taselisib [Ligand Id: 7794] activity data from GtoPdb and ChEMBL
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| ChEMBL ligand: CHEMBL2387080 (GDC-0032, RG-7604, Taselisib) |
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| DB | Assay description | Assay Type | Standard value | Standard parameter | Original value | Original units | Original parameter | Reference |
|---|---|---|---|---|---|---|---|---|
| protein kinase, DNA-activated, catalytic subunit/DNA-dependent protein kinase catalytic subunit in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL3142] [GtoPdb: 2800] [UniProtKB: P78527] | ||||||||
| ChEMBL | Inhibition of DNA-dependent protein kinase (unknown origin) | B | 5.32 | pIC50 | >4800 | nM | IC50 | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| phosphatidylinositol 3-kinase catalytic subunit type 3/Phosphatidylinositol 3-kinase catalytic subunit type 3 in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL1075165] [GtoPdb: 2152] [UniProtKB: Q8NEB9] | ||||||||
| ChEMBL | Inhibition of human VPS34 | B | 6.43 | pIC50 | 374 | nM | IC50 | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Selectivity interaction (Enzymatic assay) EUB0000685a PIK3C3 | B | 6.43 | pIC50 | 374 | nM | IC50 | Selectivity Literature for EUbOPEN Chemogenomics Library wave 3 |
| phosphoinositide-3-kinase regulatory subunit 2/Phosphatidylinositol 3-kinase regulatory subunit beta in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL4437] [GtoPdb: 2504] [UniProtKB: O00459] | ||||||||
| ChEMBL | p110alpha (Alpha) PI3K Binding Assay: PI3K Binding assays are intended for determining the biochemical potency of small molecule PI3K inhibitors. The PI3K lipid kinase reaction is performed in the presence of PIP2:3PS lipid substrate (Promega #V1792) and ATP. Following the termination if the kinase reaction, turnover of ATP to ADP by the phosphorylation of the lipid substrate is detected using the Promega ADP-Glo (Promega #V1792) assay. ReactionFinal Kinase ATP PIP2:3PS TimeKinase Source Concentration (uM) (uM) (min.)PI3K alpha Millipore 0.2 nM 40 50 120#14-602-K PI3K beta Promega 0.6 nM 40 50 120#V1751 PI3K delta Millipore 0.25 nM 40 50 120#14-604-K PI3K gamma Millipore 0.4 nM 25 50 120#14-558-KAfter 120 minutes of reaction time, the kinase reaction is terminated. Any ATP remaining after the reaction is depleted, leaving only ADP. Then the Kinase Detection Reagent is added to convert ADP to ATP, which is used in a coupled luciferin/luciferase reaction. The luminescent output is measured and is correlated with kinase activity. | B | 7.28 | pKi | 53 | nM | Ki | US-10112932-B2. Benzoxazepin oxazolidinone compounds and methods of use (2018) |
| phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha/Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL4005] [GtoPdb: 2153] [UniProtKB: P42336] | ||||||||
| ChEMBL | Inhibition of recombinant PI3K alpha (unknown origin) using PIP2 as substrate by fluorescence polarization assay | B | 9.52 | pKi | 0.3 | nM | Ki | J Med Chem (2016) 59: 985-1002 [PMID:26741947] |
| ChEMBL | Inhibition of PI3Kalpha (unknown origin) assessed as 3,4,5-inositoltriphosphate formation after 30 mins by fluorescence polarization assay | B | 9.54 | pKi | 0.29 | nM | Ki | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Affinity Biochemical interaction (Enzymatic fluorescence polarization assay) EUB0000685a PIK3CA | B | 9.54 | pKi | 0.29 | nM | Ki | Affinity Biochemical Literature for EUbOPEN Chemogenomics Library wave 3 |
| GtoPdb | - | - | 9.54 | pKi | 0.29 | nM | Ki | J Med Chem (2013) 56: 4597-610 [PMID:23662903] |
| ChEMBL | Inhibition of PI3Kalpha (unknown origin) using PIP2:3PS as substrate in presence of ATP measured after 120 mins by ADP-Glo assay | B | 10.05 | pKi | 0.09 | nM | Ki | J Med Chem (2022) 65: 16589-16621 [PMID:36455032] |
