etp 46464 Search Results


90
MedChemExpress etp 46464
Effects of mTOR inhibitors on the proliferation of pancreatic cancer cells. (A) RTCA assay. Cells were treated with PF-04691502, GSK1059615, Dactolisib, PI-103, CC-223, AZD-8055, Salidroside, Vistusertib, PP121, Apitolisib, Voxtalisib, Sapanisertib, Palomid 529, KU-0063794, and Torkinib (20 μM). (B) RTCA assay. Cells were treated with GNE-477, 3BDO, PQR620, HDACs, CZ415, mTOR inhibitor-1, Omipalisib, NSC781406, JR-AB2-011, mTOR inhibitor-3, BGT226, Temsirolimus, MHY1485, GNE-317, and Torin 2 (20 μM). (C) RTCA assay. Cells were treated with <t>ETP-46464,</t> WYE-354, Dihydromyricetin, CC-115 (hydrochloride), GDC-0349, LY3023414, WAY-600, GNE-493, PI-103 (hydrochloride), XL388, GDC-0084, CC-115, Bimiralisib, WYE-132, and VS-5584 (20 μM). (D) A statistical bar chart of RTCA results of mTOR inhibitors. (E) RTCA assay. SW1990 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (F) RTCA assay. Patu8988 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (G) RTCA assay. BxPC-3 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (H) RTCA assay. CFPAC-1 cells were treated with CC-223, NSC781406, and BGT226 (20 μM).
Etp 46464, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ETP-46464(Cat No.:I001318)is a potent and selective inhibitor of the DNA damage response kinase ataxia-telangiectasia and Rad3-related protein (ATR), a key regulator of the cellular response to DNA replication stress. By inhibiting ATR, ETP-46464 impairs the
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93
Selleck Chemicals atr inhibitor
Replication stress phenotypes depend on <t>Cdk1-,</t> <t>Plk1-</t> and <t>ATR.</t> a Mean percentages of CENP-F positive RPE1 cells; N = 3 examining NT = 1398, 200 nM Aph = 1549, 400 nM Aph = 1632 and Cdk1i = 865 interphase cells; p < 0.0001 in a one-way Anova (NT vs. 200 nM Aph p = 0.005; NT vs. 400 nM Aph p < 0.0001; NT vs. Cdk1 inhibition p < 0.0001). b Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 5 examining Aph = 210 and Aph/ATR = 221 mitoses; p = 0.0275 in paired t -test. c Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 6 examining Aph = 369, Cdk1i = 440 and Aph/Cdk1i = 457 mitoses; p < 0.0001 in a one-way Anova (400 nM Aph vs. Cdk1 inhibition p = 0.0005 and 400 nM Aph vs. 400 nM Aph + Cdk1 inhibition p = 0.003). d Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 3 examining Aph = 159 and Aph/Cdk1i = 208 mitoses; p = 0.004 in unpaired t -test. e Representative time-lapse images of metaphasic RPE centrin1-GFP cells stained with SiR-tubulin and treated with a 200 nM nocodazole pulse at t = 0 after indicated treatments; scale bars = 10 μm. f Quantification of the spindle signal as in Fig. ; N = 20 for Aph and 23 cells for Aph/Cdk1i; * p < 0.05; ** p < 0.01; *** p < 0.001 in a repeated measurement Anova test. g Quantification of the spindle signal as in Fig. ; N = 31 for Cdk1i and 34 for NT. h Mean percentage of RPE cells containing CENP-A-negative and positive micronuclei. N = 3 examining Aph = 2421 and Aph/Cdk1i = 1793 interphase cells p = 0.0339 in unpaired t -test. i Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 7 examining Aph = 321, Aph/5 nM Plk1i = 336 and Aph/10nMPlk1i = 357 mitoses; p = 0.0377 in a one-way Anova (400 nM Aph vs. 5 nM Plk1 inhibition p = 0.1787 and 400 nM Aph vs. 400 nM Aph + 10 nM PLK1 inhibition p = 0.0091). Error bars indicate sem. Source data are provided as a Source Data file
