 
        
        
        
                货号:A145872
                
                同义名:
                    
                        
                            3-甲基腺嘌呤
                            
                             / 3-MA; NSC 66389
                            
                        
                    
                
                
                
                    
                     
                
            
3-Methyladenine是一种选择性 PI3K 抑制剂,针对 Vps34 和 PI3Kγ,IC50 分别为 25 μM 和 60 μM。
 
                                 
                                
                            

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| 产品名称 | C2β ↓ ↑ | p110α ↓ ↑ | p110β ↓ ↑ | p110γ ↓ ↑ | p110δ ↓ ↑ | PI3K ↓ ↑ | Vps34 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| A66 | + C2β, IC50: 462 nM | ++ p110α, IC50: 32 nM | 99%+ | ||||||||||||||||
| Taselisib | + C2β, IC50: 292 nM | ++++ PI3Kα, Ki: 0.29 nM | +++ PI3Kβ, Ki: 9.1 nM | ++++ PI3Kγ, Ki: 0.97 nM | ++++ PI3Kδ, Ki: 0.12 nM | + hVps34, IC50: 374 nM | 99%+ | ||||||||||||
| Gedatolisib | ++++ PI3Kα, IC50: 0.4 nM | +++ PI3Kγ, IC50: 5.4 nM | mTOR | 99% | |||||||||||||||
| HS-173 | ++++ PI3Kα , IC50: 0.8 nM | 99%+ | |||||||||||||||||
| Serabelisib | +++ PI3Kα, IC50: 21 nM | 99%+ | |||||||||||||||||
| GNE-477 | ++++ PI3Kα, IC50: 4 nM | mTOR | 99% | ||||||||||||||||
| YM-201636 | + p110α, IC50: 3.3 μM | PIKfyve | 98% | ||||||||||||||||
| AS-252424 | + PI3Kα, IC50: 935 nM | ++ PI3Kγ, IC50: 33 nM | 99% | ||||||||||||||||
| Alpelisib | +++ PI3Kα, IC50: 5 nM | 99%+ | |||||||||||||||||
| AS-604850 | + PI3Kα, IC50: 4.5 μM | + PI3Kγ, IC50: 0.25 μM | 99% | ||||||||||||||||
| SF2523 | ++ PI3Kα, IC50: 34 nM | ++ PI3Kγ, IC50: 158 nM | DNA-PK,mTOR | 99%+ | |||||||||||||||
| Inavolisib | ++++ PI3K alpha, IC50: 0.038 nM | 99%+ | |||||||||||||||||
| Bimiralisib | ++++ PI3Kα, Kd: 1.5 nM | +++ PI3Kβ, Kd: 11 nM | ++ PI3Kγ, Kd: 25 nM | ++ PI3Kδ, Kd: 25 nM | mTOR | 99%+ | |||||||||||||
| GSK1059615 | ++++ PI3Kα, IC50: 0.4 nM | ++++ PI3Kβ, IC50: 0.6 nM | +++ PI3Kγ, IC50: 5 nM | ++++ PI3Kδ, IC50: 2 nM | mTOR | 98% | |||||||||||||
| GSK2636771 | ✔ | 99% | |||||||||||||||||
| Fimepinostat | +++ PI3Kα, IC50: 19 nM | ++ PI3Kβ, IC50: 54 nM | ++ PI3Kδ, IC50: 39 nM | 99%+ | |||||||||||||||
| VS-5584 | ++++ PI3Kα, IC50: 2.6 nM | +++ PI3Kβ, IC50: 21 nM | ++++ PI3Kγ, IC50: 3.0 nM | ++++ PI3Kδ, IC50: 2.7 nM | mTOR | 98% | |||||||||||||
| Dactolisib | ++++ p110α1, IC50: 4 nM | ++ p110β, IC50: 75 nM | +++ p110γ, IC50: 5 nM | +++ p110δ, IC50: 7 nM | 98+% | ||||||||||||||
| PI-103 | ++++ p110α, IC50: 2 nM | ++++ p110β, IC50: 3 nM | +++ p110γ, IC50: 15 nM | ++++ p110δ, IC50: 3 nM | DNA-PK,mTOR | 99%+ | |||||||||||||
| PI-3065 | + p110β, IC50: 1078 nM | +++ p110δ, IC50: 15 nM | 99%+ | ||||||||||||||||
| Voxtalisib | ++ PI3Kα, IC50: 39 nM | ++ PI3Kβ, IC50: 113 nM | +++ PI3Kγ, IC50: 9 nM | ++ PI3Kδ, IC50: 43 nM | DNA-PK,mTOR | 99%+ | |||||||||||||
