| Bioactivity | Tripamide is an orally active sulfonamide-derived diuretic antihypertensive agent[1]. |
| Invitro | Tripamide (less than 10 μg/ml) does not modify the membrane potential and resistance, but does suppress the spike evoked by outward current pulses in the presence of 3-5 mM TEA[1].In the mesenteric artery, Tripamide suppresses the amplitude of e.j.ps evoked by perivascular nerve stimulation. However, the facilitation process produced by repetitive stimulation is less affected by Tripamide[1]. |
| In Vivo | In rats loaded orally with 25 ml/kg of normal saline, Tripamide (0.6-160 mg/kg) increases urine volume and sodium and chloride excretion in a dose-dependent fashion. Only at a dose of 160 mg/kg, there an increase in potassiumexcretion in rats[2].Tripamide has anti-hypertensive effects, during administration to spontaneously hypertensive rats at a dose of 10 mg/kg/day for 4 weeks, tripamide doubled urine volume and sodium excretion, while potassium excretion is increased by |
| Name | Tripamide |
| CAS | 73803-48-2 |
| Formula | C16H20ClN3O3S |
| Molar Mass | 369.87 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Reference | [1]. H Asada, et al. Effects of N-(4-azo-endo-tricyclo[5.2.1.0.(2.6)]-decan-4-yl)-4-chloro-3-sulfamoylbenzamide (E614; tripamide) on vascular smooth muscles. Gen Pharmaco. 1982;13(3):215-23. [2]. Philip Hampel, et al. Azosemide is more potent than bumetanide and various other loop diuretics to inhibit the sodium-potassium-chloride-cotransporter human variants hNKCC1A and hNKCC1B. Sci Rep. 2018 Jun 29;8(1):9877. |