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                同义名:
                    
                        
                            
                                GDC-0941; GNE-0941
                            
                        
                    
                
                
                
                    
                     
                    
                     
                
            
Pictilisib(GDC-0941)是一种有效的PI3Kα/δ抑制剂,IC50为3 nM,对p110β(11倍)和p110γ(25倍)具有适度选择性。
 
                                 
                                
                            

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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 | ✔ | 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-kinases (PI3Ks) are lipid kinases that catalyze the phosphorylation of the 3-hydroxyl position of phosphatidylinositides and participate in several cellular process. Up to now, there are eight PI3 kinases have been identified, which are divided into classes IA, 1B, II, and III based on the sequence homology and substrate preference. GDC-0941 is a potent, selective and orally bioavailable inhibitor of class I PI3Ks (p110α IC50=3nM, p110δ IC50=3nM, p110β IC50=33nM, p110γ IC50=75nM, measured by scintillation proximity assay), with less potency to mTOR (IC50=0.58μM, measured by HTRF assay)[1]. GDC-0941 is a derivative of PI-103, a dual PI3K/mTOR inhibitor, and has good pharmacokinetic properties. Its oral bioavailability is up to 78% in subcutaneous U-87 MG xenograft mice and shows sustained and remarkable inhibition of Akt phosphorylation and tumor growth, up to 98%[2]. GDC-0941 barely penetrated through the intact BBB[3]. | 
| 作用机制 | GDC-0941 is a potent, ATP competitive inhibitor of p110α with Ki value of 10.2±4.4 nM.[1] | 
| Concentration | Treated Time | Description | References | |
| Human NK cells | 1 μM | 2 hours | To evaluate the effect of MLN1117 on human NK cell-mediated cytotoxicity. Results showed that selective inhibition of p110α had minimal impact on human NK cell-mediated cytotoxicity. | PLoS One. 2014 Jun 10;9(6):e99486. | 
| MEB-Med-8A cells | 1 μM | 24 h | Pictilisib significantly inhibited the migration of MEB-Med-8A cells and altered the cytoskeleton structure. | J Cell Mol Med. 2022 Dec;26(23):5832-5845. | 
| Daoy cells | 1 μM | 24 h | Pictilisib reduced the migration of Daoy cells, significantly decreased wound closure, and altered the cytoskeleton structure. | J Cell Mol Med. 2022 Dec;26(23):5832-5845. | 
| KPwmC cells | 1μM | 30 min | To observe the effect of Pictilisib on p-CREB1S133 levels, results showed that Pictilisib reduced p-CREB1S133 levels. | Cancer Discov. 2021 Aug;11(8):2094-2111. | 
| P14 CD8+ T cells | 1 μM | 3 to 4 days | Inhibition of PI3K activity, leading to defective CD3 polarity and Glut1 surface trafficking, reduced glucose uptake | Cell Rep. 2018 Jan 23;22(4):860-868. | 
| SW48-HER2 | 0.05 to 10 μM | 96 h | To evaluate the anti-proliferative effects of Pictilisib on SW48-HER2 cells. Results showed that Pictilisib as a single agent exhibited dose-dependent cell growth inhibition in HER2-amplified cells. | J Exp Clin Cancer Res. 2019 Jun 4;38(1):236. | 
| LIM1215-HER2 | 0.05 to 10 μM | 96 h | To evaluate the anti-proliferative effects of Pictilisib on LIM1215-HER2 cells. Results showed that Pictilisib as a single agent exhibited dose-dependent cell growth inhibition in HER2-amplified cells. | J Exp Clin Cancer Res. 2019 Jun 4;38(1):236. | 
| SW48-HER2 cells | 0.05 to 10 μM | 96 h | To evaluate the inhibitory effect of Pictilisib on cell proliferation, the results showed that Pictilisib monotherapy exhibited dose-dependent growth inhibition in HER2-amplified cells. | J Exp Clin Cancer Res. 2019 Jun 4;38(1):236. | 
| LIM1215-HER2 cells | 0.05 to 10 μM | 96 h | To evaluate the inhibitory effect of Pictilisib on cell proliferation, the results showed that Pictilisib monotherapy exhibited dose-dependent growth inhibition in HER2-amplified cells. | J Exp Clin Cancer Res. 2019 Jun 4;38(1):236. | 
| mIMCD3 cells | 1 µM | 10 h | Pictilisib significantly reduced phosphorylation of Akt, MAPKAP1, and GFAP, and increased the formation of Dendra2 CMA reporter puncta, indicating an increase in CMA activity. | J Cell Biol. 2020 Dec 7;219(12):e202001031. | 
| AML12 cells | 2 µM | 10 h | Pictilisib significantly reduced phosphorylation of Akt, MAPKAP1, and GFAP, and increased the formation of Dendra2 CMA reporter puncta, indicating an increase in CMA activity. | J Cell Biol. 2020 Dec 7;219(12):e202001031. | 
