric patients, including those with isolated systolic hypertension.

Black hypertensive patients generally respond better to monotherapy with calcium-channel blockers or thiazide diuretics than to other antihypertensive drug classes (e.g., ACE inhibitors, angiotensin II receptor antagonists). However, the combination of an ACE inhibitor or an angiotensin II receptor antagonist with a calcium-channel blocker or thiazide diuretic produces similar BP lowering in black patients as in other racial groups.

Nifedipine is not recommended for management of hypertensive crises.

Nifedipine is recommended by ACOG and other experts as an appropriate drug of choice in pregnant women who require antihypertensive therapy.

Raynaud’s Phenomenon

Drug of choice for the management of Raynaud’s phenomenon [off-label], preferably administered as extended-release formulations.

Preterm Labor

Has been used in selected women to inhibit uterine contractions in preterm labor [off-label] (tocolysis) and prolong gestation when beneficial.

ACOG states that because of conflicting results, there is no clear first-line tocolytic agent; data from randomized, controlled studies suggest calcium-channel blockers (principally nifedipine) may be more effective than, and preferable to, other agents (e.g., magnesium sulfate, β-adrenergic agonists).

Main benefit currently derived from tocolytic therapy may be to forestall labor providing time for patients to receive corticosteroids to increase fetal lung maturation and/or be transferred to other (e.g., tertiary-care) facilities; any other potential benefits of prolonging pregnancy are unclear.

Acute MI

Used in the early treatment and secondary prevention of acute MI [off-label]; an effective anti-ischemic agent, but mortality benefit not demonstrated.

Calcium-channel blockers generally are used for their anti-ischemic and BP-reducing properties in the MI setting, and only when β-blockers (which have been shown to reduce mortality after MI) are ineffective, not tolerated, or contraindicated.

Experts state that calcium-channel blockers may be used to relieve ischemic symptoms, lower BP, or control rapid ventricular response rate associated with atrial fibrillation in patients with ST-segment-elevation MI (STEMI) who are intolerant to β-blockers.

Experts recommend a nondihydropyridine calcium-channel blocker for ongoing or recurrent ischemia in patients with non-ST-segment-elevation MI (NSTEMI) who have a contraindication to β-blockers and who do not have clinically important left ventricular dysfunction, increased risk of cardiogenic shock, or AV block.

Use of immediate-release nifedipine generally contraindicated because of possible hypotension and reflex sympathetic activation.

Nifedipine Dosage and Administration


BP Monitoring and Treatment Goals

  • Monitor BP regularly (i.e., monthly) during therapy and adjust dosage of the antihypertensive drug until BP controlled.

  • If unacceptable adverse effects occur, discontinue drug and initiate another antihypertensive agent from a different pharmacologic class.

  • If adequate BP response not achieved with a single antihypertensive agent, either increase dosage of single drug or add a second drug with demonstrated benefit and preferably a complementary mechanism of action (e.g., ACE inhibitor, angiotensin II receptor antagonist, thiazide diuretic). Many patients will require at least 2 drugs from different pharmacologic classes to achieve BP goal; if goal BP still not achieved, add a third drug.


Oral Administration

Conventional Capsules

Administer capsules orally 3 times daily.

Swallow capsules whole.

Extended-release Tablets

Administer orally once daily.

Extended-release tablets should be swallowed intact and should not be chewed, crushed, or broken.

Manufacturer recommends that Adalat CC be administered on an empty stomach.

The shell of the extended-release tablet does not dissolve and may be passed in the stool.

Whenever extended-release tablets are dispensed or administered, care should be taken to ensure that the extended-release dosage form actually was prescribed.

Dosage of extended-release nifedipine tablets should be decreased gradually with close clinical supervision when discontinuance of the drug is required.


Manufacturer states that two 30-mg Adalat CC extended-release tablets may be interchanged with one 60-mg Adalat CC extended-release tablet; however, three 30-mg Adalat CC extended-release tablets should not be considered interchangeable with one 90-mg Adalat CC extended-release tablet.

Pediatric Patients

Hypertension† [off-label]
Extended-release Tablets

Initially, 0.2–0.5 mg/kg daily given in 1 dose or 2 divided doses recommended by some experts. Initiate drug at the low end of the dosage range; may increase dosage every 2–4 weeks until BP controlled, maximum dosage reached (3 mg/kg [up to 120 mg] daily, given in 1 or 2 divided doses), or adverse effects occur.


