Buparlisib (BKM120)

Name: Buparlisib (BKM120)
Brand: Selleck Chemicals
SKU: S2247
Rating: 5 (154 reviews)

For research use only.

Catalog No.S2247 Synonyms: NVP-BKM120

154 publications

Molecular Weight(MW): 410.39

Buparlisib (BKM120, NVP-BKM120) is a selective PI3K inhibitor of p110α/β/δ/γ with IC50 of 52 nM/166 nM/116 nM/262 nM in cell-free assays, respectively. Reduced potency against VPS34, mTOR, DNAPK, with little activity to PI4Kβ. Buparlisib induces apoptosis. Phase 2.

Selleck's Buparlisib (BKM120) has been cited by 154 publications

Cell, 2020, 25;181(7):1596-1611.e27.

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Cancer Cell, 2020, 37(2):183-199

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Nat Immunol, 2020, 21(4):442-454

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Science, 2019, 364(6441)

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Cancer Cell, 2018, 34(6):922-938

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Cancer Cell, 2018, 33(1):91-107

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Cell, 2017, 161(4):803-16

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Cancer Discov, 2017, 7(9):1018-1029

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Nature, 2016, 529(7586):413-417

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Nat Med, 2015, 10.1038/nm.3855

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Nat Med, 2015, 21(9):1038-47

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Cancer Discov, 2014, 4(1):69-79

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Cancer Discov, 2013, 4(2):232-45

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Cell, 2012, 27;149(3):656-70.

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Nat Med, 2012, 18(6):892-901

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Cancer Cell, 2012, 21(2):155-67

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Genome Med, 2020, 18;12(1):17

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Cell Rep, 2020, 31(12):107800

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Sci Signal, 2020, 3;13(621) pii: eaax2364

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Mol Cancer Res, 2020, 11

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Front Neurosci, 2020, 2;14:223

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Eur J Pharmacol, 2020, 870:172821

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Cell Biol Int, 2020, 10.1002/cbin.11322

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FASEB Bioadv, 2020, 2(2):126-144

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Mol Oncol, 2020, 10.1002/1878-0261.12673

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Small GTPases, 2020, 10.1080/21541248

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Nat Cell Biol, 2019, 21(2):226-237

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Nat Commun, 2019, 10(1):259

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Nat Commun, 2019, 10(1):2910

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Nat Commun, 2019, 10(1):1515

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J Thorac Oncol, 2019, 14(6):1061-1076

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Leukemia, 2019, 10.1038/s41375-019-0556-z

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Cell Syst, 2019, 8(2):97-108

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Theranostics, 2019, 9(8):2380-2394

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Cell Rep, 2019, 27(1):294-306

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Cell Rep, 2019, 27(2):631-647

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Cell Rep, 2019, 28(9):2317-2330

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Cell Death Differ, 2019, 10.1038/s41418-019-0422-6

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Cancer Lett, 2019, 466:23-34

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Cancers (Basel), 2019, 11(2)

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Mol Ther Oncolytics, 2019, 13:58-66

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Cancer Discov, 2019, 9(9):1306-1323

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Mol Cancer Ther, 2019, 18(4):834-844

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Aging (Albany NY), 2019, 11(18):7780-7795

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J Cell Physiol, 2019, 234(7):10907-10917

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Front Oncol, 2019, 0.87569444444

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Eur J Immunol, 2019, doi: 101002/eji201948241

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Mol Pharmacol, 2019, 95(5):528-536

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Prostate, 2019, 79(11):1347-1359

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Chem Biol Interact, 2019, 302:101-107

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Eur J Pharmacol, 2019, 842:89-98

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Biochem Biophys Res Commun, 2019, 513(3):546-552

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Leuk Lymphoma, 2019, 10.1080/10428194.2019.1594211

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Int J Hematol, 2019, 110(2):213-227

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Oncol Lett, 2019, 17(3-:3151-3162

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NPJ Breast Cancer, 2019, 05:31

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Nat Biomed Eng, 2018, 2(8):578-588

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Nat Biomed Eng, 2018, 2(4):239-253

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Nat Protoc, 2018, 13(12):2827-2843

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Nat Commun, 2018, 9(1):4550

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Nat Commun, 2018, 9(1):1357

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EMBO Mol Med, 2018, 10(5)

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Cancer Res, 2018, 78(8):2000-2013

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Cancer Res, 2018, 78(9):2383-2395

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NPJ Genom Med, 2018, 3:15

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Cancer Res, 2018, 78(14):4007-4021

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Cell Rep, 2018, 24(8):2155-2166

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Cell Rep, 2018, 24(2):463-478

