MTI-31 是一种有效的，具有口服活性的，且高度选择性的 mTORC1 和 mTORC2 抑制剂。MTI-31 高选择性作用于 mTOR，K_d 为 0.20 nM。MTI-31 对 mTOR 的 IC₅₀ 为 39 nM。MTI-31可用于乳腺癌的研究。

MTI-31 is a potent, orally active and highly selective inhibitor of mTORC1 and mTORC2. MTI-31 is selective for mTOR (K d : 0.20 nM) versus PIK3CA, PIK3CB and PIK3G with >5,000 fold selectivity in mTOR binding assays. MTI-31 shows an IC 50 of 39 nM for mTOR in LANCE assay of mTOR substrate phosphorylation with 100 μM ATP. MTI-31 can be used for the research of breast cancer.

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mTOR 0.2 nM (Ki) mTOR 39 nM (IC50, 100 μM

MTI-31 acts as a potent and selective inhibitor of mTOR enzymatic activity capable of targeting both mTORC1 and mTORC2 functions in cancer cells.
MTI-31 (0.01-100 μM) elicits a potent and more substantial inhibition of cell growth than that of Rapamycin.
Treatment with MTI-31 for 6 h demonstrates a dose-dependent inhibition of both the mTORC1 substrates P-S6K1(T389), P-S6(S235/6), P-4EBP1(T70) and mTORC2 substrate P-AKT(S473), achieving 50% inhibition at ≤0.12 μM in three representative tumor cell lines harboring mTOR pathway dysregulation (786-O renal, U87MG glioma and MDA-MB-453 breast).
MTI-31-induced apoptosis requires mTORC2-regulated Bim- and GSK3 activity. has not independently confirmed the accuracy of these methods. They are for reference only.

MTI-31 is a potent mTOR inhibitor in vivo and elicits strong antitumor efficacy. MTI-31(5-40 mg/kg; orally) is efficacious in several tumor models harboring HER2+/PIK3CAmut and/or PTEN-deficiency exemplified by MDA-MB-453 and 786-O.
Treatment of tumor bearing nude mice with orally administered MTI-31 inhibits growth of H1975 tumors (25 mg/kg/d; orally) or U87MG tumors (30 mg/kg/d; orally). has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Zhang Q, et, al. A Novel mTORC1/2 Inhibitor (MTI-31) Inhibits Tumor Growth, Epithelial-Mesenchymal Transition, Metastases, and Improves Antitumor Immunity in Preclinical Models of Lung Cancer. Clin Cancer Res. 2019 Jun 15;25(12):3630-3642.
[2]. Qian J, et, al. Molecular regulation of apoptotic machinery and lipid metabolism by mTORC1/mTORC2 dual inhibitors in preclinical models of HER2+/PIK3CAmut breast cancer. Oncotarget. 2016 Oct 11;7(41):67071-67086.

In Vitro: DMSO : 8.33 mg/mL (17.55 mM; ultrasonic and warming and heat to 60°C)配制储备液