Amlodipine is a prescription blood pressure drug from the calcium channel blocker (CCB) class. The FDA approved it in 1992 as Norvasc, and it is now one of the most widely available generic antihypertensives. It is labeled for high blood pressure and for several forms of coronary artery disease, including chronic stable angina.
Its defining features are a very long half-life (about 30–50 hours) and a dose-related side effect: ankle and leg swelling (edema). In large outcome trials such as ALLHAT and ASCOT-BPLA, amlodipine-based treatment prevented heart attacks and strokes about as well as, or better than, older comparison regimens. Amlodipine is sometimes discussed as a blood pressure option for anabolic steroid users, but no trials have tested it in that group.
This page summarizes what the FDA label and the major clinical trials report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Dihydropyridine calcium channel blocker |
| Brand / approval | Norvasc, NDA 019787, first approved July 31, 1992; generics available |
| Route | Oral tablet (amlodipine besylate) |
| Strengths | 2.5 mg, 5 mg and 10 mg |
| Labeled adult dose | 5 mg once daily to start; maximum 10 mg once daily |
| Half-life (label) | About 30–50 h; 56 h in hepatic impairment |
| Main mechanism | Blocks calcium entry into vascular smooth muscle, widening arteries |
| Most common side effect | Edema, dose-related (10.8% at 10 mg vs 0.6% placebo) |
| US status | Prescription only; not a controlled substance |
| WADA status | Not named on the 2026 Prohibited List |
What it is
Amlodipine is a 1,4-dihydropyridine molecule with the formula C₂₀H₂₅ClN₂O₅ and a molecular weight of 408.9 g/mol (PubChem). Tablets contain the besylate (benzenesulfonate) salt, a white crystalline powder with a molecular weight of 567.1. The label’s chemical name marks it as a racemic (±) mixture (Norvasc label). Pfizer’s Norvasc was approved under NDA 019787 on July 31, 1992; the application is now held by Viatris (Drugs@FDA).
Heart muscle and the smooth muscle in artery walls both need calcium to flow in through specific channels before they can contract. Per the label, amlodipine:
- blocks this calcium influx, with a greater effect on vascular smooth muscle than on heart muscle;
- acts as a direct peripheral arterial vasodilator, lowering peripheral vascular resistance and therefore blood pressure;
- binds and releases the channel slowly, which gives a gradual onset of effect;
- does not change serum calcium, sinoatrial node function or atrioventricular conduction, and did not alter ECG intervals in angina trials.
“Dihydropyridine” matters in practice. Non-dihydropyridine CCBs such as diltiazem and verapamil slow the heart rate. Amlodipine mainly relaxes arteries: with chronic dosing in people with hypertension, the label reports no significant change in heart rate or plasma catecholamines.
Amlodipine is also sold in fixed-dose combination tablets, including:
| Product | Combined with | US status (Drugs@FDA) |
|---|---|---|
| Caduet | Atorvastatin (a statin) | Prescription (FDA) |
| Exforge HCT | Valsartan (an ARB) and hydrochlorothiazide (a diuretic) | Prescription (FDA) |
| Twynsta | Telmisartan (an ARB) | Brand discontinued (FDA) |
Pharmacokinetics
From the FDA label (Norvasc label):
| Parameter | Value |
|---|---|
| Time to peak level | 6–12 h after an oral dose |
| Absolute bioavailability | 64–90%; not affected by food |
| Plasma protein binding | About 93% |
| Metabolism | About 90% converted in the liver to inactive metabolites |
| Excretion | 10% as unchanged drug and 60% as metabolites in urine |
| Terminal half-life | About 30–50 h |
| Time to steady state | 7–8 days of daily dosing |
| Hepatic impairment | Half-life 56 h; AUC (total exposure) up about 40–60% |
| Older adults, moderate to severe heart failure | AUC up about 40–60% |
| Kidney impairment | Pharmacokinetics not significantly affected |
The long half-life explains three features of the drug. Its blood pressure effect lasts the full 24-hour dosing interval, with little difference between peak and trough. The label advises waiting 7–14 days between dose increases, matching the time to steady state. And because the drug is highly protein bound, the label notes that hemodialysis is unlikely to help in an overdose.
Approved medical use
The label lists these indications, alone or with other blood pressure or angina drugs (Norvasc label):
- Hypertension, to lower blood pressure and thereby reduce the risk of fatal and nonfatal cardiovascular events, mainly strokes and heart attacks.
