Thiazesim hydrochloride

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Thiazesim hydrochloride is a CNS-penetrant GABAA receptor inhibitor, exerting anticonvulsant and antidepressant effects. Thiazesim hydrochloride depresses amygdala output, disrupts conditioned avoidance response in rats. Thiazesim hydrochloride can be used for the research of depression and epilepsy.

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Thiazesim hydrochloride Chemical Structure

CAS No. : 3122-01-8

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Other Forms of Thiazesim hydrochloride:

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Purity & Documentation
References
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Description

In Vivo

Thiazesim (1.0-10.0 mg/kg; i.p.) hydrochloride produces no significant reduction in shock-induced defensive fighting, locomotor activity, or shock reactivity in rats^[2].
Thiazesim (20 mg/kg; i.p.; daily prior to each acquisition or retention training session) hydrochloride significantly depresses conditioned avoidance response performance in rats during both acquisition and retention phases, without impairing motor escape responses or inducing state-dependent learning^[4].
Thiazesim (5-40 mg/kg; i.p.; single dose) hydrochloride blocks all tested unlearned behaviors at nondebilitating doses in rats^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	Sprague-Dawley rats (male, 120 days old, 300-325 g, shock-induced defensive fighting model)^[2]
Dosage:	1.0; 3.0; 5.0; 10.0 mg/kg
Administration:	i.p.
Result:	Recorded mean attacks of 40.00 at 1.0 mg/kg, 35.80 at 3.0 mg/kg, 41.80 at 5.0 mg/kg, and 23.60 at 10.0 mg/kg. Produced no significant reduction in shock-induced defensive fighting compared to saline or baseline conditions. Showed no significant effects on locomotor activity at 10.0 mg/kg compared to controls. Showed no significant effects on shock reactivity at 10.0 mg/kg.

Animal Model:	Holtzman albino rats (male, 275 g)^[4]
Dosage:	20 mg/kg
Administration:	i.p.; daily prior to each acquisition or retention training session
Result:	Required a significantly higher mean number of trials to reach criterion. Showed greater variability in trials to criterion. Had a mean percent CAR during acquisition of 33.1% vs. 39.6% for controls, with significantly higher variance in the drug group. Did not show significant differences in CAR latency or escape latency compared to controls. Had a significantly lower mean percent CAR during retention compared to saline-treated rats. Had significantly lower mean percent savings scores during retention compared to saline-treated rats. Showed higher mean trials to criterion during retention, though this effect was not statistically significant. Did not show significant differences in CAR latency during retention compared to controls.

Animal Model:	Sprague-Dawley male rats (200-350 g)^[5]
Dosage:	5, 10, 20, 40 mg/kg
Administration:	i.p.; single dose
Result:	Caused dose-dependent decrease in forced motor activity, with ED₅₀ of 43.89 mg/kg and no 50% reduction at 40 mg/kg. Produced linear dose-dependent decrease in spontaneous motor activity, with ED₅₀ of 29.88 mg/kg. Induced linear dose-dependent decrease in weight-adjusted food consumption, with ED₅₀ of 20.56 mg/kg. Led to linear dose-dependent decrease in water consumption lick counts, with ED₅₀ of 21.33 mg/kg. Caused linear dose-dependent decrease in mouse-killing behavior, with ED₅₀ of 33.30 mg/kg and no restoration of killing at 40 mg/kg via arousal. Produced linear dose-dependent decrease in self-grooming time, with ED₅₀ of 32.10 mg/kg. Showed ED₅₀ for conditioned avoidance response greater than the maximum tested dose of 40 mg/kg.

Molecular Weight

362.92

Formula

C₁₉H₂₃ClN₂OS

CAS No.

3122-01-8

SMILES

O=C1N(CCN(C)C)C2=C(SC(C1)C3=CC=CC=C3)C=CC=C2.Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Barratt ES. The effects of thiazesim, LSD-25, and bilateral lesions of the amygdalae on the release of a suppressed response. Recent Adv Biol Psychiatry. 1966;9:229-40. [Content Brief]

[2]. Bell R, et al. The effects of two "anti-aggressive" compounds, an indenopyridine and a benzothiazepin, on shock-induced defensive fighting in rats. Prog Neuropsychopharmacol. 1979;3(4):399-402. [Content Brief]

[3]. Dreyfuss J, et al. Metabolism of Thiazesim, 5-(2-Dimethylaminoethyl)-2,3-Dihydro-2-Phenyl-1,5-Benzothiazepin-4(5H)-One, in the Rat In Vivo and In Vitro. Journal of Pharmaceutical Sciences 1968, 57 (9), 1505-1511.

[4]. Marques, et al. Conditioned avoidance deficits induced in rats by an amygdala depressant, Thiazesim HCl.

[5]. Geyer HM 3rd, et al. Effects of a tranquilizer and two antidepressants on learned and unlearned behaviors. J Pharm Sci. 1970 Jul;59(7):964-8. [Content Brief]