Pharmaceutical Diuretic Drug CAS 2016-88-8 Amiloride Hydrochloride Amiloride HCL

1.  Quick Detail:

Pharmaceutical Raw Materials Diuretic Drug  CAS 2016-88-8 Amiloride Hydrochloride Amiloride HCL

2.  Basic Informations:

English name: amiloride hydrochloride hydrate
Alias: Amiloride Hydrochloride; Amiloride HCl; (3,5-diamino-6-chloropyrazin-2-yl) -N- (diaminomethylidene) oxomethanaminium
CAS: 2016-88-8
EINECS Number: 217-958-2
Formula: C6H9ClN7O
MW: 230.6344
Molecular Structure:

Melting point: 293-294 ℃
Boiling point: 628.1 ° C at 760 mmHg
Flash Point: 333.7 ° C
Water-soluble: <0.1 g / 100 mL at 19.5 ℃
Vapor Pressure: 1.08E-15mmHg at 25 ° C
Uses:Used as a weak diuretic drug

Assay:99%

Appearance: White or almost white fine crystalline powder

3.  Description:

Amiloride is a potassium-sparing diuretic, first approved for use in 1967 (then known as MK 870), used in the management of hypertension and congestive heart failure. 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.

4. Applications:

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 kidneys (this mechanism is the same fortriamterene).^[3] This promotes the loss of sodium and water from the body, but without depleting potassium. The drug is often used in conjunction with thiazide (e.g. co-amilozide) or loop diuretics (e.g. co-amilofruse). Due to its potassium-sparing capacities, hyperkalemia (high blood potassium levels) is occasionally observed in patients taking amiloride. The risk is high in concurrent use of ACE inhibitors or spironolactone. Patients are also advised not to use potassium-containing salt replacements.^[4] Amiloride also carries the risk of developing an acidosis.

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

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

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

Acid-sensing ion channels (ASICs) are also sensitive to inhibition by amiloride. ASICs are involved in nociceptorresponses to pH.

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