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Int J Cancer, 2018, 143(5):1188-1201

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Int J Cancer, 2018, 142(9):1926-1937

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Oncogene, 2018, 37(3):363-376

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Cancer Lett, 2018, 439:56-65

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Mol Cancer Ther, 2018, 17(2):347-354

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Mol Cancer Res, 2018, 16(4):599-609

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Oncol Rep, 2018, 40(6):3223-3234

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Oncol Rep, 2018, 40(1):479-487

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Oncol Lett, 2018, 15(3):3321-3328

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Oncotarget, 2018, 9(56):30869-30882

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J Exp Med, 2018, 215(1):159-175

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Mol Cell, 2017, 67(3):512-527

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Mol Cell, 2017, 65(6):999-1013

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Nat Commun, 2017, 8:15623

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Nat Commun, 2017, 8;8:15617

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Nat Commun, 2017, 8:15021

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Nat Commun, 2017, 8(1):1278

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Dev Cell, 2017, 43(6):673-688

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Proc Natl Acad Sci U S A, 2017, 114(41):E8628-E8636

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Cancer Res, 2017, 77(16):4448-4459

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Mol Cancer Ther, 2017, 16(4):729-738

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Mol Cancer Ther, 2017, 10.1158/1535-7163

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Mol Cancer Ther, 2017, 16(9):1779-1790

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Mol Cell Proteomics, 2017, 16(10):1864-1888

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SLAS Discov, 2017, 22(8):974-984

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Cell Stem Cell, 2017, 20(2):233-246

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Oncotarget, 2017, 8(13):21806-21817

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Nat Cell Biol, 2016, 18(12):1324-1335

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Blood, 2016, 127(10):1325-35

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Genome Biol, 2016, 17:80

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Clin Cancer Res, 2016, 22(3):644-56.

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Cancer Res, 2016, 76(24):7168-7180

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J Hematol Oncol, 2016, 9(1):113

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Cancer Discov, 2016, 6(10):1134-1147

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J Transl Med, 2016, 14:56

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Int J Biochem Cell Biol, 2016, 79:308-317

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PLoS One, 2016, 11(1):e0147682

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PLoS One, 2016, 10.1371/journal

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Oncotarget, 2016, 7(41):67277-67287

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Nature, 2016, 529(7586):413-417

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Oncotarget, 2016, 7(26):40398-40417

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Sci Rep, 2016, 6:20189

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Oncotarget, 2016, 7(45):72608-72621

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J Clin Invest, 2015, 10.1172/JCI78018

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J Clin Invest, 2015, 125(12):4559-71

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Genes Dev, 2015, 29(16):1677-82

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Cancer Res, 2015, 75(14):2851-62

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Oncogene, 2015, 10.1038/onc.2015.173

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Biomed Pharmacother, 2015, 75:40-50

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Acta Pharmacol Sin, 2015, 10.1038/aps.2015.4

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Exp Cell Res, 2015, 332(2):223-35

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Int J Biochem Cell Biol, 2015, 60C:34-42

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Int Immunopharmacol, 2015, 28(1):675-85

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PLoS One, 2015, 10(9):e0133610

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PLoS One, 2015, 10(4):e0123410

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Immunol Res, 2015, 10.1007/s12026-015-8648-y

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Oncotarget, 2015, 6(31):31792-804

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J Clin Invest, 2014, 124(12):5490-502

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J Clin Invest, 2014, 124(11):4737-52

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J Exp Med, 2014, 211(13):2497-2505

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Cancer Res, 2014, 10.1158/0008-5472.CAN-14-1392

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Cell Rep, 2014, 8(5):1265-70

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Oncogene, 2014, 10.1038/onc.2014.328

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PLoS Pathog, 2014, 10(6):e1004196

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Breast Cancer Res, 2014, 16(1):R9

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Breast Cancer Res, 2014, 16(4):406

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Cell Death Dis, 2014, 5:e1134

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Cell Death Dis, 2014, 5:e1013

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Mol Cancer Res, 2014, 12(10):1520-31

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J Biol Chem, 2014, 289(33):22785-97

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PLoS One, 2014, 9(10):e108780

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Biochem Biophys Res Commun, 2014, 10.1016/j.bbrc.2014.09.129

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Oncotarget, 2014, 5(14):5295-303

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Clin Cancer Res, 2013, 19(21):5940-51

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Cancer Res, 2013, 73(17):5459-72

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Oncogene, 2013, 10.1038/onc.2013.509

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Breast Cancer Res, 2013, 15(4):R55

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Cell Commun Signal, 2013, 11(1):3