- Chronic stable angina (chest pain on exertion).
- Vasospastic angina (Prinzmetal’s or variant angina, caused by coronary artery spasm).
- Angiographically documented coronary artery disease in patients without heart failure or an ejection fraction under 40%, to reduce hospitalization for angina and coronary revascularization procedures.
| Population | Labeled dose |
|---|---|
| Adults, hypertension | 5 mg once daily; maximum 10 mg once daily |
| Small, fragile or elderly adults, hepatic insufficiency, or add-on to other antihypertensives | May start at 2.5 mg once daily |
| Chronic stable or vasospastic angina | 5–10 mg; most patients need 10 mg |
| Coronary artery disease | 5–10 mg once daily; most trial patients needed 10 mg |
| Children 6–17 years, hypertension | 2.5–5 mg once daily; doses over 5 mg not studied |
What the research shows
Blood pressure lowering
Across 15 double-blind, placebo-controlled trials (800 patients on amlodipine, 538 on placebo) in mild to moderate hypertension, once-daily amlodipine lowered blood pressure by about 12/6 mmHg standing and 13/7 mmHg supine compared with placebo, measured 24 hours after the dose (Norvasc label). Other label findings:
- The effect was dose-related within the 2.5–10 mg range, and no tolerance developed in patients followed for up to 1 year.
- Effects were similar in Black and white patients, and on diastolic pressure in younger and older patients.
- Patients with moderate hypertension (diastolic 105–114 mmHg) responded about 50% more than those with mild hypertension (diastolic 90–104 mmHg).
- People with normal blood pressure saw no clinically significant change (+1/−2 mmHg).
ALLHAT: amlodipine vs a diuretic vs lisinopril
ALLHAT was a randomized, double-blind trial in 33,357 people aged 55 or older with hypertension and at least one other coronary risk factor. Participants received chlorthalidone (a thiazide-type diuretic, 12.5–25 mg/day), amlodipine (2.5–10 mg/day) or lisinopril (an ACE inhibitor, 10–40 mg/day), with a mean follow-up of 4.9 years (ALLHAT, JAMA 2002):
| Outcome (amlodipine vs chlorthalidone) | Amlodipine (n = 9,048) | Chlorthalidone (n = 15,255) | Relative risk (95% CI) |
|---|---|---|---|
| Fatal coronary disease or nonfatal heart attack (primary), 6-year rate | 11.3% | 11.5% | 0.98 (0.90–1.07) |
| All-cause mortality | No difference | No difference | — |
| Heart failure, 6-year rate | 10.2% | 7.7% | 1.38 (1.25–1.52) |
Systolic pressure at 5 years was 0.8 mmHg higher and diastolic 0.8 mmHg lower on amlodipine than on chlorthalidone. Apart from heart failure, other secondary outcomes were similar. Lisinopril also matched chlorthalidone on the primary outcome but had higher rates of stroke, combined cardiovascular disease and heart failure. The investigators concluded that thiazide-type diuretics should be preferred as first-step therapy, partly because they were cheaper.
ASCOT-BPLA: amlodipine-based vs atenolol-based treatment
ASCOT-BPLA randomized 19,257 people aged 40–79 with hypertension and at least three other cardiovascular risk factors. One group took amlodipine 5–10 mg, adding the ACE inhibitor perindopril 4–8 mg as needed (n = 9,639). The other took the beta blocker atenolol 50–100 mg, adding the diuretic bendroflumethiazide 1.25–2.5 mg plus potassium as needed (n = 9,618). The trial was stopped early after a median of 5.5 years (Dahlöf et al., Lancet 2005):
| Outcome | Amlodipine-based | Atenolol-based | Hazard ratio (95% CI) |
|---|---|---|---|
| Nonfatal heart attack or fatal coronary disease (primary) | 429 | 474 | 0.90 (0.79–1.02), not significant |
| Fatal and nonfatal stroke | 327 | 422 | 0.77 (0.66–0.89) |
| Total cardiovascular events and procedures | 1,362 | 1,602 | 0.84 (0.78–0.90) |
| All-cause mortality | 738 | 820 | 0.89 (0.81–0.99) |
| New-onset diabetes | 567 | 799 | 0.70 (0.63–0.78) |
The authors noted that these differences might not be fully explained by better blood pressure control. The comparison was between whole regimens, so it cannot isolate amlodipine’s contribution from perindopril’s.
