DRUGS & SUPPLEMENTS
Nicardipine capsules for oral administration each contain 20 mg or 30 mg of Nicardipine. Nicardipine capsules are a calcium ion influx inhibitor (slow channel blocker or calcium channel blocker).
Nicardipine is a dihydropyridine structure with the IUPAC (International Union of Pure and Applied Chemistry) chemical name 2-(benzyl-methyl amino)ethyl methyl 1,4-dihydro-2,6-dimethyl-4-(m-nitrophenyl)-3,5-pyridinedicarboxylate monohydrochloride, and it has the following structure:
Nicardipine is a greenish-yellow, odorless, crystalline powder that melts at about 169°C. It is freely soluble in chloroform, methanol and glacial acetic acid, sparingly soluble in anhydrous ethanol, slightly soluble in n-butanol, water, 0.01 M potassium dihydrogen phosphate, acetone and dioxane, very slightly soluble in ethyl acetate, and practically insoluble in benzene, ether and hexane. It has a molecular weight of 515.99.
Each capsule, for oral administration, contains 20 mg or 30 mg of Nicardipine. In addition, each capsule contains the following inactive ingredients: magnesium stearate, pregelatinized starch, titanium dioxide, gelatin and FD&C Blue #1. The colorants used in the capsules are black iron oxide, FD&C Blue #2, FD&C Red #40, D&C Yellow #10 and FD&C Blue #1. In addition, the 30 mg capsules also contain propylene glycol.
Mechanism of Action
Nicardipine capsules are a calcium entry blocker that inhibits the transmembrane influx of calcium ions into cardiac muscle and smooth muscle without changing serum calcium concentrations. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. The effects of Nicardipine capsules are more selective to vascular smooth muscle than cardiac muscle. In animal models, Nicardipine capsules produce relaxation of coronary vascular smooth muscle at drug levels that cause little or no negative inotropic effect.
Pharmacokinetics and Metabolism
Nicardipine capsules are completely absorbed following oral doses administered as capsules. Plasma levels are detectable as early as 20 minutes following an oral dose and maximal plasma levels are observed within 30 minutes to 2 hours (mean Tmax = 1 hour). While Nicardipine capsules are completely absorbed, it is subject to saturable first pass metabolism and the systemic bioavailability is about 35% following a 30-mg oral dose at steady-state.
When Nicardipine capsules were administered 1 or 3 hours after a high-fat meal, the mean Cmax and mean AUC were lower (20% to 30%) than when Nicardipine capsules were given to fasting subjects. These decreases in plasma levels observed following a meal may be significant, but the clinical trials establishing the efficacy and safety of Nicardipine capsules were done in patients without regard to the timing of meals. Thus, the results of these trials reflect the effects of meal-induced variability.
The pharmacokinetics of Nicardipine capsules are nonlinear due to saturable hepatic first pass metabolism. Following oral administration, increasing doses result in a disproportionate increase in plasma levels. Steady-state Cmax values following 20-, 30-, and 40-mg doses every 8 hours averaged 36, 88, and 133 ng/mL, respectively. Hence, increasing the dose from 20 to 30 mg every 8 hours more than doubled Cmax and increasing the dose from 20 to 40 mg every 8 hours increased Cmax more than threefold. A similar disproportionate increase in AUC with dose was observed. Considerable inter-subject variability in plasma levels was also observed.
Post-absorption kinetics of Nicardipine capsules are also non-linear, although there is a reproducible terminal plasma half-life that averaged 8.6 hours following 30- and 40-mg doses at steady-state (tid). The terminal half-life represents the elimination of less than 5% of the absorbed drug (measured by plasma concentrations). Elimination over the first 8 hours after dosing is much faster with a half-life of 2 to 4 hours. Steady-state plasma levels are achieved after 2 to 3 days of tid dosing (every 8 hours) and are twofold higher than after a single dose.
Nicardipine capsules are highly protein bound (>95%) in human plasma over a wide concentration range.
