benazepril (Rx)

Brand and Other Names:Lotensin
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Dosing & Uses


Dosage Forms & Strengths


  • 5mg
  • 10mg
  • 20mg
  • 40mg


Patients taking a diuretic: 5 mg/day PO initially, to avoid excessive hypotension

Patients not taking a diuretic: 10 mg/day PO

May increase to maintenance dose of 20-40 mg/day PO qDay or divided q12hr

Nephropathy-Nondiabetic (Off-label)

10-20 mg PO qDay

Dosing Modifications

Renal Impairment

  • CrCl< 30 mL/min: 5 mg PO qDay initially; not to exceed 40 mg/day

Hepatic Impairment

  • Not studied

Dosing Considerations

Consider starting an ACE inhibitor in high-risk patients, even if no hypertension or CHF

No sexual dysfunction side effect

Good choice in hyperlipidemia patients

Requires weeks for full effect; to start, use low dose and titrate q1-2wk

Abrupt discontinuance not associated with rapid increase in BP

Beneficial for many patients at risk for heart disease

Reduces risk of MI, stroke, diabetic nephropathy, microalbuminuria, new-onset diabetes mellitus

May preserve renal function in diabetes mellitus

May help to prevent migraine headaches

Dosage Forms & Strengths


  • 5mg
  • 10mg
  • 20mg
  • 40mg


<6 years: Safety and efficacy not established

≥6 years: 0.1-0.6 mg/kg PO qDay initially, not to exceed 5 mg/day; THEN  

Adjust dose based on BP response; not to exceed 0.6 mg/kg/day or 40 mg/day

Suspension preparation

  • The following prepares 150 mL of 2 mg/mL oral suspension
  • Add 75 mL of Ora-Plus oral suspending vehicle to an amber polyethylene terephthalate (PET) bottle containing fifteen benazepril 20 mg tablets, and shake for at least 2 minutes
  • Allow the suspension to stand for a minimum of 1 hr
  • After the standing time, shake the suspension for a minimum of 1 additional minute, then add 75 mL of Ora-Sweet oral syrup vehicle to the bottle and shake the suspension to disperse the ingredients
  • Store refrigerated at 2-8°C (36-46°F) for up to 30 days in the PET bottle with a child-resistant screw-cap closure
  • Shake the suspension before each use

Dosing Modification

Renal impairment (CrCl <30 mL/min): Insufficient data to recommend dosage adjustment


5-10 mg/day PO initially in single or divided doses

Maintenance: 20-40 mg/day PO adjust for renal function

Dosing Modifications

Adjust dose for renal function; benazepril and benazeprilat are substantially excreted by the kidney

Because elderly patients are more likely to have decreased renal function, take care in dose selection; it may be useful to monitor renal function



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            Adverse Effects


            Cough (1-10%)

            Headache (6%)

            Dizziness (4%)

            Fatigue (2%)

            Postural dizziness (2%)

            Serum creatinine increased (2%)

            Somnolence (2%)

            Nausea (1%)

            ARF if renal artery stenosis (1%)

            <1% (selected)

            Anaphylactoid reaction



            ECG changes




            Postural hypotension












            Hemolytic anemia






            Transaminases increased







            Stevens-Johnson syndrome

            Uric acid increased

            Postmarketing Reports

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

            Gastrointestinal: Nausea, pancreatitis, constipation, gastritis, vomiting, and melena

            Hematologic: Thrombocytopenia and hemolytic anemia

            Neurologic and psychiatric: Anxiety, decreased libido, hypertonia, insomnia, nervousness, and paresthesia






            Urinary tract infection

            Frequent urination











            Black Box Warnings

            Discontinue as soon as possible when pregnancy is detected; affects renin-angiotensin system, causing oligohydramnios, which may result in fetal injury and/or death



            History of hereditary or idiopathic angioedema

            Coadministration of neprilysin inhibitors (eg, sacubitril) with ACE inhibitors may increase angioedema risk; do not administer ACE inhibitors within 36 hr of switching to or from sacubitril/valsartan

            Concomitant administration with aliskiren in patients with diabetes mellitus or with renal impairment


            Excessive hypotension with or without syncope may occur if hypovolemia/hyponatremia present or if coadministered with diuretics

            Dual blockade of the renin-angiotensin system with ARBs, ACE inhibitors, or aliskiren associated with increased risk for hypotension, hyperkalemia, and renal function changes (including acute renal failure), compared with monotherapy

            Most patients receiving the combination of two RAS inhibitors do not obtain any additional benefit compared to monotherapy; avoid combined use of RAS inhibitors; closely monitor blood pressure, renal function and electrolytes in patients on benazepril and other agents that affect the RAS

            Not for coadministration with aliskiren in patients with diabetes; avoid use of aliskiren with benazepril in patients with renal impairment (GFR <60 ml/min/1.73 m²)

            ACE inhibition causes increased bradykinin levels, which putatively mediates angioedema (higher incidence in black patients)

