Molecular Formula | C14H16N2O3S
|
Molar Mass | 292.35 |
Density | 1.34±0.1 g/cm3 (20 ºC 760 Torr) |
Melting Point | 190-193℃ (ethanol ) |
Boling Point | 441.3±55.0 °C(Predicted) |
Solubility | DMSO (Slightly), Ethyl Acetate (Slightly), Methanol (Slightly, Heated) |
Appearance | White to light yellow solid. |
Color | White to Off-White |
pKa | 9.63±0.10(Predicted) |
Storage Condition | under inert gas (nitrogen or Argon) at 2-8°C |
Sensitive | Light Sensitive |
Use | Monastrol is an inhibitor of mitotic kinin Eg5 with high efficiency and cell permeability, with an IC50 value of 14 μM. |
In vitro study | Monastrol does not inhibit cell cycle progression through the S and G2 phases of the cell cycle or centrosome replication. The mitotic arrest of monastrol is rapidly reversible. It also inhibits bipolar spindle formation in Xenopus oocyte extracts. Monastrol blocks cells during mitosis, but does not affect microtubules or microtubule polymerization of cells during mitosis in vitro. Exposure of sympathetic neuronal cells to monastrol for several hours increases the number and growth rate of axons. However, the overall length of axons was no different from that of the control group. Sensory neurons also had this effect of a short-term increase in axonal growth rate, however, further prolonged exposure resulted in shorter axons, indicating that sensory neurons were more sensitive to the toxic effects of the drug. However, the overall culture profile of the cells was more robust than in the taxol-treated group, a drug commonly used to treat cancer. In HeLa cells, monastrol activates the spindle checkpoint, leading to mitosis arrest and apoptosis. |