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Mol Cancer Res, 2013, 11(10):1269-78

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BMC Cancer, 2013, 13:465

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Cancer Chemother Pharmacol, 2013, 71(5):1297-307

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University Gattingen, 2013, Elisabeth Hand

PubMed: ( click the link to review the publication )

Purity & Quality Control

Choose Selective PI3K Inhibitors

Biological Activity

Description

Targets

p110α ^[1] (Cell-free assay)	p110δ ^[1] (Cell-free assay)	p110β ^[1] (Cell-free assay)	p110γ ^[1] (Cell-free assay)	Vps34 ^[1] (Cell-free assay)	View More
52 nM	116 nM	166 nM	262 nM	2.4 μM	View More

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]

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Formulation	Activity Description	PMID
MCF7	NV3EUI83S3m2b4TvfIlkKEG\|c3H5		MkGzO\|IhcA>?	MV7EUXNQ	MnnWR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWNHPyClZXzsd{BmgHC{ZYPzbY5oKFCLM1vhcJBp[SCHNUS1T{BufXSjboSge4l1cCCJSUWwJI9nKDBwMECwNVU5KM7:TR?=	NGT0dFkzPDlyMEK2Oi=>
DU145	MmXpR5l1d3SxeHnjJGF{e2G7		NVHxbld7PzJiaB?=	M1rDcGROW09?	NGO3[pFEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBFXTF2NTDj[YxteyCneIDy[ZN{cW6pIFzLRlEhdXW2YX70JJdqfGhiR1m1NEBw\iByLkCwNFQ{PSEQvF2=	NGrXfIszPDlyMEK2Oi=>
A2780	NY\JZW9XS3m2b4TvfIlkKEG\|c3H5		NXTW[49xPzJiaB?=	M{DpOGROW09?	M3ztNGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KFCWRV6t[IVncWOrZX70JIh2dWGwIFGyO\|gxKGOnbHzzJJdqfGhiR1m1NEBw\iByLkCwNFY{PSEQvF2=	MoLENlQ6ODB{Nk[=
U87MG	NG\WbYJEgXSxdH;4bYMhSXO\|YYm=		MmXsO\|IhcA>?	M4[z[GROW09?	NF;YbIdEgXSxdH;4bYNqfHliYXfhbY5{fCCSVFXOMYRm\mmlaXXueEBpfW2jbjDVPFdOTyClZXzsd{B4cXSqIFfJOVAhd2ZiMD6wNFA3QThizszN	M1LZNlI1QTByMk[2
A2780	M3:3NGZ2dmO2aX;uJGF{e2G7		MV:xJIg>	NHjmdpBFVVOR	NXfOeGU1UW6qaXLpeIlwdiCxZjDQTVNMNW2nZHnheIVlKEGNVDDT[ZI1PzNicHjvd5Bpd3K7bHH0bY9vKHerdHigSWM2OCCxZjCwMlA2PSEQvF2=	M{fQRVI1QTByMk[2
DU145	Mn76SpVv[3Srb36gRZN{[Xl?		M{O3OVEhcA>?	M{XjXWROW09?	NY\keIxsUW6qaXLpeIlwdiCxZjDQTVNMNW2nZHnheIVlKEGNVDDT[ZI1PzNicHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKESXMUS1JINmdGy\|IHjhdoJwemmwZzDMT2IyKG23dHH0bY9vKHerdHigSWM2OCCxZjCwMlA4OyEQvF2=	MX:yOFkxODJ4Nh?=
A2780	Ml35SpVv[3Srb36gRZN{[Xl?		NVLKfWI1OSCq	NFPyZlFFVVOR	NIOzU\|VKdmirYnn0bY9vKG:oIGDJN2sudWWmaXH0[YQhSUuWIGPldlQ4OyCyaH;zdIhwenmuYYTpc44hcW5iUGTFUk1l\W[rY3nlcpQhcHWvYX6gRVI4QDBiY3XscJMhf2m2aDDFR\|UxKG:oIECuNFc1KM7:TR?=	M1XmbVI1QTByMk[2
MCF7	NIKwOJNHfW6ldHnvckBCe3OjeR?=		NYrESlM3OSCq	MWHEUXNQ	NXr6WnNLUW6qaXLpeIlwdiCxZjDQTVNM[WyyaHGgSVU1PUtibYX0ZY51NW2nZHnheIVlKEGNVDDT[ZI1PzNicHjvd5Bpd3K7bHH0bY9vKHerdHigSWM2OCCxZjCwMlEh\|ryP	NGDxbJMzPDlyMEK2Oi=>
