 
        
        
        ZSTK474是一种 ATP 竞争性泛 I 类 PI3K 抑制剂,对 PI3Kα 的 IC50 为 16 nM,对 PI3Kβ 为 44 nM,对 PI3Kδ 为 4.6 nM,对 PI3Kγ 为 49 nM。
 
                                 
                                
                            

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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 | Src,PKC,Sirtuin | 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 | MLCK,DNA-PK | 99%+ | ||||||||||||||||
| Samotolisib | ✔ | DNA-PK | 99%+ | ||||||||||||||||
| GNE-317 | ✔ | 99%+ | |||||||||||||||||
| Oroxin B | ✔ | Akt,PTEN | 99%+ | ||||||||||||||||
| NU 7026 | + PI3K, IC50: 13 μM | DNA-PK | 98+% | ||||||||||||||||
| Deguelin | ✔ | Akt | 99%+ | ||||||||||||||||
| Ailanthone | ✔ | Akt,CDK,ATM/ATR | 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。 | |||||||||||||||||||
| 靶点 | 
 | 
| 描述 | Phosphatidylinositol 3-kinase (PI3K), which is active in signal transduction, generates phosphatidylinositol-3,4,5-tris-phosphate (PIP3) by phosphorylating phosphatidylinositol-4,5-bisphosphate. PI3K is involved in various cellular processes, including cell survival, vesicle transport, and cytoskeletal rearrangement[3]. ZSTK474, a novel s-triazine derivative, is an ATP-competitive pan-class I PI3K inhibitor with IC50s of 16 nM, 44 nM, 4.6 nM and 49 nM for PΙ3Κα, PI3Kβ, PI3Kδ and PI3Kγ, respectively[4]. The mean logarithm of GI50 for ZSTK474 was −6.49 at 0.32 μM, which was substantially lower than that observed with LY294002 or wortmannin, indicating that ZSTK474 had stronger cell growth inhibitory activity than either of these two known PI3K inhibitors. At concentration of 1 μM, ZSTK474 reduced the PI3K activity to 4.7% of the untreated control activity. When murine embryonic fibroblast cells were incubated for 15 minutes with 1 μM ZSTK474 before the addition of platelet-derived growth factor, both membrane ruffling and the formation of PIP3 , a measure of PI3K activity, were blocked. At 10 μM, a higher concentration than its GI50, ZSTK474 induced apoptosis in OVCAR3 cells. When administered orally for 2 weeks, ZSTK474 inhibited the growth of subcutaneously implanted mouse B16F10 melanoma tumors in a dose-dependent manner. Almost complete tumor growth inhibition (i.e., tumor regression) was observed at higher dosages[3]. | 
| 作用机制 | There are three hydrogen-bonding interactions between PI3K and ZSTK474 (i.e., K802 NZ, one of the morpholino oxygens; S806 OG, the other morpholino oxygen; and V882 NH, the benzimidazole nitrogen)[3]. | 
| Concentration | Treated Time | Description | References | |
| MCF7 cells | 10 µM | 1 h | Inhibition of PI3K signaling pathway to observe its effect on ERK activation | Nat Commun. 2018 Nov 7;9(1):4673. | 
| A431 cells | 1 µM | 6 h | To evaluate the effect of ZSTK474 on apoptosis in A431 cells, results showed that CD151 knockdown increased ZSTK474-induced apoptosis. | Cell Mol Life Sci. 2019 Apr;76(8):1595-1604. | 
| LM-EV | 30 μM | 7 days | To study the effect of ZSTK474 on the viability of LM-EV cells in suspension culture, results showed that ZSTK474 significantly reduced the viability of LM-EV cells | Breast Cancer Res. 2016 Aug 5;18(1):81. | 
| BT549-EV | 30 μM | 7 days | To study the effect of ZSTK474 on the viability of BT549-EV cells in suspension culture, results showed that ZSTK474 significantly reduced the viability of BT549-EV cells | Breast Cancer Res. 2016 Aug 5;18(1):81. | 
| REH cells | 4 µM | 48 h | To evaluate the synergistic anticancer effect of ZSTK474 combined with AZD0364 on REH cells, the results showed that the combination treatment significantly reduced cell viability, increased ROS production, and induced apoptosis. | Antioxidants (Basel). 2020 Jul 17;9(7):633. | 
| MOLT-4 cells | 0.5 µM | 48 h | To evaluate the synergistic anticancer effect of ZSTK474 combined with AZD0364 on MOLT-4 cells, the results showed that the combination treatment significantly reduced cell viability, increased ROS production, and induced apoptosis. | Antioxidants (Basel). 2020 Jul 17;9(7):633. | 
