Molecular Formula | C24H25N5O3S |
Molar Mass | 463.55 |
Density | 1.263±0.06 g/cm3(Predicted) |
Melting Point | >197°C (dec.) |
Boling Point | 674.4±55.0 °C(Predicted) |
Solubility | DMSO (Slightly), Methanol (Slightly) |
Appearance | Solid |
Color | Light Yellow |
pKa | 8.88±0.10(Predicted) |
Storage Condition | Refrigerator |
In vitro study | In response to XRT and gemcitabine, VE-822(80 nM) attenuates the ATR signaling pathway and decreases tumor cell survival. In normal cells, VE-822(80 nM) attenuated the intensity of the ATR signaling pathway, but did not enhance the ability of radiation and gemcitabine to kill normal cells. VE-822(80 nM) increased residual γH2AX and 53BP1 foci elicited by XRT compared to MiaPaCa-2 and PSN-1 cells in XRT. MiaPaCa-2 and PSN-1 cells in the XRT, VE-822(80 nM) were treated before reducing the focus of RAD51. VE-822(80 nM) alone increased the rate at which MiaPaCa-2 and PSN-1 cells stayed in the G1 phase. VE-822(80 nM) reduces XRT-enriched G2/M-phase-fraction in MiaPaCa-2 and PSN-1 cells. VE-822 alone had little effect, while VE-822(80 nM),XRT and/or gemcitabine and combination enhanced early and late apoptosis in PSN-1 cells. VE-822 increased tumor response to DNA damaging agents and was associated with pChk1 Ser345 obstruction. |
In vivo study | VE-822(60 mg/kg) inhibits phosphorylation of serine 345-Chk1 in mouse PSN-1 tumors. Compared with XTR alone, VE-822(60 mg/kg) in combination with XTR increased MiaPaCa-2 tumor growth to xrt600 mm in mice by two PSN-1 and |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.157 ml | 10.786 ml | 21.573 ml |
5 mM | 0.431 ml | 2.157 ml | 4.315 ml |
10 mM | 0.216 ml | 1.079 ml | 2.157 ml |
5 mM | 0.043 ml | 0.216 ml | 0.431 ml |