U87MG	MYDGeY5kfGmxbjDBd5NigQ>?		NGjIbHQyKGh?	MV3EUXNQ	M3v4XWlvcGmkaYTpc44hd2ZiUFmzT{1u\WSrYYTl[EBCU1RiU3XyOFc{KHCqb4PwbI9zgWyjdHnvckBqdiCSVFXOMYRm\mmlaXXueEBpfW2jbjDVPFdOTyClZXzsd{B4cXSqIFXDOVAhd2ZiMD6xN{DPxE1?	M1;HO\|I1QTByMk[2
A2780	NVLkUW9JT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		MYm3NkBp	M4Ll[GROW09?	M4nCOmVEPTB;MD61NkDPxE1?	Mme0NlQ6ODB{Nk[=
SKMES-1	NVmxXlNSS3m2b4TvfIlkKEG\|c3H5	M3;HTlEh\|ryP	MkTPO\|IhcA>?		MUHJcoR2[2W\|IHPlcIwh\GWjdHi=	M4TJdlI3ODF\|M{G4
H596	MXTGeY5kfGmxbjDBd5NigQ>?	MV:xJO69VQ>?			NH\3WotKdXCjaYLzJINmdGxibXnndoF1cW:w	NEPq[3UzPjBzM{OxPC=>
HCC2450	NIDscGVHfW6ldHnvckBCe3OjeR?=	NUTPcXp7OSEQvF2=			NHzrcHpKdXCjaYLzJINmdGxiaX72ZZNqd25?	Mn3PNlYxOTN\|MUi=
A549	M4DCV2Z2dmO2aX;uJGF{e2G7	NFjudpk2ODBibl2=	MnO4OFghcA>?	NHTENVJFVVOR	MnvKTY5pcWKrdIOgRYt1KGGldHn2ZZRqd25?	MW[yOVk{PzJ7OR?=
A549	NV;hW5plT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MlnzNUDPxE1?	NHjmTFY4OiCq	M1Tv[2ROW09?	NG\rWoRKdmirYnn0d{Bk\WyuIHfyc5d1cA>?	NX;6VIQ{OjV7M{eyPVk>
H522	NIraV2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M3XMT\|Eh\|ryP	MmLCO\|IhcA>?	NVzEPG1YTE2VTx?=	M{W4WWlvcGmkaYTzJINmdGxiZ4Lve5Rp	NFvaeGczPTl\|N{K5PS=>
LNCaP	MmHmSpVv[3Srb36gRZN{[Xl?	M4D4dFEh\|ryP			MWnTeZBxemW\|c3XzJJAuSUuWIHzleoVtew>?	MXKyOVM3ODd7OR?=
LNCaP95	M1jzOmZ2dmO2aX;uJGF{e2G7	NYT5NY5xOSEQvF2=			Mmj3V5VxeHKnc4Pld{BxNUGNVDDs[ZZmdHN?	MWqyOVM3ODd7OR?=
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MDA-MB-175	NYH5S5FnT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NXXTZXBGOSEQvF2=	MV61JIQ>	MlzESG1UVw>?	Ml20TWM2ODxzIN88US=>	MWGyOFg4QTd7Nh?=
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BCR-ABL	MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NV3HSFdJOC5{NT2xNO69VQ>?	NXW3bYJiPGR?		MlrNd4lodmmoaXPhcpRtgSCrbnjpZol1KGOnbHygdJJwdGmoZYLheIlwdg>?	MXeyOFI1PDZzMh?=
LC-1/SQSF	M13peWZ2dmO2aX;uJGF{e2G7	NWXqVWluO87:TR?=	NFfwPWIzPGh?	M{jWXmROW09?	M4T0W4Rm[3KnYYPlJG5TTjJicILveIVqdiCuZY\lcC=>	NInzNHozOzl6MEC5Ny=>
Primary CLL cells	NEPFbmtCeG:ydH;zbZMhSXO\|YYm=	M3u2NVEuOTEQvF2=	M{jWSFQ5cA>?		MorjbY5lfWOnczDhdI9xfG:\|aYOgbY4hS0yOIHPlcIx{KGmwZHXw[Y5l\W62IH;mJJBzd2ewb4P0bYMhdWG{a3Xydy=>	NVHt[GxmOjN6NUC4NFc>
Primary CLL cells	M13ZcGtqdmG\|ZTDBd5NigQ>?	Ml[zNu69VQ>?	M4XJNFMxdWmw		NEjSfI1l\WO{ZXHz[YQhWEl\|SzDhZ5Rqfmm2eR?=	NEj1UlkzOzh3MEiwOy=>
Primary CLL cells	NHe2SGVEgXSxdH;4bYMhSXO\|YYm=	MWqy{txO	Mn\tNlRp		NU\t[YlWcW6mdXPld{Bk\WyuIHP5eI91d3irY3n0fS=>	M3fIZVI{QDVyOEC3
human NSCLC cell lines	NYWwVGM1SXCxcITvd4l{KEG\|c3H5	Mn;NNE4yOjVvNN88US=>	NV\xbYRKOjSq	Mn[xSG1UVw>?	NFPoe\|hKSzVyczDyZY5o\XNiZoLvcUAxNjRvMt88US=>	MkDrNlM2PjJ2N{K=
