Abstract
Thymidine phosphorylase (TP) is an angiogenic growth factor and a target for anticancer drug design. Molecular modeling suggested that 2'-aminoimidazolylmethyluracils would be potent inhibitors of TP. The novel 5-halo-2-aminoimidazolylmethyluracils (4b/4c) were very potent inhibitors of E. coli TP (IC50 approximately 20 nM). Contrastingly, the corresponding 2'-nitroimidazolylmethyluracil (as bioreductively activated) prodrugs (3b/3c) were 1000-fold less active (IC50 22-24 microM). This approach may be used to selectively deliver TP inhibitors into hypoxic regions of solid tumors where TP is overexpressed.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Angiogenesis Inhibitors / chemical synthesis*
-
Angiogenesis Inhibitors / chemistry
-
Binding Sites
-
Enzyme Inhibitors / chemical synthesis*
-
Enzyme Inhibitors / chemistry
-
Escherichia coli / chemistry
-
Humans
-
Imidazoles / chemical synthesis*
-
Imidazoles / chemistry
-
Imidazoles / pharmacology
-
Models, Molecular
-
Structure-Activity Relationship
-
Thymidine Phosphorylase / antagonists & inhibitors*
-
Thymidine Phosphorylase / chemistry
-
Uracil / analogs & derivatives*
-
Uracil / chemical synthesis*
-
Uracil / chemistry
Substances
-
Angiogenesis Inhibitors
-
Enzyme Inhibitors
-
Imidazoles
-
Uracil
-
Thymidine Phosphorylase