Species | Target name | Source | Bibliographic reference |
---|---|---|---|
Homo sapiens | retinoid X receptor, alpha | Starlite/ChEMBL | References |
Homo sapiens | peroxisome proliferator-activated receptor gamma | References | |
Homo sapiens | retinoic acid receptor, gamma | Starlite/ChEMBL | References |
Species | Potential target | Known druggable target | Length | Alignment span | Identity |
---|---|---|---|---|---|
Brugia malayi | ecdysteroid receptor | retinoid X receptor, alpha | 435 aa | 352 aa | 23.9 % |
Echinococcus granulosus | ecdysone induced protein 78C | peroxisome proliferator-activated receptor gamma | 477 aa | 447 aa | 28.2 % |
Species | Potential target | Raw | Global | Species |
---|---|---|---|---|
Echinococcus multilocularis | retinoic acid receptor rxr beta a retinoic acid receptor rxr alpha a retinoic acid receptor rxr alpha | 0.0133 | 0 | 0.5 |
Loa Loa (eye worm) | nuclear receptor nhr-7B | 0.0271 | 0.895 | 1 |
Echinococcus granulosus | retinoic acid receptor rxr beta a | 0.015 | 0.105 | 0.5 |
Brugia malayi | nuclear hormone receptor | 0.0271 | 0.895 | 0.5 |
Schistosoma mansoni | retinoic acid receptor RXR | 0.015 | 0.105 | 0.5 |
Activity type | Activity value | Assay description | Source | Reference |
---|---|---|---|---|
EC50 (functional) | = 38 nM | Antagonist activity against Retinoic acid receptor RXR-alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
EC50 (functional) | = 38 nM | Antagonist activity against Retinoic acid receptor RXR-alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
EC50 (functional) | = 167.4 nM | Synergistic activation of BRL49653 mediated PPAR gamma and retinoid X receptor alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
EC50 (functional) | = 167.4 nM | Synergistic activation of BRL49653 mediated PPAR gamma and retinoid X receptor alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
Efficacy (functional) | = 22 % | Agonist activity against Retinoic acid receptor RXR-alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
Efficacy (functional) | = 22 % | Agonist activity against Retinoic acid receptor RXR-alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
Efficacy (functional) | = 30 % | Antagonist activity against Retinoic acid receptor RXR-alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
Efficacy (functional) | = 30 % | Antagonist activity against Retinoic acid receptor RXR-alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
Efficacy (functional) | = 47 % | Synergistic activation of BRL49653 mediated PPAR gamma and retinoid X receptor alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
Efficacy (functional) | = 47 % | Synergistic activation of BRL49653 mediated PPAR gamma and retinoid X receptor alpha expressed in CV-1 cell transcriptional activation assay | ChEMBL. | 12951091 |
Ki (binding) | = 50.3 nM | Inhibition of 3[H]-9-cis-retinoic acid binding to Retinoic acid receptor RXR-alpha expressed in CV-1 cells | ChEMBL. | 12951091 |
Ki (binding) | = 50.3 nM | Inhibition of 3[H]-9-cis-retinoic acid binding to Retinoic acid receptor RXR-alpha expressed in CV-1 cells | ChEMBL. | 12951091 |
Ki (binding) | > 10000 nM | Inhibition of 3[H]ATRA binding to retinoid acid receptor gamma expressed in CV-1 cells | ChEMBL. | 12951091 |
Ki (binding) | > 10000 nM | Inhibition of 3[H]ATRA binding to retinoid acid receptor gamma expressed in CV-1 cells | ChEMBL. | 12951091 |
Synergy (functional) | = 7 | Synergistic activation of retinoid acid receptor (RAR) transcriptional activation at 3 nM TTNPB | ChEMBL. | 12951091 |
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.