| ChEMBL | Biochemical Inhibition Assay: The biochemical inhibition of four PI3K isoforms by the Formula I compounds of Table 1. In addition, two clinically tested PI3K compounds, taselisib and pictilisib are included as comparators. The representative compounds of the invention exhibit strong activity against PI3Kα, and exhibit significantly enhanced selectivity relative to the other isoforms PI3Kβ, PI3Kδ, and PI3Kγ when compared to taselisib (GDC-0032) and pictilisib (GDC-0941). In particular, the selectivity ratios in the second from the right column of Table 2A show that each Formula I compounds 101-107 has a PI3K alpha to delta selectivity ratio far higher than taselisib or pictilisib. In fact, both taselisib and pictilisib have stronger activity against PI3K delta than against PI3K alpha, i.e. their selectivity ratios are less than 1. The selectivity ratios of Formula I compound 101-107 range from 301-fold to 634-fold. | B | 10.05 | pKi | 0.09 | nM | Ki | US-10851091-B2. Benzoxazepin oxazolidinone compounds and methods of use (2020) |
| ChEMBL | Biochemical Inhibition Assay: The biochemical inhibition of four PI3K isoforms by the Formula I compounds of Table 1. In addition, two clinically tested PI3K compounds, taselisib and pictilisib are included as comparators. The representative compounds of the invention exhibit strong activity against PI3Kα, and exhibit significantly enhanced selectivity relative to the other isoforms PI3Kβ, PI3Kδ, and PI3Kγ when compared to taselisib (GDC-0032) and pictilisib (GDC-0941). In particular, the selectivity ratios in the second from the right column of Table 2A show that each Formula I compounds 101-107 has a PI3K alpha to delta selectivity ratio far higher than taselisib or pictilisib. In fact, both taselisib and pictilisib have stronger activity against PI3K delta than against PI3K alpha, i.e. their selectivity ratios are less than 1. The selectivity ratios of Formula I compound 101-107 range from 301-fold to 634-fold. | B | 10.05 | pKi | 0.09 | nM | Ki | US-10851091-B2. Benzoxazepin oxazolidinone compounds and methods of use (2020) |
| GtoPdb | - | - | 10.05 | pKi | 0.09 | nM | Ki | US20170015678. Benzoxazepin oxazolidinone compounds and methods of use (2017) |
| ChEMBL | Inhibition of PI3Kalpha in human PC3 cells assessed as reduction of AKT phosphorylation | B | 7.51 | pIC50 | 31 | nM | IC50 | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Inhibition of PI3Kalpha in human MCF7-neo/Her2 cells assessed as reduction of AKT phosphorylation at S473 | B | 8.4 | pIC50 | 4 | nM | IC50 | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Affinity Phenotypic Cellular interaction (MesoScale Discovery assay (AKT phoshorylation in MCF 7 cells)) EUB0000685a PIK3CA | B | 8.4 | pIC50 | 4 | nM | IC50 | Affinity Phenotypic Cellular Literature for EUbOPEN Chemogenomics Library wave 3 |
| ChEMBL | Inhibition of PI3K alpha (unknown origin) | B | 9.15 | pIC50 | <0.7 | nM | IC50 | ACS Med Chem Lett (2017) 8: 808-813 [PMID:28835793] |
| ChEMBL | Inhibition of PI3Kalpha H1047R mutant in human HCC1954 cells assessed as reduction in PRAS40 phosphorylation after 24 hrs by electrochemiluminescent assay | B | 7.62 | pEC50 | 24 | nM | EC50 | J Med Chem (2022) 65: 16589-16621 [PMID:36455032] |
| phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta/Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit beta isoform in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL3145] [GtoPdb: 2154] [UniProtKB: P42338] | ||||||||
| ChEMBL | Biochemical Inhibition Assay: The biochemical inhibition of four PI3K isoforms by the Formula I compounds of Table 1. In addition, two clinically tested PI3K compounds, taselisib and pictilisib are included as comparators. The representative compounds of the invention exhibit strong activity against PI3Kα, and exhibit significantly enhanced selectivity relative to the other isoforms PI3Kβ, PI3Kδ, and PI3Kγ when compared to taselisib (GDC-0032) and pictilisib (GDC-0941). In particular, the selectivity ratios in the second from the right column of Table 2A show that each Formula I compounds 101-107 has a PI3K alpha to delta selectivity ratio far higher than taselisib or pictilisib. In fact, both taselisib and pictilisib have stronger activity against PI3K delta than against PI3K alpha, i.e. their selectivity ratios are less than 1. The selectivity ratios of Formula I compound 101-107 range from 301-fold to 634-fold. | B | 7.28 | pKi | 53 | nM | Ki | US-10851091-B2. Benzoxazepin oxazolidinone compounds and methods of use (2020) |