Atr Inhibitor, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/etp+46464/ETP-46464/pmc06687892-231-45-48
Average 93 stars, based on 1 article reviews
atr inhibitor - by Bioz Stars, 2026-10
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90
ApexBio etp-46464
Replication stress phenotypes depend on <t>Cdk1-,</t> <t>Plk1-</t> and <t>ATR.</t> a Mean percentages of CENP-F positive RPE1 cells; N = 3 examining NT = 1398, 200 nM Aph = 1549, 400 nM Aph = 1632 and Cdk1i = 865 interphase cells; p < 0.0001 in a one-way Anova (NT vs. 200 nM Aph p = 0.005; NT vs. 400 nM Aph p < 0.0001; NT vs. Cdk1 inhibition p < 0.0001). b Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 5 examining Aph = 210 and Aph/ATR = 221 mitoses; p = 0.0275 in paired t -test. c Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 6 examining Aph = 369, Cdk1i = 440 and Aph/Cdk1i = 457 mitoses; p < 0.0001 in a one-way Anova (400 nM Aph vs. Cdk1 inhibition p = 0.0005 and 400 nM Aph vs. 400 nM Aph + Cdk1 inhibition p = 0.003). d Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 3 examining Aph = 159 and Aph/Cdk1i = 208 mitoses; p = 0.004 in unpaired t -test. e Representative time-lapse images of metaphasic RPE centrin1-GFP cells stained with SiR-tubulin and treated with a 200 nM nocodazole pulse at t = 0 after indicated treatments; scale bars = 10 μm. f Quantification of the spindle signal as in Fig. ; N = 20 for Aph and 23 cells for Aph/Cdk1i; * p < 0.05; ** p < 0.01; *** p < 0.001 in a repeated measurement Anova test. g Quantification of the spindle signal as in Fig. ; N = 31 for Cdk1i and 34 for NT. h Mean percentage of RPE cells containing CENP-A-negative and positive micronuclei. N = 3 examining Aph = 2421 and Aph/Cdk1i = 1793 interphase cells p = 0.0339 in unpaired t -test. i Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 7 examining Aph = 321, Aph/5 nM Plk1i = 336 and Aph/10nMPlk1i = 357 mitoses; p = 0.0377 in a one-way Anova (400 nM Aph vs. 5 nM Plk1 inhibition p = 0.1787 and 400 nM Aph vs. 400 nM Aph + 10 nM PLK1 inhibition p = 0.0091). Error bars indicate sem. Source data are provided as a Source Data file
Etp 46464, supplied by ApexBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/etp+46464/etp+46464/pm37773176-229-30-31
Average 90 stars, based on 1 article reviews
etp-46464 - by Bioz Stars, 2026-10
90/100 stars
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90
Broad Institute Inc etp-46464
