Lotensin (Benazepril)



Benazepril HCl

Angiotensin Converting Enzyme Inhibitor

Action And Clinical Pharmacology: Benazepril is an angiotensin converting enzyme (ACE) inhibitor which is used in the treatment of hypertension.

Benazepril, after hydrolytic bioactivation to benazeprilat, inhibits angiotensin converting enzyme (ACE), a peptidyl dipeptidase catalyzing the conversion of angiotensin I to the vasoconstrictor angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex, leading to sodium resorption and potassium secretion by the distal renal tubules.

Inhibition of ACE results in a decrease in plasma angiotensin II, leading to decreased vasoconstriction and a small decrease in aldosterone secretion and plasma aldosterone concentrations. Although the decrease in aldosterone is small, it can result in small increases in serum potassium. Slight increases in serum potassium have been observed in some hypertensive patients treated with benazepril alone. Essentially no change in mean serum potassium was seen in patients treated with benazepril and a thiazide diuretic (see Precautions).

Removal of inhibition of renin secretion by angiotensin II leads to increased plasma renin activity (due to removal of negative feedback of renin release).

ACE is identical to kininase II. Thus, benazepril may interfere with degradation of the potent peptide vasodilator, bradykinin. Whether increased levels of bradykinin play a role in the therapeutic effects of benazepril is unknown.

While the mechanism through which benazepril lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, benazepril has an antihypertensive effect even in patients with low renin hypertension. In particular, benazepril was antihypertensive in all races studied, although it was somewhat less effective in blacks than in nonblacks.

Pharmacokinetics: Following oral administration of benazepril, peak plasma concentrations of benazepril are reached within 0.5 to 1 hour. The extent of absorption is at least 37% as determined by urinary recovery of unchanged drug and its metabolites. Following absorption, benazepril is rapidly hydrolyzed to its active metabolite, benazeprilat. Peak plasma concentrations of benazeprilat are reached 1 to 2 hours after drug intake in the fasting state and 2 to 4 hours after drug intake in the nonfasting state. While the rate of absorption may be slowed by the presence of food in the gastrointestinal tract, the systemic availability of benazeprilat is not affected. Benazeprilat is eliminated predominantly by renal excretion and has an effective accumulation half-life of 10 to 11 hours. The serum protein binding of benazepril is about 97%, and that of benazeprilat about 95%.

Benazepril is almost completely metabolized to benazeprilat, and to the glucuronide conjugates of benazepril and benazeprilat. Only trace amounts of an administered dose of Lotensin can be recovered in the urine as unchanged benazepril, while about 20% of the dose is excreted as benazeprilat, 4% as benazepril glucuronide, and 8% as benazeprilat glucuronide. The kinetics of benazepril are approximately dose-proportional within the dosage range (10 to 40 mg).

The disposition of benazepril and benazeprilat in patients with mild to moderate renal insufficiency (creatinine clearance >30 mL/min [0.5 mL/s]) is similar to that in patients with normal renal function.

In patients with hepatic dysfunction due to cirrhosis, levels of benazeprilat are essentially unaltered. The pharmacokinetics of benazepril and benazeprilat do not appear to be influenced by age.

Pharmacodynamics: Administration of benazepril to patients with mild to moderate essential hypertension results in a reduction of both supine and standing blood pressure usually with little or no orthostatic change. Symptomatic postural hypotension is infrequent, although it may occur in patients who are salt- and/or volume-depleted (see Warnings).

After administration of a single oral dose, the onset of antihypertensive activity occurs at approximately 1 hour, with maximum reduction of blood pressure achieved by 2 to 4 hours, in most patients. At recommended doses given once daily, antihypertensive effects have persisted for at least 24 hours. In dose-response studies using once daily dosing in mild to moderate essential hypertensive patients, the minimally effective daily dose of benazepril was 10 mg. In studies comparing the same daily dose of benazepril given as a single morning dose or as a twice daily dose, blood pressure reductions at the time of morning trough blood levels were greater with the divided regimen.

During chronic therapy, the maximum reduction in blood pressure with any dose is generally achieved after 1 to 2 weeks. Abrupt withdrawal of benazepril has not been associated with a rapid increase in blood pressure.

When benazepril is given together with thiazide-type diuretics, its blood pressure lowering effect is approximately additive.

