| VLX600shows selective cytotoxicity against quiescent cancer cells |
Sample solution is provided at 25 µL, 10mM.
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| Cas No. | 327031-55-0 | SDF | Download SDF |
| Synonyms | N/A | ||
| Chemical Name | 1-(2-pyridinyl)-ethanone, 2-(6-methyl-5H-1,2,4-triazino[5,6-b]indol-3-yl)hydrazone | ||
| Canonical SMILES | C/C(C1=NC=CC=C1)=N/NC2=NC3=C(C(C=CC=C4C)=C4N3)N=N2 | ||
| Formula | C17H15N7 | M.Wt | 317.4 |
| Solubility | ≤1mg/ml in ethanol;20mg/ml in DMSO;20mg/ml in dimethyl formamide | Storage | Store at -20°C |
| Physical Appearance | A crystalline solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
VLX600 is a compound that is preferentially active against quiescent cancer cells [1].
Abnormal vascularization of solid tumors lead to the development of microenvironments deprived of oxygen and nutrients that harbour slowly growing and metabolically stressed cells, which display enhanced resistance to standard chemotherapeutic agents and repopulate tumours after therapy [1].
VLX600 shows enhanced cytotoxic activity under conditions of nutrient starvation and displays tumour growth inhibition in vivo. In HCT116 colon carcinoma multicellular spheroids (MCS), VLX600 resulted in the appearance of central necrotic areas, induced active caspase-3 and led to a strong decrease in clonogenicity of dispersed cells. VLX600 also induced the expression of genes associated with hypoxia, glycolysis and p53 signaling. In HCT116 cells, VLX600 induces an autophagic response [1].
In NMRI nu/nu mice mice, VLX600 was rapidly distributed and finally eliminated with a half-life of 4-5 h. In mice bearing HCT116 and HT29 colon cancer xenografts, VLX600 exhibited antitumour activity and induced the formation of autolysosomes [1].
Reference:Zhang X, Frykns M, Hernlund E, et al. Induction of mitochondrial dysfunction as a strategy for targeting tumour cells in metabolically compromised microenvironments. Nat Commun. 2014;5:3295.