            Cough may occur due to increased bradykinin levels

            Cholestatic jaundice reported with use

            Avoid use in bilateral renal artery stenosis

            Angioedema may occur; coadministration with mTOR inhibitors (eg, temsirolimus) may increase risk for angioedema; discontinue therapy and treat appropriately if angioedema occurs

            Discontinue immediately if pregnancy occurs (see Black Box Warnings)

            ACE inhibitors are less effective in black patients

            Renal impairment may occur

            Rare cases of agranylocytosis reported ACE inhibitor therapy

            May cause hypotension during surgery; additive hypotensive effects may occur with anesthetic agents that produce hypotension (correct by volume expansion)

            Deterioration of renal function may occur; may consider discontinuation of therapy in patients with progressive and/or significant deterioration in renal function

            Monitor for jaundice or signs of liver failure


            Pregnancy & Lactation


            Lotensin can cause fetal harm when administered to a pregnant woman; use of drugs that act on renin-angiotensin system during second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death; most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in first trimester have not distinguished drugs affecting renin-angiotensin system from other antihypertensive agents; when pregnancy is detected, discontinue Lotensin as soon as possible

            Hypertension in pregnancy increases maternal risk for pre-eclampsia, gestational diabetes, premature delivery, and delivery complications (e.g., need for cesarean section, and post-partum hemorrhage); hypertension increases fetal risk for intrauterine growth restriction and intrauterine death; pregnant women with hypertension should be carefully monitored and managed accordingly

            Oligohydramnios in pregnant women who use drugs affecting renin-angiotensin system in second and third trimesters of pregnancy can result in reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and skeletal deformations, including skull hypoplasia, hypotension, and death; in the unusual case that there is no appropriate alternative to therapy with drugs affecting renin-angiotensin system for a particular patient, apprise the mother of potential risk to fetus

            Perform serial ultrasound examinations to assess intra-amniotic environment; fetal testing may be appropriate, based on week of pregnancy; patients and physicians should be aware, however, that oligohydramnios may not appear until after fetus has sustained irreversible injury; closely observe infants with histories of in utero exposure to drug for hypotension, oliguria, and hyperkalemia; if oliguria or hypotension occur in neonates with a history of in utero exposure to drug support blood pressure and renal perfusion; exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function


            Minimal amounts of unchanged benazepril and of benazeprilat are excreted into the breast milk of lactating women receiving therapy; a newborn child ingesting entirely breast milk would receive less than 0.1% of mg/kg maternal dose of benazepril and benazeprilat

            Pregnancy Categories

            A: Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.

            B: May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk.

            C: Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done.

            D: Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk.

            X: Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist.

            NA: Information not available.



            Mechanism of Action

            Angiotensin converting enzyme (ACE) inhibitors dilate arteries and veins by competively inhibiting the conversion of angiotensin I to angiotensin II (a potent endogenous vasoconstrictor) and by inhibiting bradykinin metabolism; these actions result in preload and afterload reductions on the heart

            ACE inhibitors also promote sodium and water excretion by inhibiting angiotensin-II induced aldosterone secretion; elevation in potassium may also be observed

            ACE inhibitors also elicit renoprotective effects through vasodilation of renal arterioles

            ACE inhibitors reduce cardiac and vascular remodeling associated with chronic hypertension, heart failure, and myocardial infarction


            Bioavailability: 37%

            Onset: 1-2 hr (peak effect with 2-20 mg dose)

            Duration: 24 hr (with 5-20 mg dose)

            Peak plasma time: 0.5-1 hr (parent drug)


            Protein bound: 95-97%

            Vd: 8.7 L


            Metabolite: Benazeprilat (active)


            Half-life: 10-11 hr

            Dialyzable: Minimal

            Excretion: Urine (primarily); bile (11-12%)





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            Tier Description
            1 This drug is available at the lowest co-pay. Most commonly, these are generic drugs.
            2 This drug is available at a middle level co-pay. Most commonly, these are "preferred" (on formulary) brand drugs.
            3 This drug is available at a higher level co-pay. Most commonly, these are "non-preferred" brand drugs.
            4 This drug is available at a higher level co-pay. Most commonly, these are "non-preferred" brand drugs or specialty prescription products.
            5 This drug is available at a higher level co-pay. Most commonly, these are "non-preferred" brand drugs or specialty prescription products.
            6 This drug is available at a higher level co-pay. Most commonly, these are "non-preferred" brand drugs or specialty prescription products.
            NC NOT COVERED – Drugs that are not covered by the plan.
            Code Definition
            PA Prior Authorization
            Drugs that require prior authorization. This restriction requires that specific clinical criteria be met prior to the approval of the prescription.
            QL Quantity Limits
            Drugs that have quantity limits associated with each prescription. This restriction typically limits the quantity of the drug that will be covered.
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            Drugs that have step therapy associated with each prescription. This restriction typically requires that certain criteria be met prior to approval for the prescription.
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            Medscape prescription drug monographs are based on FDA-approved labeling information, unless otherwise noted, combined with additional data derived from primary medical literature.