1. Cell Cycle/DNA Damage
  2. Aurora Kinase


Cat. No.: HY-12054 Purity: 98.48%
Handling Instructions

Hesperadin is an ATP-competitive inhibitor of aurora B kinase with an IC50 of 250 nM.

For research use only. We do not sell to patients.

Hesperadin Chemical Structure

Hesperadin Chemical Structure

CAS No. : 422513-13-1

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Free Sample (0.5-1 mg)   Apply now  
10 mM * 1 mL in DMSO USD 123 In-stock
Estimated Time of Arrival: December 31
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10 mg USD 186 In-stock
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50 mg USD 648 In-stock
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View All Aurora Kinase Isoform Specific Products:

  • Biological Activity

  • Protocol

  • Technical Information

  • Purity & Documentation

  • References


Hesperadin is an ATP-competitive inhibitor of aurora B kinase with an IC50 of 250 nM.

IC50 & Target[1]

Aurora B

250 nM (IC50)

In Vitro

Hesperadin also inhibits other kinases such as AMPK, Lck, MKK1, MAPKAP-K1, CHK1, and PHK at 1 µM drug concentration. Hesperadin causes polyploidy in HeLa cells. Hesperadin-treated HeLa cells show alignment and segregation defects, but sister chromatid separation is intact. Hesperadin causes defects in mitosis and cytokinesis. Hesperadin inhibits Aurora B. Immunofluorescence microscopy reveals that Hesperadin-treated cells in which chromosomes are stretched toward opposite poles, i.e., which have entered anaphase, fail to assemble a central spindle and to properly localize the human centralspindlin subunits CYK-4 and MKLP1[1]. Hesperadin inhibits multiple human clinical isolates of influenza A and B viruses with single to submicromolar efficacy, including oseltamivir-resistant strains. Mechanistic studies reveal that hesperadin inhibits the early stage of viral replication by delaying the nuclear entry of viral ribonucleoprotein complex, thereby inhibiting viral RNA transcription and translation as well as viral protein synthesis[2]. Hesperadin inhibits cell cell proliferation due to appearance of multiple mitotic defects caused by Aurora B activity reduction and elimination of checkpoint proteins--such as hBUBR1 and CENP-E--from kinetochores of mitotic chromosomes[3].

Solvent & Solubility
In Vitro: 

10 mM in DMSO

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.9355 mL 9.6777 mL 19.3555 mL
5 mM 0.3871 mL 1.9355 mL 3.8711 mL
10 mM 0.1936 mL 0.9678 mL 1.9355 mL
*Please refer to the solubility information to select the appropriate solvent.
Kinase Assay

The kinase assay is performed with 10 μL beads in 20 μL kinase buffer containing 5 g histone H1, 1 μM ATP, 1 μCi [32P]ATP, and the appropriate concentration of Hesperadin or DMSO for 30 min at 37C. SDS sample buffer is added, and samples are boiled and resolved by SDS-PAGE. The gel is dried, and the radioactive signal is detected by PhosphorImager analysis[1].

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

Cell Assay

To determine cellular cytotoxicity of Hesperadin, 200 µL fresh DMEM (without FBS) medium containing serial half-log diluted Hesperadin is added to each well. After incubating for 48 h with 5% CO2 in the cell culture incubator at 37 °C, the medium is removed and 100 µL DMEM medium containing 40 µg/mL neutral red is added. The solution is incubated for another 4 h at 37 °C in the cell culture incubator. The medium is removed and the amount of neutral red that is taken by the viable cells is dissolved by adding 100 µL of destaining solution (50% ethanol, 49% H2O, and 1% acetic acid). The absorbance of the solution at 540 nm is determined[2].

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

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Cat. No.: HY-12054