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710332C

Avanti

14:0 Cardiolipin (ammonium salt)

1′,3′-bis[1,2-dimyristoyl-sn-glycero-3-phospho]-glycerol (ammonium salt), chloroform

Synonym(s):

1,1′,2,2′-tetramyristoyl cardiolipin (ammonium salt); 1,1′,2,2′-tetratetradecanoyl cardiolipin (ammonium salt); CL(1′-[14:0/14:0],3′-[14:0/14:0])

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About This Item

Empirical Formula (Hill Notation):
C65H132N2O17P2
CAS Number:
63988-20-5
Molecular Weight:
1275.69
UNSPSC Code:
51191904
NACRES:
NA.25

Assay

>99% (TLC)

form

solution

packaging

pkg of 1 × 2.5 mL (710332C-25mg)

manufacturer/tradename

Avanti Research™ - A Croda Brand 710332C

concentration

10 mg/mL (710332C-25mg)

lipid type

phospholipids
cardiolipins

shipped in

dry ice

storage temp.

−20°C

General description

14:0 Cardiolipin is an acidic phospholipid. Structurally, cardiolipin comprises three glycerol moieties and four acyl chains and is localized in the inner membrane of mitochondria. 14:0 Cardiolipin contains four myristic acid as acyl chain.

Application

14:0 Cardiolipin (1′,3′-bis[1,2-dimyristoyl-sn-glycero-3-phospho]-glycerol (ammonium salt)) has been used:
  • as a standard in tandem mass spectrometry
  • in the preparation of membrane proximal region (MPR) of human immunodeficiency virus (HIV-1) glycoprotein 41 (gp41)-lipopeptide conjugate and liposomes
  • as a component of micelle for suspending C8 ceramide substrate in ceramide kinase assay

Biochem/physiol Actions

Cardiolipin (CL) plays a key role in oxidative phosphorylation. CL is essential for energy production and in the activation of apoptosis. Deficiency of CL is associated with the development of diabetes and age-related heart failure. Anomalies associated with CL composition is observed in Barth Syndrome (BTHS).

Packaging

5 mL Clear Glass Sealed Ampule (710332C-25mg)

Legal Information

Avanti Research is a trademark of Avanti Polar Lipids, LLC

Pictograms

Skull and crossbonesHealth hazard
GHS06,GHS08

Signal Word

Danger

Hazard Classifications

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

Target Organs

Central nervous system, Liver,Kidney

WGK

WGK 3

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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Ninus Simonzadeh
Journal of chromatographic science, 47(4), 304-308 (2009-05-02)
Phospholipids, such as 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC), and 1,1',2,2'-tetramyristoyl cardiolipin, along with cholesterol, form liposomes in aqueous media and have been investigated at NeoPharm (Lake Bluff, IL) as drug-delivery systems. To accurately assess the effectiveness of various formulations involving the use of
Anja Stulz et al.
Langmuir : the ACS journal of surfaces and colloids, 35(49), 16366-16376 (2019-11-12)
Most antimicrobial peptides (AMPs) and their synthetic mimics (SMAMPs) are thought to act by permeabilizing cell membranes. For antimicrobial therapy, selectivity for pathogens over mammalian cells is a key requirement. Understanding membrane selectivity is thus essential for designing AMPs and
Fang-Cheng Bi et al.
The Plant cell, 26(8), 3449-3467 (2014-08-26)
Arabidopsis thaliana plants that lack ceramide kinase, encoded by ACCELERATED CELL DEATH5 (ACD5), display spontaneous programmed cell death late in development and accumulate substrates of ACD5. Here, we compared ceramide accumulation kinetics, defense responses, ultrastructural features, and sites of reactive
Alicja Bukowska et al.
European journal of pharmacology, 869, 172875-172875 (2019-12-27)
There is growing evidence for the contribution of the activated coagulation factor X (FXa) in the development of chronic inflammatory lung diseases. Therefore, we aimed to investigate effects of exogenous FXa on mitochondrial and metabolic function as well as the
Anastacia M Garcia et al.
American journal of physiology. Heart and circulatory physiology, 318(4), H787-H800 (2020-02-15)
Despite advances in both medical and surgical therapies, individuals with single ventricle heart disease (SV) remain at high risk for the development of heart failure (HF). However, the molecular mechanisms underlying remodeling and eventual HF in patients with SV are
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