The second pathway is the methylation of thioguanine to 2-amino-6-methylthiopurine, which is minimally effective as an anti-neoplastic and significantly less toxic than thioguanine.
12.
The second pathway is the methylation of thioguanine to 2-amino-6-methylthiopurine, which is minimally effective as an anti-neoplastic and significantly less toxic than thioguanine.
13.
Studies show that this protein provides resistance to thiopurine anticancer drugs, 6-mercatopurine and thioguanine, and the anti-HIV drug 9-( 2-phosphonylmethoxyethyl ) adenine.
14.
TPMT catalyzes the methylation of 6-mercaptopurine into the inactive metabolite 6-methylmercaptopurine-this methylation prevents mercaptopurine from further conversion into active, cytotoxic thioguanine nucleotide ( TGN ) metabolites.
15.
Thus, a cell lacking TK is resistant to bromodeoxyuridine ( BrdU ) and a cell lacking HGPRT is resistant to 6-thioguanine ( 6-TG ) and 8-azaguanine.
16.
However, the intra-cellular thio-nucleotide metabolites of thioguanine ( 6-TGN ) have longer half-lives and can therefore be measured after thioguanine is eliminated from the plasma.
17.
However, the intra-cellular thio-nucleotide metabolites of thioguanine ( 6-TGN ) have longer half-lives and can therefore be measured after thioguanine is eliminated from the plasma.
18.
Among these, albendazole, amoxicillin, amoxicillin-clavulanate, allopurinol, mercaptopurine, mupriocin, pyrimethamine, ranitidine, thioguanine, trimethoprim and zidovudine are listed on the World Health Organization's list of essential medications.
19.
The TPMT enzyme is responsible, in part, for the methylation of 6-MP into the inactive metabolite 6-methylmercaptopurine-this methylation prevents 6-MP from further conversion into active, cytotoxic thioguanine nucleotide ( TGN ) metabolites.
20.
The plasma half-life of thioguanine is short, due to the rapid uptake into liver and blood cells and conversion to 6-TGN . The median plasma half-life of 80-minutes with a range of 25 240 minutes.
