PI3K
信号通路图
研究领域
- 抑制剂选择性比较
- 溶解性比较
| 目录号 | 产品目录 | 溶解度(25°C) | ||
|---|---|---|---|---|
| 水 | DMSO | 酒精 | ||
| S1009 | Dactolisib (BEZ235, NVP-BEZ235) | <1 mg/mL | 0.01 mg/mL | <1 mg/mL |
| S1065 | Pictilisib (GDC-0941) | <1 mg/mL | 44 mg/mL | <1 mg/mL |
| S1105 | LY294002 | <1 mg/mL | 36 mg/mL | 21 mg/mL |
| S2226 | Idelalisib (CAL-101, GS-1101) | <1 mg/mL | 83 mg/mL | 23 mg/mL |
| S2247 | Buparlisib (BKM120, NVP-BKM120) | <1 mg/mL | 82 mg/mL | 2 mg/mL |
| S8752 | leniolisib(CDZ 173) | <1 mg/mL | 90 mg/mL | 13 mg/mL |
| S8738 | Bimiralisib (PQR309) | <1 mg/mL | 6 mg/mL | <1 mg/mL |
| S8560 | Seletalisib (UCB-5857) | <1 mg/mL | 97 mg/mL | 97 mg/mL |
| S8696 | 2-D08 | <1 mg/mL | 54 mg/mL | <1 mg/mL |
| S8672 | Tenalisib (RP6530) | <1 mg/mL | 75 mg/mL | 75 mg/mL |
| S7335 | IPI-3063 | <1 mg/mL | 91 mg/mL | 12 mg/mL |
| S1038 | PI-103 | <1 mg/mL | 24 mg/mL | <1 mg/mL |
| S2638 | NU7441 (KU-57788) | <1 mg/mL | 4 mg/mL | <1 mg/mL |
| S1169 | TGX-221 | <1 mg/mL | 12 mg/mL | <1 mg/mL |
| S1268 | IC-87114 | <1 mg/mL | 0.66 mg/mL | <1 mg/mL |
| S2758 | Wortmannin | <1 mg/mL | 85 mg/mL | <1 mg/mL |
| S1118 | XL147 analogue | <1 mg/mL | 3 mg/mL | <1 mg/mL |
| S1072 | ZSTK474 | <1 mg/mL | 21 mg/mL | <1 mg/mL |
| S2814 | Alpelisib (BYL719) | <1 mg/mL | 88 mg/mL | 2 mg/mL |
| S1410 | AS-605240 | <1 mg/mL | 0.4 mg/mL | <1 mg/mL |
| S1205 | PIK-75 HCl | <1 mg/mL | 4 mg/mL | <1 mg/mL |
| S2767 | 3-Methyladenine (3-MA) | 10 mg/mL | 3 mg/mL | 4 mg/mL |
| S2636 | A66 | <1 mg/mL | 79 mg/mL | 1 mg/mL |
| S1523 | Voxtalisib (SAR245409, XL765) Analogue | <1 mg/mL | 12 mg/mL | <1 mg/mL |
| S1489 | PIK-93 | <1 mg/mL | 78 mg/mL | <1 mg/mL |
| S2658 | Omipalisib (GSK2126458, GSK458) | <1 mg/mL | 100 mg/mL | <1 mg/mL |
| S1187 | PIK-90 | <1 mg/mL | 0.28 mg/mL | <1 mg/mL |
| S1462 | AZD6482 | <1 mg/mL | 82 mg/mL | 10 mg/mL |
| S2743 | PF-04691502 | <1 mg/mL | 14 mg/mL | <1 mg/mL |
| S2696 | Apitolisib (GDC-0980, RG7422) | <1 mg/mL | 20 mg/mL | <1 mg/mL |
| S1360 | GSK1059615 | <1 mg/mL | 2 mg/mL | <1 mg/mL |
| S7028 | Duvelisib (IPI-145, INK1197) | <1 mg/mL | 83 mg/mL | <1 mg/mL |
| S2628 | Gedatolisib (PF-05212384, PKI-587) | <1 mg/mL | 2 mg/mL | <1 mg/mL |
| S1352 | TG100-115 | <1 mg/mL | 9 mg/mL | <1 mg/mL |
| S2671 | AS-252424 | <1 mg/mL | 61 mg/mL | <1 mg/mL |
| S2749 | BGT226 (NVP-BGT226) | <1 mg/mL | 30 mg/mL | <1 mg/mL |
| S2759 | CUDC-907 | <1 mg/mL | 102 mg/mL | <1 mg/mL |
| S2227 | PIK-294 | <1 mg/mL | 98 mg/mL | <1 mg/mL |
| S2681 | AS-604850 | <1 mg/mL | 57 mg/mL | 5 mg/mL |
| S8002 | GSK2636771 | <1 mg/mL | 28 mg/mL | <1 mg/mL |
| S2802 | Copanlisib (BAY 80-6946) | 0.002 mg/mL | 0.002 mg/mL | 0.01 mg/mL |
| S1219 | YM201636 | <1 mg/mL | 35 mg/mL | <1 mg/mL |
| S2699 | CH5132799 | <1 mg/mL | 12 mg/mL | <1 mg/mL |
| S2682 | CAY10505 | <1 mg/mL | 58 mg/mL | <1 mg/mL |
| S2207 | PIK-293 | <1 mg/mL | 80 mg/mL | <1 mg/mL |
| S2739 | PKI-402 | <1 mg/mL | 0.4 mg/mL | <1 mg/mL |
| S2870 | TG100713 | <1 mg/mL | 2 mg/mL | <1 mg/mL |
| S7016 | VS-5584 (SB2343) | <1 mg/mL | 71 mg/mL | 3 mg/mL |
| S7103 | Taselisib (GDC 0032) | <1 mg/mL | 70 mg/mL | <1 mg/mL |
| S7018 | CZC24832 | <1 mg/mL | 5 mg/mL | <1 mg/mL |
| S7813 | AMG319 | <1 mg/mL | 77 mg/mL | 77 mg/mL |
| S7938 | GSK2292767 | <1 mg/mL | 100 mg/mL | <1 mg/mL |
| S8163 | GDC-0084 | <1 mg/mL | 8 mg/mL | <1 mg/mL |
| S8157 | GDC-0326 | <1 mg/mL | 76 mg/mL | 19 mg/mL |
| S7356 | HS-173 | <1 mg/mL | 84 mg/mL | <1 mg/mL |
| S8589 | SF2523 | <1 mg/mL | 29 mg/mL | 7 mg/mL |
