My cart
In the shopping cart is not goods, to choose and buy!
  • Product Name
  • Size
  • Quantity
  • Amount
    Selected items : 0 pieces Total : CHECK OUT()
    Buparlisib (BKM120, NVP-BKM120)
    Buparlisib (BKM120, NVP-BKM120)

    Market Price:

    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V0105
    CAS #: 944396-07-0Purity ≥98%

    Description: BKM120 (also known as NVP-BKM120, or Buparlisib) is a selective, orally bioavailable and potent Pan-class I PI3K inhibitor of p110α/β/δ/γ with IC50 of 52 nM/166 nM/116 nM/262 nM in cell-free assays, respectively. It has anticancer activity. It has reduced potency against VPS34, mTOR, DNAPK and is with little activity to PI4Kβ. BKM120 has been undergoing various clinical trials for the treatment of a variety of cancers. The intracellular phosphatidylinositol-3-kinase(PI3K) pathway regulates cellular functions including 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 experiments showed that NVP-BKM120 inhibits all four class I PI3K isoforms in biochemical assays with at least 50-fold selectivity against other protein kinases. 

    References:  Mol Cancer Ther. 2012 Feb;11(2):317-28; J Clin Oncol. 2012 Jan 20;30(3):282-90. 

    Related CAS: 1312445-63-8 (HCl)  944396-07-0 (free base)

    Customer Validation
    Official Supplier of
    • VE
    • OF
    • YALE
    • hhmi
    • 香港大学
    Publications Citing InvivoChem Products
    • Physicochemical and Storage Information
    • Protocol
    • Quality Control Documentation
    • Related Biological Data
    • Customer Review

    Molecular Weight (MW)




    CAS No.

    944396-07-0 (free); 


    -20℃ for 3 years in powder form

    -80℃ for 2 years in solvent

    Solubility (In vitro)

    DMSO: 82 mg/mL (199.8 mM)

    Water:<1 mg/mL (slightly soluble or insoluble)

    Ethanol: 2 mg/mL (4.87 mM)

    Solubility (In vivo)

    0.5% CMC Na: 6 mg/mL

    Other info

    Chemical Name: 5-[2,6-Di(4-morpholinyl)-4-pyrimidinyl]-4-(trifluoromethyl)-2-pyridinamine.


    InChi Code: InChI=1S/C18H21F3N6O2/c19-18(20,21)13-9-15(22)23-11-12(13)14-10-16(26-1-5-28-6-2-26)25-17(24-14)27-3-7-29-8-4-27/h9-11H,1-8H2,(H2,22,23)

    SMILES Code: NC1=NC=C(C2=NC(N3CCOCC3)=NC(N4CCOCC4)=C2)C(C(F)(F)F)=C1


    Buparlisib; BKM120; BKM-120; BKM 120; NVPBKM120; NVP BKM120; NV- BKM120

    • Molarity Calculator
    • Dilution Calculator
    • The molarity calculator equation

      Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

      • Mass
      • Concentration
      • Volume
      • Molecular Weight *
      • =
      • ×
      • ×
    • The dilution calculator equation

      Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

      This equation is commonly abbreviated as: C1V1 = C2V2

      • Concentration (start)
      • ×
      • Volume (start)
      • =
      • Concentration (final)
      • ×
      • Volume (final)
      • ×
      • =
      • ×
      • C1
      • V1
      • C2
      • V2

    In Vitro

    Kinase Assay: 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 Assay: 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.

    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. 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. 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. 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.

    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.  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.

    Animal model

    U87MG and A2780 xenografts are established in female nu/nu mice.

    Formulation & Dosage

    15% Captisol; 60 mg/kg; oral QD


    [1] Burger MT, et al. ACS Med Chem Lett, 2011, 2 (10), 774–779.; [2] Zheng Y, et al. J Mol Med (Berl), 2011 Dec 30.

    These protocols are for reference only. InvivoChem does not independently validate these methods.

    BKM120 (NVP-BKM120, Buparlisib)

    Analysis of buparlisib substrate affinity for ABC transporters using in vitro transport assays.  2018 Jul 17;8(1):10784.

    BKM120 (NVP-BKM120, Buparlisib)

    The impact of P-gp and BCRP on the brain and tissue penetration of buparlisib.

    BKM120 (NVP-BKM120, Buparlisib)

    Buparlisib has excellent intracranial target engagement and oral bioavailability.  2018 Jul 17;8(1):10784.

    BKM120 (NVP-BKM120, Buparlisib)

    BKM120 (NVP-BKM120, Buparlisib)

    NVP-BKM120 inhibits cancer cell proliferation and induces apoptosis in a CCA mouse model.  2018 Aug;16(2):1627-1633.

    BKM120 (NVP-BKM120, Buparlisib)

    Growth inhibition effect of NVP-BKM120 on CCA cell lines.  2018 Aug;16(2):1627-1633.


      Home Prev Next Last page / pices


      Your information is safe with us. * Required Fields.
      Products are for research use only;  We do not sell to patients
      Tel: 1-708-310-1919
      Fax: 1-708-557-7486
      Subscribe to our E-newsletter
      • Name*
      • *
      • E-mail*
      • *
      • instructions:
      • *
      Copyright 2020 InvivoChem LLC | All Rights Reserved
      Do you confirm the receipt?