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MilliporeSigma

850458C

Avanti

16:0-18:2 PC

Avanti Research - A Croda Brand

Sinónimos:

1-hexadecanoyl-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine; PC(16:0/18:2(9Z,12Z))

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About This Item

Fórmula empírica (notación de Hill):
C42H80NO8P
Número de CAS:
Peso molecular:
758.06
Número MDL:
Código UNSPSC:
51191904
NACRES:
NA.25

descripción

1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine, chloroform

Ensayo

>99% (TLC)

Formulario

liquid

envase

pkg of 1 × 2.5 mL (850458C-25mg)
pkg of 2 × 4 mL (850458C-200mg)

fabricante / nombre comercial

Avanti Research - A Croda Brand

concentración

10 mg/mL (850458C-25mg)
25 mg/mL (850458C-200mg)

tipo de lípido

cardiolipins
phospholipids

Condiciones de envío

dry ice

temp. de almacenamiento

−20°C

cadena SMILES

[O-]P(OCC[N+](C)(C)C)(OC[C@]([H])(OC(CCCCCCC/C=C\C/C=C\CCCCC)=O)COC(CCCCCCCCCCCCCCC)=O)=O

InChI

1S/C42H80NO8P/c1-6-8-10-12-14-16-18-20-21-23-25-27-29-31-33-35-42(45)51-40(39-50-52(46,47)49-37-36-43(3,4)5)38-48-41(44)34-32-30-28-26-24-22-19-17-15-13-11-9-7-2/h14,16,20-21,40H,6-13,15,17-19,22-39H2,1-5H3/b16-14-,21-20-/t40-/m1/s1

Clave InChI

JLPULHDHAOZNQI-ZTIMHPMXSA-N

Descripción general

16:0-18:2 PC or 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine is a glycerophospholipid, with substitution of palmitic acid and linolenic acid at sn-1 and sn-2 positions of the glycerol backbone, respectively.

Aplicación

16:0-18:2 PC or 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine might be used to study the effects of phosphatidylcholines (PCs) on lubrication of damaged mesothelium.[1] It has also been used to prepare liposomes with Hong Jing Tian (HJT)-small RNA-m7, in an attempt to show small plant RNA entry into human cells and the mouse lung, in vitro and in vivo.[2]

Envase

5 mL Clear Glass Sealed Ampule (850458C-200mg)
5 mL Clear Glass Sealed Ampule (850458C-25mg)

Información legal

Avanti Research is a trademark of Avanti Polar Lipids, LLC

Pictogramas

Skull and crossbonesHealth hazard

Palabra de señalización

Danger

Clasificaciones de peligro

Acute Tox. 3 Inhalation - Acute Tox. 4 Oral - Carc. 2 - Eye Irrit. 2 - Repr. 2 - Skin Irrit. 2 - STOT RE 1 Oral - STOT SE 3

Órganos de actuación

Liver,Kidney, Respiratory system

Código de clase de almacenamiento

6.1D - Non-combustible acute toxic Cat.3 / toxic hazardous materials or hazardous materials causing chronic effects

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

does not flash

Punto de inflamabilidad (°C)

does not flash


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Francesca Bodega et al.
Respiratory physiology & neurobiology, 203, 116-120 (2014-08-17)
Effect of time and phosphatidylcholines (PCs) on lubrication of damaged mesothelium has been investigated. Marked increase in coefficient of kinetic friction (μ) of pleural specimens after mesothelial blotting and rewetting decreased by 23.4±3.5%, 41.8±3.8%, and 40.5±2.7% after 30min, 1h, and
John K Eaton et al.
Nature chemical biology, 16(5), 497-506 (2020-04-02)
We recently described glutathione peroxidase 4 (GPX4) as a promising target for killing therapy-resistant cancer cells via ferroptosis. The onset of therapy resistance by multiple types of treatment results in a stable cell state marked by high levels of polyunsaturated
Giulia Coliva et al.
Molecules (Basel, Switzerland), 25(8) (2020-04-25)
Free radical driven lipid peroxidation is a chain reaction which can lead to oxidative degradation of biological membranes. Propagation vs. termination rates of peroxidation in biological membranes are determined by a variety of factors including fatty acyl chain composition, presence
Jianchao Du et al.
Science China. Life sciences, 62(3), 309-320 (2017-04-06)
Pulmonary fibrosis, a progressive chronic disease with a high mortality rate, has limited treatment options. Currently, lung transplantation remains the only effective treatment. Here we report that a small RNA, HJT-sRNA-m7, from a Chinese herbal medicine Hong Jing Tian (HJT
Eikan Mishima et al.
Journal of the American Society of Nephrology : JASN, 31(2), 280-296 (2019-11-27)
Ferroptosis, nonapoptotic cell death mediated by free radical reactions and driven by the oxidative degradation of lipids, is a therapeutic target because of its role in organ damage, including AKI. Ferroptosis-causing radicals that are targeted by ferroptosis suppressors have not

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