GGT6 Inhibitors

Ouabain is a cardiac glycoside that inhibits the Na+/K+ ATPase pump. GGT6 is a gamma-glutamyltransferase that may be influenced by cellular ionic balance alterations. Inhibition of the Na+/K+ pump by Ouabain could lead to intracellular sodium accumulation, indirectly inhibiting GGT6 by altering its substrate or product concentrations.

Acivicin is an inhibitor of gamma-glutamyltransferase enzymes. By binding to the active site of GGTs, it can block the enzyme's function, thereby inhibiting GGT6 by preventing the transfer of gamma-glutamyl functional groups.

L-azaserine is a glutamine antagonist that inhibits glutamine-utilizing enzymes. As GGT6 is involved in the metabolism of glutamine derivatives, inhibition of these pathways by L-azaserine could reduce the availability of GGT6's substrates, thereby inhibiting its activity.

DON is a glutamine analog that acts as an inhibitor of various glutamine-utilizing enzymes. By resembling glutamine, DON can inhibit GGT6 as the enzyme might bind DON instead of its natural substrates, leading to inhibition of its enzymatic activity.

Methotrexate is a dihydrofolate reductase inhibitor that affects purine and pyrimidine synthesis. While GGT6 is not directly involved in this pathway, the resulting imbalance in nucleotide pools could indirectly affect GGT6 activity by altering the cellular environment and availability of crucial co-factors.

BSO is an inhibitor of gamma-glutamylcysteine synthetase. It prevents the synthesis of glutathione, a substrate involved in the reaction catalyzed by GGT6, thereby inhibiting the function of GGT6 by depleting its substrate.

Vigabatrin is an irreversible inhibitor of GABA transaminase, which increases GABA levels. Elevated GABA can affect GGT6 activity by altering the enzyme's substrate availability or by changing the gamma-glutamyl cycle, where GGT6 is active.

Ethacrynic acid is a diuretic that inhibits glutathione S-transferases. Although a different class of enzymes, its effect on glutathione levels can indirectly affect GGT6 activity by modulating the concentration of substrates involved in GGT6-mediated reactions.

Cisplatin forms platinum-DNA adducts, which can lead to increased cellular stress and upregulation of glutathione metabolism. As GGT6 is part of glutathione metabolism, the altered levels of glutathione due to cisplatin could inhibit GGT6 activity by substrate depletion or feedback inhibition.

Levodopa is a precursor to dopamine and can influence amino acid metabolism, including glutamate and its derivatives. Since GGT6 is involved in gamma-glutamyl cycling and metabolism, changes in glutamate levels due to levodopa application could indirectly inhibit GGT6 activity.