Nicardipine capsules are metabolized extensively by the hepatic cytochrome P450 enzymes, CYP2C8, 2D6, and 3A4; less than 1% of intact drug is detected in the urine. Following a radioactive oral dose in solution, 60% of the radioactivity was recovered in the urine and 35% in feces. Most of the dose (over 90%) was recovered within 48 hours of dosing. Nicardipine capsules do not induce its own metabolism, however, nicardipine causes inhibition of certain cytochrome P450 enzymes (including CYP3A4, CYP2D6, CYP2C8, and CYP2C19). Inhibition of these enzymes may result in increased plasma levels of certain drugs, including cyclosporine and tacrolimus. The altered pharmacokinetics may necessitate dosage adjustment of the affected drug or discontinuation of treatment.
Nicardipine plasma levels were higher in patients with mild renal impairment (baseline serum creatinine concentration ranged from 1.2 to 5.5 mg/dL) than in normal subjects. After 30-mg Nicardipine tid at steady-state, Cmax and AUC were approximately twofold higher in these patients.
Because Nicardipine capsules are extensively metabolized by the liver, the plasma levels of the drug are influenced by changes in hepatic function. Nicardipine plasma levels were higher in patients with severe liver disease (hepatic cirrhosis confirmed by liver biopsy or presence of endoscopically-confirmed esophageal varices) than in normal subjects. After 20-mg Nicardipine capsules bid at steady-state, Cmax and AUC were 1.8 and fourfold higher, and the terminal half-life was prolonged to 19 hours in these patients.
The steady-state pharmacokinetics of Nicardipine capsules in elderly hypertensive patients are similar to those obtained in young normal adults. After 1 week of Nicardipine capsules dosing at 20 mg three times a day, the Cmax, Tmax, AUC, terminal plasma half-life and the extent of protein binding of Nicardipine capsules observed in healthy elderly hypertensive patients did not differ significantly from those observed in young normal volunteers
In man, Nicardipine capsules produce a significant decrease in systemic vascular resistance. The degree of vasodilation and the resultant hypotensive effects are more prominent in hypertensive patients. In hypertensive patients, nicardipine reduces the blood pressure at rest and during isometric and dynamic exercise. In normotensive patients, a small decrease of about 9 mm Hg in systolic and 7 mm Hg in diastolic blood pressure may accompany this fall in peripheral resistance. An increase in heart rate may occur in response to the vasodilation and decrease in blood pressure, and in a few patients this heart rate increase may be pronounced. In clinical studies mean heart rate at time of peak plasma levels was usually increased by 5 to 10 beats per minute compared to placebo, with the greater increases at higher doses, while there was no difference from placebo at the end of the dosing interval. Hemodynamic studies following intravenous dosing in patients with coronary artery disease and normal or moderately abnormal left ventricular function have shown significant increases in ejection fraction and cardiac output with no significant change, or a small decrease, in left ventricular end-diastolic pressure (LVEDP). Although there is evidence that Nicardipine capsules increase coronary blood flow, there is no evidence that this property plays any role in its effectiveness in stable angina. In patients with coronary artery disease, intracoronary administration of nicardipine caused no direct myocardial depression. Nicardipine capsules do, however, have a negative inotropic effect in some patients with severe left ventricular dysfunction and could, in patients with very impaired function, lead to worsened failure.
“Coronary Steal”, the detrimental redistribution of coronary blood flow in patients with coronary artery disease (diversion of blood from underperfused areas toward better perfused areas), has not been observed during nicardipine treatment. On the contrary, nicardipine has been shown to improve systolic shortening in normal and hypokinetic segments of myocardial muscle, and radio-nuclide angiography has confirmed that wall motion remained improved during an increase in oxygen demand. Nonetheless, occasional patients have developed increased angina upon receiving nicardipine. Whether this represents steal in those patients, or is the result of increased heart rate and decreased diastolic pressure, is not clear.
