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855675P

Avanti

16:0 Lyso PC

Avanti Research - A Croda Brand

Synonym(s):

1-hexadecanoyl-sn-glycero-3-phosphocholine; PC(16:0/0:0)

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About This Item

Empirical Formula (Hill Notation):
C24H50NO7P
CAS Number:
Molecular Weight:
495.63
UNSPSC Code:
51191904
NACRES:
NA.25

description

1-palmitoyl-2-hydroxy-sn-glycero-3-phosphocholine

Assay

>99% (LPC; may contain up to 10% of the 2-LPC isomer, TLC)

form

powder

packaging

pkg of 1 × 1 g (855675P-1g)
pkg of 1 × 200 mg (855675P-200mg)
pkg of 1 × 25 mg (855675P-25mg)
pkg of 1 × 500 mg (855675P-500mg)

manufacturer/tradename

Avanti Research - A Croda Brand

shipped in

dry ice

storage temp.

−20°C

SMILES string

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

InChI

1S/C24H50NO7P/c1-5-6-7-8-9-10-11-12-13-14-15-16-17-18-24(27)30-21-23(26)22-32-33(28,29)31-20-19-25(2,3)4/h23,26H,5-22H2,1-4H3/t23-/m1/s1

InChI key

ASWBNKHCZGQVJV-HSZRJFAPSA-N

Application


  • Microbubble-Mediated Drug Delivery: The role of 16:0 Lyso PC in the development of microbubble technologies for drug delivery systems emphasizes its potential in pharmaceutical formulations, enhancing the efficiency of targeted therapy applications, particularly in cancer treatment (Aron et al., 2019).

  • Photodynamic Therapy for Glioma: Research involving 16:0 Lyso PC in the context of biohybrid systems for light-activatable treatments showcases its application in medical therapies, particularly for treating challenging conditions like glioma through photodynamic therapy, underlining its potential in enhancing clinical outcomes (Inglut et al., 2019).

Packaging

20 mL Clear Glass Screw Cap Vial (855675P-1g)
20 mL Clear Glass Screw Cap Vial (855675P-500mg)
5 mL Amber Glass Screw Cap Vial (855675P-200mg)
5 mL Amber Glass Screw Cap Vial (855675P-25mg)

Legal Information

Avanti Research is a trademark of Avanti Polar Lipids, LLC

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Xinyuan Li et al.
Redox biology, 28, 101373-101373 (2019-11-16)
It has been shown that anti-inflammatory cytokines interleukin-35 (IL-35) and IL-10 could inhibit acute endothelial cell (EC) activation, however, it remains unknown if and by what pathways IL-35 and IL-10 could block atherogenic lipid lysophosphatidylcholine (LPC)-induced sustained EC activation; and
Takafumi Enomoto et al.
Langmuir : the ACS journal of surfaces and colloids, 34(3), 750-755 (2017-10-06)
A major goal of synthetic biology is the development of rational methodologies to construct self-assembling non-natural membranes, which could enable the efficient fabrication of artificial cellular systems from purely synthetic components. However, spatiotemporal control of artificial membrane formation remains both
Li V Yang et al.
Blood, 105(3), 1127-1134 (2004-09-24)
G2A is a G-protein-coupled receptor (GPCR) involved in immune regulation. Previous studies have shown that lysophosphatidylcholine (LPC), a bioactive lipid associated with atherosclerosis and autoimmunity, acts through G2A to induce diverse biologic effects. Production of LPC during cell apoptosis serves
Caius G Radu et al.
Proceedings of the National Academy of Sciences of the United States of America, 101(1), 245-250 (2003-12-19)
G2A is an immunoregulatory G protein-coupled receptor predominantly expressed in lymphocytes and macrophages. Ectopic overexpression studies have implicated G2A as a receptor for the bioactive lysophospholipid, lysophosphatidylcholine (LPC). However, the functional consequences of LPC-G2A interaction at physiological levels of receptor
Anthony J Valente et al.
Free radical biology & medicine, 70, 117-128 (2014-02-25)
Oxidized low-density lipoprotein (oxLDL) induces endothelial cell death through the activation of NF-κB and AP-1 pathways. TRAF3IP2 is a redox-sensitive cytoplasmic adapter protein and an upstream regulator of IKK/NF-κB and JNK/AP-1. Here we show that oxLDL-induced death in human primary

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