HESPERADIN
Hesperadin
CAS: 422513-13-1
Molecular Formula: C29H32N4O3S
HESPERADIN - Names and Identifiers
HESPERADIN - Physico-chemical Properties
| Molecular Formula | C29H32N4O3S |
| Molar Mass | 516.65 |
| Density | 1.326 |
| Melting Point | 228 °C |
| Solubility | DMSO, Methanol |
| Appearance | Solid |
| Color | Yellow |
| pKa | 9.14±0.20(Predicted) |
| Storage Condition | Refrigerator |
| In vitro study | Hesperadin inhibits the immunoprecipitate Aurora B, which phosphorylates histone H3, with an IC50 of 250 nM, and significantly reduces other kinases at a concentration of 1 μm (AMPK,Lck,MKK1,MAPKAP-K1,CHK1, and PHK) activity. 20-100 nM Hesperadin acts on HeLa cells, inducing loss of phosphorylation of mitotic histone H3 at the Ser10 site. Hesperadin treatment, which causes defects in mitosis and cytokinesis, leads to cessation of HeLa cell proliferation and polyploidization, as Aurora B function is inhibited during chromosome ligation. 100 nM Hesperadin restored mitotic arrest induced by paclitaxel or Monastrol instead of Nocodazole. Hesperadin and Nocodazole treated HeLa cells, abolished the centromere regionalization of BubR1, and reduced the intensity of Bub1 at the centromere, indicating that Aurora B function is necessary for efficient recruitment of BubR1 and Bub1 centroids, it can be stated that it is necessary to extend the detection point signal. In an in vitro kinase assay, Hesperadin blocked recombinant Trypanosoma histone H3 phosphorylation by T. brucei Aurora kinase -1 (TbAUK1) from pathogenic Trypanosoma brucei with an IC50 of 40 nM. Hesperadin significantly inhibited the growth of cultured Transmissibility blood form (BF) cells with an IC50 of 48 nM and weakly inhibited the growth of insect circulating phase form (PF) cells with an IC50 of 550 nM. Hesperadin inhibits Aurora B, an immunoprecipitate that phosphorylates histone H3, with an IC50 of 250 nM, and significantly reduces other kinases at a concentration of 1 μm (AMPK,Lck,MKK1,MAPKAP-K1,CHK1, and PHK) activity. 20-100 nM Hesperadin acts on HeLa cells, inducing loss of phosphorylation of mitotic histone H3 at the Ser10 site. Hesperadin treatment, causing defects in mitosis and cytokinesis, leading to cessation of HeLa cell proliferation and polyploidization, This is because Aurora B function is inhibited during chromosome joining. 100 nM Hesperadin restored mitotic arrest induced by paclitaxel or Monastrol instead of Nocodazole. Hesperadin and Nocodazole treated HeLa cells, abolished the centromere regionalization of BubR1, and reduced the intensity of Bub1 at the centromere, indicating that Aurora B function is necessary for efficient recruitment of BubR1 and Bub1 centroids, it can be stated that it is necessary to extend the detection point signal. In an in vitro kinase assay, Hesperadin blocked recombinant Trypanosoma histone H3 phosphorylation by T. brucei Aurora kinase -1 (TbAUK1) from pathogenic Trypanosoma brucei with an IC50 of 40 nM. Hesperadin significantly inhibited the growth of cultured Transmissibility blood form (BF) cells with an IC50 of 48 nM and weakly inhibited the growth of insect circulating phase form (PF) cells with an IC50 of 550 nM. |
HESPERADIN - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 1.935 ml | 9.677 ml | 19.355 ml |
| 5 mM | 0.387 ml | 1.935 ml | 3.871 ml |
| 10 mM | 0.194 ml | 0.968 ml | 1.935 ml |
| 5 mM | 0.039 ml | 0.194 ml | 0.387 ml |
Last Update：2024-01-02 23:10:35
HESPERADIN - Reference Information
