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For de novo NADPH synthesis pathway, correlation studies have revealed that thionicotinamide adenine dinucleotide (NADS) and thionicotinamide adenine dinucleotide phosphate (NADPS), converted from the pro-drug thionicotinamide (TN), act as inhibitors of NADKs through targeting the NAD-binding site of NADKs and decreasing the levels of NADPH

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We were therefore surprised to find that GSTP1 knockdown did not significantly influence cell growth rate or alter cell cycle progression in A2780 cells, although similar findings have been reported in a series of ovarian cancer cell lines made resistant to cisplatin, carboplatin and paclitaxel (Li et al, 2004), suggesting limitations of the use of immortalised cancer cell line models

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