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Cu-ATSM is a copper-containing compound with diverse biological activities.1,2,3 It inhibits ferroptotic cell death induced by RSL3, erastin (Item No. 17754), or iron(II) (EC50s = 134, 169, and 171 nM, respectively), as well as RSL3-, erastin-, or iron-induced lipid peroxidation in N27 rat mesencephalic cells when used at a concentration of 1 µM.1 Cu-ATSM (30 mg/kg per day) increases mutant superoxide dismutase (SOD1G37R) protein levels, metalation, and activity in the spinal cord in the SOD1G37R transgenic mouse model of amyotrophic lateral sclerosis (ALS).2 It also increases the number of α-motor neurons and reduces oxidatively modified proteins in the spinal cord, as well as increases the latency to fall in the rotarod test in the same ALS mouse model. Cu-ATSM containing positron-emitting copper isotopes has been used in PET imaging applications for selective labeling of hypoxic tissue.3
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1. Cu II (atsm) inhibits ferroptosis: Implications for treatment of neurodegenerative disease. Br. J. Pharmacol. 177(3), 656-667 (2020).
2. Oral treatment with CuII(atsm) increases mutant SOD1 in vivo but protects motor neurons and improves the phenotype of a transgenic mouse model of amyotrophic lateral sclerosis. J. Neurosci. 34(23), 8021-8031 (2014).
3. Cu-