High purity Methyclothiazide with best quality CAS NO.135-07-9

Product Name:

Methyclothiazide

Synonyms:

2-methyl-,1,1-dioxide;4-benzothiadiazine-7-sulfonamide,6-chloro-3-(chloromethyl)-3,4-dihydro-2h-2;6-chloro-3-(chloromethyl)-3,4-dihydro-2-methyl-2h-1,2,4-benzothiadiazine-7-sul;6-chloro-3-chloromethyl-2-methyl-7-sulfamyl-3,4-dihydro-1,2,4-benzothiadiazine;6-chloro-3-chloromethyl-3,4-dihydro-2-methyl-7-sulfamoyl-1,2,4-benzothiadiazin;aquatensen;ciba7272-su;duretic

CAS:

135-07-9

MF:

C9H11Cl2N3O4S2

MW:

360.24

Product Categories:

TYLAN

Mol File:

135-07-9.mol

Chemical Property

melting point

223-225°C

For use in the management of hypertension either as the sole therapeutic agent or to enhance the effect of other antihypertensive drugs in the more severe forms of hypertension. Also used as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy.

Methyclothiazide, a diuretic-antihypertensive agent, is a member of the benzothiadiazine (thiazide) class of drugs. Methyclothiazide has a per mg natriuretic activity approximately 100 times that of the prototype thiazide, chlorothiazide. At maximal therapeutic dosages, all thiazides are approximately equal in their diuretic/natriuretic effects. Like other benzothiadiazines, methyclothiazide also has antihypertensive properties, and may be used for this purpose either alone or to enhance the antihypertensive action of other drugs.

Methyclothiazide appears to block the active reabsorption of chloride and possibly sodium in the ascending loop of Henle, altering electrolyte transfer in the proximal tubule. This results in excretion of sodium, chloride, and water and, hence, diuresis. As a diuretic, methyclothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like methyclothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of methyclothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.