In patients with coronary artery disease nicardipine improves L.V. diastolic distensibility during the early filling phase, probably due to a faster rate of myocardial relaxation in previously underperfused areas. There is little or no effect on normal myocardium, suggesting the improvement is mainly by indirect mechanisms such as afterload reduction, and reduced ischemia. Nicardipine has no negative effect on myocardial relaxation at therapeutic doses. The clinical consequences of these properties are as yet undemonstrated.
In general, no detrimental effects on the cardiac conduction system were seen with the use of Nicardipine capsules.
Nicardipine increased the heart rate when given intravenously during acute electrophysiologic studies and prolonged the corrected QT interval to a minor degree. The sinus node recovery times and SA conduction times were not affected by the drug. The PA, AH, and HV intervals1 and the functional and effective refractory periods of the atrium were not prolonged by Nicardipine capsules and the relative and effective refractory periods of the His-Purkinje system were slightly shortened after intravenous Nicardipine.
1PA = conduction time from high to low right atrium, AH = conduction time from low right atrium to His bundle deflection or AV nodal conduction time, HV = conduction time through the His bundle and the bundle branch-Purkinje system.
There is a transient increase in electrolyte excretion, including sodium. Nicardipine capsules do not cause generalized fluid retention, as measured by weight changes, although 7% to 8% of the patients experience pedal edema.
Effects in Angina Pectoris
In controlled clinical trials of up to 12 weeks’ duration in patients with chronic stable angina, Nicardipine capsules increased exercise tolerance and reduced nitroglycerin consumption and the frequency of anginal attacks. The antianginal efficacy of Nicardipine capsules have been demonstrated in four placebo-controlled studies involving 258 patients with chronic stable angina. In exercise tolerance testing, Nicardipine capsules significantly increased time to angina, total exercise duration and time to 1 mm ST segment depression. Included among these four studies was a dose-definition study in which dose-related improvements in exercise tolerance at 1 and 4 hours postdosing and reduced frequency of anginal attacks were seen at doses of 10, 20 and 30 mg tid. Effectiveness at 10 mg tid was, however, marginal. In a fifth placebo-controlled study, the antianginal efficacy of Nicardipine capsules were demonstrated at 8 hours postdose (trough). The sustained efficacy of Nicardipine capsules have been demonstrated over long-term dosing. Blood pressure fell in patients with angina by about 10/8 mm Hg at peak blood levels and was little different from placebo at trough blood levels.
Effects in Hypertension
Nicardipine capsules produced dose-related decreases in both systolic and diastolic blood pressure in clinical trials. The antihypertensive efficacy of Nicardipine capsules administered three times daily has been demonstrated in three placebo-controlled studies involving 517 patients with mild to moderate hypertension. The blood pressure responses in the three studies were statistically significant from placebo at peak (1 hour postdosing) and trough (8 hours postdosing) although it is apparent that well over half of the antihypertensive effect is lost by the end of the dosing interval. The results from placebo controlled studies of Nicardipine capsules given three times daily are shown in the following table:
The responses are shown as differences from the concurrent placebo control group. The large changes between peak and trough effects were not accompanied by observed side effects at peak response times. In a study using 24-hour intra-arterial blood pressure monitoring, the circadian variation in blood pressure remained unaltered, but the systolic and diastolic blood pressures were reduced throughout the whole 24 hours.
When added to beta-blocker therapy, Nicardipine capsules further lower both systolic and diastolic blood pressure.
INDICATIONS AND USAGE
I. Stable Angina
Nicardipine capsules are indicated for the management of patients with chronic stable angina. Nicardipine capsules may be used alone or in combination with beta-blockers.
Nicardipine capsules are indicated for the treatment of hypertension. Nicardipine capsules may be used alone or in combination with other antihypertensive drugs. In administering Nicardipine it is important to be aware of the relatively large peak to trough differences in blood pressure effect.
