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860504P

Avanti

C4 Ceramide (d18:1/4:0)

Avanti Research - A Croda Brand 860504P, powder

Synonym(s):

N-butyroyl-D-erythro-sphingosine

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About This Item

Empirical Formula (Hill Notation):
C22H43NO3
CAS Number:
Molecular Weight:
369.58
UNSPSC Code:
12352211
NACRES:
NA.25

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

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

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

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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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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