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Buparlisib/布帕尼西 {[allProObj[0].p_purity_real_show]}

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。

Buparlisib/布帕尼西 化学结构 CAS号:944396-07-0
Buparlisib/布帕尼西 化学结构
CAS号:944396-07-0
Buparlisib/布帕尼西 3D分子结构
CAS号:944396-07-0
Buparlisib/布帕尼西 化学结构 CAS号:944396-07-0
Buparlisib/布帕尼西 3D分子结构 CAS号:944396-07-0
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Buparlisib/布帕尼西 纯度/质量文件 产品仅供科研

货号:A105286 标准纯度: {[allProObj[0].p_purity_real_show]}
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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。

Buparlisib/布帕尼西 生物活性

靶点
  • p110γ

    p110γ, IC50:262 nM

  • p110β

    p110β, IC50:166 nM

  • p110α

    p110α, IC50:52 nM

  • p110δ

    p110δ, IC50:116 nM

  • Vps34

    Vps34, IC50:2.4 μM

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]

Buparlisib/布帕尼西 细胞实验

Cell Line
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.

Buparlisib/布帕尼西 动物实验

Species
Animal Model
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.

Buparlisib/布帕尼西 动物研究

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.

Buparlisib/布帕尼西 临床研究

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 <<

Buparlisib/布帕尼西 参考文献

[1]Burger MT, Pecchi S, et al. Identification of NVP-BKM120 as a Potent, Selective, Orally Bioavailable Class I PI3 Kinase Inhibitor for Treating Cancer. ACS Med Chem Lett. 2011;2(10):774-9.

[2]Vanhaesebroeck B, Guillermet-Guibert J, et al. The emerging mechanisms of isoform-specific PI3K signalling. Nat Rev Mol Cell Biol. 2010;11(5):329-41.

[3]Zhao HF, Wang J, et al. Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development. Mol Cancer. 2017;16(1):100.

[4]Maira SM, Pecchi S, et al. Identification and characterization of NVP-BKM120, an orally available pan-class I PI3-kinase inhibitor. Mol Cancer Ther. 2012;11(2):317-28.

[5]Speranza MC, Nowicki MO, et al. BKM-120 (Buparlisib): A Phosphatidyl-Inositol-3 Kinase Inhibitor with Anti-Invasive Properties in Glioblastoma. Sci Rep. 2016 Feb 5;6:20189.

Buparlisib/布帕尼西 实验方案

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

Buparlisib/布帕尼西 技术信息

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

请根据您的动物给药指南选择适当的溶解方案。
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
方案 一
方案 二
方案 三
方案 四
方案 五
配制的工作液建议现用现配,短期内尽快用完。 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
方案 一
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