Other outcome trials
| Trial | Design | Main result |
|---|---|---|
| VALUE (Julius et al., Lancet 2004) | 15,245 high-risk hypertensive patients aged 50 or older; valsartan-based vs amlodipine-based treatment; mean 4.2 years | Cardiac composite 10.6% vs 10.4%, HR 1.04 (95% CI 0.94–1.15). Blood pressure was lower on amlodipine, by 4.0/2.1 mmHg at 1 month and 1.5/1.3 mmHg at 1 year |
| ACCOMPLISH (Jamerson et al., NEJM 2008) | 11,506 high-risk hypertensive patients; benazepril plus amlodipine vs benazepril plus hydrochlorothiazide; stopped early at mean 36 months | Primary composite 9.6% vs 11.8%, HR 0.80 (95% CI 0.72–0.90), with similar achieved blood pressure (131.6/73.3 vs 132.5/74.4 mmHg) |
| CAMELOT (Norvasc label) | 1,318 patients with angiographic coronary disease; amlodipine 5–10 mg vs placebo on top of standard care; mean 19 months | Cardiovascular composite 16.6% vs 23.1%, HR 0.691 (95% CI 0.540–0.884), driven mainly by fewer angina hospitalizations (7.7% vs 12.8%) and revascularizations (11.8% vs 15.7%) |
In an intravascular ultrasound substudy of CAMELOT (n = 274), amlodipine did not change coronary plaque volume compared with placebo. In PREVENT (825 patients with coronary disease, 3 years), it did not slow narrowing of the coronary arteries, although there were fewer angina hospitalizations and revascularizations.
Angina
In 8 placebo-controlled trials (1,038 patients with chronic stable angina, up to 6 weeks), symptom-limited exercise time rose by an average of 12.8% (63 seconds) on 10 mg and 7.9% (38 seconds) on 5 mg. In a 4-week trial in 50 patients with vasospastic angina, attacks fell by about 4 per week on amlodipine vs about 1 per week on placebo (p under 0.01) (Norvasc label).
Relevance to anabolic steroid use
Raised blood pressure in anabolic-androgenic steroid (AAS) users is documented in studies that measured it directly:
- Prospective cohort (HAARLEM study). In 100 men followed through a self-chosen steroid cycle, systolic blood pressure rose by 6.87 mmHg (95% CI 4.34–9.40) and diastolic by 3.17 mmHg (95% CI 1.29–5.04) from baseline. Blood pressure returned to baseline 3 months after the cycle (Smit et al., Andrologia 2022).
- Cross-sectional study. Among men doing recreational strength training, 37 current AAS users had higher 24-hour systolic blood pressure than 30 controls (132 vs 124 mmHg), and systolic hypertension was more common (51% vs 17%). Current users also had higher aldosterone and noradrenaline, and both current and former users had stiffer aortas (Rasmussen et al., J Hypertens 2018).
We found no published trials of amlodipine, or any calcium channel blocker, in people using anabolic steroids. A 2026 narrative review by clinicians at a Dutch clinic for androgen users suggests an ACE inhibitor or ARB as the first choice, with calcium channel blockers or thiazide-like diuretics as alternatives or add-ons. The review also notes that a cuff that is too small can overestimate readings in men with large upper arms (Bond et al., Clin Cardiol 2026). This is expert opinion, not trial evidence. Related library pages: losartan and telmisartan (ARBs) and hydrochlorothiazide (a thiazide diuretic).
Side effects and risks
Amlodipine has no boxed warning. In placebo-controlled trials (1,730 on amlodipine, 1,250 on placebo), about 1.5% stopped amlodipine because of side effects, not significantly different from placebo at about 1% (Norvasc label).
Edema (ankle and leg swelling)
Edema is the most common side effect, and it rises steeply with dose:
| Side effect | Placebo (n = 520) | 2.5 mg (n = 275) | 5 mg (n = 296) | 10 mg (n = 268) |
|---|---|---|---|---|
| Edema | 0.6% | 1.8% | 3.0% | 10.8% |
| Dizziness | 1.5% | 1.1% | 3.4% | 3.4% |
| Flushing | 0.0% | 0.7% | 1.4% | 2.6% |
| Palpitations | 0.6% | 0.7% | 1.4% | 4.5% |
Dose-related side effects, from the Norvasc label.
Edema was more common in women than men on amlodipine (14.6% vs 5.6%; placebo 5.1% vs 1.4%). Flushing and palpitations showed the same pattern.
