c10c-G1V3
c10c-G1V3 is a BRAG2 binder with a Kd value of 7.37 μM. c10c-G1V3 binds to BRAG2, thereby disrupting its interaction with GluA2 and blocking GluA2 endocytosis and AMPAR subunit switching. c10c-G1V3 reduces glutamate-induced intracellular reactive oxygen species (ROS) accumulation and cell apoptosis (apoptosis). c10c-G1V3 decreases infarct volume in the transient middle cerebral artery occlusion model. c10c-G1V3 can be used in studies related to ischemic stroke.
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- Formel: C58H78N12O19
- Molecular Weight:1247.31
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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BRAG2 7.37 μM (Kd) |
c10c-G1V3 (1.5625-100 μg/mL; 60 s association, 120 s dissociation) binds to purified human BRAG2 (AA390-763) with a Kd value of 7.37 μM[1].
c10c-G1V3 (10 μM; 24 h) shows no cytotoxicity against HT22 cells[1].
c10c-G1V3 (0.1-10 μM; 24 h preincubation prior to OGD injury) protects HT22 cells against OGD-induced damage in a dose-dependent manner[1].
c10c-G1V3 (20 μM; 4 h) exhibits stronger membrane permeability than the unmodified 3Y peptide scaffold in HEK293T cells[1].
c10c-G1V3 (200 μM; 0-8 h) exhibits superior plasma stability in rat plasma, with a half-life >8 h[1].
c10c-G1V3 (0.1-10 μM; preincubated for 2 h prior to exposure to 5 mM glutamate for 24 h) protects HT22 cells against glutamate-induced excitotoxicity, maintaining a cell viability rate of 76.34% at high concentrations[1].
c10c-G1V3 (10 μM; 30 min preincubation prior to exposure to 5 mM glutamate for 24 h) significantly inhibits glutamate-induced ROS accumulation and alleviates intracellular oxidative stress in HT22 cells[1].
c10c-G1V3 (10 μM; preincubated for 2 h prior to exposure to 10 mM glutamate for 24 h) reduces glutamate-induced apoptosis of HT22 cells[1].
c10c-G1V3 (10 μM; preincubated for 2 h prior to exposure to 10 mM glutamate for 24 h) regulates the mitochondrial apoptosis pathway in HT22 cells, and alleviates glutamate-induced apoptosis by upregulating the expression of the anti-apoptotic protein Bcl-2 and downregulating the expression of the pro-apoptotic protein Bax and cleaved-caspase 3[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HT22 hippocampal neuronal cells
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Concentration:10 μM
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Incubation Time:24 h
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Result:Did not significantly affect HT22 cell viability, with survival rates exceeding 95%.
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Cell Line:HT22 cells (oxygen-glucose deprivation injury model)
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Concentration:0.1, 1 and 10 μM
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Incubation Time:24 h preincubation before OGD injury
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Result:Maintained HT22 cell viability at 75% at 0.1 μM.
Maintained HT22 cell viability at 76.08% at 1 μM.
Maintained HT22 cell viability at 85.97% at 10 μM.
Outperformed the reference compound Tat-GluA2-3Y at equivalent concentrations.
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Cell Line:HT22 cells (glutamate-induced excitotoxicity model)
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Concentration:0.1, 1 and 10 μM
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Incubation Time:2 h preincubation before 5 mM glutamate exposure for 24 h
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Result:Maintained HT22 cell viability at 70% at 0.1 μM.
Maintained HT22 cell viability at 70% at 1 μM.
Maintained HT22 cell viability at 76.34% at 10 μM (****p < 0.0001 vs glutamate control).
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Cell Line:HT22 cells (glutamate-induced excitotoxicity model)
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Concentration:10 μM
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Incubation Time:2 h preincubation before 10 mM glutamate exposure for 24 h
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Result:Reduced total HT22 cell apoptosis rate from 12.4% to 10.7%.
Showed reduced apoptotic nuclear condensation in c10c-G1V3-treated cells compared to glutamate-only controls via Hoechst 33342 staining.
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Cell Line:HT22 cells (glutamate-induced excitotoxicity model)
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Concentration:10 μM
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Incubation Time:2 h preincubation before 10 mM glutamate exposure for 24 h
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Result:Increased Bcl-2 expression to ~90% of control, compared to 50% of control after glutamate exposure.
Downregulated Bax and cleaved-caspase 3 expression.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (SD) (adult male, transient middle cerebral artery occlusion cerebral ischemia/reperfusion model)[1]
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Dosage:8 mg/kg
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Administration:i.p.; single dose
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Result:Reduced infarct area by 9.4% compared to the tMCAO model group.
Showed no significant difference in infarct area compared to the positive control Tat-GluA2-3Y group.
Significantly improved neurological deficit scores compared to the model group.
Chemical Information
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Molecular Weight 1247.31
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Formel C58H78N12O19
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Sequence
Cyclo(Tyr-Lys-Glu-Gly-Tyr-Asn-{Val(N-Me)}-Tyr-{Gly(N-Me)}-Glu)
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Sequence Shortening
Cyclo(YKEGYN-{Val(N-Me)}-Y-{Gly(N-Me)}-E)
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)