Nicardipine capsules are contraindicated in patients with hypersensitivity to the drug. Because part of the effect of Nicardipine capsules are secondary to reduced afterload, the drug is also contraindicated in patients with advanced aortic stenosis. Reduction of diastolic pressure in these patients may worsen rather than improve myocardial oxygen balance.
About 7% of patients in short-term, placebo-controlled angina trials have developed increased frequency, duration or severity of angina on starting Nicardipine capsules or at the time of dosage increases, compared with 4% of patients on placebo. Comparisons with beta-blockers also show a greater frequency of increased angina, 4% vs 1%. The mechanism of this effect has not been established.
Use in Patients With Congestive Heart Failure
Although preliminary hemodynamic studies in patients with congestive heart failure have shown that Nicardipine capsules reduced afterload without impairing myocardial contractility, it has a negative inotropic effect in vitro and in some patients. Caution should be exercised when using the drug in congestive heart failure patients, particularly in combination with a beta-blocker.
Nicardipine capsules are not a beta-blocker and therefore gives no protection against the dangers of abrupt beta-blocker withdrawal; any such withdrawal should be by gradual reduction of the dose of beta-blocker, preferably over 8 to 10 days.
Because Nicardipine capsules decrease peripheral resistance, careful monitoring of blood pressure during the initial administration and titration of Nicardipine capsules are suggested. Nicardipine capsules like other calcium channel blockers, may occasionally produce symptomatic hypotension. Caution is advised to avoid systemic hypotension when administering the drug to patients who have sustained an acute cerebral infarction or hemorrhage. Because of prominent effects at the time of peak blood levels, initial titration should be performed with measurements of blood pressure at peak effect and just before the next dose.
Use in Patients With Impaired Hepatic Function: Since the liver is the major site of biotransformation and since Nicardipine capsules are subject to first pass metabolism, the drug should be used with caution in patients having impaired liver function or reduced hepatic blood flow. Patients with severe liver disease developed elevated blood levels (fourfold increase in AUC) and prolonged half-life (19 hours) of nicardipine.
Use in Patients With Impaired Renal Function: When Nicardipine capsules 20 mg or 30 mg tid was given to hypertensive patients with mild renal impairment, mean plasma concentrations, AUC and Cmax were approximately twofold higher in renally impaired patients than in healthy controls. Doses in these patients must be adjusted.
In controlled clinical studies, adrenergic beta-receptor blockers have been frequently administered concomitantly with Nicardipine capsules. The combination is well tolerated.
Cimetidine increases Nicardipine capsules plasma levels. Patients receiving the two drugs concomitantly should be carefully monitored.
Some calcium blockers may increase the concentration of digitalis preparations in the blood. Nicardipine capsules usually do not alter the plasma levels of digoxin; however, serum digoxin levels should be evaluated after concomitant therapy with Nicardipine capsules are initiated.
Coadministration of Maalox TC had no effect on Nicardipine capsules absorption.
Severe hypotension has been reported during fentanyl anesthesia with concomitant use of a beta-blocker and a calcium channel blocker. Even though such interactions were not seen during clinical studies with Nicardipine capsules, an increased volume of circulating fluids might be required if such an interaction were to occur.
Concomitant administration of oral or intravenous nicardipine and cyclosporine results in elevated plasma cyclosporine levels though nicardipine inhibition of hepatic microsomal enzymes, including CYP3A4. Plasma concentrations of cyclosporine should therefore be closely monitored, and its dosage reduced accordingly, in patients treated with nicardipine.
Tacrolimus: Concomitant administration of oral or intravenous nicardipine and tacrolimus may result in elevated plasma tacrolimus levels through nicardipine inhibition of hepatic microsomal enzymes, including CYP3A4. Closely monitor plasma concentrations of tacrolimus during nicardipine administration, and adjust the dose of tacrolimus accordingly.
