3-Methyladenine (3-MA)

製品コードS2767 バッチS276714

印刷

化学情報

Chemical Structure Synonyms NSC 66389 Storage
(From the date of receipt)		 3 years -20°C powder
化学式

C6H7N5
分子量 149.15 CAS No. 5142-23-4
Solubility (25°C)* 体外 DMSO (warmed with 50ºC water bath) 16 mg/mL (107.27 mM)
Water (warmed with 50ºC water bath) 10 mg/mL (67.04 mM)
Ethanol 8 mg/mL (53.63 mM)
体内 （毎回新しく調製した物を用意してください）
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Clear solution
5%DMSO 40%PEG300 5%Tween80 50%ddH2O

この製剤はselleckのラボで検証済みです。上記の溶解方法がご要望を満たさない場合、selleckの営業担当までお問い合わせ頂ければ、個別の試験を行います。

 0.500mg/ml (3.35mM) Taking the 1 mL working solution as an example, add 50 μL of 10 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify it; then continue to add 500 μL ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明 3-MA (3-Methyladenine) is a selective PI3K inhibitor for Vps34 and PI3Kγ with IC50 of 25 μM and 60 μM in HeLa cells; blocks class I PI3K consistently, whereas suppression of class III PI3K is transient, and also blocks autophagosome formation. Solutions are unstable and should be fresh-prepared.
in vitro

The slight preference for Vps34 prevention by 3-Methyladenine (3-MA) probably arises from a hydrophobic ring specific to Vps34, which encircles the 3-methyl group of this compound. [1] It has been reported to cause cancer cell death under both normal and starvation conditions, and could also suppress cell migration and invasion independently of its ability to inhibit autophagy, implying that it possesses functions other than autophagy suppression. This compound elicits caspase-dependent cell death that is independent of autophagy inhibition. Treatment with 5 mM 3-MA reduces the percentage of glucose-starved HeLa cells displaying GFP-LC3 puncta to 23%. The levels of LC3-I are increasing and the levels of LC3-II are decreasing between 12 and 48 hours in cells that are treated with it. Conversion of LC3-I to LC3-II is suppressed by 3-MA. Treatment of HeLa cells with this compound at 2.5 mM or 5 mM for one day does not affect cell viability, whereas treatment with 10 mM for one day causes a 25.0% decrease in cell viability. Treatment of cells with 2.5, 5 or 10 mM for two days causes 11.5%, 38.0% and 79.4% decrease in viability, respectively. It decreases cell viability in a time- and dose-dependent manner, and significantly shortens the duration of nocodazole-induced-prometaphase arrest. [2] Suppression of autophagy by 3-MA inhibits SU11274-induced cell death. [3] Prolonged treatment with it (up to 9 hours) induces significant LC3 I to II conversion in wild type MEFs. Prolonged treatment with 3-MA, but not wortmannin, markedly increases GFP-LC3 punctuation/aggregation. 3-MA-induced LC3 conversion and free GFP liberation are ATG7-dependent. Treatment with this compound leads to evident increase of p62 protein level. It increases the p62 level even in Atg5−/− MEFs as well as in cells with DOX-mediated deletion of ATG5. 3-MA inhibits class I and class III PI3K in different temporal patterns. 3-MA-induced LC3 I to LC3 II conversion is dramatically compromised in Tsc2−/− cells compared with wild type cells. It disrupts the anti-autophagic function of mTOR complex 1. [4]
in vivo

3-Methyladenine (3-MA) blocks autophagy through its effect on class III phosphatidylinositol 3-kinase (PI3K). Treatment with this compound does not alter the degree of hemorrhage compared with the subarachnoid hemorrhage (SAH) group. Its pretreatment significantly aggravates neurological symptoms when compared with the SAH + vehicle group. Autophagy is decreased when 3-MA treatment is applied. Conversely, cleaved caspase-3 is markedly up-regulated in the SAH + 3-Methyladenine group. In line with the up-regulation of cleaved caspase-3 expression, the number of TUNEL-positive cells in the right cortex is significantly increased in the SAH + 3-Methyladenine group compared with the SAH + vehicle group. [5]

