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The inhibition of the enzyme TRXR is proposed to be due to the stronger binding of the gold(I) to the enzymes selenocysteine, but a theoretical study found the drug could bind favorably to cysteine as well [83, 85]

For instance, P115 and GRASP65 trigger apoptosis via the ERK/p53/PUMA pathway or Fas-mediated signaling, respectively, whereas Bruce and GAAP decrease apoptosis via caspase-9, Smac and p53 inhibition, and Ca 2+ signaling downregulation [93]

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