Product Categories

BKM120 (NVP-BKM120, Buparlisib)

Catalog No.S2247

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 2.

: Selleck USA Tel: +1-832-582-8158[email protected]

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

Validation & Quality Control

Product Citations(26)

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

PubMed: 22340590

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

PubMed: 24356096

Cancer Discov,2013, 4(2):186-99

PubMed: 24302555

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

PubMed: 25488980

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

PubMed: 25401474
J Clin Invest,2014, 124(11):4737-52

PubMed: 25250573

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

PubMed: 25297634

Oncogene,2013, 10.1038/onc.2013.509

PubMed: 24292683

Oncogene,2014, 10.1038/onc.2014.328

PubMed: 25284585

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

PubMed: 23918606
Cell Rep,2014, 8(5):1265-70

PubMed: 25176649

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

PubMed: 24979463

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

PubMed: 23844554

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

PubMed: 24451154

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

PubMed: 25103565
Cell Death Dis,2014, 5:e1134

PubMed: 24651437

Cell Death Dis,2014, 5:e1013

PubMed: 24457957

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

PubMed: 24982421

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

PubMed: 25103499

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

PubMed: 25578563
Breast Cancer Res,2014, 16(4):406

PubMed: 25103565

PLoS One,2014, 9(10):e108780

PubMed: 25360799

PLoS One,2014, 9(7):e101969

PubMed: 25003333

BMC Cancer,2013, 13:465

PubMed: 24103747

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

PubMed: 25285632
University Göttingen,2013, Elisabeth Hand

Customer Reviews(3) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

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

Inhibitor Library Kinase Inhibitor Library Bioactive Compound Library Cambridge Cancer Compound Library

PI3K Inhibitors with Unique Features

Selective PI3K Inhibitors

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

Product Information

Compare PI3K Products

Research Area
Research Area
Inhibition Profile
Inhibition Profile
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 2.
Matthew T. Burger, et al. ACS Med. Chem. Lett., 2011, 2(10), 774–779
BKM120 (NVP-BKM120, Buparlisib) Mechanism
BKM120 (NVP-BKM120, Buparlisib) Mechanism
The receptor-regulated class I PI3K are heterodimeric enzymes, consisting of a 110-kDa catalytic subunit and a regulatory subunit. Different from p110α, -β, and -δ isoforms, the p110γ isoform tightly binds to the p101 regulatory subunit. The p101 structure indicates that an N-terminal domain mediates heterodimerization with the p110γ subunit, and a C-terminal interaction domain mediates the binding to Gβγ complexes. ^[1] The ATP binding site of PI3K-gamma catalytic domain is located in a cleft between the N- and the C-terminal lobes of the catalytic domain.
BKM120 is a 2,6-dimorpholino pyrimidine derivative. The crystal structure indicates that BKM120 binds in the ATP-binding site of PI3K-gamma kinase domain. Specifically, 2-morpholino group makes an interaction via the hydrogen bond from the morpholine oxygenoxygen to the backbone amino group of Val882. The exocyclic nitrogen in the 6-position pyridyl substituent as a donor also forms two bonds to Asp841 and Asp964 in the catalytic region. In addition, a water molecule makes a hydrogen bond bridge between Tyr836 and Asp810, which acts as a hydrogen bond acceptor to interact with the 6-pyridyl endocyclic nitrogen. The binding mode results in greater affinity of PI3K enzyme for BKM120 than ATP. ^[2]
References
[1] Voigt P, et al. J Biol Chem. 2005, 280(6), 5121-5127.
[2] Maira SM, et al. Mol Cancer Ther. 2012, 11(2), 317-328.
Dr. Antonino Maria Sparta demonstrates a breakthrough in leukemia research by utilizing two inhibitors produced by Selleck Chemicals.