Efficacy and safety appear to be the same for elderly (>65 years of age) and younger adult patients given the same daily dosages.

Indications And Clinical Uses: In the treatment of mild to moderate essential hypertension. It may be used alone or in association with thiazide diuretics.

In using benazepril, consideration should be given to the risk of angioedema (see Warnings).

Benazepril should normally be used in those patients in whom treatment with a diuretic or a beta-blocker was found ineffective or has been associated with unacceptable adverse effects.

Benazepril can also be tried as an initial agent in those patients in whom use of diuretics and/or beta-blockers is contraindicated or in patients with medical conditions in which these drugs frequently cause serious adverse effects.

The safety and efficacy of benazepril in congestive heart failure and renovascular hypertension have not been established and therefore, its use in these conditions is not recommended.

The safety and efficacy of concurrent use of benazepril with antihypertensive agents other than thiazide diuretics have not been established.

Pregnancy: When used in pregnancy during the second and third trimesters, ACE inhibitors can cause injury or even death of the developing fetus. When pregnancy is detected, ACE inhibitors should be discontinued as soon as possible (see Warnings, Pregnancy and Information for the Patient).

Contra-Indications: In patients with known hypersensitivity to this product or any of its components and in patients with a history of angioedema related to previous treatment with an ACE inhibitor.

Manufacturers’ Warnings In Clinical States: Angioedema: Angioedema has been reported in patients with ACE inhibitors, including benazepril. Angioedema associated with laryngeal involvement may be fatal. If laryngeal stridor or angioedema of the face, tongue, or glottis occurs, benazepril should be discontinued immediately, the patient treated appropriately in accordance with accepted medical care, and carefully observed until the swelling disappears. In instances where swelling is confined to the face and lips, the condition generally resolves without treatment, although antihistamines may be useful in relieving symptoms. Where there is involvement of tongue, glottis or larynx, likely to cause airway obstruction, appropriate therapy (including, but not limited to 0.3 to 0.5 mL of s.c. epinephrine solution 1:1 000) should be administered promptly (see Adverse Effects).

Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of angioedema while receiving an ACE inhibitor (see Contraindications).

Hypotension: Occasionally, symptomatic hypotension has occurred after administration of benazepril usually after the first or second dose or when the dose was increased. It is more likely to occur in patients who are volume depleted by diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting. In patients with ischemic heart disease or cerebrovascular disease, an excessive fall in blood pressure could result in a myocardial infarction or cerebrovascular accident (see Adverse Effects). Because of the potential fall in blood pressure in these patients, therapy with benazepril should be started under close medical supervision. Such patients should be followed closely for the first weeks of treatment and whenever the dose of benazepril is increased. In patients with severe congestive heart failure, with or without associated renal insufficiency, ACE inhibitor therapy may cause excessive hypotension and has been associated with oliguria, and/or progressive azotemia, and rarely, with acute renal failure and/or death.

If hypotension occurs, the patient should be placed in a supine position and, if necessary, receive an i.v. infusion of normal saline. A transient hypotensive response is not a contraindication to further treatment, which usually can be continued without difficulty once the blood pressure has increased after volume expansion. However, lower doses of benazepril and/or reduced concomitant diuretic therapy should be considered.

Neutropenia/Agranulocytosis: Agranulocytosis and bone marrow depression have been caused by ACE inhibitors. Current experience with benazepril shows the incidence to be rare and a causal relationship to the administration of benazepril has not been established. Periodic monitoring of white blood cell counts should be considered, especially in patients with collagen vascular disease and/or renal disease.

Pregnancy: ACE inhibitors can cause fetal and neonatal morbidity and mortality when administered to pregnant women. Several dozen cases have been reported in the world literature. When pregnancy is detected, benazepril should be discontinued as soon as possible.

In rare cases (probably less than 1 in every 1 000 pregnancies) in which there is no alternative to ACE inhibitor therapy, patients should be apprised of the potential hazards to their fetuses. Serial ultrasound examinations should be performed to assess fetal development and well-being in addition to the volume of amniotic fluid.

If oligohydramnios is observed, benazepril should be discontinued unless it is considered life-saving for the mother. A non-stress test (NST), and/or biophysical profiling (BPP) may be appropriate, depending upon the week of pregnancy. If concerns regarding fetal well-being still persist, a contraction stress testing (CST) should be considered. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury.

