Chlorambucil is an orally-active antineoplastic aromatic nitrogen mustard. Chlorambucil alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.
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Mubritinib (TAK-165) is a potent inhibitor of HER2/ErbB2 with IC50 of 6 nM.
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Mubritinib (TAK-165) is a potent inhibitor of HER2/ErbB2 with IC50 of 6 nM.
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Ponatinib is an orally available, multitargeted kinase inhibitor (IC50s: 0.37/1.1/1.5/2.2/5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively).
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SP600125 is a JNK1/2/3 inhibitor (IC50: 40/40/90 nM) and 10-fold higher selectivity than MKK4, 25-fold higher selectivity than MKK3, MKK6, PKCα, and PKB.
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Ponatinib is an orally available, multitargeted kinase inhibitor (IC50s: 0.37/1.1/1.5/2.2/5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively).
More Information Supplier Page Chlorambucil is an orally-active antineoplastic aromatic nitrogen mustard. Chlorambucil alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.
More Information Supplier Page Chlorambucil is an orally-active antineoplastic aromatic nitrogen mustard. Chlorambucil alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.
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Fabomotizole hydrochloride (CM346 hydrochloride), an anxiolytic drug, produces anxiolytic and neuroprotective effects. The mechanism of Afobazole remains poorly defined, however, with GABAergic, NGF, and BDNF release promoting, MT1 receptor antagonism, MT3 receptor antagonism, and sigma agonism suggested as potential mechanisms. Afobazole inhibits MAO-A reversibly and there might be also some involvement with serotonin receptors.
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Fabomotizole hydrochloride (CM346 hydrochloride), an anxiolytic drug, produces anxiolytic and neuroprotective effects. The mechanism of Afobazole remains poorly defined, however, with GABAergic, NGF, and BDNF release promoting, MT1 receptor antagonism, MT3 receptor antagonism, and sigma agonism suggested as potential mechanisms. Afobazole inhibits MAO-A reversibly and there might be also some involvement with serotonin receptors.
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