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Merck

H135

Sigma-Aldrich

5-羟基癸酸 钠盐

≥97% (HPLC)

别名:

5-羟基癸酸 钠盐

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About This Item

经验公式(希尔记法):
C10H19NaO3
CAS号:
分子量:
210.25
MDL號碼:
分類程式碼代碼:
12352106
PubChem物質ID:
NACRES:
NA.77

品質等級

化驗

≥97% (HPLC)

形狀

powder

儲存條件

desiccated

顏色

white to beige

溶解度

H2O: 10 mg/mL, clear

SMILES 字串

[Na+].CCCCCC(O)CCCC([O-])=O

InChI

1S/C10H20O3.Na/c1-2-3-4-6-9(11)7-5-8-10(12)13;/h9,11H,2-8H2,1H3,(H,12,13);/q;+1/p-1

InChI 密鑰

YNAGNECWEKMWRM-UHFFFAOYSA-M

生化/生理作用

阻断K+通道激活剂cromakalim的缺血后作用。

特點和優勢

该化合物在受体分类和信号转导手册的钾通道页面上有重点介绍。想要浏览手册的其他页面, 请单击此处

注意

吸湿

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

Eyeshields, Gloves, type N95 (US)


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Samy Talha et al.
Journal of applied physiology (Bethesda, Md. : 1985), 114(2), 172-179 (2012-10-30)
Brain natriuretic peptide (BNP) reduces the extent of myocardial infarction. We aimed to determine whether BNP may reduce skeletal muscle mitochondrial dysfunctions and oxidative stress through mitochondrial K(ATP) (mK(ATP)) channel opening after ischemia-reperfusion (IR). Wistar rats were assigned to four
G J Grover et al.
Journal of cardiovascular pharmacology, 16(6), 853-864 (1990-12-01)
The detailed antiischemic pharmacology of the potassium channel activator cromakalim was determined in isolated globally ischemic rat hearts and a canine model of coronary occlusion and reperfusion. Cromakalim significantly improved reperfusion function in rat hearts starting at a concentration of
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Low-flow ischemia (LFI) is consequent to coronary disease and produces cardiac stunning during reperfusion (R). Energetic performance and mechanisms of Ca2+ handling during LFI/R are not known. Moreover, cardioprotection of the phytoestrogen genistein (Gen) remains to be demonstrated in LFI/R.
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Using a new isolate of Pseudomonas aeruginosa, we obtained 7 g cell dry wt (CDW/l) using 5 % (w/v) glucose. Crude polyhydroxyalkanoates were obtained at 14.6 % of CDW. FTIR and NMR analysis confirmed that this was a new co-polymer:
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Basic research in cardiology, 108(1), 318-318 (2012-12-04)
Postconditioning (Postcon) reduces infarct size. However, its role in modulation of cardiac repair after infarction is uncertain. This study tested the hypothesis that Postcon inhibits adverse cardiac repair by reducing degradation of extracellular matrix (ECM) and synthesis of collagens via

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