Atherosclerotic vascular disease, comprising heart attacks, stroke, aortic aneurysms, and peripheral vascular disease, is the most frequent cause of death in the Western world.

Plasma and Red Blood Cell Membrane Accretion and Pharmacokinetics of RT001 (bis-Allylic 11,11-D2-Linoleic Acid Ethyl Ester) during Long Term Dosing in Patients.

The infantile neuroaxonal dystrophy rating scale (INAD-RS). INAD is an autosomal recessive neurogenetic disorder caused by biallelic pathogenic variants in PLA2G6. The downstream enzyme, iPLA2, plays a critical role in cell membrane homeostasis by helping to regulate levels of phospholipids.

Site-specifically deuterated essential lipids as new drugs against neuronal, retinal and vascular degeneration. An original approach to drug discovery and development is now in clinical and preclinical trials. The approach is based on the ‘kinetic isotope effect’ (i.e., the effect of isotopic substitution on chemical reaction rates).

Alpha synuclein aggregation drives ferroptosis: an interplay of iron, calcium and lipid peroxidation. Protein aggregation and abnormal lipid homeostasis are both implicated in neurodegeneration through unknown mechanisms. Here we demonstrate that aggregate-membrane interaction is critical to induce a form of cell death called ferroptosis.

Treatment of infantile neuroaxonal dystrophy with RT001: A di-deuterated ethyl ester of linoleic acid: Report of two cases. Infantile neuroaxonal dystrophy (INAD) is a rare, autosomal recessive disease due to defects in PLA2G6 and is associated with lipid peroxidation.

The natural history of infantile neuroaxonal dystrophy. Infantile neuroaxonal dystrophy (INAD) is a rapidly progressive neurodegenerative disorder of early onset causing premature death. It results from biallelic pathogenic variants in PLA2G6, which encodes a calcium-independent phospholipase A2.

Polyunsaturated Fatty Acid Deuteration against Neurodegeneration. Oxidative stress is a common feature of genetic and idiopathic neurological diseases that thus far have been intractable to drug therapy. Polyunsaturated fatty acids (PUFAs) form cellular, mitochondrial, retinal, and other membranes highly important in neuronal function.

Deuterated Polyunsaturated Fatty Acids Reduce Oxidative Stress and Extend the Lifespan of C. elegans. Chemically reinforced essential fatty acids (FAs) promise to fight numerous age-related diseases including Alzheimer’s, Friedreich’s ataxia and other neurological conditions.

RT001 to treat neurodegeneration—Case Study: Improvement in a single patient with Late Onset Tay-Sachs Disease (LOTS). Objective: We report on the use of RT001 in a single patient with LOTS.

Threshold Protective Effect of Deuterated Polyunsaturated Fatty Acids on Peroxidation of Lipid Bilayers. Polyunsaturated fatty acids (PUFAs) are essential components of lipid membranes, providing them with necessary fluidity. However, the very motif that makes PUFAs ‘fluid’ – the ‘skipped’ 1,4‐diene moiety – also makes PUFAs susceptible to lipid peroxidation (LPO).