| AZD-8835 | +++ PI3Kα, IC50: 6.2 nM | + PI3Kβ, IC50: 431 nM | ++ PI3Kγ, IC50: 90 nM | +++ PI3Kδ, IC50: 5.7 nM | 99% | ||||||||||||||
| Pilaralisib analogue | ++ PI3Kα, IC50: 39 nM | ++ PI3Kβ, IC50: 36 nM | +++ PI3Kγ, IC50: 23 nM | ++ PI3Kδ, IC50: 36 nM | 99%+ | ||||||||||||||
| ZSTK474 | +++ PI3Kα, IC50: 16 nM | ++ PI3Kβ, IC50: 44 nM | ++ PI3Kγ, IC50: 49 nM | +++ PI3Kδ, IC50: 4.6 nM | ++ PI3K, IC50: 37 nM | 98% | |||||||||||||
| AS-605240 | ++ PI3Kα, IC50: 60 nM | + PI3Kβ, IC50: 270 nM | +++ PI3Kγ, IC50: 8 nM | + PI3Kδ, IC50: 300 nM | 98% | ||||||||||||||
| TGX-221 | +++ p110β, IC50: 5 nM | ++ p110δ, IC50: 0.1 μM | 99%+ | ||||||||||||||||
| PF-04691502 | ++++ PI3Kα, Ki: 1.8 nM | ++++ PI3Kβ, Ki: 2.1 nM | ++++ PI3Kγ, Ki: 1.9 nM | ++++ PI3Kδ, Ki: 1.6 nM | mTOR | 98+% | |||||||||||||
| GDC-0084 | ++++ PI3Kα, Ki app: 2 nM | ++ PI3Kβ, Ki app: 46 nM | +++ PI3Kγ, Ki app: 10 nM | ++++ PI3Kδ, Ki app: 3 nM | mTOR | 99%+ | |||||||||||||
| Buparlisib | ++ p110α, IC50: 52 nM | + p110β, IC50: 166 nM | + p110γ, IC50: 262 nM | ++ p110δ, IC50: 116 nM | + Vps34, IC50: 2.4 μM | mTOR | 98% | ||||||||||||
| LY294002 | + p110α, IC50: 0.5 μM | + p110β, IC50: 0.97 μM | + p110δ, IC50: 0.57 μM | DNA-PK | 99%+ | ||||||||||||||
| AZD 6482 | + PI3Kα, IC50: 870 nM | +++ PI3Kβ, IC50: 10 nM | ++ PI3Kδ, IC50: 80 nM | DNA-PK | 99%+ | ||||||||||||||
| Pictilisib | ++++ p110α, IC50: 3 nM | ++ p110β, IC50: 33 nM | ++ p110γ, IC50: 75 nM | ++++ p110δ, IC50: 3 nM | mTOR | 99%+ | |||||||||||||
| PKI-402 | ++++ PI3Kα, IC50: 2 nM | +++ PI3Kβ, IC50: 7 nM | +++ PI3Kγ, IC50: 16 nM | +++ PI3Kδ, IC50: 14 nM | mTOR | 98% | |||||||||||||
| Copanlisib | ++++ PI3Kα, IC50: 0.5 nM | ++++ PI3Kβ, IC50: 3.7 nM | +++ PI3Kγ, IC50: 6.4 nM | ++++ PI3Kδ, IC50: 0.7 nM | 99%+ | ||||||||||||||
| Omipalisib | ++++ p110α, Ki: 0.019 nM | ++++ p110β, Ki: 0.13 nM | ++++ p110γ, Ki: 0.06 nM | ++++ p110δ, Ki: 0.024 nM | 99%+ | ||||||||||||||
| Izorlisib | +++ PI3Kα, IC50: 14 nM | ++ PI3Kβ, IC50: 0.12 μM | ++ PI3Kγ, IC50: 36 nM | + PI3Kδ, IC50: 0.50 μM | 99%+ | ||||||||||||||
| AZD8186 | ++ PI3Kα, IC50: 35 nM | ++++ PI3Kβ, IC50: 4 nM | +++ PI3Kδ, IC50: 12 nM | 99% | |||||||||||||||
| KU-0060648 | ++++ PI3Kα, IC50: 4 nM | ++++ PI3Kβ, IC50: 0.5 nM | + PI3Kγ, IC50: 0.59 μM | ++++ PI3Kδ, IC50: 0.1 nM | DNA-PK | 98% | |||||||||||||
| Apitolisib | +++ p110α, IC50: 5 nM | ++ p110β, IC50: 27 nM | +++ p110γ, IC50: 14 nM | +++ p110δ, IC50: 7 nM | mTOR | 98%+ | |||||||||||||
| CZC24832 | + PI3Kβ, IC50: 1.1 μM | ++ PI3Kγ, IC50: 27 nM | 98+% | ||||||||||||||||
| BGT226 maleate | ++++ PI3Kα, IC50: 4 nM | ++ PI3Kβ, IC50: 63 nM | ++ PI3Kγ, IC50: 38 nM | mTOR | 99%+ | ||||||||||||||
| TG 100713 | ++ PI3Kα, IC50: 165 nM | + PI3Kβ, IC50: 215 nM | ++ PI3Kγ, IC50: 50 nM | +++ PI3Kδ, IC50: 24 nM | 98%+ | ||||||||||||||
| PI3K-IN-1 | ++ PI3Kα, IC50: 39 nM | ++ PI3Kβ, IC50: 113 nM | +++ PI3Kγ, IC50: 9 nM | ++ PI3Kδ, IC50: 43 nM | DNA-PK,mTOR | 98+% | |||||||||||||
