Ischaemia modified albumin (IMA) is a recently developed biomarker of transient myocardial ischaemia.1 Circulating IMA is increased in patients with myocardial ischaemia, after percutaneous coronary intervention,2,3 or in acute coronary syndromes.4 The test has recently been licensed by the US Food and Drug Administration for diagnostic use in suspected myocardial ischaemia. IMA is serum albumin in which the N-terminus has been chemically modified. The diagnostic albumin Co2+ binding (ACB) test is based for IMA on the observation that the affinity of serum albumin for Co2+ is reduced after N-terminus modifications. It has been proposed that reactive oxygen species (ROS) such as superoxide (•O2−) and hydroxyl (•OH) radicals generated during myocardial ischaemia–reperfusion modify the N-terminus of serum albumin resulting in IMA formation but, so far, direct evidence to support this is scarce. We hypothesised that ROS generation causes the formation of IMA. Our objective was to model the formation of IMA in vitro by using chemically generated ROS and the •OH radical scavenger mercaptopropionylglycine (MPG).