| S8581 | Serabelisib (INK-1117,MLN-1117,TAK-117) | <1 mg/mL | 16 mg/mL | <1 mg/mL |
| S8330 | IPI-549 | <1 mg/mL | 100 mg/mL | 8 mg/mL |
| S2391 | Quercetin | <1 mg/mL | 61 mg/mL | 10 mg/mL |
| S8456 | VPS34 inhibitor 1 (Compound 19, PIK-III analogue) | <1 mg/mL | 78 mg/mL | <1 mg/mL |
| S7646 | Voxtalisib (XL765, SAR245409) | <1 mg/mL | 54 mg/mL | <1 mg/mL |
| S8596 | Autophinib | <1 mg/mL | 69 mg/mL | <1 mg/mL |
| S7798 | GNE-317 | <1 mg/mL | 47 mg/mL | <1 mg/mL |
| S8194 | umbralisib (TGR-1202) | <1 mg/mL | 100 mg/mL | 7 mg/mL |
| S7937 | Nemiralisib (GSK2269557) | <1 mg/mL | 88 mg/mL | 8 mg/mL |
| S8322 | LY3023414 | <1 mg/mL | 47 mg/mL | 61 mg/mL |
| S7980 | VPS34-IN1 | <1 mg/mL | 85 mg/mL | 85 mg/mL |
| S7682 | SAR405 | <1 mg/mL | 88 mg/mL | 88 mg/mL |
| S7683 | PIK-III | <1 mg/mL | 63 mg/mL | 63 mg/mL |
| S7623 | PI-3065 | <1 mg/mL | 50 mg/mL | <1 mg/mL |
| S7645 | Pilaralisib (XL147) | <1 mg/mL | 100 mg/mL | <1 mg/mL |
| S7966 | AZD8835 | <1 mg/mL | 93 mg/mL | <1 mg/mL |
| S8132 | Deguelin | <1 mg/mL | 78 mg/mL | 78 mg/mL |
| S7675 | PF-4989216 | <1 mg/mL | 76 mg/mL | 7 mg/mL |
| S7694 | AZD8186 | <1 mg/mL | 91 mg/mL | 35 mg/mL |
| S7865 | 740 Y-P (PDGFR 740Y-P) | 1 mg/mL | -1 mg/mL | -1 mg/mL |
- PI3K抑制剂（76）
- 新PI3K产品
| 产品目录 | 产品描述 | 文献引用 | 实验数据 |
|---|---|---|---|
| S1009 |
Dactolisib (BEZ235, NVP-BEZ235)Dactolisib (BEZ235, NVP-BEZ235) 是一种双重ATP竞争性 PI3K 和 mTOR 抑制剂，在无细胞试验中，抑制 p110α/γ/δ/β 和 mTOR(p70S6K) 的 IC50 分别为 4 nM /5 nM /7 nM /75 nM /6 nM。 在 3T3TopBP1-ER 细胞中抑制 ATR，IC50 为 21 nM，而对 Akt 和 PDK1 的抑制作用很弱。Phase 2。 |
Level of phospho-proteins in RTK and PI3K–Akt–mTOR pathways in treated tumours, detected with western blot.
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| S1065 |
Pictilisib (GDC-0941)Pictilisib (GDC-0941) 是一种有效的PI3Kα/δ抑制剂，在无细胞试验中IC50为 3 nM，对p110β (11倍)和p110γ (25倍)具有适度的选择性。Phase 2。 |
Clonogenic assays of TNBC cell lines grown continuously in increasing concentrations of palbociclib, divided by gene expression subtypes: LAR, luminal androgen receptor; MSL, mesenchymal stem-like; MES, mesenchymal and basal-like. All cell lines are RB1 wild-type except RB1 mutant BT549.
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| S1105 |
LY294002LY294002 是首个合成的已知抑制PI3Kα/δ/β的小分子，在无细胞测定中IC50分别为 0.5 μM/0.57 μM/0.97 μM；在溶液中比在Wortmannin中稳定，也能够阻断自噬体的形成。它不仅能够结合class I PI3Ks和其他PI3K相关的激酶，还能够结合一些与PI3K家族无关的新型靶点。 |
Type I IFNs induce ISG expression in a serine phosphorylation-independent manner. Cells were treated with kinase inhibitors (SB203580, rottlerin, Ly294002, PD98059, and SP600125) before stimulation with IFN-a and IFN-b for 6 hours. Cell lysates were used in western blotting and probed for serine phosphorylation.The relative amounts of pSTAT1 S727 in (up-graph) were quantied and normalized to an untreated control (below-graph). |
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| S2226 |
Idelalisib (CAL-101, GS-1101)Idelalisib (CAL-101, GS-1101) 是选择性p110δ抑制剂，在无细胞试验中IC50为 2.5 nM；对 p110δ 表现出的选择性是对 p110α/β/γ 的 40 到 300 倍，对p110δ的选择性是对 C2β，hVPS34，DNA-PK 和 mTOR的400到4000倍。 |
Invasive migration of RA FLS was analyzed through growth factor–reduced Matrigel-coated transwell inserts in the presence or absence of 1 µM INK007, 5 µM CAL-101, or 0.3 µM IPI-145, or 0.3 µM GDC-0941 inhibitors or DMSO. Cells were allowed to invade through Matrigel toward PDGF-BB (25 ng/ml) containing media for 24 h and were fixed and stained with Hemacolor staining kit.