Conventional Capsules

Initially, 10 mg 3 times daily.

Increase dosage gradually at 7- to 14-day intervals until optimum control of angina is obtained.

May increase more rapidly to 90 mg daily in increments of 30 mg daily over a 3-day period if symptoms so warrant and patient’s tolerance and response to therapy are frequently assessed.

In hospitalized patients who are closely monitored, dosage may be increased in 10-mg increments at 4- to 6-hour intervals, as necessary to control pain and arrhythmias caused by ischemia. Single doses usually should not exceed 30 mg.

Some experts state usual maintenance dosage is 10–20 mg 3 times daily. In some patients, especially those with evidence of coronary artery spasm, increased dosages of 20–30 mg 3 or 4 times daily and rarely, more than 120 mg daily may be necessary.

Extended-release Tablets

Initially, 30 or 60 mg once daily.

Increase dosage gradually at 7- to 14-day intervals until optimum control of angina is obtained.

Dosage may be increased more rapidly to 90 mg daily in increments of 30 mg daily after steady state is achieved (usually achieved on the second day of therapy with a given dose) if symptoms so warrant and patient’s tolerance and response are frequently assessed.

In some patients, especially those with evidence of coronary artery spasm, higher dosages may be necessary. However, experience with antianginal dosages exceeding 90 mg once daily as extended-release tablets is limited and should be employed with caution and only when clinically necessary.

Extended-release tablets can be substituted for the conventional capsules at the nearest equivalent total daily dose.

Conventional Capsules

Conventional capsules not recommended for use in the management of hypertension because of concerns about potential cardiovascular risks.

Extended-release Tablets

Initially, 30 or 60 mg once daily.

Increase dosage gradually at 7- to 14-day intervals until optimum control of BP is obtained.

Dosage may be increased more rapidly, if symptoms so warrant and the patient’s tolerance and response to therapy are frequently assessed.

Usual maintenance dosage is 30–90 mg once daily.

If unacceptable adverse effects occur, discontinue the drug and initiate another hypertensive agent from a different pharmacologic class.

Prescribing Limits

Pediatric Patients


Extended-release tablets: Maximum 3 mg/kg (up to 120 mg) daily.



Conventional liquid-filled capsules: Maximum 30 mg as a single dose. Maximum 180 mg daily.

Extended-release tablets: Maximum 120 mg daily.


Extended-release tablets: Maximum 90 mg (Adalat CC) or 120 mg (Procardia XL) once daily.

Cautions for Nifedipine


  • Known hypersensitivity to nifedipine or any ingredient in the formulation.



Excessive Hypotension

Risk of excessive, poorly tolerated hypotension in patients being treated for angina; usually occurs during initial dosage titration or subsequent upward titration and may be more likely in patients receiving concomitant β-blocker. Carefully monitor BP, especially during therapy initiation, titration, or dosage increase.

Cardiovascular Effects with Conventional Preparations

Conventional (immediate-release) nifedipine formulations generally are contraindicated in the routine management of acute MI because of negative inotropic effects and reflex sympathetic activation, tachycardia, and hypotension associated with its use. Do not administer within first 1–2 weeks after MI and avoid in acute coronary syndrome when infarction may be imminent.

Risk of profound hypotension, cerebrovascular ischemia or stroke, myocardial ischemia or infarction, and/or death with use of conventional preparations for management of hypertensive crises; similar effects reported in patients receiving such preparations for angina or pulmonary hypertension. Do not use short-acting preparations for acute BP reduction or for chronic hypertension management.

Increased Angina and/or Acute MI

Rarely, increased frequency, duration, and/or severity of angina or acute MI, particularly in patients with severe obstructive CAD, upon initiation or dosage increase of calcium-channel blockers.

β-Blocker Withdrawal

Possible increased angina in patients recently withdrawn from β-blockers after nifedipine initiation. Taper dosage of β-blockers before initiation of nifedipine. (See Interactions.)

Heart Failure

Risk of heart failure, especially in those receiving concomitant β-blockers, particularly in patients with aortic stenosis.

Sensitivity Reactions

Rash, dermatitis (including exfoliative dermatitis), erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, photosensitivity reactions, pruritus, urticaria, allergic hepatitis, and angioedema, principally oropharyngeal edema and occasionally breathing difficulty, reported.