human HCC cell lines	NUjiVJZqS2WubDD2bYFjcWyrdImgZZN{[Xl?	NHfWVm4xNjByNT2x{txO	NX7QVWlPPDiq		MmPCTWM2OD1zzszN	MoDSNlM1QDl7OUm=
Huh7	MoHMT4lv[XOnIFHzd4F6	NHP4Uncy\|ryP	M{Lwe\|Q5cA>?		MXnzbYdvce,ugXPhcpRtgSC{ZXT1Z4V{KHCqb4PwbI9zgWyjdHnvckBw\iCDa4S=	Mm\LNlM1QDl7OUm=
SK-HEP1	Mkj4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NV:x[IR3OS1{MN88US=>	NX[4O3dDPzKq	Mnj4SG1UVw>?	NVfvSGNRUUN3MP-8oFHPxE1?	MlWwNlM1PzlzM{[=
786-0	NHPvRWZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MV6xMVIx\|ryP	NI\sUlM4Omh?	NHX3WZdFVVOR	MXXJR\|Ux97zeMd88US=>	NFrxWG4zOzR5OUGzOi=>
JVM2	NYP0dWhjS3m2b4TvfIlkcXS7IHHzd4F6	MUOwMlIuOjEQvF2=	NFTXcJI4Omh?	MXzEUXNQ	NILPRXRKSzVyPUCuPe69VQ>?	MlvFNlMzOzh4M{m=
EHEB	NXzFR5Q{S3m2b4TvfIlkcXS7IHHzd4F6	M2jLbVAvOi1{MN88US=>	M3jZdlczcA>?	NXO4fIRDTE2VTx?=	NEL5VXVKSzVyPUCuO:69VQ>?	M2fRPFI{OjN6NkO5
MEC2	M37RNWN6fG:2b4jpZ4l1gSCjc4PhfS=>	NInOV3YxNjJvMkFOwG0>	M{DMbVczcA>?	MXzEUXNQ	MUXJR\|UxRTBwN988US=>	M165dlI{OjN6NkO5
primary B-CLL lymphocytes	M164UWFxd3C2b4Ppd{BCe3OjeR?=	MX\JR\|UxKG[xcjDlZYNpKHC{aX3hdpkh[2WubDDsbY5m	MlHRNlRp	MYjEUXNQ	MX7JR\|Ux97zeM988UUBnd3JiYXzsJJBifGmnboTz	NVvzWGdZOjN{M{i2N\|k>
primary B-CLL lymphocytes	M37UPGtqdmG\|ZTDBd5NigQ>?	MVPJR\|UxKG[xcjDlZYNpKHC{aX3hdpkh[2WubDDsbY5m	NF\heFMzPGh?		M2Dhc4lvcGmkaYTzJJA4OFN4SzCmJFRGNUKSMTDlfJBz\XO\|aX;u	MVmyN\|I{QDZ\|OR?=
human NSCLC	MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NGrxcG8xNjVvMt88US=>	MnXKO\|Jp		NWGx[5d2UUN3ME2x{txO	MWCyNlc5OTN7Mx?=
human NSCLC	MmmwT4lv[XOnIFHzd4F6	M1THR\|HPxE1?	NY\wfIVNOjSq		MVPpcohq[mm2czD0bIUhSWu2L33UU3Ihe2mpbnHsbY5oKHCjdHj3ZZkh[XRiM3igZYZ1\XJidILlZZRu\W62	NVHIeXk3OjJ5OEGzPVM>
Y1 cell line	NX\ZXGhnT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M3HHTFAvOc7:TT:x{txO	NHjHRYszPGh?	NUnhSVg{TE2VTx?=	M3X5U4lvcGmkaYTzJFYx97zHIHPlcIwhfmmjYnnsbZR6KGmwIF35Z{1U[3S{LYTyZY5{\mWldHXkJINmdGy\|	MV6yNlY6OjlyNB?=
PIK3CA-mutant MCF7	NFrIOWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MWnHTVUxRTF4MNMxPVFvVe,:jFzEOVA:QThywsGyO\|NvVQ>?	MoDKO\|Jp		NXn5NVExT0l3ME2xOlDDuTlzbl5vwKxNTDVyPUm4NOKyOjd\|bl2=	NFvMXW0zOjZ3M{m2Oy=>
PIK3CA-mutant MCF7	NFTPV4pMcW6jc3WgRZN{[Xl?	MUXJR\|UxRTFzNNMxN45O	MVS3Nog>		MmPiTWM2OD1zMUVCtVNvVSCrbjDy[YR2[2mwZzDBb5QheGixc4Doc5J6dGG2aX;uJIxmfmWucx?=	MVuyNlY2Ozl4Nx?=
MCF7-myr-Akt	M1TjSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NFn0VVZIUTVyPUK5PeKyPjiwTf-8kGxFPTExvK6xNEwxODCwTR?=	MV23Nog>		NWDEVXNkT0l3ME2yPVnDuTZ6bl5vwKxNTDVy78{eNVAtODBybl2=	NFfYWVMzOjZ3M{m2Oy=>
colon cancer cell lines	NH;Cd2JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MWWwMVEx\|ryP	MWi3Nog>	MUPEUXNQ	MXjJR\|UxRTIQvF2=	MlLzNlI2PDN6NUe=
gastric cancer cell lines	NGXvUW5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M4q0XFAuOTEQvF2=	NH:5UWs4Omh?	NXi0SnZkTE2VTx?=	NHnKUHBKSzVyPUKtOe69VQ>?	M3voOVIzPTR\|OEW3
