Cell viability experiments for compound 4 and TCMDC-135051 (1) were conducted using human hepatocyte-like HepG2 cells, and both demonstrated low toxicity. HepG2 cells originate from the liver, which is particularly relevant for malaria given this is where the exo-erythrocytic cycle takes place. Targeting the stage in the parasite life cycle that invades the liver is important to deliver a prophylactic treatment for malaria. Chloroacetamide 4 only fully inhibited metabolic activity of HepG2 cells at the highest concentration assessed (300 μM) (log[I] = -3.5, Fig. ), with solubility issues restricting exposure to higher concentrations. While an accurate pEC50 could not therefore be calculated, this data demonstrates chloroacetamide 4 to be much less cytostatic than TCMDC-135051 (1) with pEC50 = 5.8. This is hypothesised to be explained in part by the increase in kinase selectivity afforded by targeting Cys368. Compound 4 therefore demonstrates an excellent selectivity index for 3D7 parasites over human cells, potentially representing a very large therapeutic window.