MOEXIPRIL HYDROCHLORIDE AND HYDROCHLOROTHIAZIDE
Clinical safety rating: safe
Other antihypertensive drugs can have additive effects Lithium levels may be increased Can cause hypokalemia and hyponatremia.
Moexipril is an ACE inhibitor that inhibits the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion. Hydrochlorothiazide is a thiazide diuretic that inhibits sodium and chloride reabsorption in the distal convoluted tubule, increasing diuresis and reducing plasma volume.
| Metabolism | Moexipril is metabolized primarily via hepatic esterases to its active metabolite, moexiprilat. Hydrochlorothiazide is not significantly metabolized and is excreted unchanged in urine. |
| Excretion | Moexipril is eliminated primarily by renal excretion (about 50% as unchanged drug and metabolites) and biliary/fecal excretion (about 50%). Hydrochlorothiazide is eliminated largely unchanged by renal excretion (≥95% via glomerular filtration and tubular secretion). |
| Half-life | Moexiprilat (active metabolite) terminal half-life is approximately 2–9 hours (mean ~9 hours in hypertension; prolonged in renal impairment). Hydrochlorothiazide terminal half-life is 6–15 hours (mean ~9 hours; prolonged in renal impairment). Clinical context: Twice-daily dosing may be needed for 24-hour BP control; renal impairment requires dose adjustment. |
| Protein binding | Moexipril and moexiprilat: ~73% (primarily to albumin). Hydrochlorothiazide: ~40% (albumin and possibly alpha-1-acid glycoprotein). |
| Volume of Distribution | Moexiprilat: Vd ~180 L (approx. 2.6 L/kg for a 70 kg adult); extensive tissue distribution. Hydrochlorothiazide: Vd ~4.6–9.6 L (approx. 0.1–0.14 L/kg); primarily extracellular fluid and not extensively distributed into tissues. |
| Bioavailability | Moexipril: Absolute oral bioavailability is ~13% (converted to active metabolite moexiprilat; food reduces absorption). Hydrochlorothiazide: Oral bioavailability is ~65–70%. |
| Onset of Action | Moexipril: Onset of antihypertensive effect occurs within 1–2 hours after oral administration. Hydrochlorothiazide: Onset of diuretic effect occurs within 2 hours (peak natriuresis at 4–6 hours). |
| Duration of Action | Moexipril: Antihypertensive effect lasts approximately 24 hours with once-daily dosing, though some patients may require twice-daily dosing for full 24-hour control. Hydrochlorothiazide: Diuretic effect lasts 6–12 hours; antihypertensive effect may persist for up to 24 hours with chronic dosing. |
One tablet (7.5 mg moexipril / 12.5 mg hydrochlorothiazide or 15 mg moexipril / 25 mg hydrochlorothiazide) orally once daily.
| Dosage form | TABLET |
| Renal impairment | GFR 30-60 mL/min: initiate with 3.75 mg/12.5 mg once daily; maximum 15 mg/25 mg daily. GFR <30 mL/min: contraindicated. |
| Liver impairment | Child-Pugh A: no adjustment. Child-Pugh B or C: initiate with 3.75 mg/12.5 mg once daily; use with caution. |
| Pediatric use | Not established; safety and efficacy in pediatric patients not determined. |
| Geriatric use | Initiate at lowest dose (3.75 mg/12.5 mg once daily); monitor renal function and electrolytes. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Other antihypertensive drugs can have additive effects Lithium levels may be increased Can cause hypokalemia and hyponatremia.
| FDA category | Animal |
| Breastfeeding | Moexipril: Unknown excretion into human milk; not recommended due to potential adverse effects on infant renal function. Hydrochlorothiazide: Excreted into breast milk in trace amounts; M/P ratio 0.15-0.33. Caution recommended due to possible infant electrolyte imbalance. |
| Teratogenic Risk |
■ FDA Black Box Warning
Fetal toxicity: Drugs acting directly on the renin-angiotensin system (RAS) can cause injury and death to the developing fetus. Discontinue as soon as pregnancy is detected.
| Common Effects | edema |
| Serious Effects |
["Hypersensitivity to moexipril, hydrochlorothiazide, or other sulfonamide-derived drugs","History of ACE inhibitor-induced angioedema","Idiopathic or hereditary angioedema","Pregnancy","Anuria (due to hydrochlorothiazide)","Concomitant use with aliskiren in patients with diabetes or moderate to severe renal impairment (GFR <60 mL/min/1.73 m²)"]
| Precautions | ["Fetal/neonatal morbidity and mortality","Hypotension in salt/volume-depleted patients","Neutropenia/agranulocytosis with ACE inhibitors","Angioedema (including intestinal angioedema)","Hepatic failure and cholestatic jaundice","Renal impairment monitoring","Electrolyte disturbances (e.g., hypokalemia, hyponatremia)","Sulfonamide hypersensitivity due to hydrochlorothiazide","Acute angle-closure glaucoma (hydrochlorothiazide)","Non-melanoma skin cancer risk with hydrochlorothiazide","Systemic lupus erythematosus exacerbation","Cough and taste disturbances"] |
Loading safety data…
| First trimester: ACE inhibitors are associated with increased risk of major congenital malformations, particularly cardiovascular and central nervous system defects. Second and third trimesters: Exposure is associated with oligohydramnios, fetal renal dysfunction, skull ossification defects, hypotension, and anuria. Hydrochlorothiazide: Crosses placenta; risk of electrolyte disturbances, jaundice, and thrombocytopenia in neonate. |
| Fetal Monitoring | Monitor maternal blood pressure, serum electrolytes, renal function, and urinalysis. Fetal ultrasound to assess amniotic fluid volume, fetal growth, and renal anatomy. Neonatal monitoring for hypotension, hyperkalemia, and oliguria. |
| Fertility Effects | No specific human fertility studies. ACE inhibitors may theoretically affect spermatogenesis (based on animal data). Hydrochlorothiazide may cause reversible sexual dysfunction in males. |