Infants with a history of exposure to ACE inhibitors in utero should be closely observed for hypotension, oliguria, and hyperkalemia. If oliguria occurs, attention should be directed toward support of blood pressure and renal perfusion. Exchange transfusion or dialysis may be required as a means of reversing hypotension and/or substituting for impaired renal function, however, experience with these procedures is limited and they have not been associated with significant clinical benefit. Hemodialysis has little effect on the clearance of benazepril and benazeprilat.

Human Data: It is not known whether exposure limited to the first trimester of pregnancy can adversely affect fetal outcome. Use of ACE inhibitors during the second and third trimesters of pregnancy has been associated with fetal and neonatal injury including hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure and death. Oligohydramnios has also been reported, presumably resulting from decreased fetal renal function; oligohydramnios in this setting has been associated with fetal limb contracture, craniofacial deformation and hypoplastic lung development. Prematurity and patent ductus arteriosus have also been reported, although it is not clear whether these occurrences were due to the ACE inhibitor exposure.

Animal Data: Dose related maternal toxicity was observed in studies of pregnant rats, mice and rabbits at doses of 250 mg/kg, 150 mg/kg and 1 mg/kg respectively. No embryotoxic or teratogenic effects of benazepril were seen at doses up to 250 mg/kg in rats (300 times the maximum recommended dose in humans), 150 mg/kg in mice (90 times the maximum recommended dose in humans) and 5 mg/kg in rabbits (more than 3 times the maximum recommended dose in humans).

Precautions: Renal Impairment: As a consequence of inhibiting the renin-angiotensin-aldosterone system, changes in renal function have been seen in susceptible individuals. In patients whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, such as patients with bilateral renal artery stenosis, unilateral renal artery stenosis to a solitary kidney, or severe congestive heart failure, treatment with agents that inhibit this system has been associated with oliguria, progressive azotemia, and rarely, acute renal failure and/or death. In susceptible patients, concomitant diuretic use may further increase risk.

Use of benazepril should include appropriate assessment of renal function.

In patients with severe heart failure, whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment with ACE inhibitors, including benazepril, may be associated with oliguria and/or progressive azotemia and rarely acute renal failure and/or death.

Anaphylactoid Reactions During Membrane Exposure: Anaphylactoid reactions have been reported in patients dialyzed with high-flux membranes (e.g., polyacrylonitrile [PAN]) and treated concomitantly with an ACE inhibitor. Dialysis should be stopped immediately if symptoms such as nausea, abdominal cramps, burning, angioedema, shortness of breath and severe hypotension occur. Symptoms are not relieved by antihistamines. In these patients consideration should be given to using a different type of dialysis membrane or a different class of antihypertensive agents.

Anaphylactoid Reactions During Desensitization: There have been isolated reports of patients experiencing sustained life threatening anaphylactoid reactions while receiving ACE inhibitors during desensitizing treatment with hymenoptera (bees, wasps) venom. In the same patients, these reactions have been avoided when ACE inhibitors were temporarily withheld for at least 24 hours, but they have reappeared upon inadvertent rechallenge.

Hyperkalemia and Potassium-Sparing Diuretics: Elevated serum potassium (>5.5 mEq/L) was observed in 1.1% of hypertensive patients in clinical trials treated with benazepril alone and in 0.4% treated with benazepril and hydrochlorothiazide. In most cases these were isolated values which resolved despite continued therapy. Hyperkalemia was a cause of discontinuation of therapy in less than 0.1% of hypertensive patients.

Risk factors for the development of hyperkalemia may include renal insufficiency, diabetes mellitus, and the concomitant use of agents to treat hypokalemia (see Drug Interactions).

Valvular Stenosis: There is concern on theoretical grounds that patients with aortic stenosis might be at particular risk of decreased coronary perfusion when treated with vasodilators because they do not develop as much afterload reduction.

Surgery/Anesthesia: ACE inhibitors may augment the hypotensive effects of anesthetics and analgesics. In patients undergoing surgery or during anesthesia with agents that produce hypotension, benazepril will block the angiotensin II formation that could otherwise occur secondary to compensatory renin release. Hypotension that occurs as a result of this mechanism can be corrected by volume expansion.

Patients with Impaired Liver Function: Hepatitis (hepatocellular and/or cholestatic), elevations of liver enzymes and/or serum bilirubin have occurred during therapy with ACE inhibitors in patients with or without pre-existing liver abnormalities. In most cases the changes were reversed on discontinuation of the drug.

