Mechanism of action<unk>  produces its anti-cancer effects by interfering with DNA replication and damaging the DNA in a cell. The DNA damage induces cell cycle arrest and cellular apoptosis via the accumulation of cytosolic p53 and subsequent activation of Bcl-2-associated X protein, an apoptosis promoter.<unk>  alkylates and cross-links DNA during all phases of the cell cycle, inducing DNA damage via three different methods of covalent adduct generation with double-helical DNA: # Attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA. # DNA damage via the formation of cross-links which prevents DNA from being separated for synthesis or transcription. # Induction of mispairing of the nucleotides leading to mutations. The precise mechanisms by which<unk>  acts to kill tumor cells are not yet completely understood. Limitations to bioavailability A recent study has shown<unk>  to be detoxified by human glutathione transferase Pi (GST P1-1), an enzyme that is often found over-expressed in cancer tissues. This is important since<unk> , as an electrophile, is made less reactive by conjugation with glutathione, thereby making the drug less toxic to the cell. 800x291px Shown above,<unk>  reacts with glutathione as catalyzed by hGSTA 1-1 leading to the formation of the monoglutathionyl derivative of<unk> .
Chlorambucil
Tioguanine
Indolocarbazole
Periciazine
Hydroxycarbamide
Vindesine
Tipiracil
Milbemycin