The complete oxidation sequence of ruthenociphenol (1), an organometallic ruthenocene-based analogue of ferrocifens, a promising anticancer drug series, has been investigated by cyclic voltammetry. As for the unsubstituted ruthenocene, the oxidation of 1 produced the corresponding species 1(+), which engaged in a reversible dimerization reaction. The highest reversibility occurred in dichloromethane (DCM), a low-donor solvent, with the weakly coordinating supporting electrolyte anion B(C6F5)(4). Under these conditions, the addition of pyridine triggered a chemical sequence through which the hydroxyl group of electrogenerated 1(+) was ultimately converted into the phenoxy radical 2. Unlike analogue ferrocifen derivatives, 2 did not undergo a further electrochemical oxidation but engaged in coupling with 1(+). The slow deprotonation of the resulting species appeared to be the key step leading to the quinone methide 3 after sluggish electron transfer. Again, in contrast with the ferrocifen series, 3 was not the final and stable complex of this oxidation sequence. It was indeed shown that the quinone methide spontaneously underwent a further oxidative evolution under our conditions. This led to a five-membered-ring closure and regeneration of the phenolic species 4, which could be further oxidized irreversibly, leading presumably to the new quinone methide 6. Such distinct behavior in comparison to ferrocene analogues may explain the different cytotoxic activities observed against hormone-independent breast cancer cells for ruthenocifens and ferrocifens.