lovingscience/chembl-v37-raw-activities huggingface dataset:
Compound (SMILES): Clc1cnc2nc1NCc1cccc(c1)OCCCc1cccc(c1)N2
InChIKey: WILMKMPUMOSDLH-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK1 (SINGLE PROTEIN), Homo sapiens
UniProt: P23458
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 4.2 nM (pChEMBL 8.380000114440918)
Descriptors: MW 366.85, ALogP 4.81, HBA 5, HBD 2, PSA 59.07, QED 0.6
Compound (SMILES): C[C@H]1Nc2nc(ncc2Cl)Nc2cccc(c2)COc2cccc1c2
InChIKey: OMIMDZMFZXMMGS-GFCCVEGCSA-N
Target: Tyrosine-protein kinase JAK1 (SINGLE PROTEIN), Homo sapiens
UniProt: P23458
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 346 nM (pChEMBL 6.460000038146973)
Descriptors: MW 352.83, ALogP 4.94, HBA 5, HBD 2, PSA 59.07, QED 0.6
Compound (SMILES): Clc1cnc2nc1NCc1cccc(c1)OCCOc1cccc(c1)N2
InChIKey: JRMWFZSAQXNBSZ-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK2 (SINGLE PROTEIN), Homo sapiens
UniProt: O60674
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 8.3 nM (pChEMBL 8.079999923706055)
Descriptors: MW 368.82, ALogP 4.26, HBA 6, HBD 2, PSA 68.3, QED 0.62
Compound (SMILES): Clc1cnc2nc1NCCc1cccc(c1)OCc1cccc(c1)N2
InChIKey: BBVOVZFYMUEXGT-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK2 (SINGLE PROTEIN), Homo sapiens
UniProt: O60674
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 333 nM (pChEMBL 6.480000019073486)
Descriptors: MW 352.83, ALogP 4.42, HBA 5, HBD 2, PSA 59.07, QED 0.63
Compound (SMILES): Clc1cnc2nc1NCCc1cccc(c1)OCCc1cccc(c1)N2
InChIKey: DDEPHNOBUQYIBZ-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK1 (SINGLE PROTEIN), Homo sapiens
UniProt: P23458
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 28 nM (pChEMBL 7.550000190734863)
Descriptors: MW 366.85, ALogP 4.46, HBA 5, HBD 2, PSA 59.07, QED 0.61
Compound (SMILES): Clc1cnc2nc1NCCCc1cccc(c1)OCc1cccc(c1)N2
InChIKey: PGBXYNXDKMTLPH-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK2 (SINGLE PROTEIN), Homo sapiens
UniProt: O60674
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 117 nM (pChEMBL 6.929999828338623)
Descriptors: MW 366.85, ALogP 4.81, HBA 5, HBD 2, PSA 59.07, QED 0.6
Compound (SMILES): C[C@@H]1Nc2nc(ncc2Cl)Nc2cccc(c2)COc2cccc1c2
InChIKey: OMIMDZMFZXMMGS-LBPRGKRZSA-N
Target: Tyrosine-protein kinase JAK2 (SINGLE PROTEIN), Homo sapiens
UniProt: O60674
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 > 1000 nM (pChEMBL 6)
Descriptors: MW 352.83, ALogP 4.94, HBA 5, HBD 2, PSA 59.07, QED 0.6
Compound (SMILES): Clc1cnc2nc1NCCc1cccc(c1)OCCCc1cccc(c1)N2
InChIKey: YCEQOGSAKUVGII-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK3 (SINGLE PROTEIN), Homo sapiens
UniProt: P52333
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 315 nM (pChEMBL 6.5)
Descriptors: MW 380.88, ALogP 4.85, HBA 5, HBD 2, PSA 59.07, QED 0.58
Compound (SMILES): Clc1cnc2nc1NCCCc1cccc(c1)OCCc1cccc(c1)N2
InChIKey: NLGCDKKLEZPXLI-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK1 (SINGLE PROTEIN), Homo sapiens
UniProt: P23458
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 32 nM (pChEMBL 7.5)
