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To further define the pharmacological profile of PF-06882961, we sought to determine its binding affinity using radioligand binding assays

Steady state cellular concentrations (M) and reaction velocities (M/hr) as S varies

Further investigation revealed that the IC50 concentration of CGA, through the depletion of free iron within hepatocytes, significantly reduced the expression of iron-sulfur cluster subunits in mitochondrial complexes I-III and disrupted the oxidative-reductive homeostasis of hepatocytes, ultimately leading to hepatotoxicity

Interestingly, the bis(trifluoromethyl) substitution of thioamide 5b decreased the JAK3 inhibition

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