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Detail of "1225-55-4"

  • CAS Number:
  • 1225-55-4
  • Name:
  • 5H-Dibenzo[a,d]cycloheptene-5-propanamine,N-methyl-, hydrochloride (1:1)

  • Molecular Structure:
  • Formula:
  • C19H21 N . Cl H
  • Molecular Weight:
  • 299.87
  • Synonyms:
  • 5H-Dibenzo[a,d]cycloheptene-5-propanamine,N-methyl-, hydrochloride (9CI); 5H-Dibenzo[a,d]cycloheptene-5-propylamine,N-methyl-, hydrochloride (7CI,8CI); Concordin; MK-240; Maximed; Maximet;N-Methyl-5H-dibenzo[a,d]cycloheptene-5-propylamine hydrochloride; NormethylEX4442; Protriptyline hydrochloride; Protryptyline hydrochloride; Triptil;Triptil Hydrochloride; Vivactil
  • Hazard Symbols:
  • Risk Codes:
  • 20/21/22-36/37/38
  • Safety:
  • Poison by ingestion, intraperitoneal, intravenous, and subcutaneous routes. When heated to decomposition it emits very toxic fumes of NOx and HCl. Details

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Reference

The influence of antidepressive drugs on the level of acetylcholine and on the acetylcholinesterase activity in the brain of rats
The influence of antidepressive drugs on the level of acetylcholine and on the acetylcholinesterase activity in the brain of rats. Herman, Zbigniew S.; Sokola, Andrzej; Lenartowicz, Halina; Zielinski, Marek; Depta, Leokadia (Biol. Physiol. Inst., Silesian Med. Acad., Zabrze, Pol.). Pol. J. Pharmacol. Pharm., 28(4), 313-21 (English) 1976.In this article, certain chemicals are used. Some of their cas registry numbers are 13492-01-8 and 549-18-8 CODEN: PJPPAA. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Rats were treated i.p. with the monoamine oxidase inhibitors (MAO-I) nialamide (NL) [51-12-7], pivalylbenzylhydrazine-HCl [2971-75-7], tranylcypromine sulfate [13492-01-8], pheniprazine (Ph) [55-52-7] or pargyline [555-57-7], and the level of total, free, and bound acetylcholine (Ach) [51-84-3] as well as the acetylcholinesterase (Ach-E) [9000-81-1] activity were detd. in 4 parts of the brain 2 or 16 hr after the treatment. These parameters were detd. also after treatment with tricyclic antidepressants: desmethylimipramine-HCl (DMI) [58-28-6], amitriptyline-HCl [549-18-8] or protriptyline-HCl [1225-55-4], and under conditions of the reversal of the reserpine-like syndrome. MAO-I, 2 hr after their application and the reversal of reserpine like-syndrome, did not change the level of the fractions of Ach in the parts of the brain. DMI increased the level of all Ach fractions in the striatum. NL caused the decrease of bound Ach level in all parts of the brain, with no changes of free Ach level, 16 hr after the treatment. Ph, 16 hr after the treatment, decreased both free and bound ACh only in the cortex. All the drugs affected ACh-E activity in various parts of brain. Cholinergic mechanisms in the rat brain are involved in the central action of DMI and of some MAO-I; cholinergic function of the brain may be modulated by adrenergic activity; individual parts of the brain have different susceptibility to the influence of different MAO-I on the ACh-E activity. .
Relations between chronotropic effect, 1-3H-noradrenaline uptake and tissue concentrations of desipramine, protriptyline and doxepin in rat isolated atria
Relations between chronotropic effect, 1-3H-noradrenaline uptake and tissue concentrations of desipramine, protriptyline and doxepin in rat isolated atria. Franco, R.; Bonaccorsi, A.; Castelli, M. G.; Garattini, S.; Morselli, P. L. (Ist. Ric. Farmacol "Mario Negri", Milan, Italy). Arch. Int. Pharmacodyn. Ther., 224(1), 55-65 (English) 1976. CODEN: AIPTAK. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) The pharmacol. effects of 3 tricyclic antidepressant agents [desipramine-HCl (I-HCl) [58-28-6], protriptyline-HCl (II-HCl) [1225-55-4], and doxepine-HCl (III-HCl) [1229-29-4]] are evaluated in rat isolated atria in relation to their accumulation and efflux kinetics. 1229-29-4 and 58-28-6 which are cas registry numbers are also used here. All drugs inhibited 3H-labeled l-noradrenaline [51-41-2] uptake and potentiated noradrenaline chronotropic response (I .simeq. II > III). I and II, at concns. of 10-7 - 10-6M stimulated the spontaneous rate; higher concns. (>10-6M) depressed it. III had only a neg. chronotropic effect. When the drugs were removed from the incubation medium, the depressing effect started to disappear immediately for I and III and after 20 min for II. On the contrary, the stimulating effect persisted after repeatedly washing the prepns. The antidepressants extensively accumulated in the myocardial tissue (I .gtoreq. II > III). In the efflux studies III was washed out more rapidly than I and II. Although the kinetics of uptake and efflux of the 3 compds. were not sufficient to interpret their different pharmacol. activities in isolated atria, they give useful information on the persistance of the sympathomimetic effect and the rapid disappearing of the neg. chronotropic effect after washing. .
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