| biological activity | Hesperadin can effectively inhibit Aurora B,IC50 is 250 nM, and significantly reduce the activities of AMPK, Lck, MKK1, MAPKAP-K1, CHK1 and PHK, but will not inhibit MKK1 activity in vivo. Hesperadin can effectively inhibit Aurora B, and IC50 is 250 nM in cell-free test. It significantly reduces the activities of AMPK, Lck, MKK1, MAPKAP-K1, CHK1 and PHK, but does not inhibit MKK1 activity in vivo. |
| in vitro study | Hesperadin inhibit Aurora B,IC50 of phosphorylated histone H3, and significantly reduce the activity of other kinases (AMPK,Lck,MKK1,MAPKAP-K1,CHK1, and PHK) at a concentration of 1 μM. 20-100 nM Hesperadin acts on HeLa cells to induce the loss of phosphorylation of mitotic histone H3 at Ser10 site. Hesperadin treatment caused mitotic and cytoplasmic defects, which led to the cessation of HeLa cell proliferation and polyploidization, due to the inhibition of Aurora B function during chromosome connection. 100 nM Hesperadin restored paclitaxel or Monastrol rather than Nocodazole-induced mitotic arrest. Hesperadin and Nocodazole to treat HeLa cells, abolish the regionalization of BubR1 centromere, and reduce the strength of Bub1 at the centromere, indicating that Aurora B function is necessary for the efficient recruitment of BubR1 and Bub1 centromere points, and that it is necessary to extend the signal of the detection point. In in vitro kinase experiments, Hesperadin blocked the phosphorylation of recombinant trypanosome histone H3 by T. brucei Aurora kinase -1 (TbAUK1) from the pathogenic trypanosome genus brucei with an IC50 of 40 nM. Hesperadin significantly inhibited the growth of cultured infectious blood form (BF) cells with IC50 of 48 nM and weakly inhibited the growth of insect circulating form (PF) cells with IC50 of 550 nM. Hesperadin inhibits the immunoprecipitate Aurora B,IC50 of phosphorylated histone H3, 250 nM, and significantly reduces the activities of other kinases (AMPK,Lck,MKK1,MAPKAP-K1,CHK1, and PHK) at a concentration of 1 μM. 20-100 nM Hesperadin acts on HeLa cells to induce the loss of phosphorylation of mitotic histone H3 at Ser10 site. Hesperadin treatment caused mitotic and cytoplasmic defects, which led to the cessation of HeLa cell proliferation and polyploidization, due to the inhibition of Aurora B function during chromosome connection. 100 nM Hesperadin restored paclitaxel or Monastrol rather than Nocodazole-induced mitotic arrest. Hesperadin and Nocodazole to treat HeLa cells, abolish the regionalization of BubR1 centromere, and reduce the strength of Bub1 at the centromere, indicating that Aurora B function is necessary for the efficient recruitment of BubR1 and Bub1 centromere points, and that it is necessary to extend the signal of the detection point. In in vitro kinase experiments, Hesperadin blocked the phosphorylation of recombinant trypanosome histone H3 by T. brucei Aurora kinase -1 (TbAUK1) from the pathogenic trypanosome genus brucei with an IC50 of 40 nM. Hesperadin significantly inhibited the growth of cultured infectious blood form (BF) cells with IC50 of 48 nM and weakly inhibited the growth of insect circulating form (PF) cells with IC50 of 550 nM. |
| target | TargetValue tbauk1 (cell-free say) 40 nm aurora B (human) (cell-free say) 250 nm |
| Target | Value |
| TbAUK1 (Cell-free assay) | 40 nM |
| Aurora B (human) (Cell-free assay) | 250 nM |
Last Update：2024-04-09 20:48:19
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View History
HESPERADIN
Acide elaidique
clopidol
(4-Fluorophenyl)acetic acid
RARECHEM AR PA 0006
DADS
alpha-Furfuraldehyde
NSC 2525
Acide elaidique
clopidol
(4-Fluorophenyl)acetic acid
RARECHEM AR PA 0006
DADS
alpha-Furfuraldehyde
NSC 2525