Ibrutinib (PCI-32765)

Catalog No.S2680

Ibrutinib (PCI-32765) is a potent and highly selective Brutons tyrosine kinase (Btk) inhibitor with IC50 of 0.5 nM in cell-free assays, modestly potent to Bmx, CSK, FGR, BRK, HCK, less potent to EGFR, Yes, ErbB2, JAK3, etc.

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Ibrutinib (PCI-32765) Chemical Structure

Ibrutinib (PCI-32765) Chemical Structure
Molecular Weight: 440.5

Validation & Quality Control

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Product Information

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  • Research Area
  • Inhibition Profile

Product Description

Biological Activity

Description Ibrutinib (PCI-32765) is a potent and highly selective Brutons tyrosine kinase (Btk) inhibitor with IC50 of 0.5 nM in cell-free assays, modestly potent to Bmx, CSK, FGR, BRK, HCK, less potent to EGFR, Yes, ErbB2, JAK3, etc.
Targets BTK [1]
(Cell-free assay)
BLK [1]
(Cell-free assay)
Bmx [1]
(Cell-free assay)
CSK [1]
(Cell-free assay)

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IC50 0.5 nM 0.5 nM 0.8 nM 2.3 nM
In vitro Ibrutinib shows the potent and irreversible inhibitory effect and selectivity for Btk enzymatic activity. In BCR pathway-activated DOHH2 cell line, Ibrutinib inhibits autophosphorylation of Btk, phosphorylation of Btk's physiological substrate PLCγ, and phosphorylation of further downstream kinase, ERK with IC50 of 11 nM, 29 nM and 13 nM, respectively. [1] Ibrutinib exhibits a significant dose-dependent and time-dependent induction of cytotoxicity in chronic lymphocytic leukemia (CLL) cells. In addition, Ibrutinib induces cell death depending on caspase pathway activation and antagonizes the ability of CLL cells to proliferate after TLR signaling. [2] A recent study shows that Ibrutinib inhibits BCR-activated primary B cell proliferation with IC50 of 8 nM and results in inhibition of TNFα, IL-1β and IL-6 production in primary monocytes with IC50 of 2.6 nM, 0.5 nM and 3.9 nM, respectively. [3]
In vivo In a collagen-induced arthritis model, Ibrutinib significantly reduces clinical arthritis scores reflecting paw swelling and joint inflammation by inhibiting B-cell activation. In a MRL-Fas(lpr) lupus model, Ibrutinib reduces renal disease and autoantibody production. [1] In an adoptive transfer TCL1 mouse model of CLL, Ibrutinib (25 mg/kg/day) causes a transient early lymphocytosis, and delays CLL disease progression. [4]

Protocol(Only for Reference)

Kinase Assay:


Kinase Assays In vitro kinase IC50 values are measured using 33P filtration binding assay after 1 hour incubation of kinase, 33P-ATP, Ibrutinib, and substrate [0.2 mg/mL poly(EY)(4:1]. Assays are performed at Reaction Biology.

Cell Assay:


Cell lines Chronic lymphocytic leukemia (CLL) cells
Concentrations 0.01-100 μM
Incubation Time 48 hours

MTT (3'[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide) assays are performed to determine cytotoxicity. Briefly, cells (CLL B cells or healthy volunteer T cells or NK cells) are incubated for 48 hours with different concentrations of Ibrutinib, or vehicle control. MTT reagent is then added, and plates are incubated for an additional 20 hours before washing with protamine sulfate in phosphate-buffered saline. Dimethyl sulfoxide is added, and absorbance is measured by spectrophotometry at 540 nm in a Labsystems plate reader. Cell viability is also measured at various time points with the use of annexin/PI flow cytometry. Data are analyzed with Expo-ADC32 software package. Results are expressed as the percentage of total positive cells over untreated control. Experiments examining caspase-dependent apoptosis includes the addition of 100μM Z-VAD.

Animal Study:


Animal Models MRL-Fas(lpr) lupus model and collagen-induced arthritis model.
Formulation Ibrutinib is dissolved in DMSO.
Dosages ≤50 mg/kg
Administration Administered via p.o.

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

SpeciesMouseRatRabbitGuinea pigHamsterDog
Weight (kg)
Body Surface Area (m2)0.0070.0250.
Km factor36128520
Animal A (mg/kg) = Animal B (mg/kg) multiplied by  Animal B Km
Animal A Km

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 Km factor for a mouse and then divide by the Km 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 Km(3)  = 11.2 mg/kg
rat Km(6)


[1] Honigberg LA, et al. Proc Natl Acad Sci U S A. 2010, 107(29), 13075-13080.

[2] Herman SE, et al. Blood. 2011, 117(23), 6287-6296.

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Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2016-07-23)

NCT Number Recruitment Conditions Sponsor
Start Date Phases
NCT02757040 Not yet recruiting Leukemia, Lymphocytic, Chronic, B-Cell Peking University Peoples Hospital|Beijing Hospital December 2016 Phase 3
NCT02703272 Not yet recruiting Lymphoma, Non-Hodgkin Janssen Research & Development, LLC October 2016 Phase 3
NCT02760485 Not yet recruiting Diffuse Large B-cell Lymphoma Incyte Corporation|Pharmacyclics September 2016 Phase 1|Phase 2
NCT02815059 Not yet recruiting Acute Lymphoblastic Leukemia University of Utah|Janssen, LP August 2016 Phase 1
NCT02756897 Not yet recruiting Leukemia|Chronic Lymphocytic Leukemia|Small Lymphocytic Lymphoma M.D. Anderson Cancer Center|AbbVie August 2016 Phase 2

