lovingscience/chembl-v37-raw-activities huggingface dataset:
Compound (SMILES): C[C@H](N)C(=O)N1CC[C@]23CCN(CC4CC4)[C@H](Cc4ccc(O)cc42)[C@@H]3C1
InChIKey: BOWGWIMAPHYDBF-SKWWBAPZSA-N
Target: Kappa-type opioid receptor (SINGLE PROTEIN), Homo sapiens
UniProt: P41145
Assay: Radioligand Dose-Displacement Binding Assay: Radioligand dose-displacement binding assays for u-opioid receptors used 0.3 nM [3H]-diprenorphine (Perkin Elmer, Shelton, Conn.), with 5 mg membrane protein/well in a final volume of 500 ul binding buffer (10 mM MgCl2, 1 mM EDTA, 5% DMSO, 50 mM HEPES, pH 7.4). Reactions were carried out in the absence or presence of increasing concentrations of unlabeled naloxone. All reactions were conducted in 96-deep well polypropylene plates for 2 hours at room temperature. Binding reactions were terminated by rapid filtration onto 96-well Unifilter GF/C filter plates (Perkin Elmer, Shelton, Conn.), presoaked in 0.5% polyethylenimine using a 96-well tissue harvester (Perkin Elmer, Shelton, Conn.) followed by performing three filtration washes with 500 ul of ice-cold binding buffer. Filter plates were subsequently dried at 50 C. for 2-3 hours. BetaScint scintillation cocktail (Perkin Elmer, Shelton, Conn.) was added (50 ul/well), and plates were counted using a Packard Top-Counter.
Measurement: Ki = 0.09 nM (pChEMBL 10.050000190734863)
Descriptors: MW 369.51, ALogP 1.87, HBA 4, HBD 2, PSA 69.8, QED 0.85
Compound (SMILES): O=C(O)CN1CC[C@]23CCN(CC4CC4)[C@H](Cc4ccc(O)cc42)[C@@H]3C1
InChIKey: JQPOEJGLPPTGAT-ZVDOUQERSA-N
Target: Kappa-type opioid receptor (SINGLE PROTEIN), Homo sapiens
UniProt: P41145
Assay: Radioligand Dose-Displacement Binding Assay: Radioligand dose-displacement binding assays for u-opioid receptors used 0.3 nM [3H]-diprenorphine (Perkin Elmer, Shelton, Conn.), with 5 mg membrane protein/well in a final volume of 500 ul binding buffer (10 mM MgCl2, 1 mM EDTA, 5% DMSO, 50 mM HEPES, pH 7.4). Reactions were carried out in the absence or presence of increasing concentrations of unlabeled naloxone. All reactions were conducted in 96-deep well polypropylene plates for 2 hours at room temperature. Binding reactions were terminated by rapid filtration onto 96-well Unifilter GF/C filter plates (Perkin Elmer, Shelton, Conn.), presoaked in 0.5% polyethylenimine using a 96-well tissue harvester (Perkin Elmer, Shelton, Conn.) followed by performing three filtration washes with 500 ul of ice-cold binding buffer. Filter plates were subsequently dried at 50 C. for 2-3 hours. BetaScint scintillation cocktail (Perkin Elmer, Shelton, Conn.) was added (50 ul/well), and plates were counted using a Packard Top-Counter.
