Detail of > 22260-51-1
- CAS Number:
- 22260-51-1
- Name:
Bromocriptine mesylate
- Formula:
- C32H40BrN5O5.CH4SO3
- Molecular Structure:

- Synonyms:
- Bromocriptine mesilate (JP14);Bromocriptine mesylate (USP);Bromergon;Parlodel (TN);Pravidel;Prestwick_771;Ergotaman-3,6,18-trione, 2-bromo-12-hydroxy-2-(1-methylethyl)-5- (2-methylpropyl)-, (5alpha)-;2-Bromo-alpha-ergocryptine methanesulfonate;Bromocryptine mesylate;Parlodel;CB 154;Ergotaman-3',6',18-trione,2-bromo-12'- hydroxy-2'-(1-methylethyl)-5'-(2-methylpropyl)-,(5'R)-,monomethanesulfonate (salt);Bagren;
- Molecular Weight:
- 750.70
- EINECS:
- 244-881-1
- Boiling Point:
- 891.3 °C at 760 mmHg
- Flash Point:
- 492.8 °C
- Solubility:
- H2O: 0.8 mg/mL
- Appearance:
- white solid
- Hazard Symbols:
Xn- Risk Codes:
- 20/21/22
- Safety:
- 22-24/25-36Details
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Reference
- Effects of bromocriptine on the estrus cycle and on persistent diestrus in rats
- Effects of bromocriptine on the estrus cycle and on persistent diestrus in rats. Kun, I. (IMF, Tirgu-Mures, Rom.). Rev. Med. (Tirgu-Mures, Rom.), 29(1-2), 92-7 (Romanian) 1983. CODEN: REMTAS. ISSN: 0034-995X. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) In rats with normal estrus cycles, bromocriptine methanesulfonate (I) [22260-51-1] (5-20 mg/kg, s.c.) given before the crit. proestrus period prolonged estrus and had an antiovulatory effect. This appears to be a result of a dopaminergic agonist action of I. In animals with persistent diestrus, I at low doses (0.5 mg/kg/day for 3 days) restored cycling, apparently by lowering prolactin levels and by exerting a presynaptic effect on autoreceptors of tuberoinfundibular neurons in the hypothalamus, partially blocking their inhibitory effect on LH secretion. Only small doses of I are recommended in cases of functional amenorrhea, since high doses block ovulation as well as prolactin secretion.
- Effects of dextrofenfluramine and other anorectic drugs on experimentally induced hyperphagias
- Effects of dextrofenfluramine and other anorectic drugs on experimentally induced hyperphagias. Carruba, M. O.; Memo, M.; Missale, C.; Pizzi, M.; Garosi, V. L.; Spano, P. F.; Mantegazza, P. (Dep. Pharmacol. Chemother. Med. Toxicol., Univ. Milan, Milan 20129, Italy). Adv. Biosci., 60(Disord. Eating Behav.: Psychoneuroendocr. Approach), 353-60 (English) 1986. CODEN: AVBIB9. ISSN: 0065-3446. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 14 Anorectic drugs known to be effective in reducing food intake in rats trained to eat 4 h a day were tested for their efficacy in reducing the hyperphagic response of rats to insulin [9004-10-8] or 2-deoxy-d-glucose [154-17-6] injection. Anorectics that act through a serotoninergic mechanism, such as d-fenfluramine [3239-44-9], p-chloroamphetamine [64-12-0], quipazine hydrogen maleate [5786-68-5] and fluoxetine [54910-89-3] antagonize both insulin- and 2-DG-induced overeating, while anorectics acting through the dopaminergic system, i.e., d-amphetamine [51-64-9], diethylpropion [90-84-6], lisuride hydrogen maleate [19875-60-6], bromocriptine methane sulfonate [22260-51-1] and mazindol [22232-71-9], antagonize the hyperphagia induced by 2-DG but not that induced by insulin. Serotonin creatinine sulfate [971-74-4] itself, given s.c., was able to reduce food intake in rats trained to eat 4 h a day and to antagonize both insulin- and 2-DG-induced hyperphagia, pointing out the involvement of a peripheral serotoninergic mechanism in controlling overeating. The serotonin (5-HT) receptor blocker metergoline [17692-51-2] did not modify the hyperphagic response to insulin or 2-DG. Apparently, there are different neuronal or humoral circuits underlying the hyperphagic responses to insulin and 2-DG. In addn., these results, which show different effectiveness of anorectic drugs depending on what has provoked the hyperphagia, suggest that differences in the etiol. of the hyperphagia of obese subjects must be taken into consideration when choosing therapy.
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