| TG100-115 | + PI3Kα, IC50: 1.3 μM | + PI3Kβ, IC50: 1.2 μM | ++ PI3Kγ, IC50: 83 nM | + PI3Kδ, IC50: 235 nM | 98% | ||||||||||||||
| PIK-90 | +++ PI3Kα, IC50: 11 nM | + PI3Kβ, IC50: 350 nM | +++ PI3Kγ, IC50: 18 nM | ++ PI3Kδ, IC50: 58 nM | 99%+ | ||||||||||||||
| PIK-294 | + p110β, IC50: 490 nM | ++ p110γ, IC50: 160 nM | +++ p110δ, IC50: 10 nM | 99%+ | |||||||||||||||
| Duvelisib | ++++ PI3Kβ, Ki: 1564 pM | ++ PI3Kγ, Ki: 243 pM | ++++ PI3Kδ, Ki: 23 pM | 99%+ | |||||||||||||||
| GDC-0326 | ++++ PI3Kα, Ki: 0.2 nM | ++ PI3Kβ, Ki: 26.6 nM | +++ PI3Kγ, Ki: 10.2 nM | ++++ PI3Kδ, Ki: 4 nM | 98% | ||||||||||||||
| Quercetin Dihydrate | + PI3Kβ, IC50: 5.4 μM | + PI3Kγ, IC50: 2.4 μM | + PI3Kδ, IC50: 3.0 μM | 95% | |||||||||||||||
| Quercetin | + PI3Kβ, IC50: 5.4 μM | + PI3Kγ, IC50: 2.4 μM | + PI3Kδ, IC50: 3.0 μM | Sirtuin,Src,PKC | 95% | ||||||||||||||
| Leniolisib | + PI3Kα, IC50: 0.244 μM | + PI3Kβ, IC50: 0.424 μM | + PI3Kγ, IC50: 2.23 μM | +++ PI3Kδ, IC50: 0.011 μM | DNA-PK | 99%+ | |||||||||||||
| PIK-108 | ✔ | 99% | |||||||||||||||||
| Eganelisib | +++ PI3Kγ, IC50: 16 nM | 99%+ | |||||||||||||||||
| CAY10505 | ✔ | 99% | |||||||||||||||||
| IPI-3063 | ++++ p110δ, IC50: 2.5 nM | 99% | |||||||||||||||||
| Nemiralisib | ++++ PI3Kδ, pKi: 9.9 | 99%+ | |||||||||||||||||
| PF-4989216 | ++++ p110α, IC50: 2 nM | ++ p110γ, IC50: 65 nM | ++++ p110δ, IC50: 1 nM | 99%+ | |||||||||||||||
| PIK-75 HCl | +++ p110α, IC50: 5.8 nM | ++ p110γ, IC50: 76 nM | + p110δ, IC50: 0.51 μM | DNA-PK | 99%+ | ||||||||||||||
| Tenalisib | ++ PI3Kγ, IC50: 33.2 nM | ++ PI3Kδ, IC50: 24.5 nM | 98% | ||||||||||||||||
| Acalisib | +++ p110δ, IC50: 14 nM | 99%+ | |||||||||||||||||
| Umbralisib | +++ PI3Kδ, IC50: 22.2 nM | 99%+ | |||||||||||||||||
| AMG319 | + PI3Kγ, IC50: 850 nM | +++ PI3Kδ, IC50: 18 nM | 99% | ||||||||||||||||
| IC-87114 | + PI3Kγ, IC50: 29 μM | + PI3Kδ, IC50: 0.5 μM | 99%+ | ||||||||||||||||
| Idelalisib | ++ p110γ, IC50: 89 nM | ++++ p110δ, IC50: 2.5 nM | 98% | ||||||||||||||||
| PIK-293 | + p110γ, IC50: 10 μM | + p110δ, IC50: 0.24 μM | 99%+ | ||||||||||||||||
| Vps34-PIK-III | + PI3Kδ, IC50: 1.2μM | +++ Vps34, IC50: 0.018μM | 99%+ | ||||||||||||||||
| GSK2292767 | ✔ | 98% | |||||||||||||||||
| Seletalisib | + PI3Kγ, IC50: 282 nM | +++ PI3Kδ, IC50: 12 nM | 99%+ | ||||||||||||||||
| P110δ-IN-1 | ++++ P110δ, IC50: 0.6 nM | 99% | |||||||||||||||||
| PI3Kδ-IN-5 | ++++ PI3Kδ, IC50: 0.9 nM | 99% | |||||||||||||||||
| SRX3207 | + PI3K alpha, IC50: 244 nM | + PI3K gamma, IC50: 9790 nM | + PI3K delta, IC50: 388 nM | Syk | 98% | ||||||||||||||
| Parsaclisib HCl | ++++ PI3Kδ, IC50: 1 nM | 98% | |||||||||||||||||
| IHMT-PI3Kδ-372 | +++ PI3Kδ, IC50: 14 nM | 98% | |||||||||||||||||
| Trigonelline | ✔ | Akt | 99%+ | ||||||||||||||||
| Wortmannin | ++++ PI3K, IC50: 3 nM | DNA-PK,MLCK | 99%+ | ||||||||||||||||
| Samotolisib | ✔ | DNA-PK | 99%+ | ||||||||||||||||
| GNE-317 | ✔ | 99%+ | |||||||||||||||||