| GtoPdb | - | - | 7.28 | pKi | 53 | nM | Ki | US20170015678. Benzoxazepin oxazolidinone compounds and methods of use (2017) |
| GtoPdb | - | - | 8.04 | pKi | 9.1 | nM | Ki | J Med Chem (2013) 56: 4597-610 [PMID:23662903] |
| ChEMBL | Inhibition of PI3Kbeta (unknown origin) | B | 8.04 | pKi | 9.1 | nM | Ki | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Affinity Biochemical interaction (Enzymatic fluorescence polarization assay) EUB0000685a PIK3CB | B | 8.04 | pKi | 9.1 | nM | Ki | Affinity Biochemical Literature for EUbOPEN Chemogenomics Library wave 3 |
| ChEMBL | Affinity Phenotypic Cellular interaction (MesoScale Discovery assay (AKT phoshorylation in MCF 7 cells)) EUB0000685a PIK3CB | B | 8.4 | pIC50 | 4 | nM | IC50 | Affinity Phenotypic Cellular Literature for EUbOPEN Chemogenomics Library wave 3 |
| phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta/Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit delta isoform in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL3130] [GtoPdb: 2155] [UniProtKB: O00329] | ||||||||
| ChEMBL | p110alpha (Alpha) PI3K Binding Assay: PI3K Binding assays are intended for determining the biochemical potency of small molecule PI3K inhibitors. The PI3K lipid kinase reaction is performed in the presence of PIP2:3PS lipid substrate (Promega #V1792) and ATP. Following the termination if the kinase reaction, turnover of ATP to ADP by the phosphorylation of the lipid substrate is detected using the Promega ADP-Glo (Promega #V1792) assay. ReactionFinal Kinase ATP PIP2:3PS TimeKinase Source Concentration (uM) (uM) (min.)PI3K alpha Millipore 0.2 nM 40 50 120#14-602-K PI3K beta Promega 0.6 nM 40 50 120#V1751 PI3K delta Millipore 0.25 nM 40 50 120#14-604-K PI3K gamma Millipore 0.4 nM 25 50 120#14-558-KAfter 120 minutes of reaction time, the kinase reaction is terminated. Any ATP remaining after the reaction is depleted, leaving only ADP. Then the Kinase Detection Reagent is added to convert ADP to ATP, which is used in a coupled luciferin/luciferase reaction. The luminescent output is measured and is correlated with kinase activity. | B | 7.63 | pKi | 23.7 | nM | Ki | US-10112932-B2. Benzoxazepin oxazolidinone compounds and methods of use (2018) |
| ChEMBL | Biochemical Inhibition Assay: The biochemical inhibition of four PI3K isoforms by the Formula I compounds of Table 1. In addition, two clinically tested PI3K compounds, taselisib and pictilisib are included as comparators. The representative compounds of the invention exhibit strong activity against PI3Kα, and exhibit significantly enhanced selectivity relative to the other isoforms PI3Kβ, PI3Kδ, and PI3Kγ when compared to taselisib (GDC-0032) and pictilisib (GDC-0941). In particular, the selectivity ratios in the second from the right column of Table 2A show that each Formula I compounds 101-107 has a PI3K alpha to delta selectivity ratio far higher than taselisib or pictilisib. In fact, both taselisib and pictilisib have stronger activity against PI3K delta than against PI3K alpha, i.e. their selectivity ratios are less than 1. The selectivity ratios of Formula I compound 101-107 range from 301-fold to 634-fold. | B | 8.84 | pKi | 1.43 | nM | Ki | US-10851091-B2. Benzoxazepin oxazolidinone compounds and methods of use (2020) |
| GtoPdb | - | - | 9.68 | pKi | 0.21 | nM | Ki | J Med Chem (2013) 56: 4597-610 [PMID:23662903] |
| ChEMBL | Inhibition of PI3Kdelta (unknown origin) | B | 9.92 | pKi | 0.12 | nM | Ki | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Affinity Biochemical interaction (Enzymatic fluorescence polarization assay) EUB0000685a PIK3CD | B | 9.92 | pKi | 0.12 | nM | Ki | Affinity Biochemical Literature for EUbOPEN Chemogenomics Library wave 3 |