General Precautions

Peripheral Edema

Consider possibility of deterioration in left ventricular function, especially in patients with heart failure, if peripheral edema develops.

GI Disorders

Use extended-release tablets with caution in patients with preexisting GI narrowing; obstruction may occur.

Specific Populations


Category C.


Distributed into milk. Discontinue nursing or the drug.

Pediatric Use

Safety and efficacy remain to be fully established in children; however, some experts have recommended dosages for hypertension based on clinical experience.

Geriatric Use

Insufficient experience in patients ≥65 years of age to determine whether geriatric patients respond differently than younger adults. Select dosage with caution.

Renal Impairment

Use Adalat CC extended-release nifedipine tablets with caution in patients with renal impairment due to the possibility of altered absorption of the drug.

Common Adverse Effects

Dizziness, lightheadedness, giddiness, flushing, heat sensation, headache, tremor, nervousness, mood changes, weakness, fatigue, asthenia, muscle cramps, nausea, heartburn, peripheral edema, dyspnea, cough, wheezing, nasal congestion, sore throat.

Interactions for Nifedipine

Metabolized by CYP isoenzymes, principally CYP3A. May inhibit CYP3A; does not appear to affect CYP2D6.

Specific Drugs and Food

Drug or Food



β-Adrenergic blocking agents

Increased risk of severe hypotension, exacerbation of angina, heart failure, and arrhythmia

Monitor patient and adjust nifedipine dosage as needed; gradually reduce β-blocker dosage instead of abruptly withdrawing


Possible loss of glycemic control

Monitor glucose concentrations and adjust nifedipine dosage as needed


Increased nifedipine bioavailability

Anticoagulants (e.g., coumarins)

Possible increased PT

Antifungals, azoles (fluconazole, itraconazole, ketoconazole)

Possible increased plasma nifedipine concentrations

Monitor BP and adjust nifedipine dosage as needed

Antiretroviral agents (HIV protease inhibitors [amprenavir, atazanavir, fosamprenavir, indinavir, nelfinavir, ritonavir], nonnucleoside reverse transcriptase inhibitors [delavirdine])

Possible increased plasma nifedipine concentrations

Use concomitantly with caution; monitor patient carefully

Antituberculosis agents (rifabutin, rifampin)

Possible decreased plasma nifedipine concentrations

Adjust nifedipine dosage as needed


Possible attenuation of tachycardic effect of nifedipine


Pharmacokinetic interaction unlikely


Possible decreased plasma nifedipine concentrations

Adjust nifedipine dosage as needed


Pharmacokinetic interaction unlikely


Increased serum digoxin concentration

Monitor serum digoxin concentrations when nifedipine therapy is initiated, discontinued, or dosage is adjusted in patients receiving digoxin

Monitor for signs and symptoms of digoxin toxicity and reduce dosage if necessary


Possible increased plasma nifedipine concentrations


Pharmacokinetic interaction unlikely


Possible increased plasma nifedipine concentrations

Monitor BP and adjust nifedipine dosage as needed


Potential for severe hypotension

If patient’s condition permits, temporarily withhold nifedipine for at least 36 hours before surgery if use of high-dose fentanyl is contemplated


Insufficient clinical experience to recommend concomitant use

Grapefruit juice

Increased nifedipine bioavailability

Avoid concomitant use; discontinue grapefruit juice consumption at least 3 days prior to initiating nifedipine therapy

Histamine H2-receptor antagonists (cimetidine, ranitidine)

Decreased clearance and increased plasma nifedipine concentrations and AUC with concomitant cimetidine or (to lesser extent) ranitidine

Cautiously titrate nifedipine dosage in patients receiving cimetidine; may need to reduce nifedipine dosage in patients stabilized on the drug if cimetidine therapy is initiated

Hypotensive agents (captopril, doxazosin, hydralazine, methyldopa)

Increased incidence of severe hypotension

Observe patient closely when nifedipine is added to existing antihypertensive regimen, especially during initial titration or upward adjustment of nifedipine dosage


Pharmacokinetic interaction unlikely


Possible increased absorption of metformin


Possible increased plasma nifedipine concentrations

Monitor BP and adjust nifedipine dosage as needed


Pharmacokinetic interaction unlikely


Pharmacokinetic interaction unlikely


Possible decreased plasma nifedipine concentrations

Adjust nifedipine dosage as needed


Possible decreased phenytoin metabolism; possible decreased plasma nifedipine concentrations