Descriptors: MW 380.88, ALogP 4.85, HBA 5, HBD 2, PSA 59.07, QED 0.58
Compound (SMILES): Clc1cnc2nc1NCc1cc(ccc1Br)OCCCc1cccc(c1)N2
InChIKey: YYZSNJQQGCXQNG-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK2 (SINGLE PROTEIN), Homo sapiens
UniProt: O60674
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 91 nM (pChEMBL 7.039999961853027)
Descriptors: MW 445.75, ALogP 5.57, HBA 5, HBD 2, PSA 59.07, QED 0.47
Compound (SMILES): Clc1cnc2nc1NCc1cc(ccc1-c1ccccc1)OCCCc1cccc(c1)N2
InChIKey: JHMLRNFFLKYFAU-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK3 (SINGLE PROTEIN), Homo sapiens
UniProt: P52333
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 31 nM (pChEMBL 7.510000228881836)
Descriptors: MW 442.95, ALogP 6.48, HBA 5, HBD 2, PSA 59.07, QED 0.35
Compound (SMILES): Clc1cnc2nc1NCc1cc(Br)cc(c1)OCCCc1cccc(c1)N2
InChIKey: IBAVCNVUPMTBKJ-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK3 (SINGLE PROTEIN), Homo sapiens
UniProt: P52333
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 15 nM (pChEMBL 7.820000171661377)
Descriptors: MW 445.75, ALogP 5.57, HBA 5, HBD 2, PSA 59.07, QED 0.47
Compound (SMILES): Nc1ccc2cc1CCc1cncc(c1)Nc1ncc(Cl)c(n1)NC2
InChIKey: FKLWUWJYBORMDH-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK1 (SINGLE PROTEIN), Homo sapiens
UniProt: P23458
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 = 102 nM (pChEMBL 6.989999771118164)
Descriptors: MW 352.83, ALogP 3.56, HBA 6, HBD 3, PSA 88.75, QED 0.54
Compound (SMILES): O=C(Nc1ccc2cc1CCc1cncc(c1)Nc1ncc(Cl)c(n1)NC2)c1ccccc1
InChIKey: DZOSAHMEHFLHAZ-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK2 (SINGLE PROTEIN), Homo sapiens
UniProt: O60674
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 > 1000 nM (pChEMBL 6)
Descriptors: MW 456.94, ALogP 5.23, HBA 6, HBD 3, PSA 91.83, QED 0.38
Compound (SMILES): N#Cc1ccccc1S(=O)(=O)Nc1ccc2cc1CCc1cncc(c1)Nc1ncc(Cl)c(n1)NC2
InChIKey: AVINPMJXOWDOIE-UHFFFAOYSA-N
Target: Tyrosine-protein kinase JAK2 (SINGLE PROTEIN), Homo sapiens
UniProt: O60674
Assay: In Vitro Kinase Assay: One or more compounds herein were tested for inhibitory activity of JAK targets according to the following in vitro assay described in Park et al., Analytical Biochemistry 1999, 269, 94-104. The catalytic domains of human JAK1 (a.a. 837-1142), JAK2 (a.a. 828-1132) and JAK3 (a.a. 781-1124) with an N-terminal His tag were expressed using baculovirus in insect cells and purified. The catalytic activity of JAK1, JAK2 or JAK3 was assayed by measuring the phosphorylation of a biotinylated peptide. The phosphorylated peptide was detected by homogenous time resolved fluorescence (HTRF). IC50s of compounds were measured for each kinase in the reactions that contain the enzyme, ATP and 500 nM peptide in 50 mM Tris (pH 7.8) buffer with 100 mM NaCl, 5 mM DTT, and 0.1 mg/mL (0.01%) BSA. The ATP concentration in the reactions was 90 uM for JAK1, 30 uM for JAK2 and 3 uM for JAK3. Reactions were carried out at room temperature for 1 hr and then stopped with 20 uL 45 mM EDTA.
