Species | Target name | Source | Bibliographic reference |
---|---|---|---|
Homo sapiens | dimethylarginine dimethylaminohydrolase 1 | Starlite/ChEMBL | No references |
Species | Potential target | Raw | Global | Species |
---|---|---|---|---|
Leishmania major | hypothetical protein, unknown function | 0.0198 | 0.5 | 0.5 |
Schistosoma mansoni | ngng-dimethylarginine dimethylaminohydrolase | 0.0198 | 0.5 | 0.5 |
Onchocerca volvulus | 0.0198 | 0.5 | 0.5 | |
Leishmania major | hypothetical protein, unknown function | 0.0198 | 0.5 | 0.5 |
Echinococcus multilocularis | ng dimethylarginine dimethylaminohydrolase | 0.0198 | 0.5 | 0.5 |
Loa Loa (eye worm) | hypothetical protein | 0.0198 | 0.5 | 0.5 |
Schistosoma mansoni | ngng-dimethylarginine dimethylaminohydrolase | 0.0198 | 0.5 | 0.5 |
Echinococcus granulosus | ng dimethylarginine dimethylaminohydrolase | 0.0198 | 0.5 | 0.5 |
Activity type | Activity value | Assay description | Source | Reference |
---|---|---|---|---|
IC50 (binding) | = 13100 nM | BindingDB_Patents: Inhibition Assay. The L-citrulline assay was based upon an original test-tube method developed by Prescott and Jones in 1969 (Prescott, L. M. & Jones, M. E. Modified methods for the determination of carbamyl aspartate. Anal Biochem 32, 408-419 (1969)), which was adapted and optimized for a microplate format. Subsequently, the activity of DDAH was quantified by detecting its conversion of ADMA to citrulline using the optimized protocol. The assay was scaled up to a 384-well format for high throughput chemical screening.High Throughput Screening of Small Molecules:Over 130,000 small molecules deposited in the Stanford High-throughput Bioscience Center (HTBC) were screened using the enzymatic assay to identify chemicals that regulate DDAH activity. In brief, recombinant human DDAH1 (rhDDAH1) was mixed with ADMA in the presence of screening buffer in 384-well plates using a Staccato multidrop. Small molecules (100 nL each) were then added to the wells using a robotic arrayer to yield a final compound screening. | ChEMBL. | No reference |
IC50 (binding) | = 13100 nM | BindingDB_Patents: Inhibition Assay. The L-citrulline assay was based upon an original test-tube method developed by Prescott and Jones in 1969 (Prescott, L. M. & Jones, M. E. Modified methods for the determination of carbamyl aspartate. Anal Biochem 32, 408-419 (1969)), which was adapted and optimized for a microplate format. Subsequently, the activity of DDAH was quantified by detecting its conversion of ADMA to citrulline using the optimized protocol. The assay was scaled up to a 384-well format for high throughput chemical screening.High Throughput Screening of Small Molecules:Over 130,000 small molecules deposited in the Stanford High-throughput Bioscience Center (HTBC) were screened using the enzymatic assay to identify chemicals that regulate DDAH activity. In brief, recombinant human DDAH1 (rhDDAH1) was mixed with ADMA in the presence of screening buffer in 384-well plates using a Staccato multidrop. Small molecules (100 nL each) were then added to the wells using a robotic arrayer to yield a final compound screening. | ChEMBL. | No reference |
IC50 (binding) | = 13.1 uM | Inhibition of recombinant human DDAH1 expressed in Escherichia coli BL21 Star (DE3) using ADMA as substrate assessed as decrease in citrulline production after 4 hrs by colorimetric method | PATENT. | No reference |
Many chemical entities in TDR Targets come from high-throughput screenings with whole cells or tissue samples, and not all assayed compounds have been tested against a single a single target protein, probably because they get ruled out during screening process. Even if these compounds may have not been of interest in the original screening, they may come as interesting leads for other screening assays. Furthermore, we may be able to propose drug-target associations using chemical similarities and network patterns.