13-Methyltetradecanoic acid-d₆

Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs^[1].
13-Methyltetradecanoic acid (13-MTD; 0-140 μg/mL; 12-24 hours) inhibits cell viability and proliferation in human bladder cancer cells by inducing apoptosis^[2].
13-Methyltetradecanoic acid (13-MTD; 70 μg/mL; 2-48 hours) treatments results in significant accumulation of cells with sub-G1 DNA content in a time-dependent manner, with the proportion of sub-G1 phase DNA content ranging from 9.25% to 85.3% over 2-48 hours^[2].
13-Methyltetradecanoic acid (13-MTD; 70 μg/mL; 2-24 hours) down-regulates Bcl-2 and up-regulates Bax. This promotes mitochondrial dysfunction, leading to the release of cytochrome c from the mitochondria to the cytoplasm, as well as the proteolytic activation of caspases. 13-Methyltetradecanoic acid down-regulates AKT phosphorylation and activates phosphorylation of p38 and c-Jun N-terminal kinase (JNK)^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.