3-Methyladenine
(Synonyms: 3-甲基腺嘌呤; 3-MA) 目录号 : GC10710
3-甲基腺嘌呤是一种经典的自噬抑制剂。
Cas No.:5142-23-4
Sample solution is provided at 25 µL, 10mM.
- Redox Biol (2024)：103062.
- Autophagy (2024).PMID:38566321
- Am J Cancer Res 14.3 (2024)：1121.PMID:38590396
- Stem Cell Transl (2024)：szae028.PMID:38736295
- Inflammation (2024)：1-15.PMID:38977539
- Acta Pharmacol Sin (2024)：1-14.PMID:38992120
- Exp Eye Res(2024)：110021.PMID:39117136
- Theranostics 14.11 (2024)：4481.PMID:39113807
- Acs Nano (2024).PMID:39186478
- J Ethnopharmacol (2024)：118758.PMID:39222762
- Cell Death Dis 15.11 (2024)：826.PMID:39543094
- Langmuir (2024).PMID:39589485
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.
3-甲基腺嘌呤是一种经典的自噬抑制剂。它抑制磷脂酰肌醇3-激酶（PI3K），该激酶位于IGF/PI3K/mTOR/ULK通路的上游[1]。 3-甲基腺嘌呤能够在一系列本体不相关的人类细胞系中诱导细胞存活率持续而突然地下降。此外， 3-甲基腺嘌呤引起的细胞毒性并非由AKT/mTOR轴的抑制驱动[2]。
实验室研究表明，使用3-甲基腺嘌呤可以抑制自噬作用，从而阻止尿酸诱导肾间质成纤维细胞向肌成纤维细胞分化和转化生长因子β1（TGF-β1）、表皮生长因子受体（EGFR）以及Wnt信号通路的激活。此外，3-甲基腺嘌呤还能有效减轻肾脏中胞外基质（ECM）蛋白沉积和α平滑肌动力蛋白（α-SMA）的表达，并降低停留在G2/M期的肾上皮细胞数量。
动物实验表明，给予3-甲基腺嘌呤可以抑制Wnt/β-catenin和Notch/Jagged-1信号通路，并且还能抑制EGFR/ERK1/2信号通路。此外，3-MA治疗显著抑制了肾损伤中巨噬细胞和淋巴细胞的浸润以及多种促纤维化的细胞因子/趋化因子的释放。
| Cell experiment [1]: | |
|
Cell lines |
Rat renal interstitial fibroblasts (NRK-49F) cells |
|
Preparation Method |
Rat renal interstitial fibroblasts (NRK-49F) were cultured in DMEM with F12 containing 10% FBS, 1%penicillin and streptomycin in an atmosphere of 5%CO2, and 95% air at 37◦C. Cells were starved for 24h with DMEM containing 0.5% FBS. |
|
Reaction Conditions |
Cells were exposed to uric acid (800 μM) for 36h in the presence or absence of 3-Methyladenine (0–10 mM). |
|
Applications |
3-Methyladenine could abolish uric acid-induced α-SMA and collagen I expression. Uric acid also triggered a significant up-regulation of LC3II/I and Beclin-1. 3-Methyladenine dose-dependently suppressed these responses. In addition, treatment with 3-MA decreased TGF-βRI expression levels and the ratio of p-Smad3/Smad3 in a dose-dependent manner. |
| Animal experiment [2]: | |
|
Animal models |
male Sprague-Dawley (SD) rats (2-months old; weight 200±20 g) |
|
Preparation Method |
Mice were maintained on a 12h light/dark cycle and provided access to food and water ad libitum. All rats were pretrained to swim in the absence of a load for one week. The saline-treatment group was intravenously injected with 500 μL sterile saline by using 261/2 gauge needle via tail vein;3-MA-treatment group was intravenously injected with 500 μL 3-Methyladenine by using a 261/2 gauge needle via the tail vein. |
|
Dosage form |
15 mg/kg |
|
Applications |
3-Methyladenine could decrease the distortion of myocardium fibers as well as significantly decrease the width of cardiomyocytes of mice. In addition, 3-Methyladenine treatment obviously reduced autophagosome formation in the myocardium. 3-Methyladenine could also prevent the reduction of Bcl-2/Bax in the left ventricle of OE rats. |
|
References: [1]. Bao J, et al. Pharmacological inhibition of autophagy by 3-MA attenuates hyperuricemic nephropathy. Clin Sci (Lond). 2018 Nov 2;132(21):2299-2322. [2]. Liu H, et al. Autophagy inhibitor 3-methyladenine alleviates overload-exercise- induced cardiac injury in rats. Acta Pharmacol Sin. 2017 Jul;38(7):990-997. |
|
| Cas No. | 5142-23-4 | SDF | |
| 别名 | 3-甲基腺嘌呤; 3-MA | ||
| 化学名 | 3-methylpurin-6-amine | ||
| Canonical SMILES | CN1C=NC(=C2C1=NC=N2)N | ||
| 分子式 | C6H7N5 | 分子量 | 149.15 |
| 溶解度 | ≥ 7.45mg/mL in DMSO, ≥ 5mg/mL in Water | 储存条件 | Store at 2-8°C,Solutions of 3-MA are best fresh-prepared |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 6.7047 mL | 33.5233 mL | 67.0466 mL |
| 5 mM | 1.3409 mL | 6.7047 mL | 13.4093 mL |
| 10 mM | 0.6705 mL | 3.3523 mL | 6.7047 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >96.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
-
Related Biological Data
Autophagy inhibition augments the SAHA-mediated enhancement of NK cell cytotoxicity to BCSCs. D) The autophagy level of ALDH+ cells modulated by SAHA or 3MA, Scale bar = 2 μm.