A meta-analysis of 106 randomized trials (99,469 participants with hypertension) looked at CCB-related edema more broadly (Makani et al., J Hypertens 2011):
- Edema occurred in 10.7% on CCBs vs 3.2% on control or placebo; 2.1% vs 0.5% stopped treatment because of it.
- Both rates rose with time on treatment, reaching 24% and 5% after 6 months.
- Dihydropyridines such as amlodipine caused edema in 12.3%, vs 3.1% with non-dihydropyridines.
- High doses (more than half the usual maximum) caused edema in 16.1% vs 5.7% at low doses.
The authors describe the presumed mechanism as dilation of the small arteries feeding the capillaries, which raises pressure inside the capillaries and pushes fluid out into the tissues. A second meta-analysis of 25 randomized trials (17,206 patients) found that adding an ACE inhibitor or ARB to a CCB cut the incidence of edema by 38% (RR 0.62, 95% CI 0.53–0.74) and withdrawals due to edema by 62% (RR 0.38, 95% CI 0.22–0.66), compared with CCB alone (Makani et al., Am J Med 2011).
Other common side effects
Side effects reported in over 1% of patients that were not clearly dose-related (Norvasc label):
| Side effect | Amlodipine (n = 1,730) | Placebo (n = 1,250) |
|---|---|---|
| Fatigue | 4.5% | 2.8% |
| Nausea | 2.9% | 1.9% |
| Abdominal pain | 1.6% | 0.3% |
| Somnolence | 1.4% | 0.6% |
Less common events listed in the label include gingival hyperplasia (gum overgrowth), muscle cramps, male and female sexual dysfunction, and rash. In routine labs, the label reports no clinically relevant changes in potassium, glucose, triglycerides, total or HDL cholesterol, uric acid, urea nitrogen or creatinine.
Postmarketing reports
The label lists rare postmarketing reports where a causal link is uncertain:
- gynecomastia (breast tissue growth in men), reported infrequently;
- jaundice and liver enzyme elevations, mostly consistent with cholestasis or hepatitis, some severe enough to require hospitalization;
- extrapyramidal disorder (movement problems such as rigidity or tremor).
Heart-related warnings
- Hypotension. Symptomatic low blood pressure is possible, especially in severe aortic stenosis. Because the onset is gradual, acute hypotension is unlikely.
- Worsening angina or heart attack. These can develop after starting or increasing the dose, particularly in severe obstructive coronary artery disease.
- Heart failure. In a placebo-controlled trial of 1,153 patients with NYHA class III–IV heart failure, amlodipine had no effect on the combined endpoint of death and cardiac morbidity (39% vs 42%). In PRAISE-2 (1,654 patients), it did not change all-cause mortality, but pulmonary edema was reported more often on amlodipine. ALLHAT also found more heart failure on amlodipine than on chlorthalidone.
- Liver disease. The half-life lengthens to 56 hours, so the label advises slow titration in severe hepatic impairment.
Drug interactions
From the label (Norvasc label):
| Drug | Interaction | Label instruction |
|---|---|---|
| Simvastatin | Amlodipine 10 mg raised exposure to simvastatin 80 mg by 77% | Limit simvastatin to 20 mg daily |
| Moderate and strong CYP3A inhibitors (e.g. diltiazem, itraconazole, clarithromycin) | Diltiazem 180 mg/day raised amlodipine exposure by 60% in older patients; strong inhibitors may raise it more | Monitor for hypotension and edema; dose reduction may be needed |
| CYP3A inducers | No quantitative data | Monitor blood pressure closely |
| Sildenafil | Each drug lowers blood pressure independently | Monitor for hypotension |
| Cyclosporine | Trough levels up about 40% in 11 kidney transplant patients | Monitor trough levels; adjust dose |
| Tacrolimus | Exposure up 2.5- to 4-fold in CYP3A5 expressers | Monitor trough levels; adjust dose |
The label also reports that amlodipine does not change exposure to atorvastatin, digoxin or ethanol, or the warfarin prothrombin time. Cimetidine, aluminum/magnesium antacids, sildenafil and grapefruit juice did not change amlodipine exposure. For people on a statin, see the atorvastatin and rosuvastatin pages.
Who should not use it
The only labeled contraindication is known sensitivity to amlodipine. The label advises caution and lower starting doses in:
- older adults, whose clearance is reduced;
- people with hepatic impairment;
- small or fragile patients.