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| S2247 |
Buparlisib (BKM120, NVP-BKM120)Buparlisib (BKM120, NVP-BKM120) 是一种选择性 PI3K 抑制剂，在无细胞试验中作用于p110α/β/δ/γ的IC50分别为 52 nM/166 nM/116 nM/262 nM。对 VPS34，mTOR，DNAPK 的作用效果下降，而对 PI4Kβ几乎没有活性。Phase 2。 |
NLGN3 mRNA expression in SU-pcGBM2 cells after 12 hr exposure to vehicle, 50 nM NLGN3, 100 nM BKM120, or 50 nM NLGN3 + 100 nM BKM120.
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| S8752New |
leniolisib(CDZ 173)Leniolisib(CDZ 173)是有效的选择性PI3Kδ抑制剂，对PI3Kα, PI3Kβ, PI3Kγ和PI3Kδ的IC50分别为0.244, 0.424, 2.23和0.011 μM。 |
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| S8738New |
Bimiralisib (PQR309)Bimiralisib (PQR309)是一种新型的、可渗透入大脑的PI3K/mTOR双重抑制剂，在体内外具有抗淋巴瘤活性。相对于其他PI3K相关性脂质激酶、蛋白激酶和非相关性靶点，它对PI3K/mTOR具有较高选择性。 |
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| S8560New |
Seletalisib (UCB-5857)Seletalisib是新型的PI3Kδ小分子抑制剂，IC50为12 nM。它对PI3K具有显著的选择性，相对其他I型PI3K亚型，Seletalisib对PI3Kδ的选择性高24-303倍。 |
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| S8696New |
2-D082-D08是一种具有细胞透性的蛋白类泛素化（protein sumoylation）抑制剂。它还能抑制Axl, IRAK4, ROS1, MLK4, GSK3β, RET, KDR和PI3Kα，IC50分别为0.49, 3.9, 5.3, 9.8, 11, 11, 17和35 nM。 |
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| S8672New |
Tenalisib (RP6530)Tenalisib (RP6530)是一种有效的、选择性的PI3Kδ/γ抑制剂，对PI3Kδ和PI3Kγ的IC50值分别为24.5 nM和33.2 nM。它对δ/γ的选择性比对α和β亚型高300倍和100倍以上。 |
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| S7335New |
IPI-3063IPI-3063是有效的、选择性的p110δ抑制剂，在无细胞实验中，IC50为2.5 ± 1.2 nM。其对其他I型PI3K亚型如p110α, p110β, p110γ的IC50s至少高400倍。 |
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| S1038 |
PI-103PI-103是一种多靶点 PI3K 抑制剂，在无细胞试验中作用于p110α/β/δ/γ的IC50为 2 nM/3 nM/3 nM/15 nM，对 mTOR/DNA-PK的作用较小，IC50为30 nM/23 nM。 |
(D) IGROV parental, shControl (two independent clones) and ShPKCiota (two independent clones) were treated with 5 μM GDC-0941 and 1.5 μM PI-103 for 24 hours and subjected to western blot analysis with the indicated antibodies. Each experiment was performed in triplicate.
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| S2638 |
NU7441 (KU-57788)NU7441 (KU-57788)是一种高度有效的，选择性DNA-PK抑制剂，在无细胞试验中IC50为14 nM，也会抑制PI3K，IC50为5 μM。它可降低NHEJ的频率，而增强Cas9介导DNA剪接后发生的同源重组修复率。 |
Cells were treated with cisplatin under the following conditions: pretreatment with Nu7026 (Nu7026, 26) or Nu7441 (Nu7441, 41). Before DNA damage, wortmannin was applied at 100 nM for 30 min, Nu7026 at 10 uM for 1 h, Nu7441 at 1 uM for 1 h. Accompanying quantifications of the adjusted nucleolar EU fluorescence are shown. Each condition was normalized to cells treated with DMSO or indicated inhibitors without DNA damaging treatment. Two-way ANOVA was followed by Holm-Sidak's test for the comparison of cells with and without inhibitors. *, **, *** represent P ≤ 0.05, 0.01, 0.001, respectively.
