Copper complexes as therapeutic agents

Abstract

The importance of transition metals in biological processes has been well established. Copper (Cu) is a transition metal that can exist in oxidised and reduced states. This allows it to participate in redox and catalytic chemistry, making it a suitable cofactor for a diverse range of enzymes and molecules. Cu deficiency or toxicity is implicated in a variety of pathological conditions; therefore inorganic complexes of Cu have been investigated for their therapeutic and diagnostic potential. These Cu complexes have been shown to be effective in cancer treatment due to their cytotoxic action on tumour cells. Alternatively, Cu complexes can also modulate Cu homeostasis in the brain, resulting in protective effects in several models of neurodegeneration. In other diseases such as coronary heart disease and skin disease, the success of Cu complexes as potential therapeutics will most likely be due to their ability to increase SOD activity, leading to relief of oxidative stress. This review seeks to provide a broad insight into some of the diverse actions of Cu complexes and demonstrate the strong future for these compounds as potential therapeutic agents.

Transition Metal Complexes with 1‐Adamantoyl Hydrazones – Cytotoxic Copper(II) Complexes of Tri‐ and Tetradentate Pyridine Chelators Containing an Adamantane Ring System

“…[1,2] Numerous Cu II complexes with potent acylhydrazone chelators have been synthesized and tested for their antitumor activity. A series of salicylaldehyde pyrazole hydrazones and related copper(II) complexes induce apoptosis in A549 lung carcinoma cells.…”

Gold(I) NHC-based homo- and heterobimetallic complexes: synthesis, characterization and evaluation as potential anticancer agents

“…The gold(I) mono-and polynuclear compounds were also shown to be potent TrxR inhibitors in the nM range in vitro. In the case of the mononuclear Cu(II) complex 6 the fact that there is no correlation between its marked cytotoxic activity and the poor TrxR inhibition is not unexpected, since other mechanisms are known to be responsible for Cu(II) complex cytotoxic effects, including the inhibition of protein tyrosine phosphatases [66] and the influence on cell redox pathways, [67,68] as well as DNA damage [69].…”

Cu2+-RGDFRGDS: exploring the mechanism and high efficacy of the nanoparticle in antithrombotic therapy

“…12 Cu 2+ complexes are potential therapeutics in coronary heart disease due to their ability to increase superoxide dismutase (SOD) activity and relax oxidative stress. 13 The investigations of complexes of Cu 2+ and peptide have been correlated with nanoscale self-assembly, bioactivity, and with positron emission tomography (PET) images of arterial thrombosis. [14][15][16][17][18][19][20][21] Recently, three Cu(II)-complexes, Cu(II)-Arg-Gly-Asp-Ser-Arg-Gly-Asp-Ser (Cu(II)-4a), Cu(II)-Arg-Gly-Asp-Val-Arg-Gly-Asp-Val (Cu(II)-4b), and Cu(II)-Arg-Gly-Asp-Phe-Arg-Gly-Asp-Phe (Cu(II)-4c), were synthesized, 22 consisting of octapeptides with two repeated RGD-peptides; among the three, it was revealed that Cu(II)-4a and Cu(II)-4c possessed the highest in vitro and in vivo activities, respectively.…”