Measurement: Ki = 2.52 nM (pChEMBL 8.600000381469727)
Descriptors: MW 356.47, ALogP 2.08, HBA 4, HBD 2, PSA 64.01, QED 0.86
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(C)(=O)=O)cc2)c1
InChIKey: WLLYKTYLYHRWTC-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 10 nM (pChEMBL 8)
Descriptors: MW 492.52, ALogP 4.45, HBA 4, HBD 3, PSA 100.19, QED 0.45
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)cc2)c1
InChIKey: JZTHVVLHPZQDFA-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 66 nM (pChEMBL 7.179999828338623)
Descriptors: MW 505.56, ALogP 4.54, HBA 4, HBD 2, PSA 88.16, QED 0.47
Compound (SMILES): CC(C(=O)NCc1ccc(C(F)(F)F)nc1-c1ccccc1)c1ccc(CNS(C)(=O)=O)c(F)c1
InChIKey: HKBLLDCKVXKFIC-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 31 nM (pChEMBL 7.510000228881836)
Descriptors: MW 509.53, ALogP 4.38, HBA 4, HBD 2, PSA 88.16, QED 0.44
Compound (SMILES): CC(C(=O)NCc1ccc(C(F)(F)F)nc1-c1ccc(F)c(Cl)c1)c1ccc(CNS(C)(=O)=O)c(F)c1
InChIKey: YYWOUKCDIAGXBX-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 5 nM (pChEMBL 8.300000190734863)
Descriptors: MW 561.96, ALogP 5.17, HBA 4, HBD 2, PSA 88.16, QED 0.37
Compound (SMILES): C[C@H](C(=O)NCc1ccc(C(F)(F)F)nc1-c1ccc(F)c(Cl)c1)c1ccc(CNS(C)(=O)=O)c(F)c1
InChIKey: YYWOUKCDIAGXBX-ZDUSSCGKSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 4 nM (pChEMBL 8.399999618530273)
Descriptors: MW 561.96, ALogP 5.17, HBA 4, HBD 2, PSA 88.16, QED 0.37
Compound (SMILES): Cc1cccc(-c2nc(C3CC3)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(F)c2)c1
InChIKey: GANSXQHSCRUDLH-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 45 nM (pChEMBL 7.349999904632568)
Descriptors: MW 495.62, ALogP 4.54, HBA 4, HBD 2, PSA 88.16, QED 0.46
Compound (SMILES): Cc1cccc(-c2cc(C(C)(C)C)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(F)c2)c1
InChIKey: BZQJMVHNCWJROD-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 37 nM (pChEMBL 7.429999828338623)
Descriptors: MW 510.68, ALogP 5.57, HBA 3, HBD 2, PSA 75.27, QED 0.42
Compound (SMILES): Cc1cccc(-c2cc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(F)c2)c1
InChIKey: ZNUVGLJDHWJQSB-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 23 nM (pChEMBL 7.639999866485596)
Descriptors: MW 522.56, ALogP 5.29, HBA 3, HBD 2, PSA 75.27, QED 0.4
Compound (SMILES): Cc1cccc(-c2nc(C(C)(C)C)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(F)c2)c1
InChIKey: ZSQQWHRLJDQMJI-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 24 nM (pChEMBL 7.619999885559082)
Descriptors: MW 511.66, ALogP 4.96, HBA 4, HBD 2, PSA 88.16, QED 0.45
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(C)(=O)=O)c(F)c2)c1
InChIKey: RKDUDSFOPJMGMR-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 10 nM (pChEMBL 8)
Descriptors: MW 510.51, ALogP 4.59, HBA 4, HBD 3, PSA 100.19, QED 0.41
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNC(=O)OC(C)(C)C)c(Cl)c2)c1
InChIKey: NNZQHIUAWCQUAE-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 3 nM (pChEMBL 8.520000457763672)
Descriptors: MW 562.03, ALogP 7.17, HBA 4, HBD 2, PSA 80.32, QED 0.32
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(Cl)c2)c1
InChIKey: WFBAJBCGFOXECI-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 73 nM (pChEMBL 7.139999866485596)
Descriptors: MW 540.01, ALogP 5.2, HBA 4, HBD 2, PSA 88.16, QED 0.41
Compound (SMILES): COc1cc(C(C)C(=O)NCc2ccc(C(F)(F)F)nc2-c2cccc(C)c2)ccc1CNC(=O)OC(C)(C)C
InChIKey: ICKFOEDKZMFAAC-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 7 nM (pChEMBL 8.149999618530273)