HCT-116/HT-29/MKN-45	MnmyRZBweHSxc3nzJGF{e2G7	NYT2PIpLOs7:TR?=	M4SydlQ5cA>?		MXXzbIlnfCCrbjDHNkBxcGG\|ZR?=	NXnaOmZPOjJ3NEO4OVc>
HT-29 and HCT-116	NEDOWHpE[XOyYYPlJIF{e2G7	NVXXVIExPc7:TR?=	M2\sfFI1cA>?		MUnpcoR2[2W\|IHPhd5Bie2ViYXP0bZZqfHl?	M{HmWlIzPTR\|OEW3
MM cell lines	MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MYGxNO69VQ>?	Mm[0NlRp	NFq5NIhFVVOR	MVXJR\|UxKH[jcnnld{BidW:wZzDkbYZn\XKnboSgZ4VtdCCuaX7ld{BqdiC2aX3lJIFv\CCmb4PlJIRmeGWwZHXuZ4U>	NGm2NJczOjJyN{S4OS=>
ARP-1	MmX3RZBweHSxc3nzJGF{e2G7	NILnfWoyOM7:TR?=	NW\RbmtGOjSq	MlzxSG1UVw>?	NUjtU4hrcW6mdXPld{BOVSClZXzsJIFxd3C2b4Ppd{B1cHKxdXfoJINie3Cjc3WgZYN1cX[jdHnvci=>	NYrBXlMyOjJ{MEe0PFU>
SNU-601	NEXPOJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		NFjPXlk4Omh?	MXHEUXNQ	MXTJR\|UxRTBwOEG2xtExNjB4M988US=>	M{HrcFIzOTV7OEG0
SNU-1	NWfUdZJxT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		NX\oUVJnPzKq	MmqwSG1UVw>?	NIrmTHRKSzVyPUGuNFgzyrFyLkCyPO69VQ>?	MVKyNlE2QThzNB?=
SNU-668	M2OydWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		NXTIdmtIPzKq	M4DkemROW09?	NH\U[FRKSzVyPUGuOVc6yrFyLkC3OO69VQ>?	Mle4NlIyPTl6MUS=
AGS	MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		NGPkWHU4Omh?	NHnH[oRFVVOR	NHrReZNKSzVyPUGuO\|E1yrFyLkGxO:69VQ>?	NYK2c2Z7OjJzNUm4NVQ>
SNU-216	MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		MVS3Nog>	NH2z[oJFVVOR	MmC1TWM2OD1{Lk[5NuKyOC5yOENOwG0>	NVHNeoxCOjJzNUm4NVQ>
SNU-5	NIq0fmpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		MX[3Nog>	NWrGV\|RSTE2VTx?=	NEW1WphKSzVyPUGuN\|UyyrFyLkC5Ne69VQ>?	NFH4W5UzOjF3OUixOC=>
SNU-638	MkXDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		MlTZO\|Jp	NGrUR4ZFVVOR	MlfHTWM2OD1{LkK4NuKyOC5yNUROwG0>	NVjmPJN6OjJzNUm4NVQ>
SNU-16	NFvZ[WlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		NUX5Z5VHPzKq	M4fOZ2ROW09?	MXLJR\|UxRTFwNUezxtExNjByMd88US=>	NX:xSVZzOjJzNUm4NVQ>
SNU-484	MmHKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		NXKy[oVqPzKq	MWTEUXNQ	MWHJR\|UxRTFwN{K4xtExNjB2Nd88US=>	MnzUNlIyPTl6MUS=
SNU-620	NX[3SHRoT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		M1\qRVczcA>?	NFX1dlVFVVOR	MlLnTWM2OD1{LkmzPeKyOC5yMEJOwG0>	M{HsVVIzOTV7OEG0
SNU-719	NILVUG1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		NU\ZUI9zPzKq	MnzwSG1UVw>?	Mn7UTWM2OD1\|LkCzO:KyOC5yM{NOwG0>	MUWyNlE2QThzNB?=
glioma cell lines	NIrpeJRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		NFzuPIM4Omh?		MVnJR\|UxRTFvMt88US=>	M1HwclIzODZ3MEiw
U87	NET0fpJCeG:ydH;zbZMhSXO\|YYm=	NVu1RoEyOs7:TR?=	M3zJ[lczcA>?		Mn7kbY5lfWOnczDj[YxtKGGyb4D0c5NqeyCjbnSgZ4xm[X[nZDDQRXJRKGGwZDDjZZNx[XOnLUO=	MXeyNlA3PTB6MB?=

