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In vitro: directly inhibited FAK autophosphorylation in a dose- and time-dependent manner. Furthermore, Y15 increased pancreatic cancer cell detachment and inhibited cell adhesion in a dose-dependent manner. Inhibition of FAK pathway using Y15 significantly decreased cell survival, adhesion, and promoted apoptosis. Y15 significantly decreased viability and clonogenicity in a dose-dependent manner, increased detachment in a dose- and time-dependent manner, caused apoptosis, and inhibited cell invasion in both cell lines. In addition, Y15 treatment decreased autophosphorylation of FAK in a dose-dependent manner and changed cell morphology by causing cell rounding in DBTRG and U87 cells. In vivo: Y15 effectively caused human pancreatic tumor regression in vivo, when administered alone and its effects were synergistic with gemcitabine chemotherapy. The combination of Y15 treatment and IGF-1R knockdown also showed significant antitumor effect in vivo. Y15 was administered in an orthotopic glioma model, leading to an increase in mouse survival.
| Molecular Weight | 284.01 |
| Formula | C6H14Cl4N4 |
| CAS Number | 4506-66-5 |
| Solubility (25°C) | 10mM in DMSO |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
| Related FAK Products |
|---|
| Petunidin chloride
Petunidin chloride is an O-methylated anthocyanidin derived from delphinidin. *The compound is unstable in solutions, freshly prepared is recommended. |
| FAK-IN-11
FAK-IN-11 is a FAK inhibitor. |
| ZINC40099027
ZINC40099027 is a FAK activator. |
| FC-11
FC-11 is a PROTAC FAK degrader (DC90: 1 nM) . |
| FAK-IN-9
FAK-IN-9 is a potent and orally active FAK inhibitor with an IC50 of 27.44 nM. |
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