m-AMSA; acridinyl anisidide MedChemExpress (MCE)

Product Name	Amsacrine
Synonyms	CI-880 Amekrin Amsidyl Amsakrin Amsacrine M-AMSA, HCL M-AMSA HYDROCHLORIDE Synonyms CI-880 Amekrin Amsidyl Amsakrin Amsacrine M-AMSA, HCL M-AMSA HYDROCHLORIDE 4'-(9-Acridinylamino)methanesulfon-m-anisidide N-[4-(acridin-9-ylmethyl)-3-methoxyphenyl]methanesulfonamide N-[4-(Acridin-9-ylamino)-3-(methyloxy)phenyl]methanesulfonamide
CAS	51264-14-3
EINECS	257-094-3
Chemical Formula	C21H19N3O3S
Molecular Weight	393.46
inchi	InChI=1/C22H20N2O3S/c1-27-22-14-16(24-28(2,25)26)12-11-15(22)13-19-17-7-3-5-9-20(17)23-21-10-6-4-8-18(19)21/h3-12,14,24H,13H2,1-2H3
Package	10 mM * 1 mL;5 mg;10 mg;25 mg;50 mg;100 mg
Price	Email to quote
Descriptions	Amsacrine Amsacrine MedChemExpress (MCE) HY-13551 51264-14-3 m-AMSA Descriptions Amsacrine Amsacrine MedChemExpress (MCE) HY-13551 51264-14-3 m-AMSA acridinyl anisidide 99.91% Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year Room temperature in continental US may vary elsewhere. Amsacrine (m-AMSA acridinyl anisidide) is an inhibitor of topoisomerase II, and acts as an antineoplastic agent which can intercalates into the DNA of tumor cells. Amsacrine (m-AMSA) blocks HERG currents in HEK 293 cells and Xenopus oocytes in a concentration-dependent manner, with IC50 values of 209.4 nm and 2.0 μM, respectively. Amsacrine (m-AMSA) causes a negative shift in the voltage dependence of both activation (?7.6 mV) and inactivation (?7.6 mV). HERG current block by amsacrine is not frequency dependent[1]. In vitro studies of normal human lymphocytes with various concentrations of Amsacrine (m-AMSA), show both increased levels of chromosomal aberrations, ranging from 8% to 100%, and increase SCEs, ranging from 1.5 times the normal at the lowest concentration studied (0.005 μg/mL) to 12 times the normal (0.25 μg/mL)[3]. Amsacrine (m-AMSA)-induced apoptosis of U937 cells is characterized by caspase-9 and caspase-3 activation, increased intracellular Ca2+ concentration, mitochondrial depolarization, and MCL1 down-regulation. Amsacrine (m-AMSA) induces MCL1 down-regulation by decreasing its stability. Further, amsacrine-treated U937 cells show AKT degradation and Ca2+-mediated ERK inactivation[4]. In animals treated with different doses of amsacrine (0.5-12 mg/kg), the frequencies of micronucleated polychromatic erythrocytes increase significantly after treatment with 9 and 12 mg/kg. Furthermore, the present study demonstrates for the first time that Amsacrine (m-AMSA) has high incidences of clastogenicity and low incidences of aneugenicity whereas nocodazole has high incidences of aneugenicity and low incidences of clastogenicity during mitotic phases in vivo[2]. Amsacrine (m-AMSA) is investigated in three separated experiments. In the first experiment, animals are treated by intraperitoneal injection with 0.5, 1.5 and 4.5 mg/kg of amsacrine and bone marrow is sampled 24 h after treatment. Preliminary negative MN results at this sampling time lead to the use of 30 h sampling time for amsacrine. Thus, in the second experiment, mice are treated with 0.5, 1.5 and 4.5 mg/kg of Amsacrine (m-AMSA) and bone marrow is sampled 30 h after treatment. The doses and sampling times for amsacrine are chosen by reference to earlier studies and the selected doses are within the dose range used for human chemotherapy. The results again show that the micronuclei frequency in the bone marrow of mice is not affected by treatment with any of the selected doses of the test agent, at 30 h sampling time, thus, in the third experiment, mice are treated with 6, 9 and 12 mg/kg of amsacrine and bone marrow is sampled 24 and 30 h after treatment. Topoisomerase II \| \| \| \| \| \| \| \| \| \| [1]. Thomas D, et al. Inhibition of cardiac HERG currents by the DNA topoisomerase II inhibitor amsacrine: mode of action. Br J Pharmacol. 2004 Jun 142(3):485-94. [Content Brief] [2]. Attia SM. Molecular cytogenetic evaluation of the mechanism of genotoxic potential of amsacrine and nocodazole in mouse bone marrow cells. J Appl Toxicol. 2013 Jun 33(6):426-33. [Content Brief] [3]. Kao-Shan CS, et al. Cytogenetic effects of amsacrine on human lymphocytes in vivo and in vitro. Cancer Treat Rep. 1984 Jul-Aug 68(7-8):989-97. [Content Brief] [4]. Lee YC, et al. Amsacrine-induced apoptosis of human leukemia U937 cells is mediated by the inhibition of AKT- and ERK-induced stabilization of MCL1. Apoptosis. 2016 Oct 19 [Content Brief]
Supplier Website	https://www.medchemexpress.com/Amsacrine.html
Last Update	2025-05-21 16:50:25

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