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Literature summary extracted from

  • Garcia-Garcia, H.M.; Serruys, P.W.
    Phospholipase A2 inhibitors (2009), Curr. Opin. Lipidol., 20, 327-332.
    View publication on PubMed

Application

EC Number Application Comment Organism
3.1.1.4 drug development sPLA2s and Lp-PLA2 inhibitors darapladib and varespladib emerge as promising therapeutical options for treating patients with coronary artery disease. Lp-PLA2 inhibition may favorably affect rupture-prone lesions Homo sapiens
3.1.1.4 medicine combination of sPLA2 activity and cardiovascular reactive protein values is more useful to detect incident risk of coronary artery disease than either biomarker alone. Prognostic value of plasma concentrations and activity of Lp-PLA2 in patients with coronary heart disease Homo sapiens

Inhibitors

EC Number Inhibitors Comment Organism Structure
3.1.1.4 (3-aminooxalyl-1-benzyl-2-ethyl-6-methyl-1H-indol-4-yl)oxyacetic acid methyl ester LY374388, potent sPLA2 inhibitor Homo sapiens
3.1.1.4 1-H-indole-3-glyoxamide varespladib methyl, potent sPLA2 inhibitor Homo sapiens
3.1.1.4 3-[1-benzyl-3-(carbamoylmethyl)-2-ethylindol-5-yl]oxypropylphosphonic acid LY311727, potent sPLA2 inhibitor Homo sapiens
3.1.1.4 darapladib inhibits Lp-PLA2 activity by 59% Homo sapiens
3.1.1.4 darapladib reduces development of advanced coronary atherosclerosis in diabetic and hypercholesterolemic swine, specifically reduces plaque area and necrotic core area and medial destruction, resulting in fewer lesions with an unstable phenotype Sus scrofa
3.1.1.4 indoxam most potent sPLA2 inhibitor Homo sapiens
3.1.1.4 Me-Indoxam most potent sPLA2 inhibitor Homo sapiens
3.1.1.4 additional information substituted indoles and indolizines are the most potent sPLA2 inhibitors Homo sapiens
3.1.1.4 rilapladib
-
 Sus scrofa
3.1.1.4 sodium 2-(1-benzyl-2-ethyl)-3-oxamoylindol-4-yl oxyacetate varespladib sodium or LY315920, most potent sPLA2 inhibitor Homo sapiens

Organism

EC Number Organism UniProt Comment Textmining
3.1.1.4 Homo sapiens
-
-
-
3.1.1.4 Sus scrofa
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
3.1.1.4 inflammatory cell Lp-PLA2, cells involved in atherogenesis Homo sapiens
-
3.1.1.4 additional information Lp-PLA2 in pathologic intimal thickening plaques is nearly absent Homo sapiens
-
3.1.1.4 myocardium sPLA2 present in the limits of the infarcted myocardium Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3.1.1.4 phospholipids + H2O Lp-PLA2 rapidly degrades oxidatively modified phospholipids in modified low density lipoprotein leading to formation of proinflammatory and cytotoxic products (i.e. lysophosphatidylcholine) and oxidized nonesterified fatty acids Homo sapiens ?
-
 ?

Synonyms

EC Number Synonyms Comment Organism
3.1.1.4 lipoprotein-associated phospholipase A2
-
 Sus scrofa
3.1.1.4 lipoprotein-associated phospholipase A2 Lp-PLA2 Homo sapiens
3.1.1.4 Lp-PLA2
-
 Homo sapiens
3.1.1.4 Lp-PLA2
-
 Sus scrofa
3.1.1.4 PAF-AH
-
 Sus scrofa
3.1.1.4 PAF-AH Lp-PLA2 Homo sapiens
3.1.1.4 phospholipase A2
-
 Homo sapiens
3.1.1.4 phospholipase A2
-
 Sus scrofa
3.1.1.4 platelet-activating factor acetylhydrolase
-
 Sus scrofa
3.1.1.4 platlet-activating factor acetylhydrolase Lp-PLA2 Homo sapiens
3.1.1.4 secreted PLA2 sPLA2 Homo sapiens
3.1.1.4 sPLA2
-
 Homo sapiens
3.1.1.4 sPLA2-IIA sPLA2 Homo sapiens
3.1.1.4 type VIIA PLA2
-
 Sus scrofa
3.1.1.4 type VIIA PLA2 Lp-PLA2 Homo sapiens

Expression

EC Number Organism Comment Expression
3.1.1.4 Homo sapiens Lp-PLA2 is highly expressed in the necrotic core of atherosclerotic lesions up

General Information

EC Number General Information Comment Organism
3.1.1.4 metabolism sPLA2s and Lp-PLA2 produce biologically active metabolites that are involved in several phases of the atherosclerosis process Homo sapiens
3.1.1.4 physiological function sPLA2s (sPLA2-IIA) and Lp-PLA2 are associated with atherogenesis and its complications. Increased levels of these two phospholipases are related with an increase in complex coronary lesions and increase in major cardiovascular clinical events, respectively. sPLA2 may play an important role in atherogenesis by modifying low density lipoprotein particles in the arterial wall, thereby enhancing their aggregation, retention, and macrophage uptake. Cytotoxic compounds from Lp-PLA2 play an important in plaque vulnerability, Lp-PLA2 has a predominantly proinflammatory role in atherogenesis Homo sapiens