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经验公式(希尔记法):
C25H20N4O2
化学文摘社编号:
分子量:
408.45
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
InChI
1S/C25H20N4O2/c1-29-21-14-8-6-12-18(21)22(16-9-3-2-4-10-16)27-23(25(29)31)28-24(30)20-15-17-11-5-7-13-19(17)26-20/h2-15,23,26H,1H3,(H,28,30)/t23-/m1/s1
SMILES string
CN1C(=O)[C@@H](NC(=O)c2cc3ccccc3[nH]2)N=C(c4ccccc4)c5ccccc15
InChI key
NFHRQQKPEBFUJK-HSZRJFAPSA-N
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
color
white to off-white
solubility
DMSO: >5 mg/mL
originator
Merck & Co., Inc., Kenilworth, NJ, U.S.
storage temp.
2-8°C
Quality Level
General description
地伐西匹通过化学修饰而衍生自阿斯匹林,具有苯并二氮杂骨架。
Application
地伐西匹在人胚胎肾293T细胞和人胰腺切片中已被用作胆囊收缩素受体1(CCK1R)拮抗剂。
Biochem/physiol Actions
地伐西匹是一种CCK1受体拮抗剂。
地伐西匹是一种CCK1(CCK-A)受体拮抗剂和CCK8拮抗剂。
地伐西匹是一种胆囊收缩素受体1(CCK1R)拮抗剂。它可抑制CCK与外周型受体(CCK-A)的结合。地伐西匹可逆转胆囊收缩素八肽(CCK-8)对吗啡的拮抗作用。
Features and Benefits
该化合物是由Merck & Co., Inc., Kenilworth, NJ, U.S.开发的。想要浏览其他由制药公司开发的化合物以及已批准药物/候选药物清单, 请单击此处。
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 1 Oral
存储类别
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Shannon A Metcalf et al.
Peptides, 32(6), 1296-1302 (2011-05-12)
One of the possible mechanisms by which the weight-reducing surgical procedure ileal interposition (II) works is by increasing circulating levels of lower gut peptides that reduce food intake, such as glucagon like peptide-1 and peptide YY. However, since this surgery
Wenya Chen et al.
Bioscience, biotechnology, and biochemistry, 76(6), 1104-1109 (2012-07-14)
We have recently reported that oral gavage of a potato extract (Potein®) suppressed the food intake in rats. The satiating effect of the potato extract was compared in the present study to other protein sources, and the involvement of endogenous
Effect of devazepide reversed antagonism of CCK-8 against morphine on electrical and mechanical activities of rat duodenum in vitro
Xu MY, et al.
World Journal of Gastroenterology, 4(6), 524-524 (1998)
Involvement of endogenous CCK and CCK1 receptors in colonic motor function
Varga G, et al.
British Journal of Pharmacology, 141(8), 1275-1284 (2004)
Clémence Blouet et al.
PloS one, 7(12), e51898-e51898 (2012-12-20)
Previous evidence indicates that duodenal lipid sensing engages gut-brain neurocircuits to determine food intake and hepatic glucose production, but a potential role for gut-brain communication in the control of energy expenditure remains to be determined. Here, we tested the hypothesis
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