Abstract

A study of the electrochemical behavior of a series of antimetastatic mono- and di-ruthenium complexes, namely [Na][ trans-Ru IIICl 4(DMSO)(L)] and [Na] 2[{ trans-Ru IIICl 4(DMSO)} 2(μ-L)], L = pyrazine (pyz), pyrimidine (pym), 4,4′-bipyridine (bipy), and 1,2-bis-(4-pyridyl)ethylene (etbipy), is reported. The results obtained show that in all dimeric Ru(III) complexes linked by heterocyclic non-chelating N-donor bridges, the two redox centers behave independently (with no remarkable electrochemical interaction), thus conferring no advantage in the likely hypothesis they act as pro-drugs (activation by reduction). Moreover, electrochemical evaluation of interaction between albumin and the title complexes confirms that this protein can act as the vehicle for drugs of this type in blood.

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