| MOLM-14 cells | 0.5 µM | 48 h | To evaluate the synergistic anticancer effect of ZSTK474 combined with AZD0364 on MOLM-14 cells, the results showed that the combination treatment significantly reduced cell viability, increased ROS production, and induced apoptosis. | Antioxidants (Basel). 2020 Jul 17;9(7):633. | 
| K562 cells | 8 µM | 48 h | To evaluate the anticancer effect of ZSTK474 combined with AZD0364 on K562 cells, the results showed that the combination treatment had an antagonistic effect on K562 cells. | Antioxidants (Basel). 2020 Jul 17;9(7):633. | 
| RAW264.7 cells | 0.1 μM | 30 min | ZSTK474 suppressed the phosphorylation of Akt induced by sRANKL, indicating its inhibitory effect on the PI3-K/Akt signaling pathway. | Arthritis Res Ther. 2010;12(3):R92. | 
| mature osteoclasts | 0.1 μM | 72 h | ZSTK474 completely inhibited the bone-resorbing activity of mature osteoclasts. | Arthritis Res Ther. 2010;12(3):R92. | 
| Huh7 | 5 μM | 24 h | The combination of ZSTK474 and PIK3C3 inhibitor significantly suppressed the expression of stemness genes and effectively reduced the proportion of CD133+ cells. | Cell Death Dis. 2020 Jun 8;11(6):427. | 
| MHCC97H | 5 μM | 24 h | The combination of ZSTK474 and PIK3C3 inhibitor significantly suppressed the expression of stemness genes and effectively reduced the proportion of CD133+ cells. | Cell Death Dis. 2020 Jun 8;11(6):427. | 
| Administration | Dosage | Frequency | Description | References | ||
| C57BL/6 mice | Cerebral ischemia/reperfusion injury model | Oral | 200 mg/kg | Once daily for 3 days | ZSTK474 alleviated neurological deficits, reduced infarct volume, and shifted the phenotype of microglia/macrophages, inhibiting the inflammatory response in the cerebral ischemia/reperfusion injury model. | J Neuroinflammation. 2016 Aug 22;13(1):192 | 
| Mice | Cerebral ischemia/reperfusion injury model | Oral gavage | 200 mg/kg | Once daily for 3 days | ZSTK474 alleviated neurological deficits, reduced infarct volume, and improved neurological function in the cerebral ischemia/reperfusion injury model. | J Neuroinflammation. 2016 Aug 22;13(1):192 | 
| Mice | Collagen-induced arthritis (CIA) model | Oral | 25, 50, 100 mg/kg | Once daily until the end of the experiment | ZSTK474 significantly alleviated arthritis symptoms in the CIA model, reduced inflammatory cell infiltration and cartilage/bone destruction, and significantly decreased osteoclast formation. | Arthritis Res Ther. 2010;12(3):R92. | 
| Nude mice | Subcutaneous xenograft model | Oral | 200 mg/kg | Once daily for 10 days | The combination of ZSTK474 and PIK3C3 inhibitor significantly suppressed tumor growth and reduced the proportion of CD133+ cells in tumors. | Cell Death Dis. 2020 Jun 8;11(6):427. | 
| NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 | 
| NCT01682473 | Neoplasms | Phase 1 | Completed | - | Japan ... 展开 >> National Cancer Center Hospital East Kashiwa-city, Chiba, Japan The Cancer Institute Hospital of JFCR Koto-ku, Tokyo, Japan 收起 << | 
| NCT01280487 | Neoplasms | Phase 1 | Completed | - | United States, Massachusetts ... 展开 >> Dana Farber Cancer Institute Boston, Massachusetts, United States United States, Missouri Washington University St Louis, Missouri, United States United States, Pennsylvania Fox Chase Cancer Center Philadelphia, Pennsylvania, United States 收起 << | 
[3]Antitumor activity of ZSTK474, a new phosphatidylinositol 3-kinase inhibitor
[4]ZSTK474 is an ATP-competitive inhibitor of class I phosphatidylinositol 3 kinase isoforms
| 计算器 | ||||
| 存储液制备 |  | 1mg | 5mg | 10mg | 
| 1 mM 5 mM 10 mM | 2.40mL 0.48mL 0.24mL | 11.98mL 2.40mL 1.20mL | 23.96mL 4.79mL 2.40mL | |
| CAS号 | 475110-96-4 | 
| 分子式 | C19H21F2N7O2 | 
| 分子量 | 417.41 | 
| SMILES Code | FC(C1=NC2=CC=CC=C2N1C3=NC(N4CCOCC4)=NC(N5CCOCC5)=N3)F | 
| MDL No. | MFCD08705334 | 
| 别名 | |
| 运输 | 蓝冰 | 
| InChI Key | HGVNLRPZOWWDKD-UHFFFAOYSA-N | 
| Pubchem ID | 11647372 | 
| 存储条件 | In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Sealed in dry, store in freezer, under -20°C | 
| 溶解方案 | DMSO: 2 mg/mL(4.79 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 | 
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