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Triamterene Sodium Channel inhibitor

Cat.No.S4080

Triamterene (SKF8542) blocks epithelial Na+ channel (ENaC) in a voltage-dependent manner with IC50 of 4.5 μM.
Triamterene Sodium Channel inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 253.26

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Quality Control

Batch: Purity: 99.91%
99.91

Solubility

In vitro
Batch:

DMSO : 5 mg/mL (19.74 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

Ethanol : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 253.26 Formula

C12H11N7

Storage (From the date of receipt)
CAS No. 396-01-0 Download SDF Storage of Stock Solutions

Synonyms SKF8542 Smiles C1=CC=C(C=C1)C2=NC3=C(N=C(N=C3N=C2N)N)N

Mechanism of Action

Targets/IC50/Ki
ENaC
4.5 μM
ENaCαS583
23.9 μM
In vitro
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. This compound can achieve a modest amount of diuresis by decreasing the osmotic gradient necessary for water reabsorption from lumen to interstitium. It 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, this chemical 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 this compound and its active phase-II metabolite.
References

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