When therapeutic concentrations of furosemide, propranolol, dipyridamole, warfarin, quinidine or naproxen were added to human plasma, the plasma protein binding of Nicardipine capsules were not altered.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Rats treated with nicardipine in the diet (at concentrations calculated to provide daily dosage levels of 5, 15 or 45 mg/kg/day) for 2 years showed a dose-dependent increase in thyroid hyperplasia and neoplasia (follicular adenoma/carcinoma). One- and 3 month studies in the rat have suggested that these results are linked to a nicardipine-induced reduction in plasma thyroxine (T4) levels with a consequent increase in plasma levels of thyroid stimulating hormone (TSH). Chronic elevation of TSH is known to cause hyperstimulation of the thyroid. In rats on an iodine deficient diet, nicardipine administration for 1 month was associated with thyroid hyperplasia that was prevented by T4 supplementation. Mice treated with nicardipine in the diet (at concentrations calculated to provide daily dosage levels of up to 100 mg/kg/day) for up to 18 months showed no evidence of neoplasia of any tissue and no evidence of thyroid changes. There was no evidence of thyroid pathology in dogs treated with up to 25 mg nicardipine/kg/day for 1 year and no evidence of effects of nicardipine on thyroid function (plasma T4 and TSH) in man.
There was no evidence of a mutagenic potential of nicardipine in a battery of genotoxicity tests conducted on microbial indicator organisms, in micronucleus tests in mice and hamsters, or in a sister chromatid exchange study in hamsters.
No impairment of fertility was seen in male or female rats administered nicardipine at oral doses as high as 100 mg/kg/day (50 times the 40 mg tid maximum recommended antianginal or antihypertensive dose in man, assuming a patient weight of 60 kg).
Pregnancy Category C
Nicardipine was embryocidal when administered orally to pregnant Japanese White rabbits, during organogenesis, at 150 mg/kg/day but not at 50 mg/kg/day (25 times the maximum recommended antianginal or antihypertensive dose in man). No adverse effects on the fetus were observed when New Zealand albino rabbits were treated, during organogenesis, with up to 100 mg nicardipine/kg/day (a dose associated with significant mortality in the treated doe). In pregnant rats administered nicardipine orally at up to 100 mg/kg/day (50 times the maximum recommended human dose) there was no evidence of embryolethality or teratogenicity. However, dystocia, reduced birth weights, reduced neonatal survival, and reduced neonatal weight gain were noted. There are no adequate and well-controlled studies in pregnant women. Nicardipine capsules should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Studies in rats have shown significant concentrations of nicardipine in maternal milk following oral administration. For this reason it is recommended that women who wish to breastfeed should not take this drug.
Safety and efficacy in patients under the age of 18 have not been established.
Pharmacokinetic parameters did not differ between elderly hypertensive patients (≥65 years) and healthy controls after 1 week of Nicardipine capsules treatment at 20 mg tid. Plasma Nicardipine capsules concentrations in elderly hypertensive subjects were similar to plasma concentrations in healthy young adult subjects when Nicardipine capsules were administered at doses of 10, 20, and 30 mg tid, suggesting that the pharmacokinetics of Nicardipine capsules are similar in young and elderly hypertensive patients.
Clinical studies of nicardipine did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
In multiple-dose U.S. and foreign controlled short-term studies 1910 patients received Nicardipine capsules alone or in combination with other drugs. In these studies adverse events were reported spontaneously; adverse experiences were generally not serious but occasionally required dosage adjustment and about 10% of patients left the studies prematurely because of them. Peak responses were not observed to be associated with adverse effects during clinical trials, but physicians should be aware that adverse effects associated with decreases in blood pressure (tachycardia, hypotension, etc.) could occur around the time of the peak effect. Most adverse effects were expected consequences of the vasodilator effects of Nicardipine capsules.
The incidence rates of adverse effects in anginal patients were derived from multicenter, controlled clinical trials. Following are the rates of adverse effects for Nicardipine capsules (n=520) and placebo (n=310), respectively, that occurred in 0.4% of patients or more. These represent events considered probably drug-related by the investigator (except for certain cardiovascular events that were recorded in a different category). Where the frequency of adverse effects for Nicardipine capsules and placebo is similar, causal relationship is uncertain. The only dose-related effects were pedal edema and increased angina.