Replication stress phenotypes depend on <t>Cdk1-,</t> <t>Plk1-</t> and <t>ATR.</t> a Mean percentages of CENP-F positive RPE1 cells; N = 3 examining NT = 1398, 200 nM Aph = 1549, 400 nM Aph = 1632 and Cdk1i = 865 interphase cells; p < 0.0001 in a one-way Anova (NT vs. 200 nM Aph p = 0.005; NT vs. 400 nM Aph p < 0.0001; NT vs. Cdk1 inhibition p < 0.0001). b Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 5 examining Aph = 210 and Aph/ATR = 221 mitoses; p = 0.0275 in paired t -test. c Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 6 examining Aph = 369, Cdk1i = 440 and Aph/Cdk1i = 457 mitoses; p < 0.0001 in a one-way Anova (400 nM Aph vs. Cdk1 inhibition p = 0.0005 and 400 nM Aph vs. 400 nM Aph + Cdk1 inhibition p = 0.003). d Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 3 examining Aph = 159 and Aph/Cdk1i = 208 mitoses; p = 0.004 in unpaired t -test. e Representative time-lapse images of metaphasic RPE centrin1-GFP cells stained with SiR-tubulin and treated with a 200 nM nocodazole pulse at t = 0 after indicated treatments; scale bars = 10 μm. f Quantification of the spindle signal as in Fig. ; N = 20 for Aph and 23 cells for Aph/Cdk1i; * p < 0.05; ** p < 0.01; *** p < 0.001 in a repeated measurement Anova test. g Quantification of the spindle signal as in Fig. ; N = 31 for Cdk1i and 34 for NT. h Mean percentage of RPE cells containing CENP-A-negative and positive micronuclei. N = 3 examining Aph = 2421 and Aph/Cdk1i = 1793 interphase cells p = 0.0339 in unpaired t -test. i Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 7 examining Aph = 321, Aph/5 nM Plk1i = 336 and Aph/10nMPlk1i = 357 mitoses; p = 0.0377 in a one-way Anova (400 nM Aph vs. 5 nM Plk1 inhibition p = 0.1787 and 400 nM Aph vs. 400 nM Aph + 10 nM PLK1 inhibition p = 0.0091). Error bars indicate sem. Source data are provided as a Source Data file
Etp 46464, supplied by Broad Institute Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/etp+46464/etp+46464/pmc10081209__media___1-36-0-21
Average 90 stars, based on 1 article reviews
etp-46464 - by Bioz Stars, 2026-10
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N/A
ETP-46464 is a cell-permeable quinoline-containing heterotricyclic compound that acts as a potent inhibitor against mTOR, ATR, DNA-PK, PI 3-Kα, and ATM (IC50= 0.6, 14, 36, 170, and 545 nM, respectively).
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Effects of mTOR inhibitors on the proliferation of pancreatic cancer cells. (A) RTCA assay. Cells were treated with PF-04691502, GSK1059615, Dactolisib, PI-103, CC-223, AZD-8055, Salidroside, Vistusertib, PP121, Apitolisib, Voxtalisib, Sapanisertib, Palomid 529, KU-0063794, and Torkinib (20 μM). (B) RTCA assay. Cells were treated with GNE-477, 3BDO, PQR620, HDACs, CZ415, mTOR inhibitor-1, Omipalisib, NSC781406, JR-AB2-011, mTOR inhibitor-3, BGT226, Temsirolimus, MHY1485, GNE-317, and Torin 2 (20 μM). (C) RTCA assay. Cells were treated with ETP-46464, WYE-354, Dihydromyricetin, CC-115 (hydrochloride), GDC-0349, LY3023414, WAY-600, GNE-493, PI-103 (hydrochloride), XL388, GDC-0084, CC-115, Bimiralisib, WYE-132, and VS-5584 (20 μM). (D) A statistical bar chart of RTCA results of mTOR inhibitors. (E) RTCA assay. SW1990 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (F) RTCA assay. Patu8988 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (G) RTCA assay. BxPC-3 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (H) RTCA assay. CFPAC-1 cells were treated with CC-223, NSC781406, and BGT226 (20 μM).

