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TG6-10-1
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
TG6-10-1图片
CAS NO:1415716-58-3
规格:≥98%
包装与价格：
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议
250mg电议
500mg电议

产品介绍
理化性质和储存条件
Molecular Weight (MW) 448.43
Formula C23H23F3N2O4
CAS No. 1415716-58-3
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 10 mM
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)O=C(NCCN1C(C(F)(F)F)=CC2=C1C=CC=C2)/C=C/C3=CC(OC)=C(OC)C(OC)=C3
SynonymsTP6101; TP-6101; TP 6101; TG6-10-1; TG 6-10-1; TG-6-10-1
实验参考方法
In Vitro

In vitro activity: TG6-10-1 is a cell-permeable, highly potent, selective, and competitive antagonist of prostaglandin E2 receptor (EP2) with Kb of 17.8 nM. TG6-10-1 has sufficient pharmacokinetic profiles to be used in vivo. In the mouse pilocarpine model of status epilepticus (SE), systemic administration of TG6-10-1 completely recapitulates the effects of conditional ablation of cyclooxygenase-2 from principal forebrain neurons, namely reduced delayed mortality, accelerated recovery from weight loss, reduced brain inflammation, prevention of blood-brain barrier opening, and neuroprotection in the hippocampus, without modifying seizures acutely. Prolonged SE in humans causes high mortality and morbidity that are associated with brain inflammation and injury, but currently the only effective treatment is to stop the seizures quickly enough with anticonvulsants to prevent brain damage. The results suggest that the prostaglandin receptor EP2 is critically involved in neuroinflammation and neurodegeneration, and point to EP2 receptor antagonism as an adjunctive therapeutic strategy to treat SE.

Kinase Assay: TG6-10-1 is a cell-permeable, highly potent, selective, and competitive antagonist of prostaglandin E2 receptor (EP2) with Kb of 17.8 nM.

Cell Assay:

In VivoIn the mouse pilocarpine model of status epilepticus (SE), systemic administration of TG6-10-1 completely recapitulates the effects of conditional ablation of cyclooxygenase-2 from principal forebrain neurons, namely reduced delayed mortality, accelerated recovery from weight loss, reduced brain inflammation, prevention of blood-brain barrier opening, and neuroprotection in the hippocampus, without modifying seizures acutely. Prolonged SE in humans causes high mortality and morbidity that are associated with brain inflammation and injury, but currently the only effective treatment is to stop the seizures quickly enough with anticonvulsants to prevent brain damage. The results suggest that the prostaglandin receptor EP2 is critically involved in neuroinflammation and neurodegeneration, and point to EP2 receptor antagonism as an adjunctive therapeutic strategy to treat SE.
Animal model Mouse pilocarpine model of status epilepticus (SE)
Formulation & Dosage 5 mg/kg, i.p.
References Proc Natl Acad Sci U S A. 2013 Feb 26;110(9):3591-6.