Cat.No.	Product Name	Solubility (25°C)
S1009	BEZ235 (NVP-BEZ235, Dactolisib)	<1 mg/mL	0.01 mg/mL	<1 mg/mL
S1065	Pictilisib (GDC-0941)	<1 mg/mL	44 mg/mL	<1 mg/mL
S1105	LY294002	<1 mg/mL	36 mg/mL	21 mg/mL
S2226	CAL-101 (Idelalisib, GS-1101)	<1 mg/mL	83 mg/mL	35 mg/mL
S2247	BKM120 (NVP-BKM120, Buparlisib)	<1 mg/mL	82 mg/mL	2 mg/mL
S1038	PI-103	<1 mg/mL	24 mg/mL	<1 mg/mL
S2638	NU7441 (KU-57788)	<1 mg/mL	3 mg/mL	<1 mg/mL
S1169	TGX-221	<1 mg/mL	12 mg/mL	<1 mg/mL
S1268	IC-87114	<1 mg/mL	0.66 mg/mL	<1 mg/mL
S2758	Wortmannin	<1 mg/mL	86 mg/mL	<1 mg/mL
S1118	XL147	<1 mg/mL	3 mg/mL	<1 mg/mL
S1072	ZSTK474	<1 mg/mL	21 mg/mL	<1 mg/mL
S2814	BYL719	<1 mg/mL	88 mg/mL	2 mg/mL
S1410	AS-605240	<1 mg/mL	0.4 mg/mL	<1 mg/mL
S1205	PIK-75	<1 mg/mL	3 mg/mL	<1 mg/mL
S2767	3-Methyladenine (3-MA)	<1 mg/mL	4 mg/mL	4 mg/mL
S2636	A66	<1 mg/mL	79 mg/mL	1 mg/mL
S1523	SAR245409 (XL765)	<1 mg/mL	12 mg/mL	<1 mg/mL
S1489	PIK-93	<1 mg/mL	78 mg/mL	<1 mg/mL
S2658	GSK2126458 (GSK458)	<1 mg/mL	100 mg/mL	<1 mg/mL
S1187	PIK-90	<1 mg/mL	0.28 mg/mL	<1 mg/mL
S2743	PF-04691502	<1 mg/mL	14 mg/mL	<1 mg/mL
S1462	AZD6482	<1 mg/mL	82 mg/mL	10 mg/mL
S2696	Apitolisib (GDC-0980, RG7422)	<1 mg/mL	20 mg/mL	<1 mg/mL
S1360	GSK1059615	<1 mg/mL	2 mg/mL	<1 mg/mL
S7028	Duvelisib (IPI-145, INK1197)	<1 mg/mL	84 mg/mL	<1 mg/mL
S2628	Gedatolisib (PF-05212384, PKI-587)	<1 mg/mL	2 mg/mL	<1 mg/mL
S1352	TG100-115	<1 mg/mL	9 mg/mL	<1 mg/mL
S2671	AS-252424	<1 mg/mL	61 mg/mL	<1 mg/mL
S2749	BGT226 (NVP-BGT226)	<1 mg/mL	30 mg/mL	<1 mg/mL
S2759	CUDC-907	<1 mg/mL	102 mg/mL	<1 mg/mL
S2227	PIK-294	<1 mg/mL	98 mg/mL	<1 mg/mL
S2681	AS-604850	<1 mg/mL	57 mg/mL	5 mg/mL
S8002	GSK2636771	<1 mg/mL	28 mg/mL	<1 mg/mL
S2802	BAY 80-6946 (Copanlisib)	0.002 mg/mL	0.002 mg/mL	0.01 mg/mL
S1219	YM201636	<1 mg/mL	35 mg/mL	<1 mg/mL
S2699	CH5132799	<1 mg/mL	12 mg/mL	<1 mg/mL
S2682	CAY10505	<1 mg/mL	58 mg/mL	<1 mg/mL
S2207	PIK-293	<1 mg/mL	80 mg/mL	<1 mg/mL
S2739	PKI-402	<1 mg/mL	0.4 mg/mL	<1 mg/mL
S2870	TG100713	<1 mg/mL	2 mg/mL	<1 mg/mL
S7016	VS-5584 (SB2343)	<1 mg/mL	71 mg/mL	3 mg/mL
S7018	CZC24832	<1 mg/mL	5 mg/mL	<1 mg/mL
S7356	HS-173	<1 mg/mL	84 mg/mL	<1 mg/mL
S7623	PI-3065	<1 mg/mL	50 mg/mL	<1 mg/mL

