| Clinical data | |
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| Routes of administration | Oral |
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| Chemical and physical data | |
| Formula | C20H34D2O2 |
| Molar mass | 310.5148 g/mol g·mol−1 |
  (what is this?) | |
‘’’RT100’’’ (also known as Di-deuterated ethyl linoleate; Di-deuterated linoleic acid ethyl ester, 11,11-D2-Ethyl Linoleate, Ethyl 11,11-D2-Linoleate)[1] is an experimental, orally-bioavailable synthetic deuterated polyunsaturated fatty acid (PUFA), an isotopologue of an essential omega-6 PUFA, linoleic acid. Pre-clinical studies reveal that the isotopologue compound, while identical to linoleic acid, is resistant to lipid peroxidation.
Clinical development edit
Investigations of 11,11-D2-Ethyl linoleate are being conducted by Retrotope, Inc in several neurological indications, including Friedreich’s ataxia and Infantile Neuroaxonal Dystrophy. The drug is delivered orally at several grams per day level, typically as gelatine softgel capsules.
Phase I/II edit
A double-blind, placebo (comparator)-controlled Phase I/II clinical trial, sponsored by Retrotope, Inc and Friedreich’s Ataxia Research Alliance (FARA),[2] was conducted to determine the safety profile of and appropriate dosing for consequent trials. RT001 promptly absorbed and was found to be safe and tolerable over 28 days at the maximal dose of 9.0 g/day. RT001 statistically improved peak workload in the drug group compared to comparator group (dosed with normal, non-deuterated ethyl linoleate). Other improvement trends were recorded for the drug group, such as peak oxygen consumption. Furthermore, clear correlations were observed between multiple progression parameters measured cross-sectionally across all patient encounters (comparisons of peak workload, VO2 peak, FARS Neuro Score, and T25FW showed consistent cross-correlation).
Phase III edit
Open label trial edit
Mechanism of action edit
RT001 is recognized by cells as identical to the natural linoleic acid. But when taken up, converted into 13,13-D2-arachidonic acid, a heavy isotope version of arachidonic acid and incorporated into lipid membranes, the compound resists the non-enzymatic lipid peroxidation (LPO) through a novel, non-antioxidant based mechanism, protecting mitochondrial, neuronal and other lipid membranes and greatly reducing the levels of numerous LPO-derived toxic products such as reactive carbonyls.[3]