Elevations of liver enzymes and/or serum bilirubin have been reported with benazepril (see Adverse Effects). Should the patient receiving benazepril experience any unexplained symptoms particularly during the first weeks or months of treatment, it is recommended that a full set of liver function tests and any other necessary investigations be carried out. Discontinuation of benazepril should be considered when appropriate.

There are no adequate studies in patients with cirrhosis and/or liver dysfunction. Benazepril should be used with particular caution in patients with pre-existing liver abnormalities. In such patients baseline liver function tests should be obtained before administration of the drug and close monitoring of response and metabolic effects should apply.

Cough: A dry, persistent cough, which usually disappears only after withdrawal or lowering of the dose of benazepril has been reported. Such possibility should be considered as part of the differential diagnosis of the cough.

Lactation: Ingestion of 20 mg daily for 3 days resulted in detectable levels of benazeprilat in breast milk (0.3% of those found in plasma). In general, benazepril should not be administered to nursing mothers.

Children: Safety and effectiveness of benazepril in children have not been established; therefore, its use in this age group is not recommended.

Geriatrics: Although clinical experience has not identified differences in response between the elderly (>65 years) and younger patients, greater sensitivity of some older individuals cannot be ruled out.

Drug Interactions: Concomitant Diuretic Therapy: Patients concomitantly taking ACE inhibitors and diuretics, and especially those in whom diuretic therapy was recently instituted, may occasionally experience an excessive reduction of blood pressure after initiation of therapy. The possibility of hypotensive effects after the first dose of benazepril can be minimized by either discontinuing the diuretic or increasing the salt intake prior to initiation of treatment with benazepril. If it is not possible to discontinue the diuretic, the starting dose of benazepril should be reduced and the patient should be closely observed for several hours following initial dose and until blood pressure has stabilized (see Warnings and Dosage).

Agents Causing Renin Release: The antihypertensive effect of benazepril is augmented by antihypertensive agents that cause renin release (e.g., diuretics).

Agents Increasing Serum Potassium: Since benazepril decreases aldosterone production, increases of serum potassium may occur. Potassium sparing diuretics (e.g., spironolactone, triamterene, amiloride, etc.) or potassium supplements should be given only for documented hypokalemia and with caution and frequent monitoring of serum potassium, since they may lead to a significant increase in serum potassium. Salt substitutes which contain potassium should also be used with caution.

Agents Affecting Sympathetic Activity: Agents affecting sympathetic activity (e.g., ganglionic blocking agents or adrenergic neuron blocking agents) may be used with caution. B-adrenergic blocking agents add some further antihypertensive effect to benazepril.

Indomethacin: Indomethacin may diminish the antihypertensive efficacy of concomitantly administered benzepril.

Oral Anticoagulants: Multiple dose interaction studies failed to identify any clinically important effects on the serum concentrations, the degree of protein binding or the anticoagulant effect (measured by prothrombin time) of warfarin and nicoumalone. The bioavailability of benazeprilat was not assessed during the coadministration of benazepril with warfarin or nicoumalone.

Lithium: Increased lithium levels and symptoms of lithium toxicity have been reported in patients receiving ACE inhibitors during therapy with lithium. These drugs should be coadministered with caution and frequent monitoring of serum lithium levels is recommended. If a diuretic is also used, the risk of lithium toxicity may be increased.

Hydrochlorothiazide, Chlorthalidone and Furosemide: The bioavailability of benazepril was not altered when single doses were administered concomitantly with the diuretics hydrochlorothiazide, chlorthalidone or furosemide.

ASA: No important changes in pharmacokinetic parameters occurred when single doses of benazepril were administered concomitantly with ASA.

Digoxin: In a single dose interaction study of benazepril with multiple doses of digoxin, no important changes in pharmacokinetic parameters were observed.

Amlodipine/Nifedipine: Benazepril has been used concomitantly with the calcium channel blockers amlodipine and nifedipine, without evidence of clinically important adverse interactions.

Other: In separate single or multiple dose pharmacokinetic interaction studies, the bioavailability of benazepril was not altered by coadministration with propranolol, naproxen, atenolol, nifedipine, amlodipine or cimetidine.

