Species | Target name | Source | Bibliographic reference |
---|---|---|---|
Homo sapiens | cannabinoid receptor 1 (brain) | Starlite/ChEMBL | References |
Homo sapiens | cannabinoid receptor 2 (macrophage) | Starlite/ChEMBL | References |
Activity type | Activity value | Assay description | Source | Reference |
---|---|---|---|---|
Activity (functional) | = 95 % | Inverse agonist activity at human CB1 receptor by [35S]GTPgammaS incorporation assay relative to rimonabant | ChEMBL. | 19520572 |
EC50 (functional) | = 435 nM | Inverse agonist activity at human CB1 receptor expressed in HEK293 EBNA cells by [35S]GTPgammaS incorporation assay | ChEMBL. | 18083560 |
EC50 (functional) | = 435 nM | Inverse agonist activity at human CB1 receptor expressed in HEK293 EBNA cells by [35S]GTPgammaS incorporation assay | ChEMBL. | 18083560 |
EC50 (functional) | = 0.3 uM | Inverse agonist activity at human CB1 receptor by [35S]GTPgammaS incorporation assay | ChEMBL. | 19520572 |
Inhibition (binding) | = 98 % | Displacement of radioligand from human CB1 receptor expressed in HEK293 cells at 10 uM | ChEMBL. | 18083560 |
Inhibition (binding) | = 98 % | Displacement of radioligand from human CB1 receptor expressed in HEK293 cells at 10 uM | ChEMBL. | 18083560 |
Ki (binding) | = 92 nM | Displacement of radioligand from human CB1 receptor expressed in HEK293 cells | ChEMBL. | 18083560 |
Ki (binding) | = 92 nM | Displacement of radioligand from human CB1 receptor expressed in HEK293 cells | ChEMBL. | 18083560 |
Ki (binding) | = 3100 nM | Displacement of radioligand from human CB2 receptor expressed in HEK293 cells | ChEMBL. | 18083560 |
Ki (binding) | = 3100 nM | Displacement of radioligand from human CB2 receptor expressed in HEK293 cells | ChEMBL. | 18083560 |
Ratio Ki (binding) | = 34 | Selectivity ratio, Ki for human CB2 receptor to Ki for human CB1 receptor | ChEMBL. | 18083560 |
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.
2 literature references were collected for this gene.