Torasemide

Pharmaceuticals

Pharmaceuticals -> Listed in ZINC15

Pharmaceuticals -> Used in Switzerland

2.3

1.21

Soluble

5.96e-02 g/L

>52.3 [ug/mL] (The mean of the results at pH 7.4)

Breast Feeding; Lactation; Milk, Human; Antihypertensive Agents; Loop Diuretics

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Pharmaceuticals

Diuretics

EMA approved medicines: Veterinary medicine

EMA approved medicines: Veterinary medicine

FDA approved animal drugs -> Active ingredient

Pharmaceuticals -> UK Veterinary Medicines Directorate List

163-164 °C

164 - 164 °C

This chemical does not meet GHS hazard criteria for 2.8% (3 of 109) of reports.

Warning

H319 (86.2%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

P203, P264+P265, P280, P305+P351+P338, P318, P337+P317, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 109 reports by companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

* Electrolyte disturbances: As a result of diuresis, torsemide can cause electrolyte abnormalities, including hypokalemia, hypocalcemia, acid-base imbalance, etc., causing fatal cardiac arrhythmias. It is more common with IV administration and with higher doses.

Toxicity usually occurs with medications that can increase serum concentrations of torsemide like methotrexate, etc. No antidote is available for the treatment of toxicity. In instances of toxicity, close monitoring of kidney function and electrolytes is essential to promptly identify and treat acute kidney injury and severe electrolyte abnormalities.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Torsemide

Ambiguous-DILI-concern

2

Warnings & precautions

DOI:10.1016/j.drudis.2016.02.015

C03CA04

C - Cardiovascular system

QC - Cardiovascular system

It is widely known that administration of torasemide can attenuate renal injury and reduce the severity of acute renal failure. This effect is obtained by increasing urine output and hence, facilitating fluid, acid-base and potassium control. This effect is obtained by the increase in the excretion of urinary sodium and chloride. Several reports have indicated that torasemide presents a long-lasting diuresis and less potassium excretion which can be explained by the effect that torasemide has on the renin-angiotensin-aldosterone system. This effect is very similar to the effect observed with the administration of combination therapy with [furosemide] and [spironolactone] and it is characterized by a decrease in plasma brain natriuretic peptide and improved measurements of left ventricular function. Above the aforementioned effect, torasemide presents a dual effect .in which the inhibition of aldosterone which donates torasemide with a potassium-sparing action. Torasemide has been shown to reduce extracellular fluid volume and blood pressure in hypertensive patients suffering from chronic kidney disease. As well, some reports have indicated that torasemide can reduce myocardial fibrosis by reducing the collagen accumulation. This effect is suggested to be related to the decrease in aldosterone which in order has been shown to reduce the production of the enzyme procollagen type I carboxy-terminal proteinase which is known to be overexpressed in heart failure patients.

As mentioned above, torasemide is part of the loop diuretics and thus, it acts by reducing the oxygen demand in the medullary thick ascending loop of Henle by inhibiting the Na+/K+/Cl- pump on the luminal cell membrane surface. This action is obtained by the binding of torasemide to a chloride ion-binding site of the transport molecule. Torasemide is known to have an effect in the renin-angiotensin-aldosterone system by inhibiting the downstream cascade after the activation of angiotensin II. This inhibition will produce a secondary effect marked by the reduction of the expression of aldosterone synthase, TGF-B1 and thromboxane A2 and a reduction on the aldosterone receptor binding.