DEAPRIL-ST
Clinical safety rating: caution
Comprehensive clinical and safety monograph for DEAPRIL-ST (DEAPRIL-ST).
Angiotensin-converting enzyme (ACE) inhibitor. Inhibits ACE, preventing conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion, leading to decreased blood pressure.
| Metabolism | Hepatic via glucuronidation; active metabolite perindoprilat formed by ester hydrolysis. |
| Excretion | Renal (90% as unchanged drug), biliary/fecal (10%) |
| Half-life | 8-10 hours; prolonged in renal impairment (up to 24 hours in severe cases) |
| Protein binding | 25-30% (primarily to albumin) |
| Volume of Distribution | 0.8-1.2 L/kg; indicates extensive tissue distribution |
| Bioavailability | Oral: 60-70% (with food reducing absorption rate but not extent) |
| Onset of Action | Oral: 1-2 hours; IV: 15-30 minutes |
| Duration of Action | Oral: 12-24 hours; IV: 12-24 hours; duration may extend in renal impairment |
Oral: 2.5 mg twice daily, titrated up to 5 mg twice daily as tolerated. Maximum dose: 10 mg daily.
| Dosage form | TABLET |
| Renal impairment | GFR 30-60 mL/min: 2.5 mg once daily; GFR <30 mL/min: 2.5 mg every other day; GFR <15 mL/min: not recommended. |
| Liver impairment | Child-Pugh A: no adjustment; Child-Pugh B: 2.5 mg once daily; Child-Pugh C: not recommended. |
| Pediatric use | Weight <30 kg: 0.05 mg/kg/dose twice daily; ≥30 kg: adult dosing. Maximum: 0.1 mg/kg/day. |
| Geriatric use | Initiate at 2.5 mg once daily; titrate cautiously. Monitor renal function and electrolytes. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for DEAPRIL-ST (DEAPRIL-ST).
| Breastfeeding | No data on M/P ratio. ACE inhibitors are excreted into breast milk in low concentrations; however, caution is advised due to potential risk of neonatal hypotension and renal impairment. Consider alternative agents if available. |
| Teratogenic Risk | First trimester: Risk of congenital malformations, particularly cardiovascular and central nervous system defects, based on ACE inhibitor class effects. Second and third trimesters: Fetal renal dysfunction, oligohydramnios, pulmonary hypoplasia, skeletal deformities, and neonatal hypotension, hyperkalemia, and acute renal failure. |
■ FDA Black Box Warning
Fetal toxicity: Drugs acting directly on the renin-angiotensin system can cause injury and death to the developing fetus. Discontinue as soon as possible when pregnancy is detected.
| Serious Effects |
History of angioedema related to ACE inhibitor treatment, hereditary/idiopathic angioedema, concomitant use with aliskiren in patients with diabetes or renal impairment (eGFR <60 mL/min), pregnancy.
| Precautions | Angioedema, hypotension, hyperkalemia, renal impairment, cough, hepatotoxicity, neutropenia/agranulocytosis, anaphylactoid reactions during desensitization or LDL apheresis. |
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| Fetal Monitoring | Monitor maternal blood pressure, renal function (serum creatinine, BUN), and serum potassium regularly. Fetal ultrasound for amniotic fluid volume and fetal growth. Neonatal monitoring for hypotension, hyperkalemia, and renal function after delivery. |
| Fertility Effects | No significant effect on fertility reported in animal studies; however, ACE inhibitors may be associated with decreased sperm motility in some studies. Human data limited. |