Information for the Patient: Note: As with many other drugs, certain advice to patients being treated with benazepril is warranted. This information is intended to aid in the safe and effective use of this medication. It is not a disclosure of all possible adverse experiences or intended effects.

Angioedema: Angioedema, including laryngeal edema, may occur especially following the first dose of benazepril. Patients should be so advised and told to report immediately any signs or symptoms suggesting angioedema, such as swelling of face, extremities, eyes, lips, tongue, difficulty in swallowing or breathing. They should immediately stop taking benazepril and consult with their physician.

Hypotension: Patients should be cautioned to report light-headedness, especially during the first few days of benazepril therapy. If actual syncope occurs, the patient should be told to discontinue the drug and consult with their physician.

All patients should be cautioned that excessive perspiration and dehydration may lead to an excessive fall in blood pressure because of reduction in fluid volume. Other causes of volume depletion such as vomiting or diarrhea may also lead to a fall in blood pressure, patients should be advised to consult with their physician.

Agranulocytosis/Neutropenia: Patients should be told to report promptly to their physician any indication of infection (e.g., sore throat, fever), as this may be a sign of neutropenia.

Impaired Liver Function: Patients should be advised to return to their physician if he/she experiences any symptoms possibly related to liver dysfunction. This would include “viral-like symptoms” in the first weeks to months of therapy (such as fever, malaise, muscle pain, rash or adenopathy which are possible indicators of hypersensitivity reactions), or if abdominal pain, nausea or vomiting, loss of appetite, jaundice, itching or any other unexplained symptoms occur during therapy.

Hyperkalemia: Patients should be told not to use salt substitutes containing potassium without consulting their physician.

Pregnancy: Since the use of benazepril during pregnancy can cause injury and even death of the developing fetus, patients should be advised to report promptly to their physician if they become pregnant.

Adverse Reactions: Benazepril has been evaluated for safety in over 6 000 hypertensive patients. Over 400 elderly patients have participated in controlled hypertension trials. Long-term safety has been assessed in more than 700 patients treated for 1 year or more. There was no increase in the incidence of adverse reactions in elderly patients given the same daily dose. The overall frequency of adverse reactions was not related to duration of therapy or total daily dose.

The most severe adverse reactions occurring in clinical trials with benazepril were: angioedema (full clinical syndrome, 1 case; edema of lips or face without the other manifestations of angioedema, 0.5%), hypotension (0.3%), postural hypotension (0.4%) and syncope (0.1%).

The most frequent clinical adverse reactions in placebo-controlled clinical trials with benazepril monotherapy (N=964) were headache (6.2%), dizziness (3.6%), fatigue (2.4%), somnolence (1.6%), postural dizziness (1.5%), nausea (1.3%) and cough (1.2%). Discontinuation of therapy due to adverse experiences was required in 4% of patients treated with benazepril.

Clinical adverse reactions occurring in less than 1% of patients treated with benazepril in controlled and uncontrolled clinical trials, and postmarketing experience, are listed below by body system: Incidence less than 1%:

Body as Whole: asthenia.

Cardiovascular: excessive hypotension, angina pectoris, palpitations, myocardial infarction, cerebrovascular accident, arrhythmia.

Digestive: constipation, gastritis, vomiting, flatulence, melena, abdominal pain, pancreatitis.

Musculoskeletal: arthritis, arthralgia, myalgia.

Nervous: anxiety, depression, hypertonia, insomnia, nervousness, paresthesia, incoordination, decreased libido.

Respiratory: dyspnea, asthma, bronchitis.

Dermatologic: apparent hypersensitivity reactions (manifested by dermatitis, pruritus, or rash), photosensitivity, pemphigus, Stevens-Johnson syndrome and flushing.

Special Senses: tinnitus and taste disorders.

Urogenital: impaired renal function, impotence, urinary frequency.

Hematologic: leukopenia, eosinophilia, hemolytic anemia and thrombocytopenia.

Allergic and Immune Reactions: angioedema, lip and/or facial edema.

Abnormal Laboratory Findings: hyperkalemia (see Precautions).

Creatinine, Blood Urea Nitrogen: Increases in serum creatinine (>150% of baseline) were observed in 2% of patients treated with benazepril alone. Less than 0.1% of these patients developed simultaneous increases in blood urea nitrogen and serum creatinine. Increases are more likely to occur in patients receiving concomitant diuretic therapy than in those on benazepril alone. These increases often reversed on continued therapy.