In addition, adverse events were observed that are not readily distinguishable from the natural history of the atherosclerotic vascular disease in these patients. Adverse events in this category each occurred in <0.4% of patients receiving Nicardipine capsules and included myocardial infarction, atrial fibrillation, exertional hypotension, pericarditis, heart block, cerebral ischemia, and ventricular tachycardia. It is possible that some of these events were drug-related.
The incidence rates of adverse effects in hypertensive patients were derived from multicenter, controlled clinical trials. Following are the rates of adverse effects for Nicardipine capsules and placebo (n= 211), respectively, that occurred in 0.4% of patients or more. These represent events considered probably drug-related by the investigator. Where the frequency of adverse effects for Nicardipine capsules and placebo is similar, causal relationship is uncertain. The only dose-related effect was pedal edema.
The following rare adverse events have been reported in clinical trials or the literature:
Body as a Whole: infection, allergic reaction
Cardiovascular: hypotension, postural hypotension, atypical chest pain, peripheral vascular disorder, ventricular extrasystoles, ventricular tachycardia
Digestive: sore throat, abnormal liver chemistries
Nervous: hot flashes, vertigo, hyperkinesia, impotence, depression, confusion, anxiety
Respiratory: rhinitis, sinusitis
Special Senses: tinnitus, abnormal vision, blurred vision
Urogenital: increased urinary frequency
Overdosage with a 600-mg single dose (15 to 30 times normal clinical dose) has been reported. Marked hypotension (blood pressure unobtainable) and bradycardia (heart rate 20 bpm in normal sinus rhythm) occurred, along with drowsiness, confusion and slurred speech. Supportive treatment with a vasopressor resulted in gradual improvement with normal vital signs approximately 9 hours posttreatment.
Based on results obtained in laboratory animals, overdosage may cause systemic hypotension, bradycardia (following initial tachycardia) and progressive atrioventricular conduction block. Reversible hepatic function abnormalities and sporadic focal hepatic necrosis were noted in some animal species receiving very large doses of nicardipine.
For treatment of overdose standard measures (for example, evacuation of gastric contents, elevation of extremities, attention to circulating fluid volume, and urine output) including monitoring of cardiac and respiratory functions should be implemented. The patient should be positioned so as to avoid cerebral anoxia. Frequent blood pressure determinations are essential. Vasopressors are clinically indicated for patients exhibiting profound hypotension. Intravenous calcium gluconate may help reverse the effects of calcium entry blockade.
DOSAGE AND ADMINISTRATION
The dose should be individually titrated for each patient beginning with 20 mg three times daily. Doses in the range of 20 to 40 mg three times a day have been shown to be effective. At least 3 days should be allowed before increasing the Nicardipine capsules dose to ensure achievement of steady-state plasma drug concentrations.
Concomitant Use With Other Antianginal Agents
The dose of Nicardipine capsules should be individually adjusted according to the blood pressure response beginning with 20 mg three times daily. The effective doses in clinical trials have ranged from 20 mg to 40 mg three times daily. The maximum blood pressure lowering effect occurs approximately 1 to 2 hours after dosing. To assess the adequacy of blood pressure response, the blood pressure should be measured at trough (8 hours after dosing). Because of the prominent peak effects of nicardipine, blood pressure should be measured 1 to 2 hours after dosing, particularly during initiation of therapy. At least 3 days should be allowed before increasing the Nicardipine capsules dose to ensure achievement of steady-state plasma drug concentrations.
Concomitant Use With Other Antihypertensive Agents
1. Diuretics: Nicardipine capsules may be safety coadministered with thiazide diuretics.
2. Beta-blockers: Nicardipine capsules may be safely coadministered with beta-blocker.
Special Patient Population
Although there is no evidence that Nicardipine capsules impair renal function, careful dose titration beginning with 20 mg tid is advised.