On pregnancy, the label states that available human data are not sufficient to define a drug-associated risk of birth defects or miscarriage. In rats, a high dose given before and during pregnancy cut litter size by about 50% and prolonged labor. Amlodipine passes into breast milk at an estimated median relative infant dose of 4.2%, with no adverse effects observed in breastfed infants.
Overdose
The label expects overdose to cause excessive vasodilation with marked hypotension and possibly a fast heart rate. It recommends cardiac and respiratory monitoring, fluids and, if needed, vasopressors.
Legal status and use in sport
In the US, amlodipine is a prescription-only drug and is not a controlled substance. Amlodipine and calcium channel blockers as a class are not named on the WADA 2026 Prohibited List. Tested athletes should note that some combination tablets, such as Exforge HCT, contain hydrochlorothiazide, a diuretic that is prohibited at all times under class S5.
Key takeaways
- A long-acting artery relaxant. Amlodipine blocks calcium entry into vascular smooth muscle; its 30–50 hour half-life gives steady 24-hour control from one daily dose.
- Modest but reliable blood pressure lowering. About 12–13/6–7 mmHg vs placebo in mild to moderate hypertension, with no tolerance over a year.
- Strong outcome data. It matched a diuretic for coronary events in ALLHAT, and an amlodipine-based regimen reduced stroke, total cardiovascular events, death and new diabetes compared with an atenolol-based regimen in ASCOT-BPLA.
- Edema is the main drawback. Ankle swelling affected 10.8% at 10 mg vs 0.6% on placebo, more often in women; adding an ACE inhibitor or ARB reduces it.
- Watch the simvastatin dose. The label limits simvastatin to 20 mg daily with amlodipine; strong CYP3A inhibitors can raise amlodipine levels.
- Untested in steroid users. AAS use raises blood pressure in measured studies, but no trials have tested amlodipine in this group.
Sources
- Viatris Specialty LLC. Norvasc (amlodipine besylate) tablets prescribing information (revised February 2023). DailyMed.
- US Food and Drug Administration. Drugs@FDA: Norvasc (amlodipine besylate), NDA 019787. FDA.
- National Center for Biotechnology Information. PubChem Compound Summary for CID 2162, Amlodipine. PubChem.
- ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002;288(23):2981–2997. PubMed.
- Dahlöf B, Sever PS, Poulter NR, et al. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial. Lancet. 2005;366(9489):895–906. PubMed.
- Julius S, Kjeldsen SE, Weber M, et al. Outcomes in hypertensive patients at high cardiovascular risk treated with regimens based on valsartan or amlodipine: the VALUE randomised trial. Lancet. 2004;363(9426):2022–2031. PubMed.
- Jamerson K, Weber MA, Bakris GL, et al. Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. N Engl J Med. 2008;359(23):2417–2428. PubMed.
- Makani H, Bangalore S, Romero J, et al. Peripheral edema associated with calcium channel blockers: incidence and withdrawal rate–a meta-analysis of randomized trials. J Hypertens. 2011;29(7):1270–1280. PubMed.
- Makani H, Bangalore S, Romero J, et al. Effect of renin-angiotensin system blockade on calcium channel blocker-associated peripheral edema. Am J Med. 2011;124(2):128–135. PubMed.
- Smit DL, Grefhorst A, Buijs MM, et al. Prospective study on blood pressure, lipid metabolism and erythrocytosis during and after androgen abuse. Andrologia. 2022;54(4):e14372. PubMed.
- Rasmussen JJ, Schou M, Madsen PL, et al. Increased blood pressure and aortic stiffness among abusers of anabolic androgenic steroids: potential effect of suppressed natriuretic peptides in plasma? J Hypertens. 2018;36(2):277–285. PubMed.
- Bond P, Smit DL, Verdegaal T, de Ronde W. Preventing atherosclerotic cardiovascular disease in young male androgen abusers. Clin Cardiol. 2026;49(2):e70257. PubMed.
- US Food and Drug Administration. Drugs@FDA: Caduet (amlodipine and atorvastatin), NDA 021540. FDA.
- US Food and Drug Administration. Drugs@FDA: Exforge HCT (amlodipine, valsartan and hydrochlorothiazide), NDA 022314. FDA.
- US Food and Drug Administration. Drugs@FDA: Twynsta (telmisartan and amlodipine), NDA 022401. FDA.
- World Anti-Doping Agency. The 2026 Prohibited List. WADA 2026 Prohibited List.