EYE1118
EYE1118 is an orally active, photoactivatable VEGFR2 inhibitor without acute hepatotoxicity. EYE1118 mediates light-enhanced inhibition via azide-functionalized receptor binding, and can utilize light-guided targeting to regulate its biodistribution in vivo. EYE1118 effectively inhibits angiogenesis, endothelial cell migration, VEGF-induced retinal leakage, and the size of choroidal neovascular lesions. EYE1118 has been applied in studies related to age-related macular degeneration, diabetic retinopathy, and choroidal neovascularization.
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- No. CAS: 3037217-73-2
- Fòrmula: C23H25ClN8O3
- Peso molecular:496.95
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Actividad biológica
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VEGFR2 |
EYE1118 potently inhibits VEGFR2 in a cell-free kinase assay, with 2.7-fold increased potency (IC50=9 nM) upon illumination compared to dark conditions (IC50=24 nM)[1].
EYE1118 (0.1-100 μM; 24 h) exhibits reduced cytotoxicity relative to vorolanib (HY-109019) in NIH/3T3 fibroblasts, with significantly lower toxicity at 10 μM and only marginal toxicity at 100 μM[1].
EYE1118 (1 h inhibitor incubation; 4 h VEGF stimulation) robustly inhibits VEGFR2 signaling in VEGFR2/NFAT reporter HEK293 cells, with significant light-dependent potentiation of activity under cold white and green LED (11.85-fold increase with green light, IC50 = 4.86 nM), but no effect under red LED light[1].
EYE1118 (0.1 nM-10 μM; 10 min pre-incubation; 12 h total incubation) potently inhibits HRMEC tubulogenesis, with 3.84-fold increased potency (IC50 = 134 nM) upon cold white LED exposure compared to dark conditions (IC50 = 515 nM), and is significantly more potent than vorolanib in both light and dark conditions[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:NIH/3T3 fibroblasts
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Concentration:0.1-100 μM
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Incubation Time:24 h
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Result:Showed lower cytotoxicity against NIH/3T3 cells than its parental compound vorolanib, with this difference reaching statistical significance at 10 μM.
Exhibited only marginal toxicity at 100 μM relative to the vehicle control.
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Cell Line:VEGFR2/NFAT Reporter - HEK293
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Concentration:1-100 nM
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Incubation Time:1 h (inhibitor incubation); 10 min (VEGF stimulation)
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Result:Did not substantially inhibit VEGF-induced phosphorylation of VEGFR2 at Y951 or Y1175 in the dark, even at 100 nM.
Significantly suppressed VEGF-induced phosphorylation of VEGFR2 at Y951 and Y1175 upon cold white LED exposure, with phosphorylation reduced to baseline levels at 100 nM and statistically significantly reduced relative to VEGF alone at 50 nM.
Left total VEGFR2 and β-actin levels unchanged, confirming effects were due to inhibited phosphorylation, not receptor degradation or reduced loading.
EYE1118 (1 mg/kg; i.g.; daily; 3 days) starting 2 days before CNV induction significantly reduces CNV lesion area in C57BL/6JRj mice, with a very highly significant effect observed by day 5 post-induction[1].
EYE1118 (40 mg/kg; i.g.; single dose) does not induce acute hepatotoxicity in Balb/cJRj mice under standard or dim red light conditions[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Long Evans (male, 200-250 g, intravitreal injection of 50 ng/eye human VEGF-165)[1]
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Dosage:1 mg/kg
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Administration:i.g.; daily; 3 days
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Result:Significantly reduced VEGF-induced retinal vascular permeability, with permeability values not significantly different from control eyes and significantly lower than VEGF-only eyes (p=0.0019).
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Animal Model:C57BL/6JRj (adult, 9 weeks old, laser-induced Bruch's membrane disruption)[1]
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Dosage:1 mg/kg
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Administration:i.g.; daily; 3 days
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Result:Reduced CNV lesion area very highly significantly relative to vehicle controls by day 5 post-induction (p<0.001).
Remained significantly reduced compared to vehicle controls on day 7 post-induction.
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Animal Model:Balb/cJRj (male and female, 6-10 weeks old)[1]
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Dosage:40 mg/kg
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Administration:i.g.; single dose
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Result:Showed no evidence of liver architecture damage, necrosis, cellular stress, abnormal glycogen storage, or fibrosis via histopathological analysis, regardless of light condition.
Chemical Information
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No. CAS 3037217-73-2
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Peso molecular 496.95
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Fòrmula C23H25ClN8O3
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SMILES
CC1=C(C(N[C@H]2CCN(C(N(C)C)=O)C2)=O)C(C)=C(/C=C3C(NC4=CC(Cl)=C(N=[N+]=[N-])C=C4\3)=O)N1
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
EYE1118 Related Classifications
HY-184142 Related Classifications
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