Gefitinib (GFT) is a tyrosine kinase inhibitor used to treat advanced and metastatic non-small cell lung cancer. It is metabolized via CYP3A4 to form a variety of derivatives including the phenolic metabolites O-desmorpholinopropyl gefitinib (GFT-M1) and O-desmethyl gefitinib (GFT-M2). Both the drug and its metabolites have recently revealed to be phototoxic; the associated mechanism is related with the excited species that are formed upon irradiation of the supramolecular drug or metabolite@protein complexes with UVA light.1, 2
The photobehavior of GFT, GFT-M1 and GFT-M2 has been investigated in solution and in the presence of transport proteins of human plasma, i. e. serum albumin (HSA) and α1-acid glycoprotein (HAG). To this end, fluorescence spectroscopy, both in the steady-state and time-resolved modes, in addition to transient absorption spectroscopy have been used.
In general, excitation of the drug or its metabolites led to formation of locally excited (LE) states in non-polar organic solvents, whereas intramolecular charge transfer (ICT) states are formed in polar ones. By contrast, a different behavior has been observed in the confined environment provided by the protein. For GFT in complex with HSA or HAG, LE singlet states are mainly formed. However, since GFT-M1 is a phenol, excited state proton transfer (ESPT) to form phenolate-like excited species might become an alternative deactivation pathway in HSA. Conversely, locally excited (LE) states were also formed within HAG. The reserve was true for GFT-M2, which despite being also a phenol, led mainly to formation of LE states within HSA, and phenolate-like species (with a minor contribution of LE) inside HAG.1-3
The experimental findings are satisfactorily explained by molecular dynamics (MD) simulations. In general, the differences observed in the photobehavior of the drug and its two photoactive metabolites in protein media are consistent with their relative photosensitizing potentials.