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11787-1An inhibitor of EHMT2, also known as G9a, decreasing di- and trimethylation on lysine 9 of histone 3 (EC50 = 5 µM) induces senescence in the pancreatic cancer cell line PANC-1 without initiating apoptosis.
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11787-10An inhibitor of EHMT2, also known as G9a, decreasing di- and trimethylation on lysine 9 of histone 3 (EC50 = 5 µM) induces senescence in the pancreatic cancer cell line PANC-1 without initiating apoptosis.
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11787-25An inhibitor of EHMT2, also known as G9a, decreasing di- and trimethylation on lysine 9 of histone 3 (EC50 = 5 µM) induces senescence in the pancreatic cancer cell line PANC-1 without initiating apoptosis.
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11787-5An inhibitor of EHMT2, also known as G9a, decreasing di- and trimethylation on lysine 9 of histone 3 (EC50 = 5 µM) induces senescence in the pancreatic cancer cell line PANC-1 without initiating apoptosis.
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19834-1An HDAC inhibitor (IC<sub>50</sub>s = 29 nM, 62 nM, and 1.09 µM for HDAC1, 2, and 3, respectively) possesses preferential binding kinetics with seven-fold longer half-life on HDAC2 compared to HDAC1 (143 min vs. 20 min).
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19834-10An HDAC inhibitor (IC<sub>50</sub>s = 29 nM, 62 nM, and 1.09 µM for HDAC1, 2, and 3, respectively) possesses preferential binding kinetics with seven-fold longer half-life on HDAC2 compared to HDAC1 (143 min vs. 20 min).
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19834-5An HDAC inhibitor (IC<sub>50</sub>s = 29 nM, 62 nM, and 1.09 µM for HDAC1, 2, and 3, respectively) possesses preferential binding kinetics with seven-fold longer half-life on HDAC2 compared to HDAC1 (143 min vs. 20 min).
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19834-500An HDAC inhibitor (IC<sub>50</sub>s = 29 nM, 62 nM, and 1.09 µM for HDAC1, 2, and 3, respectively) possesses preferential binding kinetics with seven-fold longer half-life on HDAC2 compared to HDAC1 (143 min vs. 20 min).
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19836-1An HDAC inhibitor (IC<sub>50</sub>s = 21 nM, 100 nM, and 11.48 µM for HDAC1, 2, and 3, respectively) possesses six6-fold extended half-life for binding on HDAC2 compared to HDAC1 (381 min vs.
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19836-10An HDAC inhibitor (IC<sub>50</sub>s = 21 nM, 100 nM, and 11.48 µM for HDAC1, 2, and 3, respectively) possesses six6-fold extended half-life for binding on HDAC2 compared to HDAC1 (381 min vs.
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19836-5An HDAC inhibitor (IC<sub>50</sub>s = 21 nM, 100 nM, and 11.48 µM for HDAC1, 2, and 3, respectively) possesses six6-fold extended half-life for binding on HDAC2 compared to HDAC1 (381 min vs.
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16919-10A small molecule inhibitor that potently and selectively inhibits both HDAC6 and HDAC8 (IC<sub>50</sub>s = 36 and 120 nM, respectively).