M9281
3-甲基腺嘌呤
≥99% (HPLC), synthetic (organic), powder
别名:
3-MA, 6-氨基-3-甲基嘌呤
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关于此项目
经验公式（希尔记法）:
C6H7N5
化学文摘社编号:
分子量:
149.15
NACRES:
NA.51
PubChem Substance ID:
UNSPSC Code:
41106305
EC Number:
225-908-6
MDL number:
Beilstein/REAXYS Number:
146087
产品名称
3-甲基腺嘌呤, autophagy inhibitor
InChI
1S/C6H7N5/c1-11-3-10-5(7)4-6(11)9-2-8-4/h2-3H,7H2,1H3
InChI key
FSASIHFSFGAIJM-UHFFFAOYSA-N
SMILES string
Cn1cnc(N)c2ncnc12
biological source
synthetic (organic)
assay
≥99% (HPLC)
form
powder
mp
~300 °C (dec.) (lit.)
solubility
DMF: 9.80-10.20 mg/mL, clear, colorless to light yellow
storage temp.
room temp
Quality Level
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Application
3-甲基腺嘌呤作为自噬抑制剂已用于：
- 使用转染人骨髓间充质干细胞(BM-MSC)检测自噬相关基因（Beclin 1，轻链3(LC3)和p62）的表达
- 协同顺铂(cisplatin)研究A2780cp细胞的自噬抑制会否影响顺铂诱导的细胞凋亡
- 研究多黏菌素(colistin)诱导的自噬和凋亡之间的相互作用
3-甲基腺嘌呤（3-MA）用于抑制和研究多种条件下自噬（溶酶体自我降解）和细胞凋亡的机制。3-MA可通过抑制III型磷脂酰肌醇3-激酶（PI-3K）阻断自噬体的形成来对自噬进行抑制。 3-MA通常以5 mM的浓度用作自噬抑制剂。
在癌症生成过程中核酸甲基化检测的标准品。
Biochem/physiol Actions
3-甲基腺嘌呤（3-MA）用于抑制和研究多种条件下自噬（溶酶体自我降解）和细胞凋亡的机制。3-MA可通过抑制III型磷脂酰肌醇3-激酶（PI-3K）阻断自噬体的形成来对自噬进行抑制。
Other Notes
Preparation Note
该产品可溶于DMF（10 mg/mL；可能需要温和受热）。 受热情况下，其可以30 mg/ml的浓度溶于水、95％乙醇或1 N NaOH，但在冷却后会从溶液中析出。 可在DMSO中配制100 mM的3-MA溶液。
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Heng Wang et al.
Journal of dairy science, 102(9), 8264-8272 (2019-07-01)
Staphylococcus aureus is an important pathogen causing chronic and subclinical mastitis of cows. Autophagy is an important regulatory mechanism that participates in the elimination of invading pathogenic organisms. Here, we hypothesize that autophagy is involved in the process of Staph.
Jingyuan Chen et al.
Shock (Augusta, Ga.), 52(1), 111-121 (2018-10-05)
Sepsis-induced myopathy is a heavy burden for patients during respiratory failure as well as after discharge, which could be characterized with qualitative changes to nAChR in a rat model of sepsis, regulated by NRG-1. Autophagy is an innate immune defense
Ruishuang Ma et al.
Cancer biology & therapy, 20(9), 1206-1212 (2019-05-17)
Autophagy plays a complicated role in tumorigenesis, and the effects of autophagy in drug resistance have not been fully known. The aim of this study was to evaluate autophagy activity in lung cancer cells derived from different origins and explore
Halima Alsamri et al.
Frontiers in oncology, 9, 743-743 (2019-08-29)
We have previously demonstrated that carnosol, a naturally occurring diterpene, inhibited in vitro cell viability and colony growth, as well as induced cell cycle arrest, autophagy and apoptosis in human triple negative breast cancer (TNBC) cells. In the present study
Do Eun Rim et al.
Journal of biochemical and molecular toxicology, 33(8), e22348-e22348 (2019-05-09)
Golgi S-nitro-N-acetylpenicillamine receptor complex 1 (GS28) has been implicated in Golgi vesicle transport. We examined the role of GS28 and its molecular mechanisms in sodium nitroprusside (SNP)-induced cell death using GS28 siRNA (siGS28)-transfected HeLa cells. Significant inhibition of cytotoxicity was
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We presents an article on Autophagy in Cancer Promotes Therapeutic Resistance
High titer lentiviral particles for LC3 variants used for live cell analysis of cellular autophagy.
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