IROXANADINE, a pyridine derivative, is under development for the treatment of atherosclerosis and the complications of atherosclerosis such as ischaemic heart disease, peripheral arterial disease, and restenosis. It induces phosphorylation of p38 stress-activated protein kinase, which plays an important role in endothelial cells (EC) homeostasis. EC function plays a central role in vascular diseases.

Oxfenicine is a CPT-1b-specific inhibitor. It must be transaminated to its active form, 4-hydroxyphenyl-glyoxylate, which is competitive with carnitine, preventing the formation of acylcarnitine. Because CPT-1b shows the highest sensitivity to 4-hydroxyphenyl-glyoxylate, inhibition of fatty acid oxidation by oxfenicine takes place selectively in those tissues that express this CPT isoform. It may be effective for treating noninsulin-dependent diabetes mellitus which is characterized by elevated fatty acid levels and obesity. In 1980 it was also tested in preclinical models of angina pectoris and ischemia.

Meldonium (3-(2,2,2-trimethylhydrazinium)propionate; MET-88; quaterine, trade-named as Mildronate) is an antiischemic drug developed at the Latvian Institute of Organic Synthesis. It is a clinically used in the treatment of heart failure, myocardial infarction, arrhythmia, atherosclerosis, and diabetes. Mechanism of action is based on the regulation of energy metabolism pathways through l-carnitine lowering effect. L-Carnitine biosynthesis enzyme γ-butyrobetaine hydroxylase and carnitine/organic cation transporter type 2 (OCTN2) are the main known drug targets of meldonium, and through inhibition of these activities, meldonium induces adaptive changes in the cellular energy homeostasis. Since L-carnitine is involved in the metabolism of fatty acids, the decline in its levels stimulates glucose metabolism and decreases concentrations of l-carnitine related metabolites, such as long-chain acylcarnitines and trimethylamine-N-oxide. Meldonium is used in neurological clinics for the treatment of brain circulation disorders. It appears to improve patients' mood; they become more active, their motor dysfunction decreases, and asthenia, dizziness, and nausea become less pronounced. CNS effects of Meldonium could be mediated by stimulation of the nitric oxide production in the vascular endothelium by modification of the gamma-butyrobetaine and its esters pools. It is hypothesized that mildronate may increase the formation of the gamma-butyrobetaine esters. Meldonium was on the World Anti-Doping Agency’s (WADA) list of drugs being monitored until September 2015, when it was added to the list of banned substances, effective January 1, 2016.