プロトコル(参考用のみ)

キナーゼアッセイ Protein degradation assay
HeLa cells are radiolabeled for 24 hours with 0.05 mCi/mL l-[U- 14C]valine. At the end of the labeling period, cells are rinsed three times with PBS. Cells are incubated for the designated times in either full medium or EBSS with or without the presence of 10 mM 3-Methyladenine (3-MA).
細胞アッセイ 細胞株 HeLa cell line
濃度 1-10 mM
反応時間 24, 48 or 72 hours
実験の流れ

Cell (such as HeLa cell) viability is determined by a trypan blue exclusion assay after treatment with 3-Methyladenine (3-MA). Briefly, both adherent and floating cells are collected and suspended in phosphate buffered saline (PBS, pH 7.4) at a final density of 1-2 × 106/mL. An equal volume of 0.4% trypan blue solution (w/v, in PBS) is added to the cell suspension and mixed thoroughly. After incubation at room temperature for 3 min, cell counting is performed using a hemacytometer.
動物実験 動物モデル Adult male Sprague–Dawley rats weighing 300-350 g
投薬量 400 nM
投与方法 Intracerebral ventricular

参考

  • https://pubmed.ncbi.nlm.nih.gov/20574157/
  • https://pubmed.ncbi.nlm.nih.gov/22545128/
  • https://pubmed.ncbi.nlm.nih.gov/22466960/
  • https://pubmed.ncbi.nlm.nih.gov/20123989/
  • https://pubmed.ncbi.nlm.nih.gov/22521819/

カスタマーフィードバック

Data from [Data independently produced by , , Redox Biol, 2018, 18:138-157]

Data from [Data independently produced by , , Am J Cancer Res, 2015, 5(1): 125-139]

Data from [Data independently produced by , , Food Chem Toxicol, 2017, 100:183-196]

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

Cooperative nutrient scavenging is an evolutionary advantage in cancer [ Nature, 2025, 10.1038/s41586-025-08588-w] PubMed: 39972131
Host glutathione is required for Rickettsia parkeri cell division and intracellular survival [ Nat Commun, 2025, 16(1):5547] PubMed: 40593553
Viruses hijack FPN1 to disrupt iron withholding and suppress host defense [ Nat Commun, 2025, 16(1):5912] PubMed: 40595467
RNF167 mediates atypical ubiquitylation and degradation of RLRs via two distinct proteolytic pathways [ Nat Commun, 2025, 16(1):1920] PubMed: 39994288
Disrupting AGR2/IGF1 paracrine and reciprocal signaling for pancreatic cancer therapy [ Cell Rep Med, 2025, 6(2):101927] PubMed: 39914384
TBK1 is a signaling hub in coordinating stress-adaptive mechanisms in head and neck cancer progression [ Autophagy, 2025, 1-23.] PubMed: 40114316
H3K36me2 methyltransferase NSD2/WHSC1 promotes triple-negative breast cancer metastasis via activation of ULK1-dependent autophagy [ Autophagy, 2025, 21(8):1824-1842] PubMed: 40097917
Calnexin promotes glioblastoma progression by inducing protective mitophagy through the MEK/ERK/BNIP3 pathway [ Theranostics, 2025, 15(6):2624-2648] PubMed: 39990231
Glutathione reductase underlies the stability of mutant p53 by antagonizing protein glutathionylation [ Redox Biol, 2025, 81:103522] PubMed: 39983342
Carbon ion combined photon radiotherapy induces ferroptosis via NCOA4-mediated ferritinophagy in glioblastoma [ Redox Biol, 2025, 86:103865] PubMed: 40925125

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人間や獣医の診断であるか治療的な使用のためにでない。

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