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| S1169 |
TGX-221TGX-221 是一种p110β-特定的抑制剂，在无细胞试验中IC50为 5 nM，作用于p110β的选择性是作用于p110α的1000倍。 |
A p110β-selective antagonist rescues increased protein synthesis in synaptic fractions from Fmr1 KO mice and in LCLs from a patient with FXS. (A–C) Treatment of synaptoneurosomes with TGX-221 (1 μmol/L, 30 min) reduces p110β-specific PI3K activity and phosphorylation of the downstream target AKT in both WT and Fmr1 KO SNS, shown by a radioactive PI3K assay and phosphoAkt- specific western blot-ting (A). (B) Quantification of PI3K activity using a competitive ELISA showed a significant reduction in PI3K activity in both genotypes after treatment [ n = 4, 2-way ANOVA, *P (genotype) = 0.0086, * P (treatment) = 0.0087, P (interaction) = 0.7154]. (C) Densitometric quantification of phosphoAkt-specific western blots showed a significant effect of treatment (C, n = 4, 2-way ANOVA, *P (treatment) = 0.0005, P (genotype) =0.372, P (interaction) = 0.4894). |
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| S1268 |
IC-87114IC-87114是一种选择性的PI3Kδ抑制剂，无细胞试验中IC50为0.5 μM，作用于PI3Kδ比作用于PI3Kγ和PI3Kα/β选择性分别高58和100倍。 |
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| S2758 |
WortmanninWortmannin是一种首次命名的PI3K抑制剂，在无细胞试验中IC50为3 nM，对 PI3K 家族的选择性较低。也会抑制自噬体的形成，并有效抑制DNA-PK/ATM，在无细胞试验中IC50为16 nM和150 nM。 |
L3.6pl cells at 6,000 cells per well were incubated in MEM with 5% FBS in triplicate in a 96-well culture plate and then treated alone with 5 umol/L BMS-777607, 10 umol/L wortmannin, or with BMS-777607 in combination with individual inhibitors. Polyploidy was examined under BK71 Olympus microscope and photographed 72 hours after treatment. |
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| S1118 |
XL147 analogueXL147 analogue是一种选择性的，可逆的I型PI3K抑制剂，作用于PI3Kα/δ/γ，无细胞试验中IC50分别为39 nM/36 nM/23 nM，对PI3Kβ作用效果稍弱。Phase 1/2。 |
Breast cancer cells were pretreated with 100ng/ml EGF for 20 min and then treated with the indicated concentrations of XL147 for 24 hours. |
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| S1072 |
ZSTK474ZSTK474抑制I型PI3K亚型，在无细胞试验中IC50为37 nM，对PI3Kδ作用最显著。Phase 1/2。 |
j,k, Gene expression ofMYOCD (j) and ACTA2 ( SMA, k) after applying inhibitors of key components involved in the DDR2 downstream signalling pathway to HSCs cultured within 3D collagen matrix subjected to stretching (ST) (n=3, one-way ANOVA, **P=0.0036, ****P<0.0001). l,m, Expression of SMA was significantly reduced after treatment with related inhibitors in early-stage FμNs. (n=4, one-way ANOVA, ***P=0.001, ****P<0.0001). PI3K-i: ZSTK474
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| S2814 |
Alpelisib (BYL719)Alpelisib (BYL719) 是一种有效的选择性PI3Kα抑制剂，在无细胞试验中IC50为 5 nM，对PI3Kβ/γ/δ具有极弱的作用。Phase 2。 |
AN3CA (B), JHUEM2 (D), and MFE296 (H) cells were treated with the indicated doses of BGJ398 and BYL719 alone or in combination for 96 hours, and an SRB assay was subsequently performed. |
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| S1410 |
AS-605240AS-605240选择性抑制PI3Kγ，IC50为8 nM，作用于PI3Kγ比作用于PI3Kδ/β和PI3Kα选择性分别高30和7.5倍以上。 |
Wound healing assays using DMSO vehicle or 5 µM AS-605240. Resealing of the ‘wounded’ monolayer was examined after 48 h.
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| S1205 |
PIK-75 HClPIK-75 HCl是一种p110α抑制剂，IC50为5.8 nM (比作用于p110β效果强200倍)，在Ser773处功能特异性突变，也有效抑制DNA-PK，无细胞试验中IC50为2 nM。 |
A549 cells were treated with DMSO or PIK-75 (200 nM) for 1 h and subsequently stimulated with izTRAIL for 24 h. Long-term survival was visualized after 7 days by crystal violet staining. One of two independent experiments is shown.
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| S2767 |
3-Methyladenine (3-MA)3-Methyladenine (3-MA)是一种选择性PI3K抑制剂，作用于Vps34和PI3Kγ，在 HeLa细胞中IC50分别为25 μM和60 μM；永久性抑制I型PI3K，但对III型PI3K的抑制是短暂的，也会阻断自噬体的形成。现配现用（加热助溶）。 |
MDC-labeled vacuoles were induced by AZD2014 and inhibited by autophagy inhibitor (3-MA). SMMC-7721 cells were treated with AZD2014 or rapamycin at concentrations of 100 and 600 nM, respectively, for 48 hours in the presence or absence of 3-MA, and then stained with MDC. Cells were immediately observed under a confocal microscope. Cells in the control group were treated with DMSO. bars, 20 μm.
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| S2636 |
A66A66是一种有效的特异性p110α抑制剂，无细胞试验中IC50为32 nM，作用于p110α比作用于其他I类PI3K亚型选择性高100多倍。 |
(C) Western blot analyses of pAkt in MMTV-MT tumor derived cells treated with various PI3K inhibitors (in micromolar) as indicated following growth factor starvation. (D) Western blot analyses of pAkt in MMTV-NeuT tumor-derived cells treated with various PI3K inhibitors (in micromolar) as indicated. (*) P < 0.01; (**) P < 0.001 (Student’s t-test).
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| S1523 |
Voxtalisib (SAR245409, XL765) AnalogueVoxtalisib (SAR245409, XL765) Analogue是作用于mTOR/PI3K的双重抑制剂，对p110γ作用最强，IC50为9 nM；也可抑制DNA-PK和mTOR。Phase 1/2。 |
The TMZ/XL765 combination decreases serum GH and PRL of mice bearing GH3 xenografts. A and B, After treatment with DMSO, TMZ, XL765, or the XL765/TMZ combination, the blood of the nude mice xenograft with GH3 tumor was collected and serum rat-GH and rat-PRL were measured by IRMA (TMZ/XL765 combination vs TMZ or XL765 alone: ***P <.001). |
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| S1489 |
PIK-93PIK-93是第一个有效的，人工合成的PI4K(PI4KIIIβ)抑制剂，IC50为19 nM；抑制PI3Kα，IC50为39 nM。 |
After starved in serum-free medium for 24h,A549 cells incubated with the indicated concentrations of PIK-93 for 3h,followed by 20-minute stimolation of 100ng/ml EGF. |
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| S2658 |
Omipalisib (GSK2126458, GSK458)Omipalisib (GSK2126458, GSK458)是一种高选择性的，有效的p110α/β/γ/δ和 mTORC1/2抑制剂，无细胞试验中Ki分别为0.019 nM/0.13 nM/0.024 nM/0.06 nM和0.18 nM/0.3 nM。Phase 1。 |
Cells from C76N treated with indicated doses of omipalisib (GSK2126458) were lysed and electrophoresced through a 4-15% gradient gel and immunoblotted using the indicated antibodies. Dose-dependent increase in LC3 A and B (lower band) is noted.