Descriptors: MW 557.61, ALogP 6.53, HBA 5, HBD 2, PSA 89.55, QED 0.33
Compound (SMILES): COc1cc(C(C)C(=O)NCc2ccc(C(F)(F)F)nc2-c2cccc(C)c2)ccc1CNS(C)(=O)=O
InChIKey: IJLACUSCEFDWEA-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 23 nM (pChEMBL 7.639999866485596)
Descriptors: MW 535.59, ALogP 4.55, HBA 5, HBD 2, PSA 97.39, QED 0.42
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(C)(=O)=O)c(C)c2)c1
InChIKey: KMTVXPVGBSJAMY-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 74 nM (pChEMBL 7.130000114440918)
Descriptors: MW 506.55, ALogP 4.76, HBA 4, HBD 3, PSA 100.19, QED 0.43
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(N)(=O)=O)cc2)c1
InChIKey: OFVGJTFZCATUSU-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 9 nM (pChEMBL 8.050000190734863)
Descriptors: MW 493.51, ALogP 3.69, HBA 4, HBD 4, PSA 126.21, QED 0.4
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(N)(=O)=O)c(F)c2)c1
InChIKey: FBELNUQWXODYHY-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 3 nM (pChEMBL 8.520000457763672)
Descriptors: MW 524.54, ALogP 3.93, HBA 4, HBD 3, PSA 114.18, QED 0.39
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(N)(=O)=O)c(F)c2)c1
InChIKey: QEILOJQLBUVTQP-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 6 nM (pChEMBL 8.220000267028809)
Descriptors: MW 511.5, ALogP 3.83, HBA 4, HBD 4, PSA 126.21, QED 0.36
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(N)(=O)=O)cc2)c1
InChIKey: LCECPNQFXBLLTO-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 7 nM (pChEMBL 8.149999618530273)
Descriptors: MW 506.55, ALogP 3.79, HBA 4, HBD 3, PSA 114.18, QED 0.43
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(C)c2)c1
InChIKey: BFRVBYOASUJXGO-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 4 nM (pChEMBL 8.399999618530273)
Descriptors: MW 519.59, ALogP 4.85, HBA 4, HBD 2, PSA 88.16, QED 0.45
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(F)c2)c1
InChIKey: BVPHKCLFOFSJOD-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 6 nM (pChEMBL 8.220000267028809)
Descriptors: MW 523.55, ALogP 4.68, HBA 4, HBD 2, PSA 88.16, QED 0.42
Compound (SMILES): Cc1cccc(-c2nc(C(F)(F)F)ccc2CNC(=O)[C@@H](C)c2ccc(CNS(C)(=O)=O)c(F)c2)c1
InChIKey: BVPHKCLFOFSJOD-INIZCTEOSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: FLIPR Assay: The FLIPR protocol consists of 2 substance additions. First the compounds to be tested (10 uM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 uM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 uM of capsaicin (CP). After 5 minutes' incubation, 100 nM of capsaicin are applied and the Ca2+ influx is also determined.Desensitising agonists and antagonists lead to suppression of the Ca2+ influx. The % inhibition is calculated compared to the maximum achievable inhibition with 10 uM of capsazepine.Triple analyses (n=3) are carried out and repeated in at least 3 independent experiments (N=4).Starting from the percentage displacement caused by different concentrations of the compounds to be tested of general formula I, IC50 inhibitory concentrations which cause a 50-percent displacement of capsaicin were calculated.
Measurement: Ki = 15 nM (pChEMBL 7.820000171661377)
Descriptors: MW 523.55, ALogP 4.68, HBA 4, HBD 2, PSA 88.16, QED 0.42
Compound (SMILES): CC(c1cccs1)N(Cc1ccco1)C(=O)C(NS(=O)(=O)c1ccc2c(c1)CCC(=O)N2)c1ccccc1
InChIKey: KLGDKPLAQONLHF-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 1600 nM (pChEMBL 5.800000190734863)
Descriptors: MW 549.67, ALogP 5.04, HBA 6, HBD 2, PSA 108.72, QED 0.3
