| Identification | Back Directory | [Name]
tetramisole | [CAS]
5036-02-2 | [Synonyms]
Tetramizole
DL-tetramisole
6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b]thiazole
Imidazo2,1-bthiazole, 2,3,5,6-tetrahydro-6-phenyl-
6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole
(+-)-2,3,5,6-tetrahydro-6-phenylimidazo(2,1-b)thiazole | [EINECS(EC#)]
225-729-3 | [Molecular Formula]
C11H12N2S | [MOL File]
5036-02-2.mol | [Molecular Weight]
204.29 |
| Chemical Properties | Back Directory | [Melting point ]
87-89° | [Boiling point ]
344.4±45.0 °C(Predicted) | [density ]
1.32±0.1 g/cm3(Predicted) | [storage temp. ]
Sealed in dry,2-8°C | [solubility ]
DMSO; Methanol | [form ]
Solid | [pka]
10.00±0.40(Predicted) | [color ]
White (powder) | [InChI]
InChI=1S/C11H12N2S/c1-2-4-9(5-3-1)10-8-13-6-7-14-11(13)12-10/h1-5,10H,6-8H2 | [InChIKey]
HLFSDGLLUJUHTE-UHFFFAOYSA-N | [SMILES]
S1CCN2CC(C3=CC=CC=C3)N=C12 | [EPA Substance Registry System]
Tetramisole (5036-02-2) |
| Hazard Information | Back Directory | [Uses]
Tetramisol is an isolated intermediate in the synthesis of 4-Hydroxy-tetramisole (H595270), a metabolite of Tetramisole, an anthelmintic. | [Definition]
ChEBI: 6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole is an imidazothiazole that is imidazo[2,1-b][1,3]thiazole in which the double bonds at the 2-3 and 5-6 positions have been reduced to single bonds and in which one of the hydrogens at position 6 is replaced by a phenyl group. It has a role as a xenobiotic and an environmental contaminant. | [in vivo]
Tetramisole (0.54 mg/kg; intravenous injection; single dose; 3 minutes pretreatment) significantly reduces the number and duration of ventricular arrhythmias and the incidence of ventricular fibrillation in the Sprague-Dawley rat model of myocardial infarction induced by coronary artery ligation, and this effect is reversed by the IK1 channel blocker chloroquine (CQ)[2].
Tetramisole (0.54 mg/kg; intraperitoneal injection; once a day; 10 days) improves cardiac contractile function, reduces cardiomyocyte hypertrophy and interstitial fibrosis, and inhibits the activation of the PKA signaling pathway in the Sprague-Dawley rat model of isoproterenol (Iso)-induced cardiac remodeling, and the effect is dependent on the IK1 channel activity[2]. | Animal Model: | Male Sprague-Dawley rats (2 months old, weight not specified) + coronary ligation-induced acute myocardial infarction model[2] | | Dosage: | 0.18, 0.54, 1.8 mg/kg (dissolved in saline) | | Administration: | Intravenous injection 3 minutes before coronary artery occlusion; single dose | | Result: | Significantly reduced premature ventricular contractions (PVC) from 134 to 16 episodes, shortened ventricular tachycardia (VT) duration from 59.4 s to 8.1 s, and eliminated ventricular fibrillation (VF) (duration 0 s, incidence 0%), compared to control.
These anti-arrhythmic effects were largely reversed by co-administration of chloroquine (7.5 μg/kg), an IK1 antagonist. Pretreatment for 10 days (0.54 mg/kg/day) also reduced VT duration (42.7 s to 6.5 s) and abolished VF, associated with upregulated Kir2.1 protein expression in ventricular tissue. |
| Animal Model: | Male Sprague-Dawley rats (2 months old, weight not specified) + isoproterenol (3 mg/kg/day, i.p., 10 days)-induced cardiac remodeling model[2] | | Dosage: | 0.54 mg/kg/day (dissolved in saline) | | Administration: | Intraperitoneal injection once daily for 10 days | | Result: | Prevented Iso-induced increases in interventricular septum thickness and left ventricular wall thickness, normalized left ventricular ejection fraction (EF) and fractional shortening (FS), and reduced myocardial cell cross-sectional area by 22% compared to Iso group.
Masson's trichrome staining showed a 35% reduction in interstitial fibrosis, accompanied by downregulated phosphorylated PKA (p-PKA) and upregulated Kir2.1/SAP97 signaling.
Co-administration of chloroquine abolished these protective effects, confirming dependence on IK1 channel activation. |
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| Company Name: |
Merck KGaA
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| Tel: |
21-20338288 |
| Website: |
www.sigmaaldrich.cn |
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