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Amilorid - Amiloride.svg
Clinical data
Trade names Midamor, others
Synonyms MK-870
AHFS/ Monograph
  • US: B (No risk in non-human studies)
Routes of
by mouth
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability Readily absorbed, 15–25%
Protein binding ~23%
Metabolism Nil
Onset of action 2 hours (peak at 6–10 hours, duration ~24 hours)
Biological half-life 6 to 9 hours
Excretion urine (20–50%), feces (40%)
CAS Number
PubChem CID
ECHA InfoCard 100.018.205
Chemical and physical data
Formula C6H8ClN7O
Molar mass 229.627 g/mol
3D model (JSmol)

Amiloride, sold under the trade name Midamor among others, is a medication typically used with other medications to treat high blood pressure or swelling due to heart failure or cirrhosis of the liver.[1][2] Amiloride is often used with a thiazide or other loop diuretic.[2] It is taken by mouth.[1] Onset of action is about two hours and it lasts for about a day.[2]

Common side effects include high blood potassium, vomiting, loss of appetite, rash, and headache.[1] The risk of high blood potassium is greater in those with kidney problems, diabetes, and those who are older.[1] Amiloride is in the potassium-sparing diuretic family of medications.[1] It works by increasing the amount of sodium and decreasing the amount of potassium released by the distal tubule of the kidney.[2]

Amiloride was developed in 1967.[3] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[4] In the United States the wholesale price of a month of medication is about 20.10 USD.[5] In the United Kingdom a month of medication costs the NHS about 24 pounds.[6]


Amiloride is contraindicated in people with Addison's disease, hyperkalaemia, hyponatremia and anuria.[7]

Adverse effects[edit]

  • Common adverse effects:[7]


Amiloride's chemical structure contains a guanidinium group containing pyrazine derivative.

Mechanism of action[edit]

Amiloride works by directly blocking the epithelial sodium channel (ENaC) thereby inhibiting sodium reabsorption in the late distal convoluted tubules, connecting tubules, and collecting ducts in the nephron.[8] This promotes the loss of sodium and water from the body, and reduces potassium excretion. The drug is often used in conjunction with a thiazide diuretic to counteract the potassium-losing effect. Due to its potassium-sparing capacities, hyperkalemia can occur. The risk of developing hyperkalemia is increased in patients who are also on ACE inhibitors, angiotensin II receptor antagonists, other potassium-sparing diuretics, or any potassium-containing supplements.

A fraction of the effects of amiloride is inhibition of cyclic GMP-gated cation channels in the inner medullary collecting duct.[9]

Amiloride has a second action on the heart, blocking Na+/H+ exchangers sodium–hydrogen antiporter 1 or NHE-1. This minimizes re-perfusion injury in ischemic attacks.

Amiloride also blocks the Na+/H+ antiporter on the apical surface of the proximal tubule cells, in the nephron, abolishing more than 80% of the action of angiotensin II on the secretion of hydrogen ions in proximal tubule cells.[10]

Amiloride was also tested as treatment of cystic fibrosis, but it was revealed inefficient in vivo due to its short time of action, therefore longer-acting epithelial sodium channel (ENaC) inhibitors may prove more effective, e.g. benzamil.[11]

Acid-sensing ion channels (ASICs) are also sensitive to inhibition by amiloride. ASICs are involved in nociceptor responses to pH.[12]

Society and culture[edit]

It is on the World Health Organization's List of Essential Medicines, the most important medications needed in a basic health system.[4]

Amiloride is listed on the world anti-doping agency's list of banned substances, it is considered a masking agent.[13]

Formulations and trade names[edit]


  1. ^ a b c d e "Amiloride Hydrochloride". The American Society of Health-System Pharmacists. Archived from the original on 27 December 2016. Retrieved 8 December 2016. 
  2. ^ a b c d WHO Model Formulary 2008 (PDF). World Health Organization. 2009. pp. 328, 330. ISBN 9789241547659. Archived (PDF) from the original on 13 December 2016. Retrieved 8 December 2016. 
  3. ^ Progress in Drug Research/Fortschritte der Arzneimittelforschung/Progrés des recherches pharmaceutiques. Birkhäuser. 2013. p. 210. ISBN 9783034870948. Archived from the original on 2016-12-28. 
  4. ^ a b "WHO Model List of Essential Medicines (19th List)" (PDF). World Health Organization. April 2015. Archived (PDF) from the original on 13 December 2016. Retrieved 8 December 2016. 
  5. ^ "NADAC as of 2016-12-07 |". Centers for Medicare and Medicaid Services. Archived from the original on 21 December 2016. Retrieved 28 December 2016. 
  6. ^ British national formulary : BNF 69 (69 ed.). British Medical Association. 2015. p. 90. ISBN 9780857111562. 
  7. ^ a b E-Facts and Comparisons: Amiloride Adverse effects 2016
  8. ^ Loffing, Johannes; Kaissling, Brigitte (2003). "Sodium and calcium transport pathways along the mammalian distal nephron: from rabbit to human". Am J Physiol Renal Physiol. 284 (4): F628–F643. doi:10.1152/ajprenal.00217.2002. PMID 12620920. 
  9. ^ Walter F. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3.  page 875
  10. ^ M G Cogan, Angiotensin II: a powerful controller of sodium transport in the early proximal tubule, Hypertension. 1990;15:451-458, doi:10.1161/01.HYP.15.5.451, "Archived copy". Archived from the original on 2016-09-19. Retrieved 2014-03-02. 
  11. ^ (Review)Pharmacological treatment of the biochemical defect in cystic fibrosis airways, H.C. Rodgers, A.J. Knox
  12. ^ Hunt and Koltzenburg 2005 'The neurobiology of pain'
  13. ^ "S5. Diuretics and masking agents - WADA". World Anti-Doping Agency. January 2016. Archived from the original on 27 September 2016. Retrieved 1 September 2016.