22260-51-1
22260-51-1 結(jié)構(gòu)式
基本信息
甲磺酸溴隱亭
甲黃酸溴麥角環(huán)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
物理化學(xué)性質(zhì)
安全數(shù)據(jù)
22260-51-1(安全特性,毒性,儲(chǔ)運(yùn))
常見問題列表
1）溴隱亭的合成
將α-麥角隱亭12g（20.8mmoL）和二氯甲烷120mL加入反應(yīng)瓶中，攪拌溶清后依次加入5，5-二溴巴比妥酸3.69g（12.9mmoL）、33％氫溴酸的冰乙酸溶液0.2mL，控溫25～30℃反應(yīng)5～6h，過濾，濾液依次用1moL／L的硫代硫酸鈉（30mL），5％的碳酸氫鈉溶液（30mL），20％氯化鈉溶液（30mL）洗滌。有機(jī)相用無水硫酸鎂干燥，過濾，并加入硅膠36g濃縮將溶劑完全拉干。柱層析：流動(dòng)相先為二氯甲烷，后為V（二氯甲烷）∶V（丙酮）＝6∶1的混合溶液。得10.6g溴隱亭，收率７8％。
2）甲磺酸溴隱亭的合成
將溴隱亭6.0g用二氯甲烷120mL溶清后加入2-丁酮200mL，控制內(nèi)溫20～30℃，加入甲磺酸1.14g，生成結(jié)晶型沉淀，攪拌1h。濾出固體，用2-丁酮30mL洗滌，干燥得6.13g甲磺酸溴隱亭，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.