Molecular Formula | C23H20N6O3 |
Molar Mass | 428.44 |
Density | 1.38±0.1 g/cm3(Predicted) |
Melting Point | 175-177 °C |
Boling Point | 677.0±65.0 °C(Predicted) |
Solubility | Soluble in DMSO (up to 20 mg/ml). |
Appearance | solid |
Color | Yellow |
pKa | 3.40±0.20(Predicted) |
Storage Condition | 2-8°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 1 month. |
In vitro study | RK-33 specifically binds to DDX3, but does not bind to DDX5 and ddx17. RK-33 dependent on DDX3 inhibits tumor growth and sensitizes lung cancer cells to radiation. RK-33 had no effect on mitochondrial respiratory function or ATP production. It inhibits proliferation and induces apoptosis. DDX3 mediates the regulation of Wnt signaling pathway, and RK-33K can inhibit Wnt signaling pathway. RK-33 damage to radiation-induced DNA damage repair by inhibiting the activity of NHEJ. |
In vivo study | Radiation treatment in combination with RK-33 induced tumor regression in mice in a variety of lung cancer models. At the concentration dose used, RK-33 was not toxic to SCID mice. There were no significant morphological changes in RK-33 treated mice. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.334 ml | 11.67 ml | 23.34 ml |
5 mM | 0.467 ml | 2.334 ml | 4.668 ml |
10 mM | 0.233 ml | 1.167 ml | 2.334 ml |
5 mM | 0.047 ml | 0.233 ml | 0.467 ml |
biological activity | RK-33 is a small molecule inhibitor of DDX3(RNA helicase). In DDX3 overexpressed cells, it causes cell cycle arrest, induces apoptosis and promotes radiation sensitization. |
target | TargetValue DDX3 |
Target | Value | in vitro studies | RK-33 specifically bind DDX3, but do not bind DDX5 and DDX17. RK-33 relies on DDX3 to inhibit tumor growth and make lung cancer cells sensitive to radiation. RK-33 had no effect on mitochondrial respiratory function or ATP production. It can inhibit proliferation and induce apoptosis. DDX3 mediates the regulation of Wnt signaling pathway, which can RK-33K inhibit Wnt signaling pathway. RK-33 damage to radiation-induced DNA damage repair by inhibiting NHEJ activity. |
in vivo study | radiation combined with RK-33 treatment can induce tumor regression in mice with various lung cancer models. At the concentration dose used, the RK-33 was not toxic to SCID mice. Mice treated with RK-33 had no obvious morphological changes. |