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	p-AKT (T308) / p-AKT (S473) / AKT; PubMed: 27283525 J Neurooncol Left western blots showing levels of pAkt (T308), pAkt (S473) and total Akt in U87 cells exposed to buparlisib for 72 h. Right densitometric assessment of western blots, showing relative changes in phosphorylation. p-FOXO3a (S253) / FOXO3a; PubMed: 28036259 Oncotarget Cells were treated with 0.5 μM BKM120 for 24 h and cell lysates were immunoblotted with the indicated antibodies. Actin was used as the loading control. Nuclear NF-κB p65 / NF-κB p65; PubMed: 26673665 Cell Death Dis Western blots show BKM120 downregulating pAKT, nuclear NF-κB p65 and total NF-κB p65 in MDR and their parental cells. β-actin was used as a loading control for pAKT, AKT and total NF-κB p65. Lamin B was used as a loading control for nuclear NF-κB p65. p-ERK / ERK / LC3; PubMed: 27572309 Oncotarget The indicated cell lines were exposed to different concentrations of BKM120 as indicated for 8 h A. or with 2 μM BKM120 for the indicated times B. The cells were then harvested for preparation of whole-cell protein lysates and subsequent Western blot analysis to detect the given proteins. p-STAT3 / STAT3 / p-ERK / ERK / p-S6; PubMed: 29928341 Oncol Lett Western blot analysis of H460 and H2126 cell lysates using specific antibodies to phosphorylated or total proteins of STAT3, ERK1/2, AKT, S6 or GAPDH (loading control). The cells were treated with increasing concentrations of BKM120 for 24 h. p-MET / MET; PubMed: 29928341 Oncol Lett The expression of phosphorylated or total forms of MET protein was analyzed by western blotting.	27283525 28036259 26673665 27572309 29928341
Immunofluorescence	FOXO3a; PubMed: 28036259 Oncotarget Cells were cultured on coverslips to approximately 60% confluency and then treated with 1 μM BKM120 for an additional 24 h. Immunofluorescence staining was performed using an anti-FOXO3a antibody and the nuclei were stained with DAPI. Scale bar, 20 μm.	28036259
Growth inhibition assay	Cell viability; PubMed: 26673665 Cell Death Dis Dose-response curves were used to calculate the IC50 of BKM120 for MCs of MCF-7/A02 cells (upper) and CALDOX cells (lower).	26673665

