BKM120 (NVP-BKM120, Buparlisib)

BKM120 is a selective PI3K inhibitor of p110α/β/δ/γ with IC50 of 52 nM/166 nM/116 nM/262 nM, respectively. Reduced potency against VPS34, mTOR, DNAPK, with little activity to PI4Kβ. Phase 1/2.

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BKM120 (NVP-BKM120, Buparlisib) Chemical Structure

BKM120 (NVP-BKM120, Buparlisib) Chemical Structure
Molecular Weight: 410.39

Validation & Quality Control

Customer Reviews(2)

Quality Control & MSDS

Related Compound Libraries

BKM120 (NVP-BKM120, Buparlisib) is available in the following compound libraries:

PI3K inhibitors with Unique Features

Product Information

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  • Research Area
  • BKM120 (NVP-BKM120, Buparlisib) Mechanism

Product Description

Biological Activity

Description BKM120 is a selective PI3K inhibitor of p110α/β/δ/γ with IC50 of 52 nM/166 nM/116 nM/262 nM, respectively. Reduced potency against VPS34, mTOR, DNAPK, with little activity to PI4Kβ. Phase 1/2.
Targets p110α p110β p110δ p110γ
IC50 52-99 nM 166 nM 116 nM 262 nM [1]
In vitro BKM120 is not sensitive to Class III and Class IV PI3K's or PI4K. NVP-BKM120 shows great antiproliferation activity to PI3K deregulated cell lines including A2780, U87MG, MCF7 and DU145 with GI50 of 0.1-0.7 nM. [1] BKM120 induces multiple myeloma cells (ARP1, ARK, MM.1S, MM1.R and U266) apoptosis, which results in increased G1-phase cells and decreased S-phase cells. BKM120 induced CD138+ primary MM cell apoptosis and has significant lower cytotoxicity toward CD138− stromal cells. BKM120 exposure could cause upregulation of BimS and downregulation of XIAP. [2] BKM120 demonstrates antiproliferative activity in human gastric cancer cell lines by decreasing mTOR downstream signaling. BKM120 could increase either p-ERK or p-STAT3 in KRAS mutant gastric cancer cells. Combination with STAT3 blockade, BKM120 shows a synergism in cells harboring mutated KRAS by inducing apoptosis, but not in KRAS wild-type cells. [3] A recent study shows that BKM120 shows differential forms of cell death on the basis of p53 status of the cells with p53 wild-type cells undergoing apoptotic cell death and p53 mutant/deleted cells having a mitotic catastrophe cell death. BKM120 mediates mitotic catastrophe mainly through Aurora B kinase. [4]
In vivo BKM120 completely inhibits pAktser473 in A2780 xenograft tumors at doses of 30, 60, or 100 mg/kg, respectively. BKM120 also shows antitumor activity against U87MG glioma model at doses of 30 and 60 mg/kg. [1] BKM120 treatment results in significantly reduced tumor volume and level of circulating human kappa chain at 5 μM/kg/day−1in ARP1 SCID mouse model, with prolonged survival. [2]
Features

Protocol(Only for Reference)

Kinase Assay: [1]

PI3K biochemical assay (ATP depletion assay) BKM120 is dissolved in DMSO and directly distributed into a black 384-well plate at 1.25 µL per well. To start the reaction, 25 µL of 10 nM PI3 kinase and 5 µg/mL 1-α-phosphatidylinositol (PI) in assay buffer (10 mM Tris pH 7.5, 5 mM MgCl2, 20 mM NaCl, 1 mM DTT and 0.05% CHAPS) are added into each well followed by 25 µL of 2 µM ATP in assay buffer. The reaction is performed until approx 50% of the ATP is depleted and then stopped by the addition of 25 µL of KinaseGlo solution. The stopped reaction is incubated for 5 minutes and the remaining ATP is then detected via luminescence.
PI3K biochemical assay (filter binding assay) 50 µL/well of a 1:1 mixture of 100 µL/mL L-α-phosphatidylinositol and L-α-phosphatidylserine dissolved in chloroform:ethanol (2.2:7.8) is pipetted into 96-well MaxiSorpTM plates. The solvents are evaporated at room temperature and plates are washed with Tris-buffered saline (TBS, pH7.4). PI3Kα is incubated for 60 min at room temperature in coated plates in 50 µL medium containing [γ33P]-ATP (~6 kBq/well), 0.5 µM ATP (or higher), 5 mM MgCl2, 150 mM NaCl, 25 mM Tris-HCl pH7.4, and 1% DMSO. The reaction is started by adding PI3Kα (0.4 µg/ml, <2 nM) and stopped by adding 50 µL of 50 mM EDTA. Plates are washed twice with TBS and dried; 100 µL/well MicroScintTM PS is added, and bound radioactivity is determined using a TopCountTM counter.