Measurement: IC50 > 1000 nM (pChEMBL 6)
Descriptors: MW 518, ALogP 4.65, HBA 8, HBD 3, PSA 132.69, QED 0.36
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2cccc(CNS(C)(=O)=O)c2)CC1
InChIKey: WPENNJLLXZGIMX-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 102 nM (pChEMBL 6.989999771118164)
Descriptors: MW 512.6, ALogP 3.81, HBA 5, HBD 2, PSA 91.4, QED 0.56
Compound (SMILES): CC(C(=O)NCc1ccc(C(F)(F)F)nc1N1CCCC1)c1ccc(CNS(C)(=O)=O)cc1
InChIKey: YEVUHVYKRDXVSZ-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 20 nM (pChEMBL 7.699999809265137)
Descriptors: MW 484.54, ALogP 3.17, HBA 5, HBD 2, PSA 91.4, QED 0.6
Compound (SMILES): CS(=O)(=O)NCc1ccc(NC(=O)NCc2ccc(C(F)(F)F)nc2N2CCCC2)cc1
InChIKey: IMUQPNDDNHBWDX-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 26 nM (pChEMBL 7.579999923706055)
Descriptors: MW 471.51, ALogP 3.07, HBA 5, HBD 3, PSA 103.43, QED 0.58
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(C)(=O)=O)cc2)CC1
InChIKey: ROFFYOZDQKAEKC-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 4 nM (pChEMBL 8.399999618530273)
Descriptors: MW 499.56, ALogP 3.71, HBA 5, HBD 3, PSA 103.43, QED 0.54
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)cc2)CC1
InChIKey: PGNWYVDOCVWIJH-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 11 nM (pChEMBL 7.960000038146973)
Descriptors: MW 512.6, ALogP 3.81, HBA 5, HBD 2, PSA 91.4, QED 0.56
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(C)(=O)=O)c(F)c2)CC1
InChIKey: NAXMRUCVDLYTPD-UHFFFAOYSA-N
Target: Transient receptor potential cation channel subfamily V member 1 (SINGLE PROTEIN), Homo sapiens
UniProt: Q8NER1
Assay: Displacement of [3H]-resiniferatoxin from human TRPV1 expressed in CHO cells incubated for 60 mins by scintillation counting analysis
Measurement: Ki = 6.77 nM (pChEMBL 8.170000076293945)
Descriptors: MW 517.55, ALogP 3.85, HBA 5, HBD 3, PSA 103.43, QED 0.48
Compound (SMILES): CC(C(=O)NCc1ccc(C(F)(F)F)nc1N1CCCC1)c1ccc(CNS(C)(=O)=O)c(Cl)c1
InChIKey: LIVGIEWMGKYQDQ-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 80 nM (pChEMBL 7.099999904632568)
Descriptors: MW 518.99, ALogP 3.82, HBA 5, HBD 2, PSA 91.4, QED 0.55
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(C)(=O)=O)c(Cl)c2)CC1
InChIKey: ULMYDLMWPKJQDG-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 5 nM (pChEMBL 8.300000190734863)
Descriptors: MW 547.04, ALogP 4.46, HBA 5, HBD 2, PSA 91.4, QED 0.51
Compound (SMILES): COc1cc(C(C)C(=O)NCc2ccc(C(F)(F)F)nc2N2CCCC2)ccc1CNS(C)(=O)=O
InChIKey: AEEGOXCOIBDXNR-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 87 nM (pChEMBL 7.059999942779541)
Descriptors: MW 514.57, ALogP 3.18, HBA 6, HBD 2, PSA 100.63, QED 0.53
Compound (SMILES): COc1cc(NC(=O)NCc2ccc(C(F)(F)F)nc2N2CCC(C)CC2)ccc1CNS(C)(=O)=O
InChIKey: OFMHYOSDMXOYHQ-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 12 nM (pChEMBL 7.920000076293945)
Descriptors: MW 529.59, ALogP 3.72, HBA 6, HBD 3, PSA 112.66, QED 0.48
Compound (SMILES): Cc1cc(C(C)C(=O)NCc2ccc(C(F)(F)F)nc2N2CCCC2)ccc1CNS(C)(=O)=O
InChIKey: HRJSGGWXLOJFAA-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 50 nM (pChEMBL 7.300000190734863)
Descriptors: MW 498.57, ALogP 3.48, HBA 5, HBD 2, PSA 91.4, QED 0.58
Compound (SMILES): Cc1cc(NC(=O)NCc2ccc(C(F)(F)F)nc2N2CCCC2)ccc1CNS(C)(=O)=O
InChIKey: LZYGJDXTQIAIKK-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 46 nM (pChEMBL 7.340000152587891)
Descriptors: MW 485.53, ALogP 3.38, HBA 5, HBD 3, PSA 103.43, QED 0.56
Compound (SMILES): Cc1cc(NC(=O)NCc2ccc(C(F)(F)F)nc2N2CCC(C)CC2)ccc1CNS(C)(=O)=O
InChIKey: VOABDLHRSZBDAJ-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 5 nM (pChEMBL 8.300000190734863)
Descriptors: MW 513.59, ALogP 4.02, HBA 5, HBD 3, PSA 103.43, QED 0.52
