| Bioactivity | TG6-10-1 is an EP2 antagonist, shows low-nanomolar antagonist activity against only EP2, >300-fold selectivity over human EP3, EP4, and IP receptors, 100-fold selectivity over EP1 receptors[1]. | ||||||||||||
| Target | EP2 | ||||||||||||
| Invitro | TG6-10-1 robustly blocks prostaglandin E2 (PGE2) (10 μM)-induced cAMP accumulation in a concentration-dependent manner in SH-SY5Y cells[2]. | ||||||||||||
| In Vivo | TG6-10-1 (5 mg/kg; i.p.; 4-30 hours) improves survival, accelerates recovery of lost weight, and improves functional recovery following status epilepticus (SE) [1]. Animal Model: | ||||||||||||
| Name | TG6-10-1 | ||||||||||||
| CAS | 1415716-58-3 | ||||||||||||
| Formula | C23H23F3N2O4 | ||||||||||||
| Molar Mass | 448.43 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Jiang J, et al. Inhibition of the prostaglandin receptor EP2 following status epilepticus reduces delayed mortality and brain inflammation. Proc Natl Acad Sci U S A. 2013 Feb 26;110(9):3591-3596. [2]. Kang X, et al. Cyclooxygenase-2 contributes to oxidopamine-mediated neuronal inflammation and injury via the prostaglandin E2 receptor EP2 subtype. Sci Rep. 2017 Aug 25;7(1):9459. |