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| S1187 |
PIK-90PIK-90是一种PI3Kα/γ/δ抑制剂，IC50分别为11 nM/18 nM/58 nM，对PI3Kβ作用效果稍弱。 |
3D cultures expressing control (pQCXIP GFP) or K-Ras V12 (pQCXIP GFP K-Ras V12) were continuously treated with 5, 10, or 20 uM of the MEK inhibitor U0126 or 2.0 uM of the PI3K inhibitor PIK-90. At day 10, these structures were fixed and stained for aPKC and DNA. Representative images are shown. Bar, 50 um.
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| S1462 |
AZD6482AZD6482是一种PI3Kβ抑制剂，无细胞试验中IC50为10 nM，作用于PI3Kβ比作用于PI3Kδ， PI3Kα和PI3Kγ选择性分别高8，87和109倍。Phase 1。 |
Collagen-embedded melanoma spheroids were treated for 72 h with SGI-1776 [5 μM] or AZD6482 [10 μM] as single agents or in combination before staining for live (green) and dead (red) cells. Experiments were conducted in triplicate and representative images are shown. Scale bar represents 150 microns.
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| S2743 |
PF-04691502PF-04691502是一种ATP竞争性的PI3K(α/β/δ/γ)/mTOR双重抑制剂，在无细胞试验中Ki为1.8 nM/2.1 nM/1.6 nM/1.9 nM和16 nM，对Vps34， AKT， PDK1， p70S6K， MEK， ERK， p38 和 JNK 几乎没有作用活性。Phase 2。 |
BMDMs from WT animals were treated with different concentrations of PI3K inhibitors (500 nmol/L PF4691502, PI-103, BKM120 and 25 μmol/L SF1126) followed by hypoxia for 4 hours for Western blots. These macrophages were either used for lysate preparation (nuclear extracts for HIFα or WCE for pAKT and AKT) and Western blot analysis.
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| S2696 |
Apitolisib (GDC-0980, RG7422)Apitolisib (GDC-0980, RG7422)是一种有效的，I型PI3K抑制剂，作用于PI3Kα/β/δ/γ，无细胞试验中IC50分别为5 nM/27 nM/7 nM/14 nM，也是mTOR抑制剂，无细胞试验中Ki为17 nM，比作用于其他PIKK家族激酶选择性高。Phase 2。 |
Inhibition of PI3Kγ or PI3Kδ significantly decreased the migration of JVM3 cells. JVM3 cells were cultured in medium or stimulated for 24 h with CD40L/IL-4 and then incubated with the PI3Kγ-specific inhibitor CZC24832 (2 µM), the PI3Kδ-specific inhibitor idelalisib (1 µM), dual PI3Kδ/γ inhibitor duvelisib (1 µM), or the pan-PI3K inhibitor GDC0980 (1 µM) and subjected to a transwell migration assay. DMSO served as the vehicle control for the inhibitors, while SDF1α (100 ng/ml) served as the chemoattractant (n = 7).
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| S1360 |
GSK1059615GSK1059615是一种PI3Kα/β/δ/γ (可逆的)和mTOR的双重抑制剂，IC50分别为0.4 nM/0.6 nM/2 nM/5 nM和12 nM。Phase 1。 |
The PI3K/AKT pathway significantly contributes to the ligand-driven HER2 signaling activities detected by CELx HSF tests. a and b SKBr3 cells were seeded in sensor plates and then treated with a serial titration of the PI3K/AKT pathway inhibitor GSK1059615 (0 nM to 810 nM) two hours prior to maximal stimulation with NRG1b (800 pM) (a) or EGF (600 pM) (b). CELx curves are displayed using Delta CI values to demonstrate the relative signals to the time point (arrow) when the stimulus (EGF or NRG1b) was added. Dose–response curves of GSK1059615 inhibition on NRG1b and EGF-driven HER2 signals are shown in the insets
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| S7028 |
Duvelisib (IPI-145, INK1197)Duvelisib (IPI-145, INK1197) 是一种新型选择性PI3K δ/γ抑制剂，在无细胞试验中Ki和IC50分别为 23 pM/243 pM 和 1 nM/50 nM，对 PI3K δ/γ 的选择性比对其它蛋白激酶高。Phase 3。 |
MM1s were incubated with increasing doses of duvelisib for 4 h after which protein was extracted. Samples were then analysed for phospho-AKT and phospho-MAPK response using Western blotting. Blots were re-probed for total AKT and MAPK to confirm sample loading.
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| S2628 |
Gedatolisib (PF-05212384, PKI-587)Gedatolisib (PF-05212384, PKI-587)是一种高度有效的，双重PI3Kα，PI3Kγ和mTOR抑制剂，无细胞试验中IC50分别为0.4 nM， 5.4 nM和1.6 nM。Phase 2。 |
PI3K inhibitors promote apoptosis in checkpoint-defective cell lines. Two checkpoint-functional (A2058, D28) and three defective (HT144, D20, SKMel13) melanoma cell lines growth as tumour spheres as in Figure 4B were either untreated or treated with 5 uM PF-05212384 for 72 h, harvested and immunoblotted for pAkt Ser473.
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| S1352 |
TG100-115TG100-115是一种PI3Kγ/δ抑制剂，IC50为83 nM/235 nM，对PI3Kα/β几乎没有抑制效果。Phase 1/2。 |
(E) Phosphorylation of CREB affected by different concentrations of TG100-115 determined by using immunoblotting
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| S2671 |
AS-252424AS-252424是一种新型，有效的PI3Kγ抑制剂，无细胞试验中IC50为30 nM，作用于PI3Kγ比作用于PI3Kα选择性高30倍，对PI3Kδ/β具有低的抑制活性。 |
Effects of AS252424 on KL-induced cPLA 2 phosphorylation in BMMCs. BMMCs were pre-incubated with AS252424 for 1 h followed by stimulation with KL for 15 min. The phosphorylation of cPLA 2 was evaluated via immunoblot analysis. Results are representative of three independent experiments.*P<0.05, **P<0.01, ***P<0.001 and ### P<0.001, compared with BMMCs with KL induction but without pretreatment by AS252424.