| Oroxin B | ✔ | PTEN,Akt | 99%+ | ||||||||||||||||
| NU 7026 | + PI3K, IC50: 13 μM | DNA-PK | 98+% | ||||||||||||||||
| Deguelin | ✔ | Akt | 99%+ | ||||||||||||||||
| Ailanthone | ✔ | CDK,ATM/ATR,Akt | 98% | ||||||||||||||||
| Resibufogenin | ✔ | ROS | 98% | ||||||||||||||||
| KU-57788 | + PI3K, IC50: 5 μM | DNA-PK,mTOR | 99%+ | ||||||||||||||||
| Cinobufagine | ✔ | Akt | 99% | ||||||||||||||||
| α-Linolenic acid | ✔ | 97% (GC) | |||||||||||||||||
| MTX-211 | ✔ | EGFR | 98% | ||||||||||||||||
| PI3K/mTOR Inhibitor-2 | ++++ PI3K, IC50: 3.4 nM | mTOR | 99%+ | ||||||||||||||||
| SPP-86 | ✔ | 99%+ | |||||||||||||||||
| (E)-Akt inhibitor-IV | ✔ | 98% | |||||||||||||||||
| Vps34-IN-1 | ++ Vps34, IC50: 25 nM | 98% | |||||||||||||||||
| SAR405 | ++++ Vps34, IC50: 1.2 nM | 98+% | |||||||||||||||||
| 3-Methyladenine | + PI3Kγ, IC50: 60 μM | + Vps34, IC50: 25 μM | Autophagy | 98% | |||||||||||||||
| Vps34-IN-4 | +++ VPS34, IC50: 15 nM | 98%+ | |||||||||||||||||
| Autophinib | +++ Vps34, IC50: 19 nM | Autophagy | 99% | ||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | Autophagy ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| SBI-0206965 | +++ ULK1, IC50: 108 nM ULK2, IC50: 711 nM | 95% | |||||||||||||||||
| Hydroxychloroquine sulfate | ✔ | 99% | |||||||||||||||||
| Valproic acid sodium | ✔ | HDAC | 97% | ||||||||||||||||
| PFK-015 | ++ PFKFB3, IC50: 207 nM | 99%+ | |||||||||||||||||
| MRT68921 HCl | ++++ ULK1, IC50: 2.9 nM ULK2, IC50: 1.1 nM | 99%+ | |||||||||||||||||
| ROC-325 | ✔ | 99%+ | |||||||||||||||||
| Autophinib | +++ Autophagy, IC50: 40 nM | 99% | |||||||||||||||||
| Lys05 | ✔ | 99%+ | |||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 靶点 | 
 | 
| 描述 | Vps34 is one kind of PI3K isoform, which plays an essential role in endosomal trafficking of proteins to the vacuole/lysosome, autophagy and phagocytosis. 3-Methyladenine (3-MA) shows inhibition of Vps34 in vitro, with an IC50 of 25 μM as compared with 60 μM for PI3Kγ. 3-Methyladenine is typically employed at a concentration of 10 mM in cellular studies[1]. It is usually served as the inhibitor for both autophagy[1] and type 1 mitophagy through suppression of class III PI3K activity [2]. However, now it was found that 3-Methyladenine play a dual role in modulation of autophagy. Prolonged treatment with 3-Methyladenine (5mM) up to 9 h can induce LC3 I to II conversion in wild type MEFs, L929 and 293T cells cultured in full-medium, whereas it is still effective in suppressing LC3 II conversation in cells induced by starvation. And this observation is consistent with result of punctuate formation of GFP-LC3 study. These results demonstrate that prolonged treatment with 3-Methyladenine under nutrient-rich conditions can enhance autophagic flux. This may due to its different temporal patterns of inhibition on Class I and III PI3K[3]. | 
| 作用机制 | May due to the specific hydrophobic ring to Vps34 encircles the 3-methyl group of 3-MA.[1] | 
