For the SAR generated in this study to inform future pantothenamide design, it will be important to determine the extent to which they reflect relative efficacy against the target, relative cell permeabilities, relative rates of BTS 54-505 hydrochloride pantetheinase-mediated hydrolysis, and inactivation by other mechanisms including serum binding. In light of the demonstration in this study that pantothenamides are hydrolyzed by serum BADGE pantetheinase in vitro, it is likely that they will also be subject to pantetheinase-mediated hydrolysis in vivo, and thereby rendered ineffective as antiplasmodial agents in vivo. Consistent with this, compound 12 had little-to-no effect on parasite growth at concentrations up to in the presence of human serum. Therefore to exploit the antiplasmodial potency of pantothenamides it will be important to consider strategies for circumventing pantetheinase-mediated hydrolysis in vivo. This is also crucial for the future development of pantothenamides as antibacterial agents, as serum stability will be required for all but topical applications. One strategy is to develop antiplasmodial pantothenamide analogues that are resistant to degradation by pantetheinases by, for example, using a bioisosteric replacement strategy to replace the key hydrolyzable amide bond. Another strategy for circumventing pantetheinase-mediated pantothenamide hydrolysis in vivo is to simultaneously inhibit host pantetheinase. Recently, however, genetic studies in mice have provided evidence that a reduction in pantetheinase activity increases susceptibility to malaria, perhaps as a result of modulation of the inflammatory response. The design of pantetheinase-resistant pantothenamides may therefore be a preferable strategy for circumventing pantetheinase-mediated degradation. In conclusion, in this study we present, for the first time, analogues of pantothenate that inhibit growth of P. falciparum at sub-micromolar concentrations through inhibition of pantothenate and/or CoA utilization, and propose the identification of pantetheinase-resistant pantothenamide analogues as a viable strategy for the discovery of antimalarial agents. The more recently developed Chronic Kidney Disease Epidemiology Collaboration serum creatinine equation has been shown to improve accuracy of estimation of eGFR and of prediction of mortality risk and risk of progression to end stage kidney disease over the MDRD equation. As a result, the 2012 Kidney Disease Improving Global Outcomes recommendations advocate the routine use of the CKDEPI equation for reporting of eGFR as do the recently revised CKD guidelines from the UK National Institute of Health and Care Excellence. In a large retrospective study of routine creatinine requests, O��Callaghan et al showed that routine use of CKDEPI Scr equation in place of MDRD in a UK clinical biochemistry laboratory would result in a lower overall prevalence of CKD, but an increase in higher risk CKD stage 3�C5 among older people. However, the study was not able to derive population prevalence of CKD for each equation nor to assess proteinuria, an important independent risk factor.