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| S2749 |
BGT226 (NVP-BGT226)BGT226 (NVP-BGT226)是一种新型I型PI3K/mTOR抑制剂，作用于PI3Kα/β/γ，IC50为4 nM/63 nM/38 nM。Phase 1/2。 |
IGROV1-R10 cells were treated with BGT266(250nM) for 8 h.The effect of BGT226 on PI3K/Akt/mTOR pathway activation (A) and on expression of Mcl-1 and Bim (B). |
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| S2759 |
CUDC-907CUDC-907是一种PI3K和HDAC双重抑制剂，作用于PI3Kα和HDAC1/2/3/10，IC50分别为19 nM和1.7 nM/5 nM/1.8 nM/2.8 nM。Phase 1。 |
Representative Oil Red O staining of lipid-filled mature adipocytes on day 7 for uninduced cells (a), adipocyteinduced hMSCs exposed to the vehicle control (b) or CUDC-907-treated cells (500 nM) (c). Nile red staining (d and e) on day 7 of post-adipocytic induction in hMSCs and after exposure to CUDC-907. Images were captured at ×20 magnification using the FLoid Cell Imaging Station. The level of Nile red staining was quantified using the Molecular Devices M5 Microplate Reader (f). Data are presented as mean ± S.E (n = 16) from three independent experiments, ***P <0.0005.
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| S2227 |
PIK-294PIK-294是一种高度选择性p110δ抑制剂，IC50为10 nM，作用于PI3Kα/β/γ效果分别低1000，49和16倍。 |
After starved in serum-free medium for 24 h,A549 cells incubated with the indicated concentrations of PIK-294 for 3 h,followed by 20-minute stimolation of 100ng/ml EGF. |
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| S2681 |
AS-604850AS-604850是一种选择性的，ATP竞争性的PI3Kγ抑制剂，IC50为250 nM，作用于PI3Kγ比作用于PI3Kδ/β选择性高80倍以上，作用于PI3Kγ比作用于PI3Kα选择性高18倍。 |
Numbers of AID on-target (Igh and Igk loci) and off-target hot spots from WT and AID−/− B cells. Data pooled from at least n = 3 biological replicates
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| S8002 |
GSK2636771GSK2636771是一种口服生物有效的PI3Kβ选择性抑制剂，其对PI3Kβ的选择性比对PI3Kα/PI3Kγ高900倍以上，比对PI3Kδ的选择性大10倍以上。对PTEN缺失细胞系敏感。 |
Cells were treated as indicated. Medium and drug were refreshed every 2 to 3 days, and protein lysates were analyzed as above. |
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| S2802 |
Copanlisib (BAY 80-6946)Copanlisib (BAY 80-6946)是一个高效的泛I型 PI3K抑制剂，其对PI3Kα/β/γ/δ抑制的IC50分别为0.5, 3.7, 6.4, and 0.7 nM。Phase 3。 |
(A) Total cell lysates were immunoblotted with the indicated antibodies. β-actin served as the loading control.
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| S1219 |
YM201636YM201636是一种选择性的PIKfyve抑制剂，IC50为33 nM，对p110α作用效果稍弱，对Fabl(酵母同源基因)不敏感。 |
Validation study for vacuolin-1 and YM201636. (A) HeLa cells were treated with 3 lM vacuolin-1 or YM201636 in the presence or absence of the lysosomal protease inhibitor E64d (10 μg/mL) and pepstatin A (10 μg/mL). After 24 h of treatment, cell lysates (10 μg) were separated by 10% polyacrylamide gel electrophoresis, and LC3 was detected via immunoblotting.
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| S2699 |
CH5132799CH5132799抑制I型PI3Ks，尤其是PI3Kα，IC50为14 nM；对PI3Kβδγ作用效果稍弱，对PIK3CA突变型细胞系敏感。Phase 1。 |
Effect of selected compounds on MLC phosphorylation induced by 2-AG. Washed platelets (1.0 x 109 platelets/mL) were preincubated at 37 ℃ for 10 min with saline or 20 uM LY294002 (L), 10 uM CH5132799 (C), 10 uM TGX221 (T), 10 uM MK2206 (M), 20 uM Y27632 (Y), 1 uM PIK-75 (P), 1 U/mL apyrase (AP), 5 uM AS252424 (AS), 1 uM IC87114 (IC) and then stimulated for 30 s with 10 uM 2-AG. At the end of incubation suitable aliquots were immunoblotted with anti-p-MLC (thr18/ser19) as detailed in Methods. Blot is representative of four independent experiments.
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| S2682 |
CAY10505CAY10505是AS-252424的羟基化合物，是一种PI3Kγ抑制剂，IC50为30 nM. |
(D) Box plots showing the results of primary MM cell treatment (n = 22; in co-culture with BMSCs) with PI3K inhibitors (10 umol/l each). BYL-719 exerted the strongest anti-myeloma effects of TGX-221, CAY10505 or CAL-101. The mean survival value is indicated by a horizontal bar and the end of the whiskers show the values of the most sensitive and most resistant sample, respectively. (E) Treatment of PBMCs (n = 5) for 5 d with PI3K isoform-specific inhibitors (10 umol/l each).
