Four new bis(N,N-dialkylbenzimidazol-2-ylidene)dichlorido platinum(ii) complexes 2 featuring N-alkyl substituents of increasing size (a: Me, b: Et, c: n-butyl, d: n-octyl) were synthesised and oxidised with PhICl2 to give the corresponding [PtIVCl4(N,N-dialkylbenzimidazol-2-ylidene)2] complexes 4 as potential anticancer prodrugs. The known bis(N,N-dibenzylimidazol-2-ylidene)dichlorido platinum(ii) complex 1 was likewise oxidised to [PtIVCl4(N,N-dibenzylimidazol-2-ylidene)2] 3. In contrast, oxidation of complexes 1 and 2 with H2O2 or hypochlorites, or exchange of chlorido for hydroxo ligands in tetrachlorido complexes 4 failed to give isolable complexes of type [PtIVCl4-n(OH)n(NHC)2]. In MTT assays the [PtIICl2(NHC)2]/[PtIVCl4(NHC)2] complex couples 1/3, 2c/4c, and trans-2c/trans-4c, bearing either N-benzyl or N-butyl substituents, each showed similar single-digit micromolar IC50 values against at least three out of five human cancer cell lines, presumably due to an intracellular reduction of the PtIV complexes to their active PtII congeners. Unlike cisplatin, whose anticancer effect requires functional p53, each of them was active both in wildtype and in p53-negative HCT116 colon carcinoma cells. In ethidium bromide saturation assays with isolated DNA, cis-(bis-NHC)PtII complexes such as 1 caused morphological DNA changes more pronounced than those initiated by cisplatin, while the corresponding cis-(bis-NHC)PtIV complexes such as 3 interacted with DNA in a less structure-modifying way.