ATC Code C03BA11
Formula C16H16ClN3O3S
Molar Mass (g·mol−1) 365,83
Physical State solid
Melting Point (°C) 160–162
PKS Value 8,3
CAS Number 26807-65-8
PUB Number 3702
Drugbank ID DB00808


Indapamide is a drug from the group of thiazides used to treat high blood pressure (hypertension) and to "flush out" edema in decompensated heart failure.

Indications and use

Indapamide is most commonly used as monotherapy or in combination with other antihypertensive agents to treat hypertension. It may also be used to treat fluid and salt retention associated with heart failure. Unlike other diuretics, indapamide produces only a small reduction in urine volume, making it well suited for combination therapies with other antihypertensive agents.

Indapamide is usually administered orally in the form of a film-coated tablet or as a sustained-release tablet (sustained-release tablet). The dosages of indapamide are usually 0.625 mg, 1.25 mg, or 1.5 mg.

Indapamide is available only against a prescription.


Indapamide was first synthesized and patented by Servier Laboratories in the late 1960s. It was first approved in 1977. Indapamide is on the WHO's essential medicines list.


Pharmacology and mechanism of action

Indapamide acts on the nephron (the smallest functional unit of the kidney), specifically in the proximal segment of the distal tubule. There it inhibits the  Na+/Cl-cotransporter, resulting in decreased sodium reabsorption. As a result, sodium and water are retained in the lumen of the nephron and excreted in the urine. Subsequent effects include decreased plasma volume, decreased venous return, decreased cardiac output, and ultimately low blood pressure.

It is likely that thiazide-like diuretics such as indapamide have additional blood pressure-lowering mechanisms unrelated to diuresis. The exact mechnism behind this additional mechanism of action is not clear. Some studies suggest that indapamide reduces responsiveness to pressor agents (substances that can increase blood pressure). Other studies suggest that indapamide may decrease peripheral resistance by an unexplained mechanism.


The bioavailability of indapamide is virtually complete after an oral dose and is not affected by food or antacids. Indapamide is highly lipophilic due to its indoline moiety. This property probably explains why the renal clearance of indapamide is less than 10% of the total systemic clearance. The maximum plasma concentration is reached after approximately 2 to 3 hours. Approximately 75-80% of indapamide is present in protein-bound form. Indapamide binds primarily to acid alpha-1-glycoprotein and less strongly to serum albumin. In blood, indapamide is additionally strongly bound to erythrocytes. As a result of extensive metabolism in the liver, most of the given dose is metabolized. Only about 7% remains unchanged. There are several metabolic pathways by which indapamide can be metabolized. The major enzyme that metabolizes indapamide is the liver enzyme CYP3A4. Indapamide is excreted approximately 60-70% in urine and 15-25% in feces. The elimination half-life is usually between 14 and 18 hours.

Drug Interactions

When indapamide is combined with lithium and drugs that may cause prolonged QT interval or arrhythmias.

Substances that may cause interaction with indapamide include:

  • Amiodarone and other antiarrhythmic agents.
  • Lithium
  • Digitoxin and related substances
  • Terfenadine
  • Ketoconazole
  • Erythromycin and related substances



Indapamide is contraindicated if:

  • there is an allergy to the active substance or other sulfonamides
  • there is severe renal impairment or renal insufficiency
  • hepatic encephalopathy is present
  • liver failure is present
  • potassium level is particularly low or hypokalemia is present.

Side effects

Common side effects are:

  • Dizziness
  • weakness and fatigue
  • back pain and muscle cramps
  • anxiety or restlessness
  • headache
  • runny nose
  • hypokalemia

Pregnancy and lactation

There are very few reliable data on adequate safety for use during pregnancy and lactation. Therefore, its use is not recommended.

Markus Falkenstätter

Markus Falkenstätter

Markus Falkenstätter ist Autor zu pharmazeutischen Themen in der Medizin-Redaktion von Medikamio. Er befindet sich im letzten Semester seines Pharmaziestudiums an der Universität Wien und liebt das wissenschaftliche Arbeiten im Bereich der Naturwissenschaften.

Mag. pharm Stefanie Lehenauer

Mag. pharm Stefanie Lehenauer

Stefanie Lehenauer ist seit 2020 freie Autorin bei Medikamio und studierte Pharmazie an der Universität Wien. Sie arbeitet als Apothekerin in Wien und ihre Leidenschaft sind pflanzliche Arzneimittel und deren Wirkung.

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