Species | Target name | Source | Bibliographic reference |
---|---|---|---|
Homo sapiens | acetylcholinesterase (Yt blood group) | References | |
Anopheles gambiae | Acetylcholinesterase | References |
Species | Potential target | Known druggable target | Length | Alignment span | Identity |
---|---|---|---|---|---|
Echinococcus multilocularis | BC026374 protein (S09 family) | Acetylcholinesterase | 737 aa | 651 aa | 34.6 % |
Echinococcus granulosus | BC026374 protein S09 family | Acetylcholinesterase | 737 aa | 650 aa | 34.5 % |
Brugia malayi | Carboxylesterase family protein | acetylcholinesterase (Yt blood group) | 614 aa | 510 aa | 26.5 % |
Schistosoma mansoni | family S9 non-peptidase homologue (S09 family) | Acetylcholinesterase | 737 aa | 636 aa | 24.2 % |
Schistosoma mansoni | gliotactin | Acetylcholinesterase | 737 aa | 616 aa | 27.3 % |
Species | Potential target | Raw | Global | Species |
---|---|---|---|---|
Loa Loa (eye worm) | acetylcholinesterase 1 | 0.0205 | 0.5 | 0.5 |
Echinococcus multilocularis | acetylcholinesterase | 0.0205 | 0.5 | 0.5 |
Brugia malayi | Carboxylesterase family protein | 0.0205 | 0.5 | 0.5 |
Echinococcus granulosus | carboxylesterase 5A | 0.0205 | 0.5 | 0.5 |
Echinococcus multilocularis | acetylcholinesterase | 0.0205 | 0.5 | 0.5 |
Loa Loa (eye worm) | hypothetical protein | 0.0205 | 0.5 | 0.5 |
Echinococcus granulosus | acetylcholinesterase | 0.0205 | 0.5 | 0.5 |
Loa Loa (eye worm) | carboxylesterase | 0.0205 | 0.5 | 0.5 |
Echinococcus granulosus | acetylcholinesterase | 0.0205 | 0.5 | 0.5 |
Loa Loa (eye worm) | hypothetical protein | 0.0205 | 0.5 | 0.5 |
Echinococcus multilocularis | carboxylesterase 5A | 0.0205 | 0.5 | 0.5 |
Schistosoma mansoni | family S9 non-peptidase homologue (S09 family) | 0.0205 | 0.5 | 0.5 |
Activity type | Activity value | Assay description | Source | Reference |
---|---|---|---|---|
Activity (functional) | NOVARTIS: Antimalarial liver stage activity measured as a greater than 50% reduction in Plasmodium yoelii schizont area in HepG2-A16-CD81 cells at 10uM compound concentration, determined by immuno-fluorescence. | ChEMBL. | 22096101 | |
CC50 (functional) | > 68.36 uM | Huh7 cytotoxicity for Pf inhibitors | Novartis-GNF Malaria Box. | No reference |
CC50 | > 68.36 uM | NOVARTIS: Cytotoxicity against human hepatocellular carcinoma cell line (Huh7) | ChEMBL. | 18579783 |
EC50 (functional) | = 0.0348 uM | W2 Pf proliferation inhibition | Novartis-GNF Malaria Box. | No reference |
EC50 (functional) | = 0.0348 uM | NOVARTIS: Inhibition of Plasmodium falciparum W2 (drug-resistant) proliferation in erythrocyte-based infection assay | ChEMBL. | 18579783 |
EC50 (functional) | = 0.0858 uM | PF proliferation inhibition 3D7 | Novartis-GNF Malaria Box. | No reference |
EC50 (functional) | = 0.0858 uM | NOVARTIS: Inhibition of Plasmodium falciparum 3D7 (drug-susceptible) proliferation in erythrocyte-based infection assay | ChEMBL. | 18579783 |
IC50 (binding) | = 5.1 uM | Inhibition of human recombinant AChE using acetylthiocholine iodide as substrate measured over 60 secs by Ellman assay | LITERATURE. | 27598521 |
IC50 (binding) | = 8.3 uM | Inhibition of Anopheles gambiae recombinant AChE1 expressed in baculovirus infected insect Sf9 cells using acetylthiocholine iodide as substrate measured over 60 secs by Ellman assay | LITERATURE. | 27598521 |
IFI promiscuity index | = 0.02837 | IFI promiscuity index | Novartis-GNF Malaria Box. | No reference |
Inhibition (binding) | = 94 % | Inhibition of Anopheles gambiae recombinant AChE1 expressed in baculovirus infected insect Sf9 cells at 50 uM using acetylthiocholine iodide as substrate measured over 60 secs by Ellman assay relative to control | LITERATURE. | 27598521 |
Species name | Source | Reference | Is orphan |
---|---|---|---|
Plasmodium falciparum | ChEMBL23 | 18579783 |
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.