Control# 115011
Table of Contents
SUMMARY PRODUCT INFORMATION 3 INDICATIONS AND CLINICAL USE 3 CONTRAINDICATIONS 4 WARNINGS AND PRECAUTIONS 4 ADVERSE REACTIONS 8 DRUG INTERACTIONS 11 DOSAGE AND ADMINISTRATION 12 OVERDOSAGE 13 ACTION AND CLINICAL PHARMACOLOGY. 13 STORAGE AND STABILITY 15 DOSAGE FORMS, COMPOSITION AND PACKAGING 15
PHARMACEUTICAL INFORMATION 17 CLINICAL TRIALS 18 DETAILED PHARMACOLOGY 21 TOXICOLOGY 22 REFERENCES 25
Pr
APO-BENAZEPRIL
Benazepril Hydrochloride
| Route of Administration | Dosage Form / Strength | Clinically Relevant Nonmedicinal Ingredients |
| Oral | tablet / 5 mg, 10 mg and 20 mg | None. For a complete listing see Dosage Forms, Composition and Packaging section. |
APO-BENAZEPRIL (benazepril hydrochloride) indicated in the treatment of mild to moderate essential hypertension. It may be used alone or in association with thiazide diuretics. In using APO-BENAZEPRIL, consideration should be given to the risk of angioedema (see WARNINGS AND PRECAUTIONS). APO-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. APO-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 APO-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 APO-BENAZEPRIL with antihypertensive agents other than thiazide diuretics have not been established.
APO-BENAZEPRIL (benazepril hydrochloride) is contraindicated 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.
Angioedema has been reported in patients with ACE inhibitors, including benazepril hydrochloride. Angioedema associated with laryngeal involvement may be fatal. If laryngeal stridor or angioedema of the face, tongue, or glottis occurs, benazepril hydrochloride 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 subcutaneous epinephrine solution 1:1000) should be administered promptly (see ADVERSE REACTIONS). The incidence of angioedema during ACE inhibitor therapy has been reported to be higher in black patients of African origin than in non-black patients. 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).
Occasionally, symptomatic hypotension has occurred after administration of benazepril hydrochloride 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 REACTIONS). Because of the potential fall in blood pressure in these patients, therapy with benazepril hydrochloride 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 hydrochloride 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 intravenous 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 hydrochloride and/or reduced concomitant diuretic therapy should be considered.
Agranulocytosis and bone marrow depression have been caused by ACE inhibitors. Current experience with benazepril hydrochloride shows the incidence to be rare and a causal relationship to the administration of benazepril hydrochloride 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.
ACE inhibitors can cause fetal and neonatal morbidity and mortality when administered to pregnant women. When pregnancy is detected, benazepril hydrochloride should be discontinued as soon as possible. The 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, associated with fetal limb contractures, craniofacial deformation, and hypoplastic lung development. Prematurity, and patent ductus arteriosus and other structural cardiac malformations, as well as neurologic malformations, have also been reported following exposure in the first trimester of pregnancy. Infants with a history of in utero exposure to ACE inhibitors 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, limited experience with those procedures has not been associated with significant clinical benefit. It is not known if benazepril hydrochloride can be removed from the body by hemodialysis.
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 hydrochloride 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).
The presence of concentrations of ACE inhibitor have been reported in human milk. Use of ACE inhibitors is not recommended during breast-feeding.
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 APO-BENAZEPRIL (benazepril hydrochloride) should include appropriate assessment of renal function.
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.
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 challenge.
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).
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.
Patients on 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.
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 hydrochloride (see ADVERSE REACTIONS). Should the patient receiving benazepril hydrochloride 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 hydrochloride should be considered when appropriate. There are no adequate studies in patients with cirrhosis and/or liver dysfunction. Benazepril hydrochloride 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.
A dry, persistent cough, which usually disappears only after withdrawal or lowering of the dose of benazepril hydrochloride has been reported. Such possibility should be considered as part of the differential diagnosis of the cough.
Safety and effectiveness of benazepril hydrochloride in children have not been established, therefore its use in this age group is not recommended.
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.