Nicardipine capsules should be administered cautiously in patients with severely impaired hepatic function. A suggested starting dose of 20 mg twice a day is advised with individual titration based on clinical findings maintaining the twice a day schedule.
Congestive Heart Failure
Caution is advised when titrating Nicardipine capsules dosage in patients with congestive heart failure.
Nicardipine 20 mg capsules are available in light blue opaque/white opaque hard gelatin capsules imprinted “E501” in black ink on cap and body, filled with yellow powder. These are supplied in bottles of 90, 100, 500 and 1000.
Nicardipine 30 mg capsules are available in light blue opaque hard gelatin capsules imprinted “E502” with black ink on cap and body, filled with yellow powder. These are supplied in bottles of 90, 100, 500 and 1000.
Store at 20° to 25°C (68° to 77°F). Dispense contents in a tight, light-resistant container with a child-resistant closure.
The brands listed are trademarks of their respective owners.
Epic Pharma, LLC
Laurelton, NY 11413
Manufactured in USA
Nicardipine Capsules, 20 mg
Nicardipine Capsules, 30 mg
Nicardipine pharmaceutical active ingredients containing related brand and generic drugs:
Active ingredient is the part of the drug or medicine which is biologically active. This portion of the drug is responsible for the main action of the drug which is intended to cure or reduce the symptom or disease. The other portions of the drug which are inactive are called excipients; there role is to act as vehicle or binder. In contrast to active ingredient, the inactive ingredient's role is not significant in the cure or treatment of the disease. There can be one or more active ingredients in a drug.
Nicardipine available forms, composition, doses:
Form of the medicine is the form in which the medicine is marketed in the market, for example, a medicine X can be in the form of capsule or the form of chewable tablet or the form of tablet. Sometimes same medicine can be available as injection form. Each medicine cannot be in all forms but can be marketed in 1, 2, or 3 forms which the pharmaceutical company decided based on various background research results.
Composition is the list of ingredients which combinedly form a medicine. Both active ingredients and inactive ingredients form the composition. The active ingredient gives the desired therapeutic effect whereas the inactive ingredient helps in making the medicine stable.
Doses are various strengths of the medicine like 10mg, 20mg, 30mg and so on. Each medicine comes in various doses which is decided by the manufacturer, that is, pharmaceutical company. The dose is decided on the severity of the symptom or disease.
Nicardipine destination | category:
Destination is defined as the organism to which the drug or medicine is targeted. For most of the drugs what we discuss, human is the drug destination.
Drug category can be defined as major classification of the drug. For example, an antihistaminic or an antipyretic or anti anginal or pain killer, anti-inflammatory or so.
Nicardipine Anatomical Therapeutic Chemical codes:
A medicine is classified depending on the organ or system it acts [Anatomical], based on what result it gives on what disease, symptom [Therapeutical], based on chemical composition [Chemical]. It is called as ATC code. The code is based on Active ingredients of the medicine. A medicine can have different codes as sometimes it acts on different organs for different indications. Same way, different brands with same active ingredients and same indications can have same ATC code.
Nicardipine pharmaceutical companies:
Pharmaceutical companies are drug manufacturing companies that help in complete development of the drug from the background research to formation, clinical trials, release of the drug into the market and marketing of the drug.
Researchers are the persons who are responsible for the scientific research and is responsible for all the background clinical trials that resulted in the development of the drug.
Frequently asked QuestionsCan i drive or operate heavy machine after consuming Nicardipine?
Depending on the reaction of the Nicardipine after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Nicardipine not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.Is Nicardipine addictive or habit forming?
Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
Reviewsdrugs.com conducted a study on Nicardipine, and the result of the survey is set out below. It is noteworthy that the product of the survey is based on the perception and impressions of the visitors of the website as well as the views of Nicardipine consumers. We, as a result of this, advice that you do not base your therapeutic or medical decisions on this result, but rather consult your certified medical experts for their recommendations.
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The information was verified by Dr. Arunabha Ray, MD Pharmacology