| GtoPdb | - | - | 10.1 | pKi | 0.08 | nM | Ki | US20170015678. Benzoxazepin oxazolidinone compounds and methods of use (2017) |
| ChEMBL | p110alpha (Alpha) PI3K Binding Assay: PI3K Binding assays are intended for determining the biochemical potency of small molecule PI3K inhibitors. The PI3K lipid kinase reaction is performed in the presence of PIP2:3PS lipid substrate (Promega #V1792) and ATP. Following the termination if the kinase reaction, turnover of ATP to ADP by the phosphorylation of the lipid substrate is detected using the Promega ADP-Glo (Promega #V1792) assay. ReactionFinal Kinase ATP PIP2:3PS TimeKinase Source Concentration (uM) (uM) (min.)PI3K alpha Millipore 0.2 nM 40 50 120#14-602-K PI3K beta Promega 0.6 nM 40 50 120#V1751 PI3K delta Millipore 0.25 nM 40 50 120#14-604-K PI3K gamma Millipore 0.4 nM 25 50 120#14-558-KAfter 120 minutes of reaction time, the kinase reaction is terminated. Any ATP remaining after the reaction is depleted, leaving only ADP. Then the Kinase Detection Reagent is added to convert ADP to ATP, which is used in a coupled luciferin/luciferase reaction. The luminescent output is measured and is correlated with kinase activity. | B | 10.1 | pKi | 0.08 | nM | Ki | US-10112932-B2. Benzoxazepin oxazolidinone compounds and methods of use (2018) |
| ChEMBL | Affinity Phenotypic Cellular interaction (MesoScale Discovery assay (AKT phoshorylation in MCF 7 cells)) EUB0000685a PIK3CD | B | 8.4 | pIC50 | 4 | nM | IC50 | Affinity Phenotypic Cellular Literature for EUbOPEN Chemogenomics Library wave 3 |
| ChEMBL | Inhibition of PI3K delta (unknown origin) | B | 9.15 | pIC50 | <0.7 | nM | IC50 | ACS Med Chem Lett (2017) 8: 808-813 [PMID:28835793] |
| phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma/Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit gamma isoform in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL3267] [GtoPdb: 2156] [UniProtKB: P48736] | ||||||||
| GtoPdb | - | - | 8.84 | pKi | 1.43 | nM | Ki | US20170015678. Benzoxazepin oxazolidinone compounds and methods of use (2017) |
| ChEMBL | p110alpha (Alpha) PI3K Binding Assay: PI3K Binding assays are intended for determining the biochemical potency of small molecule PI3K inhibitors. The PI3K lipid kinase reaction is performed in the presence of PIP2:3PS lipid substrate (Promega #V1792) and ATP. Following the termination if the kinase reaction, turnover of ATP to ADP by the phosphorylation of the lipid substrate is detected using the Promega ADP-Glo (Promega #V1792) assay. ReactionFinal Kinase ATP PIP2:3PS TimeKinase Source Concentration (uM) (uM) (min.)PI3K alpha Millipore 0.2 nM 40 50 120#14-602-K PI3K beta Promega 0.6 nM 40 50 120#V1751 PI3K delta Millipore 0.25 nM 40 50 120#14-604-K PI3K gamma Millipore 0.4 nM 25 50 120#14-558-KAfter 120 minutes of reaction time, the kinase reaction is terminated. Any ATP remaining after the reaction is depleted, leaving only ADP. Then the Kinase Detection Reagent is added to convert ADP to ATP, which is used in a coupled luciferin/luciferase reaction. The luminescent output is measured and is correlated with kinase activity. | B | 8.84 | pKi | 1.43 | nM | Ki | US-10112932-B2. Benzoxazepin oxazolidinone compounds and methods of use (2018) |
| GtoPdb | - | - | 9.01 | pKi | 0.97 | nM | Ki | J Med Chem (2013) 56: 4597-610 [PMID:23662903] |
| ChEMBL | Inhibition of PI3Kgamma (unknown origin) | B | 9.01 | pKi | 0.97 | nM | Ki | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Affinity Biochemical interaction (Enzymatic fluorescence polarization assay) EUB0000685a PIK3CG | B | 9.01 | pKi | 0.97 | nM | Ki | Affinity Biochemical Literature for EUbOPEN Chemogenomics Library wave 3 |