Cell Assay: [1]

Cell lines A2780 cells.
Concentrations 0-6.6 μM
Incubation Time 3 days.
Method A2780 cells are cultured in DMEM supplemented with 10% FBS, L-glutamine, sodium pyruvate, and antibiotics. Cells are plated in the same medium at a density of 103 cells per well, 100 μL per well into black-walled-clear-bottom plates and incubated for 3-5 hours. BKM120 supplied in DMSO (20 mM) is diluted. The diluted BKM120 solution (2 μL), is then added to cell medium (500 μL) cell medium (concentration from 0-6.6 μM). Equal volumes of this solution (100 μL) are added to the cells in 96 well plates and incubated at 37 °C for 3 days and developed using Cell Titer Glo. Inhibition of cell proliferation is determined by luminescence read using Trilux.

Animal Study: [1]

Animal Models U87MG and A2780 xenografts are established in female nu/nu mice.
Dosages ~60 mg/kg.
Administration Dosed orally daily (q.d.).
Solubility 15% Captisol, pH 4 6 mg/mL
1

References

Clinical Trial Information( data from http://clinicaltrials.gov)

NCT Number Recruitment Conditions Sponsor
/Collaborators
Start Date Phases
NCT01852292 Not yet recruiting Platinum Pre-treated Recurrent or Metastatic Head and Neck Squamous Cell Carcinoma. Novartis|Novartis Pharmaceuticals 2013-08 Phase 2
NCT01870726 Not yet recruiting Recurrent Glioblastoma Novartis|Novartis Pharmaceuticals 2013-09 Phase 1|Phase 2
NCT01550380 Not yet recruiting Endometrial Cancer University of Utah|Novartis 2013-12 Phase 2
NCT01613677 Not yet recruiting Treatment for Metastatic or Locally Advanced Cervical Cancer Novartis|Novartis Pharmaceuticals 2014-01 Phase 4
NCT01723800 Not yet recruiting Adenocarcinoma of the Lung|Bronchoalveolar Cell Lung Cancer|Large Cell Lung Cancer|Recurrent Non-small Cell Lung Cancer|Stage IV Non-small Cell Lung Cancer City of Hope Medical Center|National Cancer Institute (NCI) 2014-01 Phase 1

Chemical Information

Download BKM120 (NVP-BKM120, Buparlisib) SDF
Molecular Weight (MW) 410.39
Formula

C18H21F3N6O2

CAS No. 944396-07-0
Storage 3 years -20℃Powder
6 months-80℃in DMSO
Syonnyms N/A
Solubility (25°C) * In vitro DMSO 82 mg/mL (199 mM)
Water <1 mg/mL (<1 mM)
Ethanol 2 mg/mL (4 mM)
In vivo 15% Captisol, pH 4 6 mg/mL
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Chemical Name 5-(2,6-dimorpholinopyrimidin-4-yl)-4-(trifluoromethyl)pyridin-2-amine

Preparing Stock Solutions

Stock Solution (1ml DMSO) 1mM 10mM 20mM 30mM
Mass(mg) 0.41039 4.1039 8.2078 12.3117

Research Area

Customer Reviews (2)


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Rating
Source One customer. BKM120 (NVP-BKM120, Buparlisib) purchased from Selleck
Method Cell growth inhibition assay
Cell Lines Melanoma cell lines
Concentrations 0.00000512-10 μM
Incubation Time 72 h
Results BKM120 treatment inhibited Melanoma cells growth in a does-dependent manner.

Click to enlarge
Rating
Source Dr. Zhang of Tianjin Medical University. BKM120 (NVP-BKM120, Buparlisib) purchased from Selleck
Method Western blot
Cell Lines A549 cells
Concentrations 0-10 μM
Incubation Time 3 h
Results BKM120 treatment resulted in a reduction of Akt-308 phosphorylation in A549 cells.

Product Citations (8)

Tech Support & FAQs

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