22260-51-1
基本信息
甲磺酸溴隐亭
甲黄酸溴麦角环肽
(+)-2-bromo-12'-hydroxy-2'-(1-methylethyl)-5'-(2-methylpropyl)ergotaman-3',6'-18-trione methanesulfonate salt
2-BROMO-12'-HYDROXY-2'-(1-METHYLETHYL)-5'-(2-METHYL-PROPYL)ERGOTAMAN-3',6',18-TRIONE-METHANESULFONATE
2-BROMO-ALPHA-ERGOCRYPTINE METHANESULFONATE
2-BROMO-ALPHA-ERGOCRYPTINE METHANESULFONATE SALT
2-BROMOERGOCRYPTINE MONOMETHANESULFONATE SALT
(5'A)-2-BROMO-12'-HYDROXY-2'-(1-METHYLETHYL)-5'-(2-METHYLPROPYL)ERGOTAMAN-3',6',18-TRIONE MESYLATE
BCT
BRC
(+)-BROMOCRIPTINE MESYLATE
BROMOCRIPTINE MESYLATE
(+)-BROMOCRIPTINE METHANESULFONATE
BROMOCRIPTINE METHANESULPHONATE
BROMOCRYPTINE MESYLATE METHANESULFONATE SALT
2-bromo-alpha-ergocryptinemesylate
2-bromo-alpha-ergocryptinmethanesulfonate
2-bromo-alpha-ergokryptine-mesilate
bromocriptinemesilate
bromocryptinemethanesulfonate
cb-154
物理化学性质
安全数据
22260-51-1(安全特性,毒性,储运)
常见问题列表
1)溴隐亭的合成
将α-麦角隐亭12g(20.8mmoL)和二氯甲烷120mL加入反应瓶中,搅拌溶清后依次加入5,5-二溴巴比妥酸3.69g(12.9mmoL)、33%氢溴酸的冰乙酸溶液0.2mL,控温25~30℃反应5~6h,过滤,滤液依次用1moL/L的硫代硫酸钠(30mL),5%的碳酸氢钠溶液(30mL),20%氯化钠溶液(30mL)洗涤。有机相用无水硫酸镁干燥,过滤,并加入硅胶36g浓缩将溶剂完全拉干。柱层析:流动相先为二氯甲烷,后为V(二氯甲烷)∶V(丙酮)=6∶1的混合溶液。得10.6g溴隐亭,收率78%。
2)甲磺酸溴隐亭的合成
将溴隐亭6.0g用二氯甲烷120mL溶清后加入2-丁酮200mL,控制内温20~30℃,加入甲磺酸1.14g,生成结晶型沉淀,搅拌1h。滤出固体,用2-丁酮30mL洗涤,干燥得6.13g甲磺酸溴隐亭,收率86%。
pKi: 8.05±0.2 (dopamine D2 receptor)
Bromocriptine stimulates [ 35 S]-GTPγS binding at D2 dopamine receptor expressed in CHO cells with pEC 50 of 8.15±0.05. Bromocriptine also is a strong inhibitor of brain nitric oxide synthase. The ergot alkaloid Bromocriptine (BKT) is found to act as a strong inhibitor of purified neuronal nitric oxide synthase (NOS) (IC 50 =10±2 μM) whereas it is poorly active towards inducible macrophage NOS (IC 50 >100 μM) . Bromocriptine is found to inhibit the activity of at least one human cytochrome P450 enzyme. Bromocriptine is a potent inhibitor of CYP3A4 with a calculated IC 50 value for the interaction of 1.69 μM.
Bromocriptine mesylate (2 mg/kg, i.p.) is administered for 7 days in groups of mice in forced swimming test (FST) and tail suspension test (TST). Bromocriptine group shows significant anti-immobility action as compared to control. When Bromocriptine administered 30 min after the last dose of 7 days MPE treatment and subjected to FST, this dopaminergic agonist produces significant and dose dependent potentiation of anti-immobility action of MPE (200 mg/kg, p.o.) as compared to MPE treatment alone. Bromocriptine treatment group shows a significant reduction of immobility time as compared to control. Bromocriptine administration after 7 days pretreatment with MPE (100 and 200 mg/kg, p.o.) shows significant and dose dependent potentiation of anti-immobility action of MPE as compared to MPE treatment alone. Intracisternal administration of Bromocriptine decreases significantly the static mechanical allodynia (SMA) score compared to that of sham (saline-injected rats) and its effect lasted for 30 min. Intraperitoneal administration of Bromocriptine induces a significant, dose dependent (0.1 mg and 1 mg/kg) decrease in pain scores in CCI-IoN group when compared to sham and its effect lasted for 6 h. The highest dose induces the highest score decrease (P<0.01). Bromocriptine effect lasts for 20 min. Intraperitoneal administration of Bromocriptine induces a significant dose dependent decrease in SMA score in CCI-IoN+6-OHDA lesioned group compared to that of sham. Its effect lasts for 6 h.