Activity type | Activity value | Assay description | Source | Reference |
---|---|---|---|---|
Clp (functional) | = 60 | Cumulative lesions in HSV-1 infected mice, after administration of 0.1 % of compound intracutaneously | ChEMBL. | 2842506 |
CMP (functional) | = 25 | Cumulative mortality in percent of HSV-1 infected mice, after intraperitoneal administration of 5 mg/kg of compound | ChEMBL. | 2842506 |
CMP (functional) | = 50 | Cumulative mortality in percent of HSV-1 infected mice,after peroral administration of 10 mg/kg of compound | ChEMBL. | 2842506 |
CMP (functional) | = 50 | Cumulative mortality in percent of HSV-1 infected mice, after intraperitoneal administration of 0.5 mg/kg of compound | ChEMBL. | 2842506 |
CMP (functional) | = 58 | Cumulative mortality in percent of HSV-1 infected mice, after intraperitoneal administration of 1 mg/kg of compound | ChEMBL. | 2842506 |
CMP (functional) | = 92 | Cumulative mortality in percent of HSV-1 infected mice, after peroral administration of 5 mg/kg of compound | ChEMBL. | 2842506 |
CMP (functional) | = 100 | Cumulative mortality in percent of HSV-1 infected mice, after peroral administration of 1 mg/kg of compound | ChEMBL. | 2842506 |
MDL (functional) | = 5.3 day | Mean duration of lesions in HSV-1 infected mice, after administration of 0.1 % of compound intracutaneously | ChEMBL. | 2842506 |
MIC (functional) | = 2.3 uM | Minimum inhibitory concentration causing 25% inhibition of cytopathic effect induced by Herpes simplex virus-1 (Brand) in vero cells | ChEMBL. | 2842506 |
MIC (functional) | = 2.3 uM | Minimum inhibitory concentration causing 25% inhibition cytopathic effect induced by Herpes simplex virus-1 (Brand) in HEp-2 cells | ChEMBL. | 2842506 |
MIC (functional) | = 23.2 uM | Minimum inhibitory concentration causing 25% inhibition of cytopathic effect induced by Herpes simplex virus(HSV) -1 (thymidine kinase deficient) in vero cells | ChEMBL. | 2842506 |
MIC (functional) | = 23.2 uM | Minimum inhibitory concentration causing 25% inhibition of cytopathic effect induced by Herpes simplex virus(HSV) -1 (thymidine kinase deficient) in HEp-2 cells | ChEMBL. | 2842506 |
MIC (functional) | = 69.6 uM | Minimum inhibitory concentration causing 25% inhibition of cytopathic effect induced by Herpes simplex virus-1 (K979) in HEp-2 cells | ChEMBL. | 2842506 |
MIC (functional) | = 232 uM | Minimum inhibitory concentration causing 25% inhibition of cytopathic effect induced by herpes simplex virus (HSV)-1 (K979) in vero cells. | ChEMBL. | 2842506 |
MIC (functional) | > 232 uM | Minimum inhibitory concentration causing 25% inhibition cytopathic effect induced by Herpes simplex virus(HSV) -2 (thymidine kinase deficient) in vero cells | ChEMBL. | 2842506 |
MIC (functional) | = 232 uM | Minimum inhibitory concentration causing 25% inhibition of cytopathic effect induced by Herpes simplex virus(HSV) -2 (thymidine kinase deficient) in HEp-2 cells | ChEMBL. | 2842506 |
MST (functional) | = 8.6 day | Mean survival time in HSV-1 infected mice, after peroral administration of 1 mg/kg of compound | ChEMBL. | 2842506 |
MST (functional) | = 11.2 day | Mean survival time in HSV-1 infected mice, after peroral administration of 5 mg/kg of compound | ChEMBL. | 2842506 |
MST (functional) | = 14.1 day | Mean survival time in HSV-1 infected mice, after intraperitoneal administration of 1 mg/kg of compound | ChEMBL. | 2842506 |
MST (functional) | = 14.2 day | Mean survival time in HSV-1 infected mice, after intraperitoneal administration of 0.5 mg/kg of compound | ChEMBL. | 2842506 |
MST (functional) | = 15.3 day | Mean survival time in HSV-1 infected mice, after peroral administration of 10 mg/kg of compound | ChEMBL. | 2842506 |
MST (functional) | = 17.3 day | Mean survival time in HSV-1 infected mice, after intraperitoneal administration of 5 mg/kg of compound | ChEMBL. | 2842506 |
MTC (functional) | = 766 uM | Minimum cytotoxic concentration causing toxic effects on uninfected cells in rabbit | ChEMBL. | 2842506 |
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.
1 literature reference was collected for this gene.