TMPA 是一种具有高亲和力的 Nur77 拮抗剂，与 Nur77 结合导致 LKB1 在细胞质中释放和穿梭，以激活 AMPKα。TMPA 能有效地降低血糖，减轻 II 型 db/db、高脂饮食和链脲霉素诱导的糖尿病小鼠的胰岛素抵抗。TMPA 能减少人类 T 细胞的 RICD，也可用于癌症和 T 细胞凋亡失调的研究。

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.

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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.
TMPA (10 μM; 6 h) enhances the LKB1-AMPKα interaction but decreases the LKB1-Nur77 interaction under physio logical conditions in Lo2 cells.
TMPA binds directly to LBD in specific conformation.
TMPA (10, 20 μM; 6 h) induces LKB1 nuclear export to activate AMPKα in Lo2 cells.
TMPA (10, 50, 100 μM; 4 h) impairs human T-cell RICD (restimulation-induced cell death). has not independently confirmed the accuracy of these methods. They are for reference only.

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. has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model:

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Powder -20°C 3 years；4°C 2 years

[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).

In Vitro: DMSO : ≥ 100 mg/mL (262.83 mM)配制储备液