| Concentration | Treated Time | Description | References | |
| THLE2 cells | 5 mM | 6 h | To inhibit autophagy and study the protective role of YAP in hepatic ischemia-reperfusion injury. Results showed that inhibition of autophagy weakened YAP-mediated cell protection, accompanied by a significant upregulation of apoptosis levels. | Chin Med J (Engl). 2024 Mar 20;137(6):657-668. | 
| mouse primary cortical neurons | 5 mM | 24 h | To inhibit autophagy and evaluate its effect on neuronal survival. Results showed that 3-MA at appropriate concentrations significantly increased neuronal survival after oxygen-glucose deprivation (OGD). | J Extracell Vesicles. 2020 Oct;10(1):e12024. | 
| COV434 cells | 5 mM | 24 h | Inhibited autophagy but did not significantly alleviate CDDP-induced ER stress and apoptosis | Reprod Biol Endocrinol. 2018 Sep 3;16(1):85. | 
| KGN cells | 5 mM | 24 h | Inhibited autophagy but did not significantly alleviate CDDP-induced ER stress and apoptosis | Reprod Biol Endocrinol. 2018 Sep 3;16(1):85. | 
| cardiomyocytes | 10 mM | 3 h | inhibited autophagy, significantly attenuated or ablated lethal toxin-induced cardiomyocyte contractile anomalies | BMC Med. 2012 Nov 7;10:134. | 
| osteoclasts | 0.5 mM | 72 h | 3-MA reversed the enhanced autophagy levels by DOX, indicating that enhanced autophagy was responsible for the effects of DOX. | Antioxidants (Basel). 2022 Jul 28;11(8):1476. | 
| HEK293T cells | 5 mg/mL | 8 h | To investigate the effect of 3-MA on BinCARD1 degradation, it was found that 3-MA inhibited TBK1-mediated autophagic degradation of BinCARD1. | Cell Mol Immunol. 2022 Oct;19(10):1168-1184. | 
| Newborn mouse ovarian cells | 1 mM | 3 days | Inhibited autophagy, leading to a decreased percentage of primordial follicles | Cell Death Dis. 2020 Sep 10;11(9):737. | 
| Mouse embryonic fibroblasts (MEFs) | 5 mM | Inhibition of autophagy, leading to increased toxicity in glucose-starved wild-type MEFs, similar to the effect of RelA inactivation. | Nat Cell Biol. 2011 Aug 28;13(10):1272-9. | |
| Administration | Dosage | Frequency | Description | References | ||
| Mice | Hepatic ischemia-reperfusion injury model | Intraperitoneal injection | 15 mg/kg | Once, 1 hour before I/R model establishment | To inhibit autophagy and study the protective role of YAP in hepatic ischemia-reperfusion injury. Results showed that inhibition of autophagy weakened YAP-mediated liver protection, accompanied by a significant upregulation of apoptosis levels. | Chin Med J (Engl). 2024 Mar 20;137(6):657-668. | 
| C57BL/6 male mice | Transverse aortic constriction (TAC)-induced cardiac hypertrophy model | Intraperitoneal injection | 20 mg/kg | Once daily for 4 weeks | 3-MA inhibited PKD siRNA-induced increase in autophagy and prevented the ameliorative effects of PKD siRNA on cardiac hypertrophy | Int J Biol Sci. 2017 Feb 12;13(3):276-285 | 