Compound (SMILES): Cc1cc(C)c(NC(=O)C(NS(=O)(=O)c2ccc3c(c2)CCC(=O)N3)c2ccccc2)c(C)c1
InChIKey: JHMPLCCJSHNUMD-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 5600 nM (pChEMBL 5.25)
Descriptors: MW 477.59, ALogP 4.15, HBA 4, HBD 3, PSA 104.37, QED 0.5
Compound (SMILES): CC(C)N(Cc1ccccc1)C(=O)C(NS(=O)(=O)c1ccc2c(c1)CCC(=O)N2)c1ccccc1
InChIKey: XPIMMZXDWLLRGV-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 5700 nM (pChEMBL 5.239999771118164)
Descriptors: MW 491.61, ALogP 4.03, HBA 4, HBD 2, PSA 95.58, QED 0.5
Compound (SMILES): CCN(CC)C(=O)C(NS(=O)(=O)c1ccc2c(c1)CCC(=O)N2)c1ccccc1
InChIKey: FLQWFUHYGSYGKX-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 21000 nM (pChEMBL 4.679999828338623)
Descriptors: MW 415.52, ALogP 2.46, HBA 4, HBD 2, PSA 95.58, QED 0.73
Compound (SMILES): O=C(O)CC(NS(=O)(=O)c1ccc2c(c1)CCC(=O)N2)c1cccc(Cl)c1
InChIKey: CUOSEWIVEPUJKI-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 15000 nM (pChEMBL 4.820000171661377)
Descriptors: MW 408.86, ALogP 2.72, HBA 4, HBD 3, PSA 112.57, QED 0.68
Compound (SMILES): CCOc1ccccc1N(C)S(=O)(=O)c1ccc2[nH]c(=O)ccc2c1
InChIKey: WAFATMGHCBOETO-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 50000 nM (pChEMBL 4.300000190734863)
Descriptors: MW 358.42, ALogP 2.75, HBA 4, HBD 1, PSA 79.47, QED 0.76
Compound (SMILES): Cc1ccc(N2CCN(C(=O)C(NS(=O)(=O)c3ccc4c(c3)CCC(=O)N4)c3ccccc3)CC2)cc1
InChIKey: NWNTVXCJXSIQMG-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 9000 nM (pChEMBL 5.050000190734863)
Descriptors: MW 518.64, ALogP 3.25, HBA 5, HBD 2, PSA 98.82, QED 0.52
Compound (SMILES): CN(CC(=O)Nc1nc2ccc(Cl)cc2s1)S(=O)(=O)c1ccc2[nH]c(=O)ccc2c1
InChIKey: KQODEWWFTJHAAI-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 60000 nM (pChEMBL 4.21999979019165)
Descriptors: MW 462.94, ALogP 3.05, HBA 6, HBD 2, PSA 112.23, QED 0.47
Compound (SMILES): COc1cc2c(cc1OC)C(C)N(S(=O)(=O)c1ccc3[nH]c(=O)ccc3c1)CC2
InChIKey: DQFBHOKHGWQFEW-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 50000 nM (pChEMBL 4.300000190734863)
Descriptors: MW 414.48, ALogP 2.85, HBA 5, HBD 1, PSA 88.7, QED 0.71
Compound (SMILES): O=C1CCc2cc(S(=O)(=O)NC(C(=O)N(Cc3ccco3)Cc3cccs3)c3ccccc3)ccc2N1
InChIKey: VVGGETLFAOTUSD-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 4000 nM (pChEMBL 5.400000095367432)
Descriptors: MW 535.65, ALogP 4.47, HBA 6, HBD 2, PSA 108.72, QED 0.33
Compound (SMILES): O=C(C(NS(=O)(=O)c1ccc2[nH]c(=O)ccc2c1)c1ccccc1)N(Cc1ccco1)Cc1cccs1
InChIKey: FUPKFFJNRCYVCY-UHFFFAOYSA-N
Target: UDP-N-acetylglucosamine--peptide N-acetylglucosaminyltransferase 110 kDa subunit (SINGLE PROTEIN), Homo sapiens
UniProt: O15294
Assay: Inhibition Assay: 384-well plates (Costar #3654) were filled using a liquid handling robot with 20 uL of a mixture of 50 nM of a fluorescein-linked UDP-GlcNAc analog (see Gross et al, 2003), 1-2 uM sOGT, and buffer (20 mM potassium phosphate, pH=7.4 with 500 uM tris(hydroxypropyl)phosphine). The 1249 compound library was serially diluted in DMSO from the 5 mg/ml plates fivefold 3 times, such that 4 different concentrations of compounds were prepared. Compound libraries of the 4 concentrations in duplicated were then transferred to the assay plates using a 100 nL pin array, resulting in a final compound concentration of 25 ug/mL or 70 uM at the highest of the four concentrations, assuming an average compound MW of 350. Using a Perkin Elmer Envision microplate reader, the sample was excited at 480 nm in the vertical plane, and simultaneous emission intensity (535 nm) of the vertical and horizontal polarization planes was measured.
