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878119P

Avanti

C16 Lyso PAF

Avanti Research™ - A Croda Brand 878119P, powder

Sinónimos:

1-O-hexadecyl-2-hydroxy-sn-glycero-3-phosphocholine

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About This Item

Fórmula empírica (notación de Hill):
C24H52NO6P
Número de CAS:
52691-62-0
Peso molecular:
481.65
MDL number:
MFCD00042932
UNSPSC Code:
12352211
NACRES:
NA.25

form

powder

packaging

pkg of 1 × 5 mg (878119P-5mg)

manufacturer/tradename

Avanti Research™ - A Croda Brand 878119P

lipid type

bioactive lipids
phosphoglycerides

shipped in

dry ice

storage temp.

−20°C

SMILES string

O[C@](COP([O-])(OCC[N+](C)(C)C)=O)([H])COCCCCCCCCCCCCCCCC

InChI

1S/C24H52NO6P/c1-5-6-7-8-9-10-11-12-13-14-15-16-17-18-20-29-22-24(26)23-31-32(27,28)30-21-19-25(2,3)4/h24,26H,5-23H2,1-4H3/t24-/m1/s1

InChI key

VLBPIWYTPAXCFJ-XMMPIXPASA-N

Categorías relacionadas

Application

C16 Lyso PAF is suitable for the use in thin layer chromatography for the synthesis of acyl-platelet activating factor (PAF). It is also suitable for intraperitoneal injection into mice to compare the relative inhibitory actions of acyl-PAF, lyso-PC and lyso-PAF on alkyl PAF-induced death.

Packaging

5 mL Amber Glass Screw Cap Vial (878119P-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

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Modulation of inflammatory platelet-activating factor (PAF) receptor by the acyl analogue of PAF
Chaithra VH, et al.
Journal of Lipid Research, 59(11), 2063-2074 (2018)
Kelsey B Law et al.
Autophagy, 13(5), 868-884 (2017-05-20)
Peroxisome biogenesis disorders (PBDs) are metabolic disorders caused by the loss of peroxisomes. The majority of PBDs result from mutation in one of 3 genes that encode for the peroxisomal AAA ATPase complex (AAA-complex) required for cycling PEX5 for peroxisomal
Michael A Kennedy et al.
PLoS genetics, 10(1), e1004010-e1004010 (2014-01-28)
Unbiased lipidomic approaches have identified impairments in glycerophosphocholine second messenger metabolism in patients with Alzheimer's disease. Specifically, we have shown that amyloid-β42 signals the intraneuronal accumulation of PC(O-16:0/2:0) which is associated with neurotoxicity. Similar to neuronal cells, intracellular accumulation of

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