The cobalt(II) complex salts [Co(bpy)(az)2](PF6)2 and [Co(az)4](PF6), each bearing the unusual cis-N,N′-diphenylazodioxide ligand, were both screened as possible anticancer agents against SK-HEP-1 liver cancer cells. Both compounds were found to induce substantial apoptosis as an increasing function of concentration and time. Measurement of apoptosis-related proteins indicated that both the extrinsic and intrinsic pathways of apoptosis were activated. The apoptotic activity induced by these salts is not displayed either by simple cobalt(II) salts or complexes or by the free nitrosobenzene ligand. Additionally, these compounds did not induce apoptosis, as assessed by poly(adenosine diphosphate-ribose) polymerase cleavage, in several other cell lines.

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Removal of chloride from CoCl 2 with TlPF 6 in acetonitrile, followed by addition of excess nitrosobenzene, yielded the eight-coordinate cobalt(II) complex salt [Co{Ph(O)NN(O)Ph} 4 ](PF 6 ) 2 , shown by single-crystal X-ray analysis to have a distorted tetragonal geometry. The analogous treatment of the bipyridyl complex Co(bpy)Cl 2 yielded the mixed-ligand cobalt(II) complex salt [Co(bpy){Ph(O)NN(O)Ph} 2 ](PF 6 ) 2 , whose single-crystal X-ray structure displays a trigonal prismatic geometry, similar to that of the iron(II) cation in the previously known complex salt [Fe{Ph(O)NN(O)Ph} 3 ](FeCl 4 ) 2 . The use of TlPF 6 to generate solvated metal complex cations from chloride salts or chlorido complexes, followed by the addition of nitrosobenzene, is shown to be a useful synthetic strategy for the preparation of azodioxide complex cations with the noncoordinating, diamagnetic PF 6 – counteranion. Coordination number appears to be more important than d electron count in determining the geometry and metal–ligand bond distances of diphenylazodioxide complexes.

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Genomic aberrations comprise hallmarks of multiple myeloma (MM), a plasma cell malignancy with an overall poor prognosis. MM is heterogeneous and has different molecularly-defined subtypes according to varying clinical and pathological features. Hyperdiploidy or non-hyperdiploidy has usually been identified as early initiating genetic events that can be followed by secondary aberrations, including copy number changes, secondary translocations, and different epigenetic modifications, which cause immortalization of plasma cell and disease progression. Even though recent advances in drug discovery have offered new perspectives of treatment, MM remains incurable. However, understanding the molecular complexity of MM would allow patients to get precision treatment. Our review focuses on current evidence in myeloma biology with special attention to genomic and molecular variations.