Levuglandins are reactive aldehydes formed by the spontaneous rearrangement of prostaglandin H (PGH).

Enantiomerically pure levuglandin (LG) E2 can also be formed through the cyclooxygenase (COX) pathway by a rearrangement of the prostaglandin (PG) endoperoxide PGH 2.

[2][3] Levuglandins and isolevuglandins can damage proteins by covalent adduction, thereby interfering with their normal functions.

Elevated plasma levels of isoLG-protein epitopes are associated with atherosclerosis but are independent of total cholesterol, a classical risk factor.

[4][5] Prof. Robert Salomon at Case Western Reserve University discovered that a novel alternative rearrangement also occurs that producing two γ-ketoaldehydes[6] and named them levuglandins LGD2 and LGE2 as they are derivatives of levulinaldehyde with prostanoid side chains.