Species | Target name | Source | Bibliographic reference |
---|---|---|---|
Mus musculus | receptor (TNFRSF)-interacting serine-threonine kinase 1 | References | |
Homo sapiens | receptor (TNFRSF)-interacting serine-threonine kinase 1 | References |
Species | Potential target | Raw | Global | Species |
---|---|---|---|---|
Brugia malayi | Immunoglobulin I-set domain containing protein | 0.0052 | 0.5 | 0.5 |
Onchocerca volvulus | Netrin receptor homolog | 0.0052 | 0.5 | 0.5 |
Schistosoma mansoni | hypothetical protein | 0.0052 | 0.5 | 0.5 |
Echinococcus granulosus | death domain containing protein | 0.0052 | 0.5 | 0.5 |
Echinococcus granulosus | ankyrin repeat and death domain containing protein | 0.0052 | 0.5 | 0.5 |
Schistosoma mansoni | netrin receptor unc5 | 0.0052 | 0.5 | 0.5 |
Loa Loa (eye worm) | hypothetical protein | 0.0052 | 0.5 | 0.5 |
Echinococcus multilocularis | netrin receptor unc 5 | 0.0052 | 0.5 | 0.5 |
Echinococcus multilocularis | ankyrin repeat and death domain containing protein | 0.0052 | 0.5 | 0.5 |
Echinococcus granulosus | Ankyrin | 0.0052 | 0.5 | 0.5 |
Echinococcus multilocularis | Ankyrin | 0.0052 | 0.5 | 0.5 |
Schistosoma mansoni | ankyrin 23/unc44 | 0.0052 | 0.5 | 0.5 |
Brugia malayi | Death domain containing protein | 0.0052 | 0.5 | 0.5 |
Echinococcus granulosus | netrin receptor unc 5 | 0.0052 | 0.5 | 0.5 |
Schistosoma mansoni | retinoblastoma-binding protein 4 (rbbp4) | 0.0052 | 0.5 | 0.5 |
Loa Loa (eye worm) | immunoglobulin I-set domain-containing protein | 0.0052 | 0.5 | 0.5 |
Loa Loa (eye worm) | hypothetical protein | 0.0052 | 0.5 | 0.5 |
Brugia malayi | Protein kinase domain containing protein | 0.0052 | 0.5 | 0.5 |
Activity type | Activity value | Assay description | Source | Reference |
---|---|---|---|---|
IC50 (binding) | = 1.6 nM | Inhibition of human RIP1 (1 to 375 residues) after 4 hrs by ADP-Glo reagent based assay | ChEMBL. | 26854747 |
IC50 (binding) | = 2.8 nM | Inhibition of human WT RIP1 infected in HEK293T cells assessed as reduction in S166 phosphorylation by ELISA | ChEMBL. | 26854747 |
IC50 (binding) | = 10 nM | Inhibition of human RIP1 in human U937 cells assessed as inhibition of TNF/zVAD.fmk induced necroptosis after 24 hrs by Cell titer-Glo luminescence assay | ChEMBL. | 26854747 |
IC50 (binding) | = 10 nM | Binding affinity to human RIP1 (1 to 375 residues) preincubated for 10 mins measured after 20 mins by fluorescence polarization assay | ChEMBL. | 26854747 |
IC50 (binding) | = 3.2 uM | Binding affinity to mouse RIP1 (1 to 378 residues) preincubated for 10 mins measured after 20 mins by fluorescence polarization assay | ChEMBL. | 26854747 |
IC50 (binding) | = 3.2 uM | Inhibition of mouse RIP1 in mouse L929 cells assessed as inhibition of TNF/zVAD.fmk induced necroptosis by Cell titer-Glo luminescence assay | ChEMBL. | 26854747 |
IC50 (binding) | > 10 uM | Inhibition of mouse WT RIP1 transfected in HEK293T cells assessed as reduction in S166 phosphorylation by ELISA | ChEMBL. | 26854747 |
Inhibition (binding) | Inhibition of human RIP1 in human HT-29 cells assessed as reduction in of TNF/SMAC-mimetic/zVAD.fmk induced RIP1 autophosphorylation at Ser166 at 10 times IC90 concentration pre-incubated for 1 hr measured after 2.5 hrs by ELISA | ChEMBL. | 26854747 | |
Inhibition (binding) | = 100 % | Inhibition of human RIP1 at 10 uM | ChEMBL. | 26854747 |
K (binding) | = 0.66 /uM/s | Binding affinity to human RIP1 (1 to 375 residues) by stopped flow kinetic study | ChEMBL. | 26854747 |
Ki (binding) | = 0.8 nM | Competitive inhibition of human RIP1 (1 to 375 residues) in presence of increasing ATP by ADP-Glo reagent based assay | ChEMBL. | 26854747 |
T1/2 (binding) | = 64 min | Binding affinity to human RIP1 (1 to 375 residues) assessed as half life preincubated for 10 mins measured after 20 mins by fluorescence polarization assay | ChEMBL. | 26854747 |
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.