| Bioactivity | TMPA is a high-affinity Nur77 antagonist that binds to Nur77 leading to the release and shuttling of LKB1 in the cytoplasm to activate AMPKα. TMPA effectively lowers blood glucose and attenuates insulin resistance in type II db/db, high-fat diet and streptozotocin-induced diabetic mice. TMPA reduces RICD (restimulation-induced cell death) in human T cells, can also be used in studies of cancer and T-cell apoptosis dysregulation[1][2]. | ||||||||||||
| Invitro | TMPA (5, 10, 20, 40, 80 µM; 6 h or 10 µM; 0.5, 1, 3, 6, 12, 24, 36, 48 h) antagonizes the Nur77-LKB1 interaction in a dose- and time-dependent manner in hepatic LO2 cells[1].TMPA (10 µM; 6 h) enhances the LKB1-AMPKα interaction but decreases the LKB1-Nur77 interaction under physio logical conditions in Lo2 cells[1].TMPA binds directly to LBD in specific conformation[1].TMPA (10, 20 µM; 6 h) induces LKB1 nuclear export to activate AMPKα in Lo2 cells[1].TMPA (10, 50, 100 µM; 4 h) impairs human T-cell RICD (restimulation-induced cell death)[2]. Cell Viability Assay[2] Cell Line: | ||||||||||||
| In Vivo | TMPA (50 mg/kg; i.p.; single daily for 19 days) is capable of lowering blood glucose and improving glucose tolerance in type II diabetic mice[1]. Animal Model: | ||||||||||||
| Name | TMPA | ||||||||||||
| CAS | 1258275-73-8 | ||||||||||||
| Formula | C21H32O6 | ||||||||||||
| Molar Mass | 380.48 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Zhan YY, et al. The orphan nuclear receptor Nur77 regulates LKB1 localization and activates AMPK. Nat Chem Biol. 2012 Nov;8(11):897-904. [2]. Recher, et al. Modulation of T-cell apoptosis by small molecule compounds targeting the nuclear orphan receptor Nur 77. (2018). |