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| S2207 |
PIK-293PIK-293是 一种PI3K抑制剂，最有效作用于PI3Kδ，IC50为0.24 μM，作用于PI3Kα/β/γ效果分别低500，100和50倍。 |
After starved in serum-free medium for 24 h,A549 cells incubated with the indicated concentrations of PIK-293 for 3 h,followed by 20-minute stimolation of 100ng/ml EGF. |
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| S2739 |
PKI-402PKI-402是一种有效的，pan-PI3K/mTOR双重抑制剂，靶向作用于PI3Kα/β/γ/δ和mTOR，IC50分别为2 nM/7 nM/16 nM/14 nM和3 nM，也有效作用于PI3Kα突变型E545K和H1047R。 |
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| S2870 |
TG100713TG100713是一种pan-PI3K抑制剂，作用于PI3Kγ， PI3Kδ， PI3Kα和PI3Kβ，IC50分别为50 nM， 24 nM， 165 nM和215 nM。 |
The compounds BAY80-6946 and TG100713, which are respectively an alpha/beta- and a pan-isoforms inhibitors, demonstrated a very good ability to block Jurkat E6.1 proliferation with an IC50 slightly higher than 1 mM. |
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| S7016 |
VS-5584 (SB2343)VS-5584 (SB2343)是一种有效的，选择性，PI3K/mTOR双重抑制剂，抑制mTOR和PI3Kα/β/δ/γ，IC50分别为3.4 nM和2.6-21 nM。Phase 1。 |
VS-5584 inhibits melanoma cell survival and proliferation-Established melanoma cell lines (A375, A-2058 and SK-MEL-3), patient-derived primary melanoma cells, B10BR melanocytes and primary human keratinocytes (“Kera”) were treated with applied concentration of VS-5585 (“VS”) or vehicle control (“C”, 0.1% of DMSO), cell survival was tested by MTT assay (A, E and F) and trypan blue exclusion assay (B, for A375 cells); Cell proliferation was analyzed by through [H3] Thymidine incorporation assay (C, for A375 cells) and clonogenicity assay (D, for A375 cells). Data were expressed as mean ± SD, experiments were repeated three times. *p<0.05 vs group “C”.
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| S7103 |
Taselisib (GDC 0032)Taselisib (GDC 0032)是一种有效，下一代的β亚型PI3K抑制剂，作用于PI3Kα/δ/γ， IC50分别为0.29 nM/0.12 nM/0.97nM，比作用于PI3Kβ选择性高10倍以上。 |
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| S7018 |
CZC24832CZC24832是第一个PI3Kγ选择性抑制剂，IC50为27 nM，比作用于PI3Kβ选择性高10倍，比作用于PI3Kα和PI3Kδ选择性高100倍以上。 |
(c) MM primary cells were treated with idelalisib (1 μm), CZC24832 (1 μm) and duvelisib (1 μm) for 72 h and then assessed for apoptosis by PI/Annexin V staining (n=4). |
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| S7813 |
AMG319AMG319是一种有效的选择性PI3Kδ抑制剂，IC50为18 nM，选择性比作用于其他PI3Ks高47倍多。Phase 2。 |
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| S7938 |
GSK2292767GSK2292767是一种有效的、选择性的PI3Kδ抑制剂。 |
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| S8163 |
GDC-0084GDC-0084是一种能透过血脑屏障的PI3K和mTOR的抑制剂，对PI3Kα, PI3Kβ, PI3Kδ, PI3Kγ 和mTOR的Kiapp分别为2 nM, 46 nM, 3 nM, 10 nM和70 nM。 |
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| S8157 |
GDC-0326GDC-0326是一种有效的、选择性的PI3Kα抑制剂，Ki值为0.2 nM。在酶活性实验中，对PI3Kα的选择性显著高于其它I类亚型。 |
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| S7356 |
HS-173HS-173 是强效的PI3Kα抑制剂，其IC50为0.8 nM。 |
b, d Serum-deprived MG-63 (b) and U20S cells (d) were pre-treated with 1 nmol/L HS-173 (PI3Kα inhibitor), 10 nmol/L TGX-221 (PI3Kβ inhibitor), 10 nmol/L CZC24832 (PI3Kγ inhibitor) and 10 nmol/L CAL-101 (PI3Kδ inhibitor) for 1 h, then were incubated with 100 ng/mL Wnt5a and harvested at 30 min after the start of Wnt5a treatment. Data were presented as mean ± SD of 3 determinations. The relative RhoA activity was normalized to the average value of each inhibitor-untreated group |
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| S8589 |
SF2523SF2523是一种有效的、具有高度选择性的PI3K抑制剂，对PI3Kα, PI3Kγ, DNA-PK, BRD4 和 mTOR的IC50分别为34 nM, 158 nM, 9 nM, 241 nM 和 280 nM。 |
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| S8581 |
Serabelisib (INK-1117,MLN-1117,TAK-117)Serabelisib (INK-1117,MLN-1117,TAK-117)是一种有效的、选择性的，可用于口服的PI3Kα抑制剂，IC50为21 nM。对PI3Kα的选择性比对其他I类PI3K家族成员高100倍以上。 |
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| S8330 |
IPI-549IPI-549是PI3K-γ的有效抑制剂，选择性是对其他脂质和蛋白激酶的100倍以上。生化IC50为16 nM。 |
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| S2391 |
QuercetinQuercetin是蔬菜水果和白酒中的天然黄酮类化合物，是一种体外重组Sirt1蛋白的激活剂同时也是PI3K抑制剂，IC50为2.4 – 5.4 μM。 |
After starved in serum-free medium for 24h,A549 cells incubated with the indicated concentrations of Quercetin for 3h,followed by 20-minute stimolation of 100ng/ml EGF. |
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| S8456 |
VPS34 inhibitor 1 (Compound 19, PIK-III analogue)VPS34 inhibitor 1 (Compound 19, PIK-III analogue)是有效的、选择性的VPS34抑制剂，IC50为15 nM。 |
Confirmation of selective growth inhibition using VPS34-IN1 inhibitor. Proliferation of Tsc2+/+ and Tsc2-/- MEFs treated with vehicle control (DMSO), CQ (5 uM), VPS34-IN1 (500 nM) or the combination for 72 hours (crystal violet staining). Two sample t-test was carried out between CQ and SAR405 and each drug alone. Results are representative of three independent experiments. Bar graph represent means ±SD.
