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BKM120 Inhibitor of pan-Class I PI3K

Catalog No.A3015
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10mM (in 1mL DMSO)
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Sample solution is provided at 25 µL, 10mM.

Product Citations

1. Peng T, Dou QP. "Everolimus Inhibits Growth of Gemcitabine-Resistant Pancreatic Cancer Cells via Induction of Caspase-Dependent Apoptosis and G(2) /M Arrest." J Cell Biochem. 2017 Feb 6. PMID:28165150

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Chemical structure


Related Biological Data

Annexin V assay analyzing stages of apoptosis 48 h following drug treatments [BKM120 (2 μM)] for U87Mg cells; Experiments were repeated 3 times. The mean ± SEM from at least 2–3 independent experiments containing 4 replicates each were obtained. Students t test was used to determine significance (p < 0.05) between groups. AV annexin V, PI propidium iodide.

Related Biological Data

BKM120 almost completely blocked the phosphorylation of Akt at concentration of 2.5 μM. High concentrations of BKM120 such as 5 μM and 10 μM induced cell death.
Method:Western Blot; Cell Lines:Primary HUVECs; Concentrations:2.5 μM; Incubation Time:2 h.

Related Biological Data


Biological Activity

Description BKM120(NVP-BKM120, Buparlisib) is a selective PI3K inhibitor of p110α/β/δ/γ with IC50 of 52 nM/166 nM/116 nM/262 nM, respectively.
Targets p110α p110β p110δ p110γ    
IC50 52-99 nM 166 nM 116 nM 262 nM    


Cell experiment: [1]

Cell lines

MM cell lines (RPMI-8226, OPM1, MM.1S, OPM2 and H929)

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reaction Conditions

IC50: 0.5-1μM, 48 hours


The effect of the pan-PI3K inhibition, mediated by increased concentrations of buparlisib on MM cell survival was tested by MTT assay. Buparlisib induced cell toxicity after 48 hr treatment in all MM cell lines tested; with an IC50 between 0.5 and 1 μM. In addition, buparlisib decreased the activation of signaling proteins downstream of PI3K including pAkt, pS6R, pP70S6K, and p-mTOR in MM.1S cells in a dose dependent manner.

Animal experiment: [1]

Animal models

Female SCID-Bg mice injected with MM.1S-GFP+/luc+ cells

Dosage form

Oral administration, 50 mg/kg, once a day for 5 weeks


Treatment of mice with buparlisib significantly decreased the rate of tumor progression compared with the vehicle treated group, as shown in representative images of the BLI and quantification of the BLI. These results were further confirmed by fluorescence microscopy, showing that the number of MM.1S- GFP+/luc+ cells present in the BM of mice treated with buparlisib decreased significantly compared with those present in the BM of mice treated with vehicle, as shown in representative images of immunofluorescence.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Sahin I, Azab F, Mishima Y, Moschetta M, Tsang B, Glavey SV, Manier S, Zhang Y, Sacco A, Roccaro AM, Azab AK, Ghobrial IM. Targeting survival and cell trafficking in multiple myeloma and Waldenstrom macroglobulinemia using pan-class I PI3K inhibitor, buparlisib. Am J Hematol. 2014 Jul 24.

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Chemical Properties

Cas No. 944396-07-0 SDF Download SDF
Synonyms BKM-120,Buparlisib,BKM 120,NVP-BKM120,NVP-BKM-120
Chemical Name 5-(2,6-dimorpholin-4-ylpyrimidin-4-yl)-4-(trifluoromethyl)pyridin-2-amine
Formula C18H21F3N6O2 M.Wt 410.39
Solubility ≥20.52mg/mL in DMSO Storage Store at -20°C
Physical Appearance A solid Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.