| ChEMBL | Biochemical Inhibition Assay: The biochemical inhibition of four PI3K isoforms by the Formula I compounds of Table 1. In addition, two clinically tested PI3K compounds, taselisib and pictilisib are included as comparators. The representative compounds of the invention exhibit strong activity against PI3Kα, and exhibit significantly enhanced selectivity relative to the other isoforms PI3Kβ, PI3Kδ, and PI3Kγ when compared to taselisib (GDC-0032) and pictilisib (GDC-0941). In particular, the selectivity ratios in the second from the right column of Table 2A show that each Formula I compounds 101-107 has a PI3K alpha to delta selectivity ratio far higher than taselisib or pictilisib. In fact, both taselisib and pictilisib have stronger activity against PI3K delta than against PI3K alpha, i.e. their selectivity ratios are less than 1. The selectivity ratios of Formula I compound 101-107 range from 301-fold to 634-fold. | B | 10.1 | pKi | 0.08 | nM | Ki | US-10851091-B2. Benzoxazepin oxazolidinone compounds and methods of use (2020) |
| ChEMBL | Biochemical Inhibition Assay: The biochemical inhibition of four PI3K isoforms by the Formula I compounds of Table 1. In addition, two clinically tested PI3K compounds, taselisib and pictilisib are included as comparators. The representative compounds of the invention exhibit strong activity against PI3Kα, and exhibit significantly enhanced selectivity relative to the other isoforms PI3Kβ, PI3Kδ, and PI3Kγ when compared to taselisib (GDC-0032) and pictilisib (GDC-0941). In particular, the selectivity ratios in the second from the right column of Table 2A show that each Formula I compounds 101-107 has a PI3K alpha to delta selectivity ratio far higher than taselisib or pictilisib. In fact, both taselisib and pictilisib have stronger activity against PI3K delta than against PI3K alpha, i.e. their selectivity ratios are less than 1. The selectivity ratios of Formula I compound 101-107 range from 301-fold to 634-fold. | B | 10.1 | pKi | 0.08 | nM | Ki | US-10851091-B2. Benzoxazepin oxazolidinone compounds and methods of use (2020) |
| ChEMBL | Affinity Phenotypic Cellular interaction (MesoScale Discovery assay (AKT phoshorylation in MCF 7 cells)) EUB0000685a PIK3CG | B | 8.4 | pIC50 | 4 | nM | IC50 | Affinity Phenotypic Cellular Literature for EUbOPEN Chemogenomics Library wave 3 |
| phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha/Phosphatidylinositol 4-phosphate 3-kinase C2 domain-containing subunit alpha in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL1075102] [GtoPdb: 2150] [UniProtKB: O00443] | ||||||||
| ChEMBL | Inhibition of PI3KC2alpha (unknown origin) | B | 5 | pIC50 | >10000 | nM | IC50 | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta/Phosphatidylinositol 4-phosphate 3-kinase C2 domain-containing subunit beta in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL5554] [GtoPdb: 2151] [UniProtKB: O00750] | ||||||||
| ChEMBL | Inhibition of PI3KC2beta (unknown origin) | B | 6.53 | pIC50 | 292 | nM | IC50 | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
| ChEMBL | Selectivity interaction (Enzymatic assay) EUB0000685a PIK3C2B | B | 6.53 | pIC50 | 292 | nM | IC50 | Selectivity Literature for EUbOPEN Chemogenomics Library wave 3 |
| mechanistic target of rapamycin kinase/Serine/threonine-protein kinase mTOR in Human (target type: SINGLE PROTEIN) [ChEMBL: CHEMBL2842] [GtoPdb: 2109] [UniProtKB: P42345] | ||||||||
| ChEMBL | Inhibition of mTOR (unknown origin) | B | 5.92 | pKi | 1200 | nM | Ki | J Med Chem (2013) 56: 4597-4610 [PMID:23662903] |
ChEMBL data shown on this page come from version 36:
Zdrazil B, Felix E, Hunter F, Manners EJ, Blackshaw J, Corbett S, de Veij M, Ioannidis H, Lopez DM, Mosquera JF, Magarinos MP, Bosc N, Arcila R, Kizilören T, Gaulton A, Bento AP, Adasme MF, Monecke P, Landrum GA, Leach AR. (2024). The ChEMBL Database in 2023: a drug discovery platform spanning multiple bioactivity data types and time periods. Nucleic Acids Res., 52(D1). DOI: 10.1093/nar/gkad1004. [EPMCID:10767899] [PMID:37933841]
Davies M, Nowotka M, Papadatos G, Dedman N, Gaulton A, Atkinson F, Bellis L, Overington JP. (2015) 'ChEMBL web services: streamlining access to drug discovery data and utilities.' Nucleic Acids Res., 43(W1). DOI: 10.1093/nar/gkv352. [EPMCID:25883136]