Measurement: Kd = 400 nM (pChEMBL 6.400000095367432)
Descriptors: MW 533.63, ALogP 4.43, HBA 6, HBD 2, PSA 112.48, QED 0.29
Compound (SMILES): Cn1cc(CNc2cc(OC[C@H]3C[C@@H]3c3ccccn3)nc3ccnn23)cn1
InChIKey: YLPZTDCVMOWRPZ-CVEARBPZSA-N
Target: Cytochrome P450 3A4 (SINGLE PROTEIN), Homo sapiens
UniProt: P08684
Assay: Inhibition of CYP3A4 (unknown origin)
Measurement: IC50 > 50000 nM (pChEMBL 4.301000118255615)
Descriptors: MW 375.44, ALogP 2.65, HBA 8, HBD 1, PSA 82.16, QED 0.53
Compound (SMILES): c1ccc([C@H]2C[C@@H]2COc2cc(NCc3cn[nH]c3)n3nccc3n2)nc1
InChIKey: ZFWAJANXDQOOAB-CABCVRRESA-N
Target: cAMP and cAMP-inhibited cGMP 3',5'-cyclic phosphodiesterase 10A (SINGLE PROTEIN), Homo sapiens
UniProt: Q9Y233
Assay: Inhibition Assay: In a typical experiment the PDE10 inhibitory activity of the compounds of the present invention was determined in accordance with the following experimental method. PDE10A2 was amplified from human fetal brain cDNA (Clontech, Mountain View, Calif.) using a forward primer corresponding to nucleotides 56-77 of human PDE10A2 (Accession No. AF127480, Genbank Identifier 4894716), containing a Kozak consensus sequence, and a reverse primer corresponding to nucleotides 2406-2413 of human PDE10A2 (Accession No. AF127480, Genbank Identifier 4894716). Amplification with Easy-A polymerase (Stratagene, La Jolla, Calif.) was 95Â° C. for 2 minutes followed by thirty three cycles of 95Â° C. for 40 seconds, 55Â° C. for 30 seconds, and 72Â° C. for 2 minutes 48 seconds. Final extension was 72Â° C. for 7 minutes. The PCR product was TA cloned into pcDNA3.2-TOPO (Invitrogen, Carlsbad, Calif.) according to standard protocol.
Measurement: Ki = 0.24 nM (pChEMBL 9.619999885559082)
Descriptors: MW 361.41, ALogP 2.64, HBA 7, HBD 2, PSA 93.02, QED 0.53
Compound (SMILES): COc1ccc([C@H]2C[C@@H]2COc2cc(NCc3nnc(C)s3)n3nccc3n2)nc1
InChIKey: LJBJWAVTNDCFGF-HIFRSBDPSA-N
Target: cAMP and cAMP-inhibited cGMP 3',5'-cyclic phosphodiesterase 10A (SINGLE PROTEIN), Homo sapiens
UniProt: Q9Y233
Assay: Inhibition Assay: In a typical experiment the PDE10 inhibitory activity of the compounds of the present invention was determined in accordance with the following experimental method. PDE10A2 was amplified from human fetal brain cDNA (Clontech, Mountain View, Calif.) using a forward primer corresponding to nucleotides 56-77 of human PDE10A2 (Accession No. AF127480, Genbank Identifier 4894716), containing a Kozak consensus sequence, and a reverse primer corresponding to nucleotides 2406-2413 of human PDE10A2 (Accession No. AF127480, Genbank Identifier 4894716). Amplification with Easy-A polymerase (Stratagene, La Jolla, Calif.) was 95Â° C. for 2 minutes followed by thirty three cycles of 95Â° C. for 40 seconds, 55Â° C. for 30 seconds, and 72Â° C. for 2 minutes 48 seconds. Final extension was 72Â° C. for 7 minutes. The PCR product was TA cloned into pcDNA3.2-TOPO (Invitrogen, Carlsbad, Calif.) according to standard protocol.
Measurement: Ki = 0.012 nM (pChEMBL 10.920000076293945)
Descriptors: MW 423.5, ALogP 3.09, HBA 10, HBD 1, PSA 99.35, QED 0.46