There has been an intense renewal of interest in primaquine (PQ) after over 60 years since its introduction into clinical medicine [1, 2]. This is understandably so because, despite spirited research efforts, no suitable alternative has yet been approved to rival the unique therapeutic profile of PQ. As the prototype 8-aminoquinoline (8-AQ), PQ is the only licensed drug capable of treating the relapsing liver stages (hypnozoites) of Plasmodium vivax . It is gametocytocidal against Plasmodium falciparum and capable of blocking transmission. Additionally, PQ has been used as a prophylactic option against all forms of malaria . It has found use in the treatment of artemisinin-resistant P. falciparum strains . The major limitation in the clinical utility of PQ is its haemolytic toxicity in individuals with genetic deficiency in glucose-6-phosphate dehydrogenase (G6PD). Both the therapeutic and haemotoxic effects of PQ have been strongly linked to its metabolite(s) [6–8]. While a number of human metabolites of PQ have been described , the identity of the specific PQ metabolites responsible for efficacy and toxicity are not well understood .