| NIH3T3 cells | 500 nM | 10 h | Pictilisib significantly reduced phosphorylation of Akt, MAPKAP1, and GFAP, and increased the accumulation of Dendra2 CMA reporter puncta, indicating an increase in CMA activity. | J Cell Biol. 2020 Dec 7;219(12):e202001031. | 
| Administration | Dosage | Frequency | Description | References | ||
| Mice | T-ALL JW81 model | Oral and intraperitoneal injection | 100 mg/kg/day | GDC0941 once daily, VCR twice weekly, until mice developed progressive disease | To evaluate the efficacy of GDC0941 and VCR combination therapy in T-ALL mouse model | Cell Rep. 2019 Apr 9;27(2):631-647. e5 | 
| Nude mice | LIM1215-HER2 and SW48-HER2 tumor xenograft models | Oral | 75 mg/kg | Once daily for 4 weeks | To evaluate the antitumor activity of Pictilisib in LIM1215-HER2 and SW48-HER2 tumor xenograft models. Results showed that Pictilisib as a single agent had little effect on tumor growth, but the combination with Refametinib almost completely suppressed tumor growth. | J Exp Clin Cancer Res. 2019 Jun 4;38(1):236. | 
| Nude mice | LIM1215-HER2 and SW48-HER2 tumor xenografts | Oral | 75 mg/kg | Every day, for 4 weeks | To evaluate the inhibitory effect of Pictilisib monotherapy and its combination with Refametinib on tumor growth, the results showed that the combination therapy significantly suppressed tumor growth and lasted up to 20 weeks after the end of treatment. | J Exp Clin Cancer Res. 2019 Jun 4;38(1):236. | 
| Mice | Normal 3-month-old mice | Oral | 100 mg/kg | Once per day for 7 days | Pictilisib significantly increased CMA substrate uptake in liver lysosomes and reduced lysosomal GFAP phosphorylation in mice, indicating an increase in CMA activity. | J Cell Biol. 2020 Dec 7;219(12):e202001031. | 
| Mice | MR86 patient-derived xenograft (PDX) model | Oral | 150 mg/kg | Once daily for up to 40 days | To evaluate the inhibitory effect of Pictilisib in combination with Erdafitinib on tumor growth, the results showed that the combination treatment significantly inhibited tumor growth | Cancer Discov. 2023 Sep 6;13(9):1998-2011 | 
| Dose | Mice: min = 75 mg/kg[4], max = 150 mg/kg[5] Nude Mice: min = 25 mg/kg bid, max = 50 mg/kg bid[6] | 
| Administration | p.o | 
| NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 | 
| NCT02430363 | Glioblastoma | Phase 1 Phase 2 | Unknown | June 2018 | United States, Massachusetts ... 展开 >> Dana-Farber Cancer Institute Boston, Massachusetts, United States, 02115 United States, Texas M D Anderson Cancer Center Houston, Texas, United States, 77030 Belgium UCL- Cliniques Universitaires Saint Luc Brussels, Belgium Germany St Johannes Hospital Duisburg, Germany, 47166 Italy Spedali Civili di Brescia Brescia, Italy IRCCS San Raffaele Milan, Italy Poland Lower-Silesian Oncology Centre Wroclaw, Lower-Silesian, Poland, 53413 Russian Federation Pavlov State Medical University St. Petersburg, Russian Federation, 197089 Spain Hospital Universitario Germans Trias I Pujol Barcelona,, Spain Switzerland Universitätsklinik für Frauenheilkunde Bern, Switzerland Ukraine Regional Cancer Center Dnepropetrovsk, Ukraine, 49000 National Institute of Cancer Kiev, Ukraine, 03035 United Kingdom Royal Victoria Hospital Belfast, Ulster, United Kingdom, BT12 6BA 收起 << | 
| NCT02389842 | Advanced Solid Tumours ... 展开 >> Breast Cancer 收起 << | Phase 1 | Unknown | August 2017 | United Kingdom ... 展开 >> The Royal Marsden NHS Foundation Trust Recruiting London, United Kingdom, SM2 5PT Contact: Timothy Yap, PhD 02086613539 timothy.yap@icr.ac.uk Principal Investigator: Timothy Yap, PhD The Christie NHS Foundation Trust Not yet recruiting Manchester, United Kingdom, M20 4BX Contact: Anne Amstrong, MBBS 0161 446 3746 elaine.mercer@christie.nhs.uk Principal Investigator: Anne Armstrong, MBBS 收起 << | 
| NCT02092831 | Healthy Volunteer | Phase 1 | Completed | - | United States, Wisconsin ... 展开 >> Madison, Wisconsin, United States, 53704 收起 << | 
| 计算器 | ||||
| 存储液制备 |  | 1mg | 5mg | 10mg | 
| 1 mM 5 mM 10 mM | 1.95mL 0.39mL 0.19mL | 9.73mL 1.95mL 0.97mL | 19.47mL 3.89mL 1.95mL | |
| CAS号 | 957054-30-7 | 
| 分子式 | C23H27N7O3S2 | 
| 分子量 | 513.64 | 
| SMILES Code | CS(=O)(=O)N1CCN(CC2=CC3=C(S2)C(=NC(=N3)C2=C3C=NNC3=CC=C2)N2CCOCC2)CC1 | 
| MDL No. | MFCD11616196 | 
| 别名 | GDC-0941; GNE-0941; Pictrelisib; RG7321 | 
| 运输 | 蓝冰 | 
| InChI Key | LHNIIDJUOCFXAP-UHFFFAOYSA-N | 
| Pubchem ID | 17755052 | 
| 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: 105 mg/mL(204.43 mM),配合低频超声,并水浴加热至45℃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 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶 
 
 
 
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