Molecular Formula | C14H15N5S |
Molar Mass | 285.37 |
Solubility | DMSO: ≥5mg/mL |
Appearance | powder |
Color | yellow to orange |
Storage Condition | 2-8°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO may ne stored at -20°C for 1 month. |
Sensitive | Light Sensitive |
In vitro study | Dp44mT is cytotoxic to breast cancer cells, at least in part, due to selective inhibition of top2α. Dp44mT alone induced selective cell killing in the breast cancer cell line MDA-MB-231 when compared with healthy mammary epithelial cells (MCF-12A). It induces G1 cell cycle arrest and reduces cancer cell clonogenic growth at nanomolar concentrations. Dp44mT, but not the iron chelator desferal, induces DNA double-strand breaks quantified as S139 phosphorylated histone foci (γ-H2AX) and Comet tails induced in MDA-MB-231 cells. Doxorubicin-induced cytotoxicity and DNA damage are both enhanced significantly in the presence of low concentrations of Dp44mT. The chelator caused selective poisoning of DNA topoisomerase IIα (top2α) as measured by an in vitro DNA cleavage assay and cellular topoisomerase-DNA complex formation. Dp44mT targets lysosome integrity through copper binding. Copper binding is essential for the potent antitumor activity of Dp44mT, as coincubation with nontoxic copper chelators markedly attenuated its cytotoxicity. |
Hazard Symbols | Xn - Harmful |
Risk Codes | 22 - Harmful if swallowed |
UN IDs | UN 2811 6.1 / PGIII |
WGK Germany | 3 |
Hazard Class | 6.1 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 3.504 ml | 17.521 ml | 35.043 ml |
5 mM | 0.701 ml | 3.504 ml | 7.009 ml |
10 mM | 0.35 ml | 1.752 ml | 3.504 ml |
5 mM | 0.07 ml | 0.35 ml | 0.701 ml |
biological activity | Dp44mT is an iron chelating agent (iron chelator) with selective anti-cancer activity. |
target | target: Iron chelator |
in vitro research | Dp44mT is cytotoxic to breakfast cancer cells, at least in part, due to selective inhibition of top2α. Dp44mT alone induced selective cell killing in the breast cancer cell line MDA-MB-231 when compared with healthy mammary epithelial cells (MCF-12A). It induces G1 cell cycle arrest and reduces cancer cell clonogenic growth at nanomolar concentrations. Dp44mT, but not the iron chelator desferal, induces DNA double-strand breaks quantified as S139 phosphorylated histone foci (γ-H2AX) and Comet tails induced in MDA-MB-231 cells. Doxorubicin-induced cytotoxicity and DNA damage are both enhanced significantly in the presence of low concentrations of Dp44mT. The chelator led selective poisoning of DNA topoisomerase II α (top2α) as measured by an in Vitro DNA cleavage may and cellular topoisomerase-DNA complex formation. Dp44mT targets lysosome integrity through copper binding. Copper binding is essential for the potent antitumor activity of Dp44mT, as coincubation with nontoxic copper chelators markedly attenuated its cytotoxicity. |