Muzolimine - CAS 55294-15-0
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Muzolimine is a pyrazole and high-ceiling loop diuretic with long duration and high capacity of action. It was used for kidney failure and hypertension but was withdrawn worldwide because of severe neurological effects.
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Solid powder
Soluble in DMSO, not in water
-20°C Freezer
Muzolimine was used for kidney failure and hypertension.
Quality Standard:
In-house standard
Boiling Point:
401.4±55.0 °C | Condition: Press: 760 Torr
Melting Point:
127-129 °C
1.51±0.1 g/cm3 | Condition: Temp: 20 °C Press: 760 Torr
Canonical SMILES:
Current Developer:
Muzolimine was withdrawn worldwide because of severe neurological effects.
1.Triclinic and monoclinic polymorphs of meso-(E,E)-1,1'-[1,2-bis(4-chlorophenyl)ethane-1,2-diyl]bis(phenyldiazene): the high-yield synthesis of an unexpected product, concomitant polymorphism and configurational disorder.
Mohamed SK1, Younes SH2, Abdel-Raheem EM2, Horton PN3, Akkurt M4, Glidewell C5. Acta Crystallogr C Struct Chem. 2016 Jan 1;72(Pt 1):57-62. doi: 10.1107/S2053229615023578. Epub 2016 Jan 1.
Pyrazolidine-3,5-diones and their derivatives exhibit a wide range of biological activities. Seeking to explore the effect of combining a hydrocarbyl ring substituent, as present in sulfinpyrazone (used to treat gout), with a chlorinated aryl ring, as present in muzolimine (a diuretic), we explored the reaction between 1-phenylpyrazolidine-3,5-dione and 4-chlorobenzaldehyde under mildly basic conditions in the expectation of producing the simple condensation product 4-(4-chlorobenzylidene)-1-phenylpyrazolidine-3,5-dione. However, the reaction product proved to be meso-(E,E)-1,1'-[1,2-bis(4-chlorophenyl)ethane-1,2-diyl]bis(phenyldiazene), C26H20Cl2N4, and a tentative mechanism is proposed. Crystallization from ethanol produces two concomitant polymorphs, i.e. a triclinic form, (I), in the space group P-1, and a monoclinic form, (II), in the space group C2/c. In both polymorphs, the molecules lie across centres of inversion, but in (II), the molecules are subject to whole-molecule disorder equivalent to configurational disorder with occupancies of 0.
2.Effects of diuretics on renal excretory function.
Reyes AJ1. Eur Heart J. 1992 Dec;13 Suppl G:15-21.
From a clinicopharmacological standpoint, the urinary excretory potency of diuretics should be assessed comparatively, on the basis of placebo-controlled changes in 24 h natriuresis, following single oral doses administered to healthy adult subjects who are in steady-state habitual external sodium balance. The potency of 30 diuretic formulations has been evaluated. Two formulations of loop diuretics (muzolimine 20 mg and torasemide 2.5 mg) are non-diuretic. The majority of the other formulations of loop diuretics studied (e.g. furosemide 40 mg and torasemide 5 and 10 mg) are comparatively less potent than most of the common formulations of early distal tubular diuretics studied (e.g. hydrochlorothiazide 25 and 50 mg, xipamide 10, 20 and 40 mg). Hydrochlorothiazide 25 mg and furosemide 80 mg have similar potencies. The presence of a rebound in natriuresis between 6 and 24 h after administration of loop diuretics make the majority of the common formulations of these drugs less potent than most common formulations of thiazide-type diuretics.
3.Effect of various diuretics on membrane voltage of macula densa cells. Whole-cell patch-clamp experiments.
Schlatter E1. Pflugers Arch. 1993 Apr;423(1-2):74-7.
The tubuloglomerular feedback mechanism is inhibited by diuretics such as furosemide. For the macula densa (MD) cells similar transport systems, as present in thick ascending limb (TAL) cells, have been suggested. To examine this further, membrane voltages (Vm) of MD cells were recorded with the fast or slow whole-cell patch-clamp method. The effects of diuretics on voltages and the conductance properties of these cells were examined. Vm of MD cells measured with the whole-cell patch-clamp method were as high as those in TAL cells: -72 +/- 1 mV (n = 21). An increase in the extracellular K+ concentration by 15 mmol/l depolarized Vm of MD cells by 11 +/- 1 mV (n = 18). Ba2+ (1 mmol/l) reversibly depolarized MD cells by 10 +/- 2 mV (n = 10). Thus, MD cells possess a K+ conductance that could allow for the recycling of K+ taken up by the Na(+)-2 Cl(-)-K+ cotransporter. MD cells hyperpolarized reversibly upon addition of the loop diuretics furosemide, piretanide and torasemide, whereas muzolimine and hydrochlorothiazide, neither one acting on this cotransport system in other preparations including the TAL, had no effect on Vm.
4.Mechanisms of the inhibition of human erythrocyte pyridoxal kinase by drugs.
Lainé-Cessac P1, Cailleux A, Allain P. Biochem Pharmacol. 1997 Oct 15;54(8):863-70.
The aim of this study was to investigate the interaction between drugs chosen for their clinical neurotoxicity or chemical structure and vitamin B6 metabolism. After a preliminary screening of drugs to determine their potential inhibitory effect on erythrocyte nonpurified pyridoxal kinase (PLK) (EC, additional investigations, including kinetic studies and detection of chemical reactivity between the inhibiting drugs and pyridoxal (PL) or pyridoxal-5'-phosphate (PLP), using UV-visible spectrophotometry and mass analysis, were carried out to specify the mechanism of PLK inhibition. Depending on the results, the inhibiting drugs were divided into three groups. The first group included theophylline and progabide and inhibited PLK using either PL or pyridoxamine (PM) as substrate and thereby were true inhibitors. Moreover, they did not form covalent complexes with PL or PLP. The second group, which included cycloserine, dopamine, isoniazid, and thiamphenicol glycinate, inhibited PLK using PL, but not PM, as substrate.
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CAS 55294-15-0 Muzolimine

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