C0424
PK 11195
peripheral benzodiazepine antagonist, powder
别名:
1-（2-氯苯基）-N-甲基-N-（1-甲基丙基）-3-异喹啉羧
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关于此项目
经验公式（希尔记法）:
C21H21ClN2O
化学文摘社编号:
分子量:
352.86
MDL编号:
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77
产品名称
PK 11195,
表单
powder
质量水平
SMILES字符串
CCC(C)N(C)C(=O)c1cc2ccccc2c(n1)-c3ccccc3Cl
InChI
1S/C21H21ClN2O/c1-4-14(2)24(3)21(25)19-13-15-9-5-6-10-16(15)20(23-19)17-11-7-8-12-18(17)22/h5-14H,4H2,1-3H3
InChI key
RAVIZVQZGXBOQO-UHFFFAOYSA-N
基因信息
human ... BZRAP1(9256), TSPO(706)
rat ... Gabra2(29706), Tspo(24230)
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相关类别
应用
PK 11195 已被用作胚胎原始红细胞和骨肉瘤细胞质杂交体中外周苯二氮卓受体（PBR）类似物的抑制剂。它还被用作心脏组织切片体外放射自显影实验中的未标记竞争性结合剂。
生化/生理作用
PK 11195是一种外周苯二氮卓拮抗剂。它还是人组成型雄烷受体（hCAR）和人孕烷 X 受体（PXR）的拮抗剂。在人原代肝细胞中，PK 11195通过反甲基化诱导对受体hCAR的激动剂功能。PK 11195还是B细胞淋巴瘤2（Bcl-2）的拮抗剂，有望成为线粒体靶向治疗和肝胆管型肝癌治疗的化合物。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Pk11195, a mitochondrial benzodiazepine receptor antagonist, reduces apoptosis threshold in Bcl-XL and Mcl-1 expressing human cholangiocarcinoma cells
Okaro AC, et al.
Gut, 51(4), 556-561 (2002)
A S Hazell et al.
Neuroscience letters, 271(1), 5-8 (1999-09-02)
Alterations of 'peripheral-type' benzodiazepine receptors (PTBRs) in brain are a feature of hepatic encephalopathy (HE). Although ammonia toxicity has been implicated in the disorder, recent findings suggest an accumulation of manganese in the brains of cirrhotic patients dying in hepatic
M Okubo et al.
European journal of pharmacology, 359(2-3), 243-249 (1998-12-01)
This study examined the influence of benzodiazepine receptors on amylase release from rat parotid acinar cells. Diazepam (10(-8)-10(-6) M), which is a potent agonist of both central- and peripheral-type benzodiazepine receptors, dose dependently decreased amylase release induced by isoprenaline and
18-kDa translocator protein ligand 18 F-FEMPA: biodistribution and uptake into atherosclerotic plaques in mice
Hellberg S, et al.
Journal of Nuclear Cardiology : Official Publication of the American Society of Nuclear Cardiology, 24(3), 862-871 (2017)
Identification of small molecules that improve ATP synthesis defects conferred by Leber's hereditary optic neuropathy mutations
Datta S, et al.
Mitochondrion, 30, 177-186 (2016)
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