1. Cell Cycle/DNA Damage
  2. Topoisomerase

Amsacrine (Synonyms: AMSA; m-AMSA; CI-880; SN-11841; acridinyl anisidide)

Cat. No.: HY-13551 Purity: 99.98%
Handling Instructions

Amsacrine is an inhibitor of topoisomerase II, and acts as an antineoplastic agent which can intercalates into the DNA of tumor cells.

For research use only. We do not sell to patients.
Amsacrine Chemical Structure

Amsacrine Chemical Structure

CAS No. : 51264-14-3

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Free Sample (0.5-1 mg)   Apply now  
10 mM * 1 mL in DMSO USD 92 In-stock
10 mg USD 84 In-stock
50 mg USD 192 In-stock
100 mg USD 264 In-stock
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Other Forms of Amsacrine:

  • Biological Activity

  • Protocol

  • Technical Information

  • Purity & Documentation

  • References


Amsacrine is an inhibitor of topoisomerase II, and acts as an antineoplastic agent which can intercalates into the DNA of tumor cells.

IC50 & Target

Topoisomerase II[1]

In Vitro

Amsacrine 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 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 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-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 induces MCL1 down-regulation by decreasing its stability. Further, amsacrine-treated U937 cells show AKT degradation and Ca2+-mediated ERK inactivation[4].

In Vivo

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 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].

Clinical Trial
Preparing Stock Solutions
Concentration Volume Mass 1 mg 5 mg 10 mg
1 mM 2.5416 mL 12.7078 mL 25.4155 mL
5 mM 0.5083 mL 2.5416 mL 5.0831 mL
10 mM 0.2542 mL 1.2708 mL 2.5416 mL
Please refer to the solubility information to select the appropriate solvent.
Animal Administration

Amsacrine 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 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. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Molecular Weight








Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month

Room temperature in continental US; may vary elsewhere

Solvent & Solubility

DMSO: 9.3 mg/mL

* "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

Purity: 99.98%

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