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关于此项目
经验公式(希尔记法):
C31H41N6O7 Na
化学文摘社编号:
分子量:
632.68
NACRES:
NA.32
PubChem Substance ID:
UNSPSC Code:
12352204
MDL number:
Quality Level
assay
≥99%
form
lyophilized powder
storage temp.
−20°C
SMILES string
[H][C@@]12CCCN1C(=O)[C@@H](CC(O)=O)NC(=O)[C@@H](Cc3c[nH]c4ccccc34)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](NC2=O)C(C)C
InChI
1S/C31H42N6O7/c1-16(2)12-21-27(40)33-22(13-18-15-32-20-9-6-5-8-19(18)20)28(41)35-23(14-25(38)39)31(44)37-11-7-10-24(37)29(42)36-26(17(3)4)30(43)34-21/h5-6,8-9,15-17,21-24,26,32H,7,10-14H2,1-4H3,(H,33,40)(H,34,43)(H,35,41)(H,36,42)(H,38,39)/t21-,22+,23+,24-,26+/m0/s1
InChI key
VYCMAAOURFJIHD-PJNXIOHISA-N
Gene Information
human ... EDNRA(1909), EDNRB(1910)
rat ... Ednra(24326), Ednrb(50672)
Application
BQ-123已用作选择性内皮素-A受体拮抗剂,研究其对肿瘤坏死因子α(TNFα)诱导的人气道平滑肌细胞(HASMC)增殖的影响。作为内皮素-A受体拮抗剂,它还用于研究其对TNFα诱导的粒细胞-巨噬细胞集落刺激因子(GM-CSF) 表达的影响。
Biochem/physiol Actions
BQ-123是一种内皮素(Et)受体拮抗剂,对内皮素A(ETA)受体敏感。它是一种环五肽。
选择性ETA内皮素受体拮抗剂。
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
法规信息
常规特殊物品
此项目有
F Cosentino et al.
Journal of cardiovascular pharmacology, 22 Suppl 8, S332-S335 (1993-01-01)
The present study was designed to determine whether an endothelinA (ETA)-receptor antagonist BQ-123 (cyclo[Dtrp, Dasp, pro-D-Val-Leu]) or an ET-converting enzyme inhibitor phosphoramidon may prevent development of cerebral vasospasm after subarachnoid hemorrhage (SAH). A "double hemorrhage" canine model of the disease
M Clozel et al.
Life sciences, 52(9), 825-834 (1993-01-01)
The aim of this study was to evaluate the role of endothelin and endothelin ETA receptor in the early cerebral vasoconstriction following subarachnoid hemorrhage (SAH) in the rat. SAH induced by injection of autologous blood in the cisterna magna reduced
J Knobloch et al.
Thorax, 64(12), 1044-1052 (2009-10-24)
There is an urgent need to inhibit endothelin-1 (ET-1) induced chronic inflammatory processes in early stages of lung diseases in order to prevent untreatable irreversible stages often accompanied by lung fibrosis and pulmonary hypertension. Nothing is known about the airway
Jürgen Knobloch et al.
Biochemical pharmacology, 116, 188-199 (2016-07-17)
Pathological proliferation of human airway smooth muscle cells (HASMCs) causes hyperplasia in chronic lung diseases. Signaling pathways that link airway inflammation to HASMC proliferation might provide therapeutic targets for the prevention of airway remodeling and chronic lung diseases. Endothelin-1 (ET-1)
Sarah Pisarcik et al.
American journal of physiology. Lung cellular and molecular physiology, 304(8), L549-L561 (2013-02-19)
Numerous cellular responses to hypoxia are mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1). HIF-1 plays a central role in the pathogenesis of hypoxic pulmonary hypertension. Under certain conditions, HIF-1 may utilize feedforward mechanisms to amplify its activity. Since hypoxia
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