| C57BL/6 mice | Middle cerebral artery occlusion (MCAO) model | Intraperitoneal injection | 15 mg/kg | Single injection at the beginning of reperfusion or 12 hours later | To evaluate the inhibitory effect of 3-MA on autophagy after cerebral ischemia and its impact on neuroprotection and neurological recovery. Results showed that 3-MA injection at 12 hours after reperfusion significantly reduced brain injury and improved neurological recovery. | J Extracell Vesicles. 2020 Oct;10(1):e12024. | 
| C57BL/6J mice | Cisplatin-induced premature ovarian insufficiency model | Intraperitoneal injection | 10 mg/kg | Consecutively for 7 days | Inhibiting autophagy did not significantly alleviate CDDP-induced ovarian damage and hormone dysregulation | Reprod Biol Endocrinol. 2018 Sep 3;16(1):85. | 
| Mice | TAC-induced heart failure model | Intraperitoneal injection | 15 mg/kg | Every 3 days | To inhibit autophagic induction and evaluate its effect on TAC-induced heart failure | JACC Basic Transl Sci. 2023 Jul 19;8(9):1215-1239 | 
| C57BL/6J female mice | DOX-induced bone loss model | Intraperitoneal injection | 5 mg/kg | DOX once per week for three weeks; 3-MA daily for four weeks | Injection of 3-MA reversed DOX-induced bone loss and reduced the area of OCs on the bone surface. | Antioxidants (Basel). 2022 Jul 28;11(8):1476. | 
| Mice | Heterotopic transplant model of intestinal fibrosis | Intraperitoneal injection | 10 mg/kg | Once daily for 7 days | 3-MA further inhibited autophagy in the grafted tissue and aggravated fibrosis. | Cells. 2019 Sep 13;8(9):1078 | 
| BALB/C nude mice | A2780 tumor xenograft model | Not specified | 5 mg/kg | 3 weeks | To investigate the effect of 3-MA on A2780 tumor growth, it was found that 3-MA could completely suppress autophagy induced by the combination of erlotinib and AZD2281 and attenuate its antitumor activity. | Drug Des Devel Ther. 2015 Jun 22;9:3183-90 | 
| Animal Administration | Rats: 15 mg/kg[4] Mice: 35 mg/kg[5] | 
| Dose | Mice: 35 mg/kg[5] Rats: 15 mg/kg[4] | 
| Administration | i.v., i.p. | 
| 计算器 | ||||
| 存储液制备 |  | 1mg | 5mg | 10mg | 
| 1 mM 5 mM 10 mM | 6.70mL 1.34mL 0.67mL | 33.52mL 6.70mL 3.35mL | 67.05mL 13.41mL 6.70mL | |
| CAS号 | 5142-23-4 | 
| 分子式 | C6H7N5 | 
| 分子量 | 149.15 | 
| SMILES Code | NC1=C2N=CN=C2N(C)C=N1 | 
| MDL No. | MFCD00010531 | 
| 别名 | 3-甲基腺嘌呤 ;3-MA; NSC 66389; 3-Methyladenine, NSC 66389 | 
| 运输 | 蓝冰 | 
| InChI Key | ZPBYVFQJHWLTFB-UHFFFAOYSA-N | 
| Pubchem ID | 135398661 | 
| 存储条件 | In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Sealed in dry,2-8°C | 
| 溶解方案 | DMSO: 7 mg/mL(46.93 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO H2O: 5 mg/mL(33.52 mM),配合低频超声助溶 细胞培养中,3-MA 的浓度可能会用到 0.5-10 mM,工作浓度较高,不推荐使用 DMSO 储备液。建议在实验前称量需要的 3-MA 的量,然后将其直接溶解在培养基中,并用 0.22 μm 滤膜过滤除菌,现用现配。 
 
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			沪公网安备 31011702889066号
			
			沪ICP备2024050318号-1