Research Update

1. Effects of PI3K inhibitor NVP-BKM120 on acquired resistance to gefitinib of human lung adenocarcinoma H1975 cells. J Huazhong Univ Sci Technolog Med Sci. 2013 Dec;33(6):845-51. doi: 10.1007/s11596-013-1209-5. Epub 2013 Dec 13.
NVP-BKM120, a class I PI3K inhibitor, concentration-dependently inhibited the growth of H1975 cells, which increased the proportion of H1975 cells in G0-G1 phase at 1 umol/L and promoted apoptosis at 2 umol/L. Moreover, NVP-BKM120 overcame acquired gefitinib resistance in H1975 cells though down-regulation of phosphorylated protein in PI3K/AKT signal pathways, including Akt, S6 and 4E-BP1.
2. The phosphatidylinositol-3-kinase inhibitor NVP-BKM120 overcomes resistance signals derived from microenvironment by regulating the Akt/FoxO3a/Bim axis in chronic lymphocytic leukemia cells. Haematologica. 2013 Nov;98(11):1739-47. doi: 10.3324/haematol.2013.088849. Epub 2013 Jul 12.
NVP-BKM120 is an orally-available inhibitor of class I phosphatidylinositol-3-kinase that promoted mitochondrial apoptosis in chronic lymphocytic leukemia primary cells through blocking phosphatidylinositol-3-kinase signaling, decreasing Akt and FoxO3a phosphorylation and inducing Bim expression. NVP-BKM120 disrupts phosphatidylinositol-3-kinase pathway in chronic lymphocytic leukemia primary cells by inhibiting microenvironment signals, including B-cell receptor- and stroma-dependent Akt pathway activation, B-cell receptor stimulation induced chemokines secretion and CXCL12 triggered cell chemotaxis and actin polymerization upon CXCR4.
3. Inhibition of pan-class I phosphatidyl-inositol-3-kinase by NVP-BKM120 effectively blocks proliferation and induces cell death in diffuse large B-cell lymphoma. Leuk Lymphoma. 2014 Feb;55(2):425-34. doi: 10.3109/10428194.2013.806800. Epub 2013 Jul 25.
Inhibition of PI3K/Akt/mammalian target of mTOR signaling pathway by NVP-BKM120, a pan-class I PI3K inhibitot, in DLBCL cells results in decreased cell proliferation, increased apoptotic cell death, increased expression of Puma and Bim and down-regulation of Bcl-xL and Mcl-1.
4. The PI3 kinase inhibitor NVP-BKM120 induces GSK3/FBXW7-dependent Mcl-1 degradation, contributing to induction of apoptosis and enhancement of TRAIL-induced apoptosis. Cancer Lett. 2013 Sep 28;338(2):229-38. doi: 10.1016/j.canlet.2013.03.032. Epub 2013 Apr 2.
BKM120, a PI3 kinase inhibitor, induced apoptosis and enhanced TRAIL-induced apoptosis in human lung cancer cells through facilitating Mcl-1 degradation involving a GSK3/FBXW7-dependent mechanism.
5. Activity of the pan-class I phosphoinositide 3-kinase inhibitor NVP-BKM120 in T-cell acute lymphoblastic leukemia. Leukemia. 2013 Nov 6. doi: 10.1038/leu.2013.369. [Epub ahead of print]
BKM120, an orally-available pan-PI3K inhibitor, has the potential to treat T-ALL for its abilities to induce G2/M phase cell cycle arrest and apoptosis T-ALL cells and patient T lymphoblasts, significantly delay tumor growth in a subcutaneous xenotransplant model of human T-ALL and synergize with chemotherapeutic agents for treating T-ALL patients.


BKM120(NVP-BKM120, Buparlisib) is a selective PI3K inhibitor of p110α/β/δ/γ with IC50 of 52 nM/166 nM/116 nM/262 nM, respectively.

The intracellular phosphatidylinositol-3-kinase(PI3K) pathway regulates cellular functions incuding cell proliferation, growth, survival, apoptosis, protein synthesis, and glucose metabolism. BKM120, a biologic characterization of the 2-morpholino pyrimidine derivative, is a pan-PI3K inhibitor.

In vitro: NVP-BKM120 inhibits all four class I PI3K isoforms in biochemical assays with at least 50-fold selectivity against other protein kinases. NVP-BKM120 is also active against the most common somatic PI3Ka mutations but does not significantly inhibit the related class III (Vps34) and class IV (mTOR, DNA-PK) PI3K kinases. Consistent with its mechanism of action, NVP-BKM120 decreases the cellular p-Akt levels in mechanistic models and relevant tumor cell lines. In a panel of 353 cell lines test, NVP-BKM120 showed preferential inhibition of tumor cells with PIK3CA mutations, rather than either KRAS or PTEN mutant models [1].

In vivo: NVP-BKM120 shows dose-dependent in vivo pharmacodynamic activity as measured by significant inhibition of p-Akt and tumor growth inhibition in mechanistic xenograft models. In addition, NVP-BKM120 behaves synergistically when combined with either targeted agents such as MEK or HER2 inhibitors or with cytotoxic agents such as docetaxel or temozolomide [1].

Clinical trial: A phase I dose-escalation study investigated the maximum-tolerated dose (MTD), safety, preliminary activity, PK, and PD of BKM120. This study demonstrates feasibility and proof-of-concept of class I PI3K inhibition in cancer patients. BKM120 at the MTD of 100 mg d-1 is safe and well tolerated, with a good PK profile, clear evidence of target inhibition, and preliminary antitumor activity [2].

[1] Maira SM, Pecchi S, Huang A, Burger M, Knapp M, Sterker D, Schnell C, Guthy D, Nagel T, Wiesmann M, Brachmann S, Fritsch C, Dorsch M, Chène P, Shoemaker K, De Pover A, Menezes D, Martiny-Baron G, Fabbro D, Wilson CJ, Schlegel R, Hofmann F, García-Echeverría C, Sellers WR, Voliva CF.  Identification and characterization of NVP-BKM120, an orally available pan-class I PI3-kinase inhibitor. Mol Cancer Ther. 2012;11(2):317-28.
[2] Bendell JC, Rodon J, Burris HA, de Jonge M, Verweij J, Birle D, Demanse D, De Buck SS, Ru QC, Peters M, Goldbrunner M, Baselga J.  Phase I, dose-escalation study of BKM120, an oral pan-Class I PI3K inhibitor, in patients with advanced solid tumors. J Clin Oncol. 2012;30(3):282-90.