Monitor plasma phenytoin concentrations when nifedipine is initiated or discontinued; monitor BP and adjust nifedipine dosage as needed


Possible increased plasma nifedipine concentrations; possible decreased serum quinidine concentrations

Monitor heart rate and adjust nifedipine dosage as needed; monitor serum quinidine concentrations whenever nifedipine is initiated or discontinued; adjust quinidine dosage accordingly

Quinupristin and dalfopristin

Possible increased plasma nifedipine concentrations

Monitor BP and adjust nifedipine dosage as needed


Pharmacokinetic interaction unlikely

St. John’s wort

Possible decreased plasma nifedipine concentrations

Adjust nifedipine dosage as needed


Possible increased plasma tacrolimus concentrations

Monitor tacrolimus blood concentrations and adjust tacrolimus dosage as needed


Pharmacokinetic interaction unlikely

Valproic acid

Possible increased plasma nifedipine concentrations

Monitor BP and adjust nifedipine dosage as needed


Possible increased plasma nifedipine concentrations

Monitor BP and adjust nifedipine dosage as needed

Nifedipine Pharmacokinetics



Following oral administration of conventional capsules, approximately 90% of a dose is absorbed with peak serum concentrations usually attained within 0.5–2 hours.

Oral bioavailability of extended-release tablets is approximately 75–89% of that achieved with same doses as conventional capsules.

Peak plasma concentrations for extended-release tablets are attained within about 2.5–6 hours.


Food decreases the rate but not extent of absorption from conventional capsules.

Food can increase the early rate of GI absorption of extended-release tablets but does not affect overall bioavailability.

Special Populations

Bioavailability is increased in patients with liver cirrhosis and may be particularly increased in those with portacaval shunts.

Following oral administration of extended-release tablets (Adalat CC), , absorption of nifedipine may be altered in patients with renal impairment.

Substantial reductions in GI retention time for prolonged periods (e.g., in patients with short-bowel syndrome) can result in decreased absorption from extended-release tablets.

Increased mean peak plasma concentrations and average plasma concentrations compared with those in younger adults have been reported in healthy subjects >60 years of age receiving Adalat CC extended-release tablets.



Nifedipine is distributed into milk.

Plasma Protein Binding

Approximately 92–98%.

Special Populations

Plasma protein binding may be decreased in patients with renal or hepatic impairment.



Extensively metabolized in the liver by CYP isoenzymes, including CYP3A, to highly water soluble, inactive metabolites.

Elimination Route

Metabolites excreted in urine (60–80%) and feces (possibly via biliary elimination).


2 hours (conventional capsules); 7 hours (Adalat CC extended-release tablets).

Special Populations

Elimination may be altered in patients with hepatic impairment. Elimination half-life of 7 hours reported in patients with cirrhosis.

Following IV administration, decreased total body clearance in geriatric individuals compared with that in young adults .





Tight, light resistant containers at 15–25°C; protect from light and moisture.

Extended-release Tablets

Tight, light resistant containers at <30°C; protect from light and moisture.


  • Inhibits transmembrane influx of extracellular calcium ions across the membranes of myocardial cells and vascular smooth muscle cells, without changing serum calcium concentrations.

  • Peripheral arterial vasodilator; acts directly on vascular smooth muscle causing reduction in peripheral vascular resistance (afterload) and BP.

Advice to Patients

  • Importance of swallowing extended-release tablets whole; do not chew, crush, or break.

  • Importance of advising patients receiving extended-release tablets that tablet core may be excreted in stools without affecting drug efficacy.

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.

  • Importance of informing patients of other important precautionary information. (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name



Dosage Forms


Brand Names



Capsules, liquid-filled

10 mg*

NIFEdipine Capsules



20 mg*

NIFEdipine Capsules

Tablets, extended-release, film-coated

30 mg*

Adalat CC


Afeditab CR


Nifedical XL


NIFEdipine ER

Procardia XL


60 mg*

Adalat CC


Afeditab CR


Nifedical XL


NIFEdipine ER

Procardia XL


90 mg*

Adalat CC


NIFEdipine ER

Procardia XL


AHFS DI Essentials™. © Copyright 2023, Selected Revisions November 5, 2018. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Off-label: Use is not currently included in the labeling approved by the US Food and Drug Administration.

Reload page with references included