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Chemical Information

Download Ibrutinib (PCI-32765) SDF
Molecular Weight (MW) 440.5


CAS No. 936563-96-1
Storage 3 years -20℃powder
6 months-80℃in solvent
Synonyms N/A
Solubility (25°C) * In vitro DMSO 88 mg/mL (199.77 mM)
Water <1 mg/mL (<1 mM)
Ethanol <1 mg/mL (<1 mM)
In vivo 2% DMSO+Castor oil 10mg/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 (R)-1-(3-(4-amino-3-(4-phenoxyphenyl)-1H-pyrazolo[3,4-d]pyrimidin-1-yl)piperidin-1-yl)prop-2-en-1-one

Customer Product Validation(7)

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Source J Cell Sci 2015 128(2), 251-65. Ibrutinib (PCI-32765) purchased from Selleck
Method Immunoprecipitation
Cell Lines THP-1 cells
Concentrations 250, 500, 1000 nM
Incubation Time 2 h
Results Btk inhibition had an apparently total inhibitory effect on the tyrosine phosphorylation of WIP at all pharmacologically relevant concentrations of PCI-32765 tested, demonstrating that this kinase is a key mediator of WIP phosphorylation in these cells.

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Source Br J Haematol 2014 166(6), 849-61. Ibrutinib (PCI-32765) purchased from Selleck
Method Western blotting assays
Cell Lines Mantle cell lymphoma cells
Concentrations 0.2-1 uM
Incubation Time 1, 4 h
Results It then determined whether the phosphorylation of BTK responds to ibrutinib. It performed immunoblotting assays in MCL cells treated with or without ibrutinib. Phosphorylated BTK (Y223) expression was reduced by ibrutinib not only in the sensitive cell line Jeko-1 (left panel) but also in resistant cell lines Mino and Granta-519 (right and bottom panels). As a control, total BTK remained unchanged by the treatment. These results suggest that ibrutinib indeed directly inhibits the activity of BTK in MCL cells.

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Source J Biol Chem 2015 290(18), 11557-68. Ibrutinib (PCI-32765) purchased from Selleck
Method Western blotting assays
Cell Lines CLEC-2, GPVI cells
Concentrations 5 nM
Incubation Time 5 min
Results Another study in platelets has shown that a Tec family kinase inhibitor abolished CLEC-2 mediated microparticle generation. These results suggest a crucial role of Tec family kinases in CLEC-2 signaling. It elucidated the role of Tec family kinases in CLEC-2 signaling by using Ibrutinib, a Tec family kinase inhibitor. Ibrutinib is known as a highly potent small molecule inhibitor of Btk. Due to the structural similarity between Btk, Itk and Tec, Ibrutinib is known to affect all these Tec family kinases. Ibrutinib abolished platelet aggregation and Syk phosphorylation induced by rhodocytin and other CLEC-2 agonists.

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Source Cell Signal 2013 25, 106-12. Ibrutinib (PCI-32765) purchased from Selleck
Method Western blotting/Proliferation/death assays
Cell Lines MM cell lines
Concentrations 1/10 μM
Incubation Time 48 h
Results Ibrutinib induces signifi cant cell death (7–46%) in MM cells at 10 μM(Fig. C) as measured by the Cell Titer GLO assay. We also observed a similar effect with ibrutinib in MM cell lines ( Fig. D).

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Source Cell Signal 2013 25, 106-12. Ibrutinib (PCI-32765) purchased from Selleck
Method flow cytometry/Cell Titer GLO assay
Cell Lines RPMI8226 cells/Primary human monocytes
Concentrations 1/10 μM
Incubation Time 48 h
Results Ibrutinib significantly increased cytotoxicity of malignant plasma cells, with the effectin- vitro appearing greater in combination with bortezomib (Fig. A). We also observed a similar effect with ibrutinib in combination with either lenalidomide or bortezomi b in MM ce ll lines (Fig. B). These observations were further confirmed using an annexin-V/ propidium iodide apoptosis assay (Fig. C). Furthermore, we observed that BTK inhibition had no cytotoxic effects on primary monocytes suggesting the effect on malignant plasma cells is not through non-specific cytotoxicity (Fig. D).

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Source Cell Signal 2013 25, 106-12. Ibrutinib (PCI-32765) purchased from Selleck
Method Western blotting/Cell Titer GLO assay/Real-time PCR
Cell Lines MM cells
Concentrations 10 μM
Incubation Time 48 h
Results We found that FLIPL, Bcl-xL and survivin are inhibited by ibrutinib alone and in combination with bortezomib (Fig. A and B). Since both FLIPL and Bcl-xL negatively regulate caspase-induced cell death we looked to establish whether cell death observed in the MM cells was the result of caspase activation. Thepan-caspase inhibitor zVAD-fmk was able to protect MM cells from cell death induced by ibrutinib alone or in co mb in ation with bortezomib establishing that ibrutinib induced MM cell death is caspase-dependent(Fig. C).

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Source Blood Cancer J 2014 4, e181. Ibrutinib (PCI-32765) purchased from Selleck
Method Western blotting assays
Cell Lines Nalm6, MHH-CALL4, MHH-CALL3 cells
Concentrations 50, 150 uM
Incubation Time 4 h
Results In correspondence, the level of phosphorylated ERK1/2, which is an important downstream effector of BTK contributing to cell survival, decreased upon a 4-h exposure to Ibrutinib in the TCF3-rearranged MHH-CALL3 but not in both non-TCF3-rearranged cell lines Nalm6 and MHH-CALL4.

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