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Merck
CN

860504P

Avanti

C4 Ceramide (d18:1/4:0)

Avanti Research - A Croda Brand

别名:

N-butyroyl-D-erythro-sphingosine

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关于此项目

经验公式(希尔记法):
C22H43NO3
化学文摘社编号:
分子量:
369.58
MDL number:
UNSPSC Code:
12352211
NACRES:
NA.25
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产品名称

C4 Ceramide (d18:1/4:0), Avanti Research - A Croda Brand 860504P, powder

SMILES string

OC[C@]([H])(NC(CCC)=O)[C@]([H])(O)/C=C/CCCCCCCCCCCCC

InChI

1S/C22H43NO3/c1-3-5-6-7-8-9-10-11-12-13-14-15-16-18-21(25)20(19-24)23-22(26)17-4-2/h16,18,20-21,24-25H,3-15,17,19H2,1-2H3,(H,23,26)/b18-16+/t20-,21+/m0/s1

InChI key

UCBLGIBMIAFISC-CQLAPORSSA-N

assay

>99% (TLC)

form

powder

packaging

pkg of 1 × 5 mg (860504P-5mg)

manufacturer/tradename

Avanti Research - A Croda Brand 860504P

lipid type

sphingolipids

shipped in

dry ice

storage temp.

−20°C

General description

C4 Ceramide (d18:1/4:0) or N-butyroyl-D-erythro-sphingosine is a synthetic ceramide containing sphingosine with butyric acid. It is a non-toxic, short-chain sphingolipid.

Application

C4 Ceramide (d18:1/4:0) has been used to study its role in rescuing and stabilizing ΔF508-cystic fibrosis transmembrane conductance regulator (ΔF508-CFTR).

Biochem/physiol Actions

C4 Ceramide (d18:1/4:0) is implicated in a series of mutual autophosphorylation and phosphorylation actions between 3-phosphoinositide-dependent kinase 1 (PDK1) and serum/glucocorticoid-induced protein kinase 1 (SGK1). It stimulates cyclic adenosine monophosphate (cAMP)-activated chloride secretion and represses hypersecretion of interleukin-8 (IL-8). C4 Ceramide might be a potential therapeutic for cystic fibrosis (CF).

Packaging

5 mL Amber Glass Screw Cap Vial (860504P-5mg)

Legal Information

Avanti Research is a trademark of Avanti Polar Lipids, LLC

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Hung Caohuy et al.
The Journal of biological chemistry, 289(52), 35953-35968 (2014-11-12)
Cystic fibrosis (CF) is due to a folding defect in the CF transmembrane conductance regulator (CFTR) protein. The most common mutation, ΔF508, prevents CFTR from trafficking to the apical plasma membrane. Here we show that activation of the PDK1/SGK1 signaling

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