Catalog No.S4080 Synonyms: SKF8542
Molecular Weight(MW): 253.26
Triamterene blocks epithelial Na+ channel (ENaC) in a voltage-dependent manner with IC50 of 4.5 μM.
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Choose Selective Sodium Channel Inhibitors
|Description||Triamterene blocks epithelial Na+ channel (ENaC) in a voltage-dependent manner with IC50 of 4.5 μM.|
Triamterene inhibits the epithelial sodium channels on principal cells in the late distal convoluted tubule and collecting tubule, which are responsible for 1-2% of total sodium reabsorption. Triamterene can achieve a modest amount of diuresis by decreasing the osmotic gradient necessary for water reabsorption from lumen to interstitium. Triamterene also has a potassium-sparing effect. Normally, the process of potassium excretion is driven by the electrochemical gradient produced by sodium reabsorption. As sodium is reabsorbed, it leaves a negative potential in the lumen, while producing a positive potential in the principal cell. This potential promotes potassium excretion through apical potassium channels. By inhibiting sodium reabsorption, triamterene also inhibits potassium excretion. 
|In vivo||4'-hydroxylation of triamterene in humans appears to be mediated exclusively by CYP1A2. Inhibition or induction of CYP1A2 will change the time course of both triamterene and its active phase-II metabolite.|
|In vitro||DMSO||20 mg/mL (78.97 mM)|
|In vivo||Add solvents individually and in order:
0.5% CMC Na+1% Tween 80
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02522650||Recruiting||Proteinuria||Georgetown University||July 2013||Phase 4|
|NCT00000525||Completed||Cardiovascular Diseases|Death, Sudden, Cardiac|Heart Arrest|Heart Diseases|Hypertension||University of California, San Francisco|National Heart, Lung, and Blood Institute (NHLBI)||July 1986||Phase 3|
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