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Increase in renal glutathione in cholestatic liver disease is due to a direct effect of bile acids | American Journal of Physiology-Renal Physiology | American Physiological Society

and coworkers discovered that inhA —which they also found to encode an NADH-specific enoyl-acyl carrier protein reductase—as isoniazid's primary target [31] [29] : 7 The isoniazid-NAD adduct was also shown to bind and inhibit InhA, the protein product of inhA

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COA, HPLC/MS, salt form, and blend document review is treated as search context, not as a protocol or outcome claim