货号:A105286
同义名:
BKM120; NVP-BKM120
Buparlisib (BKM120; NVP-BKM120) 是一种泛 I 类 PI3K 抑制剂,对 p110α 的 IC50 为 52 nM,对 p110β 为 166 nM,对 p110δ 为 116 nM,对 p110γ 为 262 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 | PI3Ks (Phosphatidylinositol-4,5-bisphosphate 3-kinase) participate in a diverse array of process, including the regulation of cellular survival, differentiation and stem cell-like properties, growth, proliferation, metabolism, migration, and angiogenesis[2]. BKM120 is an orally bioavailable pan-PI3K inhibitor with IC50 value of IC50=52nM, IC50=116nM, IC50=166nM, IC50=262nM, IC50=2.4μM, IC50=4.6μM on p110α, p110δ, p110β, p110γ(measured by filter binding assay), Vps34 (measured by ATP depletion assay), mTOR (measured by TR-FRET assay), respectively, most potent on Class I PI3Ks. Treatment of BKM120 can cause decrease of p-AKT-ser473 (downstream of PI3Ks) both in vitro and in vivo. BKM120 has good pharmacokinetic properties, exhibiting medium to high oral bioavailability across species as 80%, 50%, 44% and 100% observed in mouse, rat, dog, and monkey, respectively[1]. For BKM120 is well-tolerated and permeable to the blood–brain barrier, it is the most frequently-used PI3K inhibitor in the clinical trials for glioblastoma multiforme treatment[3]. |
| 作用机制 | Mechanism: BKM120 has greater affinity for the free PI3K enzyme,relative to the ATP bound.[4] |
| Concentration | Treated Time | Description | References | |
| MDA-MB-453 cells | 0.5 µM | 48 h | Induced apoptosis | Theranostics. 2021 Jan 20;11(8):3552-3564. |
| BT20 cells | 0.5 µM | 48 h | Induced apoptosis | Theranostics. 2021 Jan 20;11(8):3552-3564. |
| HER2+/PIK3CAH1047R primary tumor cells | 1 μM | 24 h | Evaluate the effect of Buparlisib on primary tumor cells, showing upregulation of ECM gene expression | Cancer Res. 2017 Jun 15;77(12):3280-3292. |
| HCC1954 cells | 1 μM | 24 h | Evaluate the effect of Buparlisib on HER2+ breast cancer cells, showing upregulation of ECM gene expression | Cancer Res. 2017 Jun 15;77(12):3280-3292. |
| MDA-MB 453 cells | 1 μM | 24 h | Evaluate the effect of Buparlisib on HER2+ breast cancer cells, showing upregulation of ECM gene expression | Cancer Res. 2017 Jun 15;77(12):3280-3292. |
| H10 cells | 10 µM | 72 h | To assess the effect of Buparlisib on cell viability, results showed that Buparlisib significantly reduced cell viability. | Int J Mol Sci. 2019 Aug 29;20(17):4235. |
| H3 cells | 10 µM | 72 h | To assess the effect of Buparlisib on cell viability, results showed that Buparlisib significantly reduced cell viability. | Int J Mol Sci. 2019 Aug 29;20(17):4235. |
| H2 cells | 10 µM | 72 h | To assess the effect of Buparlisib on cell viability, results showed that Buparlisib significantly reduced cell viability. | Int J Mol Sci. 2019 Aug 29;20(17):4235. |
| H1 cells | 10 µM | 72 h | To assess the effect of Buparlisib on cell viability, results showed that Buparlisib significantly reduced cell viability. | Int J Mol Sci. 2019 Aug 29;20(17):4235. |
| WHIM12 cells | 0-1 uM | 24 h | To evaluate the cytotoxic effect of Buparlisib in combination with other drugs on WHIM12 cells, results showed synergistic anti-tumor effects. | Cancer Res. 2018 May 15;78(10):2732-2746. |
| WHIM12 cells | 1 uM | 6 days | To evaluate the effect of Buparlisib on the growth of WHIM12 cells, results showed that Buparlisib significantly inhibited cell growth. | Cancer Res. 2018 May 15;78(10):2732-2746. |
| C-26 tumor cells | 2.5 μM and 5 μM | 72 h | To evaluate the effect of buparlisib on the growth of C-26 tumor cells, results showed that buparlisib significantly reduced tumor growth. | Mol Cancer Ther. 2017 Feb;16(2):344-356. |
| H460 cells | 1 μM | 24 h | Buparlisib reduced glucose consumption in H460 cells by inhibiting the PI3K signaling pathway. | Nat Commun. 2019 Nov 29;10(1):5444. |
| WHIM12 cells | 0-1 μM | To evaluate the cytotoxic effect of Buparlisib on WHIM12 cells, results showed that Buparlisib in combination with other drugs had synergistic or additive cytotoxic effects. | Cancer Res. 2018 May 15;78(10):2732-2746. | |
| WHIM12 cells | 1 μM | 6 days | To evaluate the effect of Buparlisib on the clonogenic ability of WHIM12 cells, results showed that Buparlisib significantly inhibited colony formation. | Cancer Res. 2018 May 15;78(10):2732-2746. |
| Administration | Dosage | Frequency | Description | References | ||
| Nude mice | HER2+/PIK3CAH1047R transgenic mammary tumor model | Oral gavage | 30 mg/kg | Once daily for over 3 weeks | Evaluate the effect of Buparlisib on HER2+/PIK3CAH1047R tumors, showing resistance to combination therapy | Cancer Res. 2017 Jun 15;77(12):3280-3292. |
| Mice | TNBC cell line xenograft model | Oral | 30 mg/kg | Once daily for 7 days | Combination treatment resulted in a ~40% decrease in tumor volume after 7 days, while tumors in single agent groups showed slight growth. The combination significantly reduced lung metastatic burden. | NPJ Breast Cancer. 2017 Apr 26;3:17 |