Benazepril hydrochloride 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 hydrochloride 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%). Hypotension or postural dizziness was a cause for discontinuation of therapy in < 0.2% of patients treated with benazepril alone. Myocardial infarction and cerebral vascular accident occurred, possibly secondary to excessive hypotension in high risk patients (see WARNINGS AND PRECAUTIONS). The most frequent clinical adverse reactions in placebo-controlled clinical trials with benazepril hydrochloride 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 hydrochloride. Adverse reactions occurring in 1 % or more of the 2004 patients in controlled hypertension trials who were treated with benazepril hydrochloride monotherapy, are listed below:
| Body System | Patients (N=2004) | |
| Nervous System | Headache | 10.2% |
| Dizziness | 4.2% | |
| Somnolence | 1.1% | |
| Vertigo | 1.1% | |
| Respiratory | Upper respiratory symptoms | 5.4% |
| Increased cough | 3.4% | |
| Flu symptoms | 1.2% | |
| Gastrointestinal | Nausea | 2.5% |
| Abdominal pain | 2.4% | |
| Diarrhea | 2.0% | |
| Dyspepsia | 1.2% | |
| Musculoskeletal | Musculoskeletal pain | 2.6% |
| Other | Fatigue | 3.6% |
| Rhinitis | 2.4% | |
| Pharyngitis | 1.7% | |
| Back Pain | 1.7% | |
| Chest Pain | 1.2% | |
Clinical adverse reactions occurring in less than 1% of patients treated with benazepril hydrochloride 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, flushing, Stevens-Johnson Syndrome Special Senses: tinnitus, taste disorders Urogenital: impaired renal function, impotence, urinary frequency Hematologic: leucopenia, eosinophilia, hemolytic anemia and thrombocytopenia Allergic and immune reactions: angioedema, lip and/or facial edema Liver: hepatitis (predominantly cholestatic), cholestatic jaundice
Abnormal Laboratory Findings
Hyperkalemia
(see WARNINGS AND PRECAUTIONS)
Creatinine, Blood Urea Nitrogen:
Increases in serum creatinine (> 150% of baseline) were observed in 2% of patients treated with benazepril hydrochloride 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 hydrochloride alone. These increases often reversed on continued therapy.
Neutropenia: Neutrophil counts of less than 1500/mm3 occurred 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. No patient developed a persistent neutrophil count < 1000/mm3 and no patient developed a serious infection in association with a reduced neutrophil or WBC count. No patient treated with benazepril developed agranulocytosis (see WARNINGS AND PRECAUTIONS).
Hemoglobin:
Decreases in hemoglobin (a low value and a decrease of 5 g/dL) occurred in only one of 2014 patients receiving benazepril hydrochloride alone and in 1 of 1357 patients receiving benazepril hydrochloride plus a diuretic.
Hepatic:
Elevations of liver enzymes and/or serum bilirubin have occurred (see WARNINGS AND PRECAUTIONS).
Other:
Elevations of uric acid and blood glucose have been reported, as have scattered incidents of hyponatremia and proteinuria.
Drug-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 hydrochloride can be minimized by either discontinuing the diuretic or increasing the salt intake prior to initiation of treatment with benazepril hydrochloride. If it is not possible to discontinue the diuretic, the starting dose of benazepril hydrochloride 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 PRECAUTIONS and DOSAGE AND ADMINISTRATION).
The antihypertensive effect of benazepril hydrochloride is augmented by antihypertensive agents that cause renin release (e.g. diuretics).
Since benazepril hydrochloride 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 (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 hydrochloride.
lndomethacin may diminish the antihypertensive efficacy of concomitantly administered benazepril hydrochloride.
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.
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.
The bioavailability of benazepril hydrochloride was not altered when single doses were administered concomitantly with the diuretics hydrochlorothiazide, chlorthalidone or furosemide.
No important changes in pharmacokinetic parameters occurred when single doses of benazepril hydrochloride were administered concomitantly with aspirin.
In a single dose interaction study of benazepril hydrochloride with multiple doses of digoxin, no important changes in pharmacokinetic parameters were observed.
Benazepril hydrochloride has been used concomitantly with the calcium channel blockers amlodipine and nifedipine, without evidence of clinically important adverse interactions.
