3-Methyladenine (Synonyms: 3-MA) |
| カタログ番号GC10710 |
3-メチルアデニンは、古典的なオートファジー阻害剤です。
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Cas No.: 5142-23-4
Sample solution is provided at 25 µL, 10mM.
3-Methyladenine is a classic autophagy inhibitor. It inhibits phosphatidylinositol 3-kinase (PI3K), which is located upstream of the IGF/PI3K/mTOR/ULK pathway.[1] 3-Methyladenine is capable to induce a consistent and abrupt decrease in cell viability across a series of ontologically unrelated human cell lines. In addition, 3-Methyladenine-induced cytotoxicity was not driven by the inhibition of the AKT/mTOR axis.[2]
In vitro study indicated that the inhibition of autophagy by 3-Methyladenine abolished uric acid-induced differentiation of renal fibroblasts to myofibroblasts and activation of transforming growth factor-β1 (TGF-β1), epidermal growth factor receptor (EGFR), and Wnt signaling pathways in cultured renal interstitial fibroblasts. Moreover, 3-Methyladenine was effective in attenuating renal deposition of extracellular matrix (ECM) proteins and expression of α-smooth muscle actin (α-SMA) and reducing renal epithelial cells arrested at the G2/M phase of cell cycle.[3]
In vivo study demonstrated that the administration of 3-Methyladenine inhibited Wnt/β-catenin and Notch/Jagged-1 signaling pathways as well as suppresses EGFR/ERK1/2 signaling pathway. Furthermore, 3-MA treatment remarkably inhibited the infiltration of macrophages and lymphocytes as well as release of multiple profibrogenic cytokines/chemokines in the injured kidney.[3]
References:
[1]. Yang F, et al. Rapamycin and 3-Methyladenine Influence the Apoptosis, Senescence, and Adipogenesis of Human Adipose-Derived Stem Cells by Promoting and Inhibiting Autophagy: An In Vitro and In Vivo Study. Aesthetic Plast Surg. 2021 Jun;45(3):1294-1309.
[2].Chicote J, et al. Cell Death Triggered by the Autophagy Inhibitory Drug 3-Methyladenine in Growing Conditions Proceeds With DNA Damage. Front Pharmacol. 2020 Oct 15;11:580343.
[3].Bao J, et al. Pharmacological inhibition of autophagy by 3-MA attenuates hyperuricemic nephropathy. Clin Sci (Lond). 2018 Nov 2;132(21):2299-2322.
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