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]

Protocol

Kinase Assay:^[1]	- Collapse 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.
Cell Research:^[1]	- Collapse 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. (Only for Reference)
Animal Research:^[1]	- Collapse Animal Models: U87MG and A2780 xenografts are established in female nu/nu mice. Dosages: ~60 mg/kg. Administration: Dosed orally daily (q.d.). (Only for Reference)

References

[4] Koul D, et al. Clin Cancer Res, 2012, 18(1), 184-195.

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Solubility (25°C)

In vitro	DMSO	82 mg/mL (199.8 mM)
	Water	Insoluble
	Ethanol	'2 mg/mL
In vivo	Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 5% DMSO+30% PEG 300+ddH2O For best results, use promptly after mixing.	15mg/mL

* 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 Information Download Buparlisib (BKM120) SDF

Molecular Weight	410.39
Formula	C₁₈H₂₁F₃N₆O₂
CAS No.	944396-07-0
Storage	3 years-20°C powder 2 years-80°C in solvent
Synonyms	NVP-BKM120
Smiles	NC1=CC(=C(C=N1)C2=NC(=NC(=C2)N3CCOCC3)N4CCOCC4)C(F)(F)F

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

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mg/kg

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Step 2: Enter the in vivo formulation (Different batches have different solubility ratios, please contact Selleck to provide you with the correct ratio)

% DMSO+ % + % Tween 80+ % ddH₂O

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Working concentration： mg/ml；

Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL， Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation：Take DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH₂O，mix and clarify.

Note：1.Please make sure the liquid is clear before adding the next solvent.
2.Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.

Bio Calculators

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

Serial Dilutions
Concertration (start):
Dilution-folds:

Computed Result

C1=C0/X	C1:	LOG(C1):
C2=C1/X	C2:	LOG(C2):
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Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

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To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2020-05-15)

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT04338399	Not yet recruiting	Drug: Buparlisib & Paclitaxel	Head and Neck Cancer	Adlai Nortye Biopharma Co. Ltd.	July 31 2020	Phase 3
NCT02614508	Terminated	Drug: Buparlisib\|Drug: Ibrutinib\|Biological: Ofatumumab	Recurrent Chronic Lymphocytic Leukemia\|Recurrent Small Lymphocytic Lymphoma\|Refractory Chronic Lymphocytic Leukemia\|Refractory Small Lymphocytic Lymphoma	Emory University\|Novartis	January 2016	Phase 1
NCT01613677	Withdrawn	Drug: BKM120	Treatment for Metastatic or Locally Advanced Cervical Cancer	Novartis Pharmaceuticals\|Novartis	November 2015	Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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PI3K Signaling Pathway Map

PI3K Inhibitors with Unique Features

Selective PI3K Inhibitors

CAL-101 (Idelalisib, GS-1101) : p110δ-selective, IC50=2.5 nM.
Selective PI3K Inhibitors

TGX-221 : p110β-specific, IC50=5 nM.
Most Potent PI3K Inhibitor

BEZ235 (NVP-BEZ235, Dactolisib) : p110α/γ/δ/β, IC50=4 nM/5 nM/7 nM/75 nM.
FDA-approved PI3K Inhibitor

CAL-101 (Idelalisib, GS-1101) : Approved by FDA for Relapsed Chronic Lymphocytic Leukemia, Follicular Lymphoma and Small Lymphocytic Lymphoma.
Newest PI3K Inhibitor

VS-5584 (SB2343) ^New : Potent and selective dual PI3K/mTOR inhibitor for mTOR, PI3Kα/β/δ/γ with IC50 of 3.4 nM and 2.6-21 nM, respectively.

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Taselisib (GDC 0032) is a potent, next-generation β isoform-sparing PI3K inhibitor targeting PI3Kα/δ/γ with K_i of 0.29 nM/0.12 nM/0.97nM, >10 fold selective over PI3Kβ.

Features:A beta isoform-sparing PI3K inhibitor.
Pilaralisib (XL147) ^New

Pilaralisib (XL147) is a selective and reversible class I PI3K inhibitor for PI3Kα/δ/γ with IC50 of 39 nM/36 nM/23 nM in cell-free assays, less potent to PI3Kβ. Phase 1/2.
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LY294002

LY294002 is the first synthetic molecule known to inhibit PI3Kα/δ/β with IC50 of 0.5 μM/0.57 μM/0.97 μM, respectively; more stable in solution than Wortmannin, and also blocks autophagosome formation. It not only binds to class I PI3Ks and other PI3K-related kinases, but also to novel targets seemingly unrelated to the PI3K family. LY294002 also inhibits CK2 with IC50 of 98 nM. LY294002 is a non-specific DNA-PKcs inhibitor and activates autophagy and apoptosis.
3-Methyladenine (3-MA)

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Idelalisib (CAL-101, GS-1101)

Idelalisib (CAL-101, GS-1101) is a selective p110δ inhibitor with IC50 of 2.5 nM in cell-free assays; shown to have 40- to 300-fold greater selectivity for p110δ than p110α/β/γ, and 400- to 4000-fold more selectivity to p110δ than C2β, hVPS34, DNA-PK and mTOR. Idelalisib also stimulates autophagy.
Wortmannin

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Pictilisib (GDC-0941)

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Buparlisib (BKM120)