In separate single or multiple dose pharmacokinetic interaction studies, the bioavailability of benazepril hydrochloride was not altered by coadministration with propranolol, naproxen, atenolol, nifedipine or cimetidine.
Dosage of APO-BENAZEPRIL (benazepril hydrochloride) 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 APO-BENAZEPRIL may need to be adjusted.
The recommended initial dose of APO-BENAZEPRIL is 10 mg once daily. Dosage should be adjusted according to blood pressure response, generally, at intervals of at least two weeks. The usual maintenance dose is 20 mg daily. The maximum daily dose of APO- 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 APO-BENAZEPRIL alone, a diuretic may be added. After the addition of a diuretic, it may be possible to reduce the dose of APO-BENAZEPRIL.
Symptomatic hypotension occasionally may occur following the initial dose of APO-BENAZEPRIL and is more likely in patients who are currently being treated with a diuretic. The diuretic should, if possible, be discontinued for two to three days before beginning therapy with APO-BENAZEPRIL to reduce the likelihood of hypotension (see WARNINGS AND PRECAUTIONS). 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 APO-BENAZEPRIL should subsequently be titrated (as described above) to the optimal response.
The usual dose of APO-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 < 30 mL/min [0.5 mL/s]), the initial daily dose is 5 mg. Titration must be individualized. The dosage may be titrated upwards to 10 mg/day. For further reductions in blood pressure the addition of a diuretic or another antihypertensive should be considered or alternatively, the dose of APO-BENAZEPRIL can be increased.
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 intravenous infusion of normal saline solution. If ingestion is recent, then emesis should be induced. Although the active metabolite, benazeprilat, is only slightly dialysable, renal dialysis may be useful in overdosed patients with severely impaired renal function.
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 hydrochloride alone. Essentially no change in mean serum potassium was seen in patients treated with benazepril hydrochloride and a thiazide diuretic (see WARNINGS AND 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 hydrochloride 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 hydrochloride was antihypertensive in all races studied, although it was somewhat less effective in blacks than in nonblacks.
Following oral administration of benazepril hydrochloride, peak plasma concentrations of benazepril are reached within 0.5-1.0 hours. 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 1-2 hours after drug intake in the fasting state and 2-4 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 10-11 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 benazepril hydrochloride 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 (10-40 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 creatinine clearance < 30 mL/min [0.5 mL/s], peak benazeprilat levels and the initial (alpha phase) half-life increase, and time to steady state may be delayed (see DOSAGE AND ADMINISTRATION). 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.
Administration of benazepril hydrochloride 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 AND PRECAUTIONS). After administration of a single oral dose, the onset of antihypertensive activity occurs at approximately one hour, with maximum reduction of blood pressure achieved by 2-4 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 hydrochloride was 10 mg. In studies comparing the same daily dose of benazepril hydrochloride 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 1-2 weeks. Abrupt withdrawal of benazepril hydrochloride has not been associated with a rapid increase in blood pressure. When benazepril hydrochloride 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.
Store at room temperature (15degC - 30degC).
In addition to the active ingredient, benazepril hydrochloride, each film-coated tablet also contains microcrystalline cellulose, crospovidione, colloidal silicon dioxide, zinc stearate, hydroxypropyl methylcellulose, hydroxypropyl cellulose, polyethylene glycol, titanium dioxide, yellow iron oxide (5 mg and 10 mg only) and red iron oxide (20 mg only). APO-BENAZEPRIL 5 mg Tablets: Each light yellow, capsule-shaped, scored film-coated tablet with "APO" engraved on one side and "BE" over "5" on the other side contains 5 mg of benazepril hydrochloride. Available in bottles of 100. APO-BENAZEPRIL 10 mg Tablets: Each yellow, capsule-shaped, scored film-coated tablet with "APO" engraved on one side and "BE" over "10" on the other side contains 10 mg of benazepril hydrochloride. Available in bottles of 100. APO-BENAZEPRIL 20 mg Tablets: Each light pink, round-shaped, unscored film-coated tablet with "APO" engraved on one side and "BE" over "20" on the other side contains 20 mg of benazepril hydrochloride. Available in bottles of 100.