| NOD/SCID mice | Subcutaneous H1_DL2 tumor model | Oral | 50 mg/kg | Once daily for 30 days | To assess the effect of Buparlisib on tumor growth, results showed that Buparlisib significantly inhibited tumor growth. | Int J Mol Sci. 2019 Aug 29;20(17):4235. |
| Mice | PDX model | Oral | 20 mg/kg | Once daily, 5 days/week for 3 weeks | To test the growth inhibitory effect of buparlisib on PIK3R1W624R PDXs, results showed that buparlisib delayed tumor growth. | Cells. 2020 Feb 14;9(2):442 |
| Mice | TNBC PDX models | Oral gavage | 30mg/kg | Days 1-5 each week for 24-32 days | To evaluate the effect of Buparlisib on tumor growth in TNBC PDX models, results showed varying responsiveness across models, with some exhibiting resistance. | Cancer Res. 2018 May 15;78(10):2732-2746. |
| NSG mice | BT20 xenograft model | Intraperitoneal injection | 25 mg/kg | Once daily for 2 weeks | Inhibited tumor growth and metastasis | Theranostics. 2021 Jan 20;11(8):3552-3564. |
| Mice | Colon-26 tumor model | Oral | 25 mg/kg | Daily for 16 days | To evaluate the effect of buparlisib on the growth of C-26 tumors, results showed that buparlisib significantly reduced tumor growth and preserved skeletal muscle mass. | Mol Cancer Ther. 2017 Feb;16(2):344-356. |
| Mice | Patient-derived xenograft models of TNBC | Oral | 30 mg/kg | Days 1-5 each week for 24-32 days | To evaluate the antitumor effect of Buparlisib on PDX models, results showed significant variability in response among different models, with some models exhibiting resistance to Buparlisib. | Cancer Res. 2018 May 15;78(10):2732-2746. |
| Dose | Nude Mice: min = 2 mg/kg, max = 20 mg/kg[5] Mice: min = 30 mg/kg, max = 60 mg/kg[4] |
| Administration | p.o., i.v., i.p. |
| NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 |
| NCT01820364 | Melanoma | Phase 2 | Terminated(Study was withdrawn... 展开 >> due to scientific and business considerations.) 收起 << | - | United States, Tennessee ... 展开 >> Sarah Cannon Research Institute Onc Dept Nashville, Tennessee, United States, 37203 Australia, Victoria Novartis Investigative Site East Melbourne, Victoria, Australia, 3002 Canada, Alberta Novartis Investigative Site Edmonton, Alberta, Canada, T6G 1Z2 Germany Novartis Investigative Site Heidelberg, Germany, 69120 Spain Novartis Investigative Site Barcelona, Catalunya, Spain, 08035 Switzerland Novartis Investigative Site Zuerich, Switzerland, 8091 收起 << |
| NCT01820364 | - | Terminated(Study was withdrawn... 展开 >> due to scientific and business considerations.) 收起 << | - | - | |
| NCT02159066 | Melanoma | Phase 2 | Active, not recruiting | March 30, 2019 | United States, Arizona ... 展开 >> Mayo Clinic - Arizona onc Dept Scottsdale, Arizona, United States United States, California University of California at Los Angeles Onc Dept Los Angeles, California, United States, 90095 United States, Massachusetts Massachusetts General Hospital Dept of Onc. Boston, Massachusetts, United States, 02115 United States, New York Memorial Sloan Kettering Cancer Center Dept Oncology New York, New York, United States, 90033 United States, Oregon Oregon Health & Science University Onc. Dept Portland, Oregon, United States, 97239 United States, Tennessee Sarah Cannon Research Institute Onc. Dept Nashville, Tennessee, United States, 37203 Australia, Victoria Array BioPharma Investigative Site East Melbourne, Victoria, Australia, 3002 Canada, Ontario Array BioPharma Investigative Site Toronto, Ontario, Canada, M5G 2M9 Canada, Quebec Array BioPharma Investigative Site Montreal, Quebec, Canada, H3T 1E2 Germany Array BioPharma Investigative Site Heidelberg, Germany, 69120 Array BioPharma Investigative Site Köln, Germany, 50937 Array BioPharma Investigative Site Muenchen, Germany, 80336 Array BioPharma Investigative Site Würzburg, Germany, 97080 Italy Array BioPharma Investigative Site Napoli, Italy, 80131 Netherlands Array BioPharma Investigative Site Amsterdam, Netherlands, 1066 CX Spain Array BioPharma Investigative Site Barcelona, Catalunya, Spain, 08035 Switzerland Array BioPharma Investigative Site Zuerich, Switzerland, 8091 United Kingdom Array BioPharma Investigative Site Oxford, United Kingdom, OX3 7LJ 收起 << |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
2.44mL 0.49mL 0.24mL |
12.18mL 2.44mL 1.22mL |
24.37mL 4.87mL 2.44mL |
|
| CAS号 | 944396-07-0 |
| 分子式 | C18H21F3N6O2 |
| 分子量 | 410.39 |
| SMILES Code | NC1=NC=C(C2=CC(=NC(=N2)N2CCOCC2)N2CCOCC2)C(=C1)C(F)(F)F |
| MDL No. | MFCD18251596 |
| 别名 | BKM120; NVP-BKM120 |
| 运输 | 蓝冰 |
| InChI Key | CWHUFRVAEUJCEF-UHFFFAOYSA-N |
| Pubchem ID | 16654980 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Inert atmosphere, store in freezer, under -20°C |
| 溶解方案 |
DMSO: 105 mg/mL(255.85 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 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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