Journal: Frontiers in Pharmacology

Article Title: CC-223, NSC781406, and BGT226 Exerts a Cytotoxic Effect Against Pancreatic Cancer Cells via mTOR Signaling

doi: 10.3389/fphar.2020.580407

Figure Lengend Snippet: Effects of mTOR inhibitors on the proliferation of pancreatic cancer cells. (A) RTCA assay. Cells were treated with PF-04691502, GSK1059615, Dactolisib, PI-103, CC-223, AZD-8055, Salidroside, Vistusertib, PP121, Apitolisib, Voxtalisib, Sapanisertib, Palomid 529, KU-0063794, and Torkinib (20 μM). (B) RTCA assay. Cells were treated with GNE-477, 3BDO, PQR620, HDACs, CZ415, mTOR inhibitor-1, Omipalisib, NSC781406, JR-AB2-011, mTOR inhibitor-3, BGT226, Temsirolimus, MHY1485, GNE-317, and Torin 2 (20 μM). (C) RTCA assay. Cells were treated with ETP-46464, WYE-354, Dihydromyricetin, CC-115 (hydrochloride), GDC-0349, LY3023414, WAY-600, GNE-493, PI-103 (hydrochloride), XL388, GDC-0084, CC-115, Bimiralisib, WYE-132, and VS-5584 (20 μM). (D) A statistical bar chart of RTCA results of mTOR inhibitors. (E) RTCA assay. SW1990 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (F) RTCA assay. Patu8988 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (G) RTCA assay. BxPC-3 cells were treated with CC-223, NSC781406, and BGT226 (20 μM). (H) RTCA assay. CFPAC-1 cells were treated with CC-223, NSC781406, and BGT226 (20 μM).

Article Snippet: mTOR inhibitors PF-04691502 (purity of 99.64%), GSK1059615 (purity of 98.91%), Dactolisib (purity of 99.13%), PI-103 (purity of 99.86%), CC-223 (purity of 99.43%), AZD-8055 (purity of 99.19%), Salidroside (purity of 98.63%), Vistusertib (purity of 98.82%), PP121 (purity of 98.89%), Apitolisib (purity of 99.26%), Voxtalisib (purity of 99.93%), Sapanisertib (purity of 99.06%), Palomid 529 (purity of 99.47%), KU-0063794 (purity of 99.23%), Torkinib (purity of 98.76%), GNE-477 (purity of 95.81%), 3BDO (purity of 99.67%), PQR620 (purity of 98.06%), HDACs (purity of 99.12%), CZ415 (purity of 98.43%), mTOR inhibitor-1 (purity of 99.29%), Omipalisib (purity of 99.31%), NSC781406 (purity of 99.91%), JR-AB2-011 (purity of 98.09%), mTOR inhibitor-3 (purity of 98.54%), BGT226, Temsirolimus (purity of 99.56%), MHY1485 (purity of 99.86%), GNE-317 (purity of 99.26%), Torin 2 (purity of 99.93%), ETP-46464 (purity of 99.13%), WYE-354 (purity > 98.0%), Dihydromyricetin (purity of 99.54%), CC-115 (hydrochloride, purity of 96.64%), GDC-0349 (purity of 98.2%), LY3023414 (purity of 99.77%), WAY-600 (purity of 95.12%), GNE-493 (purity of 95.12%), PI-103 (hydrochloride, purity of 99.86%), XL388 (purity of 98.46%), GDC-0084 (purity of 99.28%), CC-115 (purity of 96.64%), Bimiralisib (purity of 98.90%), WYE-132 (purity of 98.98%), and VS-5584 (purity of 98.01%) were purchased from MCE (China).

Techniques:

Replication stress phenotypes depend on Cdk1-, Plk1- and ATR. a Mean percentages of CENP-F positive RPE1 cells; N = 3 examining NT = 1398, 200 nM Aph = 1549, 400 nM Aph = 1632 and Cdk1i = 865 interphase cells; p < 0.0001 in a one-way Anova (NT vs. 200 nM Aph p = 0.005; NT vs. 400 nM Aph p < 0.0001; NT vs. Cdk1 inhibition p < 0.0001). b Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 5 examining Aph = 210 and Aph/ATR = 221 mitoses; p = 0.0275 in paired t -test. c Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 6 examining Aph = 369, Cdk1i = 440 and Aph/Cdk1i = 457 mitoses; p < 0.0001 in a one-way Anova (400 nM Aph vs. Cdk1 inhibition p = 0.0005 and 400 nM Aph vs. 400 nM Aph + Cdk1 inhibition p = 0.003). d Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 3 examining Aph = 159 and Aph/Cdk1i = 208 mitoses; p = 0.004 in unpaired t -test. e Representative time-lapse images of metaphasic RPE centrin1-GFP cells stained with SiR-tubulin and treated with a 200 nM nocodazole pulse at t = 0 after indicated treatments; scale bars = 10 μm. f Quantification of the spindle signal as in Fig. ; N = 20 for Aph and 23 cells for Aph/Cdk1i; * p < 0.05; ** p < 0.01; *** p < 0.001 in a repeated measurement Anova test. g Quantification of the spindle signal as in Fig. ; N = 31 for Cdk1i and 34 for NT. h Mean percentage of RPE cells containing CENP-A-negative and positive micronuclei. N = 3 examining Aph = 2421 and Aph/Cdk1i = 1793 interphase cells p = 0.0339 in unpaired t -test. i Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 7 examining Aph = 321, Aph/5 nM Plk1i = 336 and Aph/10nMPlk1i = 357 mitoses; p = 0.0377 in a one-way Anova (400 nM Aph vs. 5 nM Plk1 inhibition p = 0.1787 and 400 nM Aph vs. 400 nM Aph + 10 nM PLK1 inhibition p = 0.0091). Error bars indicate sem. Source data are provided as a Source Data file

