The ability to image caspase activation provides a powerful tool for the evaluation of the oncologic therapeutic response via the apoptotic cascade. Research efforts have focused on the development of radiolabelled non-peptidyl caspase inhibitors to be utilised for imaging purposes. Isatin sulfonamides are of particular interest because of their specificity and potency for inhibiting the 'apoptotic executioner' caspase-3. However, imaging attempts using the radiolabelled lead isatin have shown low target-to-background radiotracer uptake. The research aim was to explore alternative series of caspase-3 inhibitors as radioligands with optimal properties for the PET imaging of apoptosis. The series based on the pyrimidoindolone, triazoleindolone and imidazoleindolone heterocycles are structurally similar to the isatin core heterocycle, with all containing the crucial ketone responsible for caspase inhibition via the formation of a thiohemiketal with an active site cysteine residue. Using computational modelling studies combined with UV-vis titrations, these heterocycles were shown to have the propensity to favourably form thiohemiketals and therefore potentially inhibit caspase-3. Initial target structures, modelled on the structure of the lead isatin, were subsequently designed for synthesis and biological characterisation. Pyrimidoindolone target was synthesised and radiolabelled using modified literature conditions. Biological results showed the pyrimidoindolone to have a similar biological profile to isatin. Four different synthetic strategies were investigated for the synthesis of the imidazoleindolone and triazoleindolone heterocycles including, the use isatin sulfonamide intermediates, an intramolecular SNAr cyclisation process, Friedel-Crafts cyclisation method and nucleophilic addition to a benzonitrile. Preparation of imidazoleindolone was achieved with the SNAr cyclisation route. Preparation of triazoleindolone proved challenging with synthesis of only the core heterocyclic precursors, hydrazone and ketal achieved using the SNAr cyclisation route. Acid-sensitivity of the ring system hindered deprotection reactions and led to ring destruction.