Cisplatin-based combination chemotherapies are used in the daily clinical routine against a variety of tumours. However, intrinsic and acquired resistance, as well as adverse effects limit their application. To avoid these problems several novel metal-based anticancer drugs have been investigated. In this study we focused on KP1537 and KP1691, two novel analogues of the approved drug oxaliplatin, and on KP46, a novel gallium complex. Aim of the study was to determine the in vitro and in vivo anticancer properties and the underlying molecular mechanisms with respect to the structure-activity-relationship in case of the oxaliplatin analogues. Moreover, we were interested in how far drug-resistance mechanisms may limit their application in the clinics. In the first part of the thesis it could be shown that KP1537 and KP1691 displayed, beside several comparable activities with its parental compound, improved anticancer characteristics. The analogues were less vulnerable to resistance mechanisms including p53 mutations, less dependent on immunogenic cell death, and displayed a broader therapeutic window with significant reduced adverse effects, such as weight loss and cold hyperalgesia. Beside this, KP1537 was more active against a leukaemia xenograft mouse model than oxaliplatin. Furthermore, drug accumulation was distinctly influenced by the substitution and stereoisomerism of the methyl group. Studies on the resistance profile of the platinum drugs revealed that different mechanisms were developed to cope with the platinum drugs. Apart from an impact of p53 on the level of genomic or epigenetic changes, a deletion in DEPDC-1B in the p53/ko oxR3 and an amplicon in Notch1 in the p53/ko oxR2 cell models were found. Both were confirmed by further molecular studies. With regard to KP46, in vivo anticancer activity against a solid tumour model could be proven. Furthermore, the study elucidated a novel mechanism contributing to the anticancer activity of KP46. The gallium complex induced disassembly of adhesion complexes, rapid cell rounding, de-attachment and an activation of Bax and cell death, by a mechanism involving calpain. Consequently, co-incubation with a calpain inhibitor could reverse the anticancer activity of KP46. Summarizing, this study demonstrated that the investigated substances harbour characteristics which qualify them for further (pre-) clinical development.