Product Description

Biological Activity Protocol Clinical Trial Information Chemical Information Customer Reviews Product Citations Tech Support & FAQs

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 2.
Targets	p110α ^[1]	p110δ ^[1]	p110β ^[1]	p110γ ^[1]	Vps34 ^[1]	View More
IC50	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]
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 MaxiSorp^TM plates. The solvents are evaporated at room temperature and plates are wa

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 MaxiSorp^TM plates. The solvents are evaporated at room temperature and plates are wa

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.
Formulation	In 15% Captisol.
Dosages	~60 mg/kg.
Administration	Dosed orally daily (q.d.).
Solubility	0.5% CMC Na, 6 mg/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.

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

Species	Baboon	Dog	Monkey	Rabbit	Guinea pig	Rat	Hamster	Mouse
Weight (kg)	12	10	3	1.8	0.4	0.15	0.08	0.02
Body Surface Area (m²)	0.6	0.5	0.24	0.15	0.05	0.025	0.02	0.007
K_m factor	20	20	12	12	8	6	5	3

Animal A (mg/kg) = Animal B (mg/kg) multiplied by	Animal B K_m
	Animal A K_m

For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the K_m factor for a mouse and then divide by the K_m factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.

Rat dose (mg/kg) = mouse dose (22.4 mg/kg) ×	mouse K_m(3)	= 11.2 mg/kg
	rat K_m(6)

References

[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.

view more

Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2015-02-07)

NCT Number	Recruitment	Conditions	Sponsor /Collaborators	Start Date	Phases
NCT01613677	Not yet recruiting	Treatment for Metastatic or Locally Advanced Cervical Cancer	Novartis Pharmaceuticals\|Novartis	July 2015	Phase 2
NCT01613677	Not yet recruiting	Treatment for Metastatic or Locally Advanced Cervical Cancer	Novartis Pharmaceuticals\|Novartis	July 2015	Phase 2
NCT01971489	Not yet recruiting	Recurrent Non-small Cell Lung Cancer\|Stage IIIA Non-small Cell Lung Cancer\|Stage IIIB Non-small Cell Lung Cancer\|Stage IV Non-small Cell Lung Cance ...more	Roswell Park Cancer Institute\|National Cancer Institute ( ...more	February 2015	Phase 1
NCT01971489	Not yet recruiting	Recurrent Non-small Cell Lung Cancer\|Stage IIIA Non-small Cell Lung Cancer\|Stage IIIB Non-small Cell Lung Cancer\|Stage IV Non-small Cell Lung Cance ...more	Roswell Park Cancer Institute\|National Cancer Institute ( ...more	February 2015	Phase 1
NCT02340780	Not yet recruiting	Chronic Lymphocytic Leukemia	NCIC Clinical Trials Group\|Novartis	January 2015	Phase 2

view more

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
Storage	6 months-80℃in solvent (DMSO, water, etc.)
Synonyms

Solubility (25°C) *	In vitro	DMSO	82 mg/mL (199.8 mM)
		Water	<1 mg/mL (<1 mM)
		Ethanol	2 mg/mL (4.87 mM)
	In vivo	0.5% CMC Na	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

Molarity Calculator Dilution Calculator Molecular Weight Calculator

Research Area

Customer Reviews (3)

Click to enlarge

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.

Click to enlarge

Rating

Source

Dr. Pilar Eroles of INCLIVA Biomedical Research Institute.. BKM120 (NVP-BKM120, Buparlisib) purchased from Selleck

Method

MTT assay

Cell Lines

JIMT-1 cells

Concentrations

1-1000 nM

Incubation Time

48 h

Results

JIMT-1 cells were seeded in 96 well plates (8x10<SUP>3</SUP>cells per well) andtreated with medium containing DMSO as a control and inhibitor BKM-120 (1nM, 5nM, 10nM, 50nM, 100nM, 500nM, 1000nM). Cell growth was measured after 48 hours by MTT assay.Results are expressed as a percent over DMSO control.