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| S7646 |
Voxtalisib (XL765, SAR245409)Voxtalisib (SAR245409, XL765)是作用于mTOR/PI3K的双重抑制剂，对p110γ作用最强，IC50为9 nM；也可抑制DNA-PK和mTOR。Phase 1/2。 |
Cell viability measurements. The IMR-32, LA-N-1 and CHP‑134 cells were treated with mTOR/PI3K inhibitor SAR245409 alone or in combination with the 14G2a mAb (40 μg/ml) for 72 h. The cell viability was
determined by measuring ATP content, and compared to respective controls treated with appropriate diluents (DMSO or water, set as 1). P-values for t-test were as follows: *p<0.05, **p<0.01, ***p<0.001.
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| S8596 |
AutophinibAutophinib是有效的自噬 (autophagy)抑制剂，在饥饿诱导的自噬试验和rapamycin诱导的自噬试验中，其IC50分别为90 nM和40 nM。它还是Vps34的抑制剂，IC50为19 nM。 |
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| S7798 |
GNE-317GNE-317 是一种有效的，大脑渗透性 PI3K 抑制剂。 |
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| S8194 |
umbralisib (TGR-1202)TGR-1202是一种新型的PI3Kδ抑制剂，在酶学研究中和在细胞研究中，其抑制PI3Kδ活性的IC50和EC50分别为22.2 nM和24.3 nM。 |
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| S7937 |
Nemiralisib (GSK2269557)Nemiralisib，又名GSK-2269557，是有效的、选择性的PI3Kδ抑制剂（pKi=9.9）。 |
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| S8322 |
LY3023414LY3023414是一种口服的ATP竞争性抑制剂，抑制I类PI3K亚型、mTOR和DNA-PK。 |
The structure and formula weight of LY3023414 were presented (A). Established human glioma cells (U251MG and A172 lines), primary human astrocytes (“Astrocytes”) or primary human glioma cells [three lines, “Glioma (L1/2/3)”], were either left untreated (“Ctrl”) or treated with LY3023414 at 1-1000 nM, cells were further cultured for indicated time; Cell survival was tested (B, C, and E) (n=5). Cell proliferation was also tested by the BrdU ELISA assay (D and F) (n=5). *p < 0.05 vs. “Ctrl”. Experiments in this figure were repeated three times.
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| S7980 |
VPS34-IN1Vps34-IN1 是Vps34的抑制剂，在体外实验中所测得的IC50为25 nM, 对1型和2型 PI3K没有显著抑制作用。 |
C. Lysosomal and endosomal inhibition selectively targets Tsc2−/− MEFs. Proliferation of Tsc2+/+ and Tsc2−/− MEFs treated with vehicle control (DMSO), CQ (5uM), Vps34 inhibitor (SAR405; 1uM) or the combination for 72 hours (crystal violet staining). D. Confirmation of selective growth inhibition using VPS34-IN1 inhibitor. Proliferation of Tsc2+/+ and Tsc2−/− MEFs treated with vehicle control (DMSO), CQ (5uM), VPS34-IN1 (500nM) or the combination for 72 hours (crystal violet staining). Two-sample t-test was carried out between CQ and SAR405 and each drug alone. Results are representative of three independent experiments. Bar graph represent means ±SD.
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| S7682 |
SAR405SAR405是一种低分子量的Vps34抑制剂（Kd=1.5 nM），具有高选择性，在浓度高达10 μM时，对I类和Ⅱ类PI3Ks及mTOR没有活性。 |
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| S7683 |
PIK-IIIPIK-III, 一种选择性VPS34酶活性的抑制剂，抑制细胞自噬以及LC3的重新脂化，稳定自噬底物。其对VPS34和 PI(3)Kδ的IC50值分别为0.018 μM和1.2 μM。 |
LC3 and DAPI immunofluorescence staining were performed to detect autophagy in VSC4.1 cells treated with 25 mM HD alone, 25 mM HD + 5 μM PIK-III, 5 μM PIK-III and 0.1% DMSO alone (control group). Scale bar: 20 μm |
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| S7623 |
PI-3065PI-3065是一种选择性p110δ抑制剂，IC50为15 nM,选择性比其他PI3K家族成员高出70多倍。 |
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| S7645 |
Pilaralisib (XL147)Pilaralisib (XL147)是一种选择性的可逆I型PI3K抑制剂，作用于PI3Kα/δ/γ，在无细胞试验中IC50为 39 nM/36 nM/23 nM，对PI3Kβ作用较低。Phase 1/2。 |
G, tumor growth response of HR6 tumors grown in athymic nude mice and treated with single and combination treatments. H, table of earliest detectable (P < 0.05) reduction in tumor size for control
versus treated mice. ^, tumors that initially shrank and then grew; NS, not significant. I, OMI index initially decreases in HR6 organoids treated with paclitaxel, XL147, and combination therapies at 24 hours. J, OMI index of HR6 organoids treated for 72 hours. Red bars, significant reductions in OMI index; P< 0.05, for treated organoids versus control. Blue bars, significant increases in OMIindex;P< 0.05, for treated organoids versus control.
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| S7966 |
AZD8835AZD8835是一种新型的PI3Kα和PI3Kδ混合型抑制剂，IC50分别为6.2 nM和5.7 nM。对PI3Kβ和PI3Kγ同样具有选择性，IC50分别为431 nM和90 nM。 |
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| S8132 |
DeguelinDeguelin，一种从植物中分离出来的天然产物，是PI3K/Akt的抑制剂。 |
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| S7675 |
PF-4989216PF-4989216 是一种有效的选择性PI3K抑制剂，对p110α，p110β，p110γ，p110δ，和 VPS34的 IC50 分别为 2 nM，142 nM，65 nM，1 nM，和 110 nM。 |
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| S7694 |
AZD8186AZD8186是一种有效的选择性PI3Kβ和PI3Kδ抑制剂，IC50分别为 4 nM 和 12 nM。Phase 1。 |
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| S7865 |
740 Y-P (PDGFR 740Y-P)740 Y-P是具有细胞可透过性的PI3K磷酸肽激活剂。 |
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