Journal: Nature Communications

Article Title: Mild replication stress causes chromosome mis-segregation via premature centriole disengagement

doi: 10.1038/s41467-019-11584-0

Figure Lengend Snippet: Replication stress phenotypes depend on Cdk1-, Plk1- and ATR. a Mean percentages of CENP-F positive RPE1 cells; N = 3 examining NT = 1398, 200 nM Aph = 1549, 400 nM Aph = 1632 and Cdk1i = 865 interphase cells; p < 0.0001 in a one-way Anova (NT vs. 200 nM Aph p = 0.005; NT vs. 400 nM Aph p < 0.0001; NT vs. Cdk1 inhibition p < 0.0001). b Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 5 examining Aph = 210 and Aph/ATR = 221 mitoses; p = 0.0275 in paired t -test. c Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 6 examining Aph = 369, Cdk1i = 440 and Aph/Cdk1i = 457 mitoses; p < 0.0001 in a one-way Anova (400 nM Aph vs. Cdk1 inhibition p = 0.0005 and 400 nM Aph vs. 400 nM Aph + Cdk1 inhibition p = 0.003). d Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 3 examining Aph = 159 and Aph/Cdk1i = 208 mitoses; p = 0.004 in unpaired t -test. e Representative time-lapse images of metaphasic RPE centrin1-GFP cells stained with SiR-tubulin and treated with a 200 nM nocodazole pulse at t = 0 after indicated treatments; scale bars = 10 μm. f Quantification of the spindle signal as in Fig. ; N = 20 for Aph and 23 cells for Aph/Cdk1i; * p < 0.05; ** p < 0.01; *** p < 0.001 in a repeated measurement Anova test. g Quantification of the spindle signal as in Fig. ; N = 31 for Cdk1i and 34 for NT. h Mean percentage of RPE cells containing CENP-A-negative and positive micronuclei. N = 3 examining Aph = 2421 and Aph/Cdk1i = 1793 interphase cells p = 0.0339 in unpaired t -test. i Mean percentages of disengaged RPE1 centrin1-GFP cells; N = 7 examining Aph = 321, Aph/5 nM Plk1i = 336 and Aph/10nMPlk1i = 357 mitoses; p = 0.0377 in a one-way Anova (400 nM Aph vs. 5 nM Plk1 inhibition p = 0.1787 and 400 nM Aph vs. 400 nM Aph + 10 nM PLK1 inhibition p = 0.0091). Error bars indicate sem. Source data are provided as a Source Data file

Article Snippet: Cells were treated with 200 nM, 400 nM (for RPE1) or 1 μM Aphidicolin (for MCF10A; for 16 h), 1 mM Hydroxyurea (for 3 h), 10 ng/ml Nocodazole (for 16 h), 9 μM RO3306, 5 nM or 10 nM Plk1 inhibitor (BI2536; Sigma), 800 nM ATR inhibitor (ETP-46464; Selleckchem) or 6 nM Taxol (added 3 h before the beginning of the movie, all Sigma Aldrich).

Techniques: Inhibition, Staining