NK cell infusion with intratumor injection of hydrogel encapsulating SAHA and 3MA (GlpBio, USA), or NK cell infusion with intravenous injection of SAHA (15mg kg−1) and 3MA (10mg kg−1).
Advanced Science 9.23 (2022): 2201271. PMID: 35712750 IF: 15.1004 -
Related Biological Data
Autophagosome accumulation is critical for efficient RABV VLP budding ACCEPTED MANUSCRIPT in cells and viral virulence in mice. (C) N2a cells were infected with RABV at an MOI of 0.01 for indicated time points, and treated with 3-MA (1mM) for 24h. Cell culture supernatants were collected for viral titration.
RABV-infected (MOI = 0.01, 36h) N2a cells were mock-treated or treated with 3-MA (1mM) (GlpBio, USA) for 24h.
Autophagy just-accepted (2024). PMID: 38566321 IF: 13.3003 -
Related Biological Data
VDR activated mitophagy was beneficial for ameliorating fibrosis and mitochondrial function. L. MitoSOX Red and JC-1 staining (magnification ×630, scale bar: 5μm).
HK-2 cells were randomly divided into several groups: control group: D-glucose 5mM, high glucose (30mM) and TGF-β(50ng/ml) intervention group, high glucose and TGF-β with or without other interventions: paricalcitol (200nM), 3-MA (10mM)(GlpBio, USA) for indicated time (72h) based on previous studies.
Redox Biology (2024): 103062. PMID: 38320454 IF: 11.3997 -
Related Biological Data
Autophagy inhibitors exacerbated TGF-β1-induced fibrosis in primary ConFB. (C) Invasive ability of primary ConFB stimulated with 1ng/ml TGF-β1 for 48h, with cotreatment of 2mM 3-MA or 2μM CQ for 18h, determined by Transwell assay (left).
Cells were treated with 1ng/ml TGF-β1 (100-21) for 48h, with or without co-treatment of 2μM rapamycin, serum starvation (0.5% FBS), 2mM 3-MA (GC10710, GLPBIO), or 2μM CQ (GC19549, GLPBIO) for 18h.
J Mol Cell Biol(2023): mjad009. PMID: 36792067 IF: 8.185 -
Related Biological Data
Melatonin enhances autophagy in HSFs. (F) Western blot indicated that treatment with 3-MA blocked the melatonin-enhanced autophagy in HSFs.
HSFs were treated with vehicle (DMSO) or 200µM melatonin in the presence or absence of 5mM 3-MA(GlpBio, USA) for 24h.
Bba-Mol Basis Dis(2023): 166887. PMID: 37739092 IF: 6.2001 -
Related Biological Data
Inhibition of autophagy increased upregulated S100P-enhanced chemosensitivity. D. Inhibition of autophagy reversed upregulated S100P-enhanced cells death. HL-60 and Jurkat cells were transfected with S100P shRNA or control shRNA and then pre-treated with 3-MA. Cells were subsequently treated for 24h with ADM, then active caspase-3 levels were assayed by western blot.
HL-60 and Jurkat cells were transfected with S100P vector or empty vector and then pre-treated with 3-MA (10mM)(GlpBio, USA) for 1h.
Am J Cancer Res 14.3 (2024): 1121. PMID: 38590396 IF: 5.2999