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Iprindole Sale

(Synonyms: 伊普吲哚) 目录号 : GC60938

Iprindole具有抗抑郁的生物活性,是一种弱的去甲肾上腺素和5-HT摄取的抑制剂。

Iprindole Chemical Structure

Cas No.:5560-72-5

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10mM (in 1mL DMSO)
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10mg
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25mg
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50mg
¥3,780.00
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100mg
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产品描述

Iprindole, a tricyclic indole antidepressant, is a weak inhibitor of the uptake of noradrenaline and 5-HT[1].

Iprindole produces less than 50% inhibition of the uptake of noradrenaline as well as that of 5-HT at 100 mg/kg i .p..

[1]. M I Gluckman, et al. The pharmacology of iprindole, a new antidepressant. Psychopharmacologia. 1969;15(3):169-85.

Chemical Properties

Cas No. 5560-72-5 SDF
别名 伊普吲哚
Canonical SMILES CN(C)CCCN1C2=C(CCCCCC2)C3=C1C=CC=C3
分子式 C19H28N2 分子量 284.44
溶解度 DMSO: 120 mg/mL (421.88 mM); Water: < 0.1 mg/mL (insoluble) 储存条件 4°C, protect from light
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1 mM 3.5157 mL 17.5784 mL 35.1568 mL
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Research Update

Metabolism of some "second"- and "fourth"-generation antidepressants: Iprindole, viloxazine, bupropion, mianserin, maprotiline, trazodone, nefazodone, and venlafaxine

Cell Mol Neurobiol 1999 Aug;19(4):427-42.PMID:10379419DOI:10.1023/a:1006953923305.

1. This review summarizes the major known aspects of the metabolism of second-generation (Iprindole, viloxazine, bupropion, mianserin, maprotiline, and trazodone) and fourth-generation (nefazodone and venlafaxine) antidepressants. 2. Discussions about specific enzymes involved and about possible pharmacokinetic drug-drug interactions, particularly as they relate to cytochrome P450 enzymes, are provided.

Jaundice due to Iprindole

Gut 1971 Sep;12(9):705-8.PMID:4106521DOI:10.1136/gut.12.9.705.

Twenty-one patients treated for depression with Iprindole developed evidence of liver damage: 15 were jaundiced, five had bilirubinuria, and one had pruritus. These complications occurred between four and 21 days after initial exposure to the drug. All patients recovered. Light and electron microscopic findings in liver biopsies of one of these patients were those of cholestasis without inflammation.

The effects of Iprindole on noradrenergic transmission in the rat anococcygeus muscle

Naunyn Schmiedebergs Arch Pharmacol 1983 Aug;323(4):321-7.PMID:6314151DOI:10.1007/BF00512470.

The effects of Iprindole on the contractile responses to field stimulation and to exogenously applied agents have been studied in the rat anococcygeus muscle. In addition the effects on the spontaneous overflow of 3H and that induced by field stimulation (following preloading of the tissue with [3H]-noradrenaline) are reported. Iprindole (10(-7)-5 X 10(-6) M) had no effect on the contractile responses to acetylcholine. Iprindole at 10(-7) or 10(-6) M was equieffective in potentiating the contractile responses to either field stimulation or to noradrenaline. With a higher concentration of Iprindole (5 X 10(-6) M) the potentiation was greater. The responses to oxymetazoline were potentiated and inhibited by Iprindole at 10(-8) and 10(-7) M, respectively. Iprindole at 10(-6) M potentiated the responses to tyramine. The effects of Iprindole at 10(-7) and 5 X 10(-6) M on the responses to field stimulation and to noradrenaline were not altered by the presence of ouabain (5 X 10(-5) M), neostigmine (10(-6) M) or yohimbine (10(-7) M). In the presence of desipramine (10(-6) M), Iprindole at 10(-7) M potentiated the contractile responses to field stimulation and to noradrenaline. The higher concentrations of Iprindole (10(-6) and 5 X 10(-6) M) inhibited the contractile responses to field stimulation and to noradrenaline in the presence of desipramine. Iprindole (10(-7) M) had no effect on the relaxant responses to field stimulation. Iprindole at 10(-7) or 10(-6) M had no effect on the spontaneous overflow of 3H or that induced by field stimulation at 2 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)

Iprindole reverses the lamellar body deficiency of cultured L-2 cells. Possible implications in the reversal of surfactant deficiency

Am J Pathol 1987 Oct;129(1):34-43.PMID:2821815doi

Type II alveolar epithelial cells in long-term culture typically lose the ability to synthesize surfactant together with a loss of the characteristic lamellar bodies in the cytoplasm of the cells. Iprindole, a cationic amphiphilic drug, induces lamellar body formation in cultured L-2 cells, a cell line derived from rat Type II cells, but devoid of lamellar bodies. With concentrations of 10(-7)-10(-5) M Iprindole, which approximate therapeutic plasma concentrations in human subjects, the drug induced the formation of lamellar bodies within 8 hours of incubation. This effect on cell morphology was rapidly lost after withdrawal of the drug. At concentrations of Iprindole which induced lamellar body formation, there was a significant increase in phospholipid content of the L-2 cells as well as an increase in disaturated phosphatidylcholine, an important constituent of surfactant. These studies suggest that the use of drugs such as Iprindole may represent a novel approach in the augmentation of phospholipid (and possibly surfactant) content of Type II cells in the lung.

Effect of D-amphetamine on the extracellular concentrations of glutamate and dopamine in iprindole-treated rats

Brain Res 1993 Nov 5;627(1):1-8.PMID:7904885DOI:10.1016/0006-8993(93)90741-5.

A single administration of D-amphetamine and Iprindole has been reported to produce selective, long-lasting decreases in brain dopamine (DA) content because of axon terminal degeneration. It has been found that the noncompetitive glutamate (GLU) antagonist, MK 801, blocks D-amphetamine-induced DA depletion in iprindole-treated rats. In the present study, the effect of D-amphetamine (9.2 mg/kg) and Iprindole (10 mg/kg) on the extracellular concentrations of DA and GLU was determined in the striatum of awake, freely moving rats by the use of in vivo microdialysis. D-Amphetamine significantly increased DA and GLU efflux in the striatum of iprindole-treated rats as compared to the vehicle-treated group. The increase in the extracellular concentration of GLU occurred 4-6 hr following drug administration. The concentration of DA was decreased significantly in the striatum of D-amphetamine and iprindole-treated rats 7 days following administration as compared to the vehicle-treated group. Inhibition of tyrosine hydroxylase after alpha-methylparatyrosine (150 mg/kg) administration attenuated D-amphetamine-induced DA and GLU release. The DA antagonist, haloperidol (1 mg/kg), blocked D-amphetamine-induced GLU release without affecting the increase in the extracellular concentration of DA produced by the combination of D-amphetamine and Iprindole. Both alpha-methylparatyrosine and haloperidol blocked the depletion of DA in the striatum 7 days after D-amphetamine and Iprindole as compared to the vehicle group. In addition, administration of MK-801 (2 mg/kg) 2 hr after D-amphetamine significantly attenuated the long-term (7 day) decrease in striatal DA content produced by the combination of D-amphetamine and Iprindole.2+