Levuglandins are reactive aldehydes formed by the spontaneous rearrangement of prostaglandin H (PGH). Enantiomerically pure levuglandin (LG) E<sub>2</sub> can also be formed through the cyclooxygenase (COX) pathway by a rearrangement of the prostaglandin (PG) endoperoxide PGH <sub>2</sub>. They are nonclassic eicosanoids. One species, levuglandin E<sub>2</sub>, (LGE<sub>2</sub>), forms neurotoxic adducts with amyloid beta. Levuglandins and isolevuglandins can damage proteins by covalent adduction, thereby interfering with their normal functions. These lipid-derived protein modifications may serve as dosimeters of oxidative injury. Elevated plasma levels of isoLG-protein epitopes are associated with atherosclerosis but are independent of total cholesterol, a classical risk factor.
Though spontaneous rearrangements of PGH2 are known to generate prostaglandins (PG) PGD2 and PGE2. Prof. Robert Salomon at Case Western Reserve University discovered that a novel alternative rearrangement also occurs that producing two ó-ketoaldehydes and named them levuglandins LGD2 and LGE2 as they are derivatives of levulinaldehyde with prostanoid side chains.