since the molecular properties and structure with this enzyme are not well understood, specific approaches to modulation of ATE1 action and features in vitro and in vivo haven’t been undertaken before. A few natural and synthetic compounds that influence natural product libraries activity in different systems have been identified through the past studies of ATE1 controlled procedures, however many of them have none, or limited activity and none of the compounds have high specificity for ATE1 enzyme in cells. Tri peptide GluVal Phe can prevent arginylation by working as a substrate copy that saturates ATE1, making it unavailable for arginyl shift to its natural goals, however this peptide acts only at high concentrations and is not very successful in biological assays. Bifunctional phenylarsenoxide was shown to prevent ATE1 through interaction with reactive Cys residues in the critical roles within the molecule, however this inhibitor is not only hazardous but relatively non specific, as it exerts its effect likewise on all proteins whose activity is dependent on reactive Cys teams. ATE1 reaction is inhibited by heparin, a widely used anticoagulant, in vitro, perhaps through its motion on Arg tRNA synthetase which produces Arg charged tRNA used for arginyl transfer. Equally protease inhibitors indirectly restrict protein arginylation in brain extracts by interfering with the charging of tRNA. Finally, hemin, the Fe3 kind of heme, was shown to prevent Lymphatic system ATE1 and promote its degradation in cells through ubiquitin dependent proteolysis an indirect result, likely linked to hemins action on proteasome, and perhaps on RRS. Ergo, no natural or synthetic compounds are proven to date which may particularly modulate ATE1 activity and/or its intracellular functions. Here we report the development of a chemical assay for detection of small molecule inhibitors of ATE1 and program of this assay to screening of a molecule library of 3280 known chemicals. Our screen determined four elements that may specifically inhibit the experience of ATE1, including two compounds which specifically affect ATE1 controlled functions in cells. One of these substances tannic acid has been previously proven to prevent angiogenesis and protein degradation in mouse and cell models and to act as a treatment of heart disease and cancer and agent in prevention Cabozantinib clinical trial. Our data claim that these measures of tannic acid are mediated by its immediate impact on ATE1, which regulates protein degradation and angiogenesis in vivo. Deborah terminally arginylated b actin peptide RDDIAALC was used to raise polyclonal anti R b antibody in rabbits. Collection and immunizations of antisera were done by Sigma Genosys.