Neutropenia: Neutrophil counts of less than 1 500/mmoccurred in 2% of patients treated with benazepril alone. No patient was discontinued from a study because of a low neutrophil or white blood cell (WBC) count.

Hemoglobin: Decreases in hemoglobin (a low value and a decrease of 5 g/dL) occurred in only 1 of 2 014 patients receiving benazepril alone and in 1 of 1 357 patients receiving benazepril plus a diuretic.

Hepatic: Elevations of liver enzymes and/or serum bilirubin have occurred (see Precautions).

Other: Elevations of uric acid and blood glucose have been reported, as have scattered incidents of hyponatremia and proteinuria.

Symptoms And Treatment Of Overdose: Symptoms and Treatment: No data are available on overdosage in humans.

The most likely clinical manifestation of overdosage would be symptoms attributable to severe hypotension, for which the usual treatment is i.v. infusion of normal saline solution.

If ingestion is recent, then emesis should be induced. Although the active metabolite, benazeprilat, is only slightly dialyzable, renal dialysis may be useful in overdosed patients with severely impaired renal function.

Dosage And Administration: Dosage must be individualized. Initiation of therapy requires consideration of recent antihypertensive drug treatment, the extent of blood pressure elevation and salt restriction. The dosage of other antihypertensive agents being used with benazepril may need to be adjusted.

Monotherapy: The recommended initial dose of benazepril is 10 mg once daily. Dosage should be adjusted according to blood pressure response, generally, at intervals of at least 2 weeks. The usual maintenance dose is 20 mg daily. The maximum daily dose of benazepril is 40 mg.

In some patients treated once daily, the antihypertensive effect may diminish towards the end of the dosing interval. This can be evaluated by measuring blood pressure just prior to dosing to determine whether satisfactory control is being maintained for 24 hours. If it is not, either twice daily administration with the same total daily dose, or an increase in dose should be considered.

If blood pressure is not controlled with benazepril alone, a diuretic may be added. After the addition of a diuretic, it may be possible to reduce the dose of benazepril.

Concomitant Diuretic Therapy: Symptomatic hypotension occasionally may occur following the initial dose of benazepril and is more likely in patients who are currently being treated with a diuretic. The diuretic should, if possible, be discontinued for 2 to 3 days before beginning therapy with benazepril to reduce the likelihood of hypotension (see Warnings). If the diuretic cannot be discontinued, an initial dose of 5 mg benazepril should be used with careful medical supervision for several hours and until blood pressure has stabilized. The dosage of benazepril should subsequently be titrated (as described above) to the optimal response.

Dosage Adjustment in Renal Impairment: The usual dose of benazepril is recommended for patients with a creatinine clearance >30 mL/min [0.5 mL/s]. For patients with severe renal impairment (creatinine clearance of

Availability And Storage: 5 mg: Each light yellow, capsule-shaped, biconvex, film-coated tablet, engraved CG on one side and LV on the other side, fully bisected on both sides between the C and G, and the L and V, contains: benazepril HCl 5 mg. Nonmedicinal ingredients: cellulose compounds, colloidal silicon dioxide, cornstarch, hydrogenated castor oil, iron oxide, lactose, polyethylene glycol, povidone, talc and titanium dioxide. Bottles of 100.

10 mg: Each dark yellow, capsule-shaped, biconvex, film-coated tablet, engraved CG on one side and HO on the other side, fully bisected on both sides between the C and G, and the H and O, contains: benazepril HCl 10 mg. Nonmedicinal ingredients: cellulose compounds, colloidal silicon dioxide, cornstarch, hydrogenated castor oil, iron oxide, lactose, polyethylene glycol, povidone, talc and titanium dioxide. Bottles of 100.

20 mg: Each reddish-orange, capsule-shaped, biconvex, film-coated tablet, engraved CG on one side and HP on the other side, fully bisected on both sides between the C and G, and the H and P, contains: benazepril HCl 20 mg. Nonmedicinal ingredients: cellulose compounds, colloidal silicon dioxide, cornstarch, hydrogenated castor oil, iron oxide, lactose, polyethylene glycol, povidone, talc and titanium dioxide. Bottles of 100.

Protect from heat (i.e., store at 15 to 30°C) and humidity.

LOTENSIN® Novartis Benazepril HCl Angiotensin Converting Enzyme Inhibitor

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