Compound (SMILES): CCS(=O)(=O)NCc1ccc(C(C)C(=O)NCc2ccc(C(F)(F)F)nc2N2CCCC2)cc1F
InChIKey: HDAZZIHJSYAMFR-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 76 nM (pChEMBL 7.119999885559082)
Descriptors: MW 516.56, ALogP 3.7, HBA 5, HBD 2, PSA 91.4, QED 0.5
Compound (SMILES): CCS(=O)(=O)NCc1ccc(C(C)C(=O)NCc2ccc(C(F)(F)F)nc2N2CCC(C)CC2)cc1F
InChIKey: DNFJEOQWECTZFD-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 4 nM (pChEMBL 8.399999618530273)
Descriptors: MW 544.62, ALogP 4.34, HBA 5, HBD 2, PSA 91.4, QED 0.46
Compound (SMILES): NS(=O)(=O)NCc1ccc(NC(=O)NCc2ccc(C(F)(F)F)nc2N2CCCC2)cc1
InChIKey: HMCIMBQBQAEJFG-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 85 nM (pChEMBL 7.070000171661377)
Descriptors: MW 472.49, ALogP 2.32, HBA 5, HBD 4, PSA 129.45, QED 0.49
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)Nc2ccc(CNS(N)(=O)=O)cc2)CC1
InChIKey: OTVBHAAUANCTTG-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 1 nM (pChEMBL 9)
Descriptors: MW 500.55, ALogP 2.95, HBA 5, HBD 4, PSA 129.45, QED 0.46
Compound (SMILES): NS(=O)(=O)NCc1ccc(NC(=O)NCc2ccc(C(F)(F)F)nc2N2CCCC2)cc1F
InChIKey: YIRGIFCCCSSQIZ-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 20 nM (pChEMBL 7.699999809265137)
Descriptors: MW 490.48, ALogP 2.45, HBA 5, HBD 4, PSA 129.45, QED 0.44
Compound (SMILES): Cc1ccc(CNC(=O)Nc2ccc(CNS(N)(=O)=O)c(F)c2)c(N2CCC(C)CC2)n1
InChIKey: XFFRGHGSUNXKDD-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 1 nM (pChEMBL 9)
Descriptors: MW 464.57, ALogP 2.38, HBA 5, HBD 4, PSA 129.45, QED 0.5
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CNS(N)(=O)=O)c(F)c2)CC1
InChIKey: FHVGITBZDXWOSJ-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 4 nM (pChEMBL 8.399999618530273)
Descriptors: MW 531.58, ALogP 3.19, HBA 5, HBD 3, PSA 117.42, QED 0.45
Compound (SMILES): CC1CCN(c2nc(C(F)(F)F)ccc2CNC(=O)C(C)c2ccc(CN(C)S(C)(=O)=O)c(F)c2)CC1
InChIKey: XNNMKUJTBOKRLK-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 μM) are pipetted onto the cells and the Ca2+ influx is compared with the control (capsaicin 10 μM). This provides the result in % activation based on the Ca2+ signal after the addition of 10 μM 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 μM of capsazepine. 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. K1 values for the test substances were obtained by conversion by means of the Cheng-Prusoff equation (Cheng, Prusoff; Biochem. Pharmacol. 22, 3099-3108, 1973).
Measurement: Ki = 55 nM (pChEMBL 7.260000228881836)
Descriptors: MW 544.62, ALogP 4.29, HBA 5, HBD 1, PSA 82.61, QED 0.5
Compound (SMILES): C[C@@H](c1ccc(Br)cc1)N1CCC2(CC=CC2)OC1=O
InChIKey: JWBPAUHMRIEGNU-LBPRGKRZSA-N
Target: 11-beta-hydroxysteroid dehydrogenase 1 (SINGLE PROTEIN), Homo sapiens
UniProt: P28845
Assay: Homogeneous Time-Resolved Fluorescence Assay: In vitro inhibition of 11beta -HSD1 by test compounds is determined with HTRF (Homogeneous Time-Resolved Fluorescence) technology (cisbio international, France) detecting cortisol generated from cortisterone by human liver microsomes. Briefly, compounds are incubated for 1 hour at 37C. in Tris buffer (20 mM tris, 5 mM EDTA, pH 6.0) containing NADPH (200 uM) and cortisone (80 nM). Cortisol generated in the reaction is then detected with a competitive immunoassay, involving two HTRF conjugates: cortisol linked to XL665 and anti-cortisol antibody labeled with Europium cryptate. The incubation period for detection reaction is typically 2 hours. The amount of cortisol is determined by reading the time-resolved fluorescence of the wells (Ex 320/75 nm; Em 615/8.5 nm and 665/7.5 nm). The ratio of the two emission signals is then calculated (Em665X10000/Em615).
Measurement: IC50 = 320 nM (pChEMBL 6.5)
Descriptors: MW 336.23, ALogP 4.44, HBA 2, HBD 0, PSA 29.54, QED 0.75