Product Citations (26)

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BEZ235 (NVP-BEZ235, Dactolisib)
BEZ235 (NVP-BEZ235) is a dual ATP-competitive PI3K and mTOR inhibitor for p110α/γ/δ/β and mTOR(p70S6K) with IC50 of 4 nM /5 nM /7 nM /75 nM /6 nM, respectively. Inhibits ATR with IC50 of 21 nM, whileshown to be a poor inhibitor to Akt and PDK1. Phase 2.
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BYL719
BYL719 is a potent and selective PI3Kα inhibitor with IC50 of 5 nM, and minimal effect on PI3Kβ/γ/δ. Phase 2.
CAL-101 (Idelalisib, GS-1101)
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Tech Support & FAQs

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

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

* Indicates a Required Field

Related PI3K Products

HS-173
HS-173 is a potent PI3Kα inhibitor with IC50 of 0.8 nM.
PI-3065
PI-3065 is a selective p110δ inhibitor with IC50 of 15 nM, >70-fold selectivity over other PI3K family members.
VE-822
VE-822 is an ATR inhibitor with IC50 of 19 nM.

Features:VE-822 is a highly selective and potent derivative of the ATR inhibitor VE-821.
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.
BEZ235 (NVP-BEZ235, Dactolisib)
BEZ235 (NVP-BEZ235) is a dual ATP-competitive PI3K and mTOR inhibitor for p110α/γ/δ/β and mTOR(p70S6K) with IC50 of 4 nM /5 nM /7 nM /75 nM /6 nM, respectively. Inhibits ATR with IC50 of 21 nM, whileshown to be a poor inhibitor to Akt and PDK1. Phase 2.
3-Methyladenine (3-MA)
3-Methyladenine is a selective PI3K inhibitor for Vps34 and PI3Kγ with IC50 of 25 μM and 60 μM; blocks class I PI3K consistently, whereas suppression of class III PI3K is transient, and also blocks autophagosome formation.
CAL-101 (Idelalisib, GS-1101)
CAL-101 (Idelalisib, GS-1101) is a selective p110δ inhibitor with IC50 of 2.5 nM; shown to have 40- to 300-fold greater selectivity for p110δ thanp110α/β/γ, and 400- to 4000-fold more selectivity to p110δ than C2β, hVPS34, DNA-PK and mTOR.
Pictilisib (GDC-0941)
Pictilisib (GDC-0941) is a potent inhibitor of PI3Kα/δ with IC50 of 3 nM, with modest selectivity against p110β (11-fold) and p110γ (25-fold). Phase 2.
Wortmannin
Wortmannin is the first described PI3K inhibitor with IC50 of 3 nM, with little selectivity within the PI3K family. Also blocks autophagosome formation and potently inhibits DNA-PK/ATM with IC50 of 16 nM and 150 nM.
BYL719
BYL719 is a potent and selective PI3Kα inhibitor with IC50 of 5 nM, and minimal effect on PI3Kβ/γ/δ. Phase 2.

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Product Categories

BKM120 (NVP-BKM120, Buparlisib)

Validation & Quality Control

Product Citations(26)

Customer Reviews(3) in vivo invitation

Quality Control & MSDS

Anti-DYKDDDDK(Flag) Affinity Gel

Protease Inhibitor Cocktail

Mouse Tail Direct PCR Kit

Related Compound Libraries

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

PI3K Inhibitors with Unique Features

Selective PI3K Inhibitors

Most Potent PI3K Inhibitor

FDA-approved Inhibitor

Newest PI3K Inhibitor

Product Information

Compare PI3K Products

Research Area

Inhibition Profile

BKM120 (NVP-BKM120, Buparlisib) Mechanism

Product Description

Biological Activity

Protocol(Only for Reference)

Kinase Assay: [1]

Cell Assay: [1]

Animal Study: [1]

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

References

view more

Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2015-02-07)

view more

Chemical Information

Research Area

Customer Reviews (3)

Product Citations (26)

Customers Who Bought This Item Also Bought

Tech Support & FAQs

If you have any other enquiries, please leave a message.

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Kinase Assay: ^[1]

Cell Assay: ^[1]

Animal Study: ^[1]