Ibrutinib (PCI-32765)

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.

Price Stock Quantity  
USD 272 In stock
USD 170 In stock
USD 320 In stock
USD 970 In stock
Bulk Inquiry

Massive Discount Available

Free Overnight Delivery on all orders over $ 500.

Ibrutinib (PCI-32765) Chemical Structure

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

Validation & Quality Control

Customer Product Validation(7)

Quality Control & MSDS

Related Compound Libraries

Product Information

  • Compare BTK Inhibitors
    Compare BTK Products
  • 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)

 View  More

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.

view more

Clinical Trial Information( data from http://clinicaltrials.gov, updated on 2015-11-14)

NCT Number Recruitment Conditions Sponsor
Start Date Phases
NCT02581930 Not yet recruiting Metastatic Melanoma|Recurrent Melanoma of the Skin|Stage IV Skin Melanoma National Cancer Institute (NCI) May 2016 Phase 2
NCT02272686 Not yet recruiting Lymphoma M.D. Anderson Cancer Center|Pharmacyclics January 2016 Phase 2
NCT02532257 Not yet recruiting Lymphoma|Follicular Lymphoma (FL) M.D. Anderson Cancer Center|Janssen, LP December 2015 Phase 2
NCT02518555 Not yet recruiting Chronic Lymphocytic Leukemia|Small Lymphocytic Lymphoma Farrukh Awan|Pharmacyclics|Ohio State University Comprehe  ...more Farrukh Awan|Pharmacyclics|Ohio State University Comprehensive Cancer Center December 2015 Phase 2
NCT02587299 Not yet recruiting Follicular Lymphoma|Diffuse Large B-cell Lymphoma|Peripheral T-cell Lymphoma Pharmacyclics December 2015 Phase 1|Phase 2

view more

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 10 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 (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)

Click to enlarge
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.

Click to enlarge
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.

Click to enlarge
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.

Click to enlarge
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).

Click to enlarge
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).

Click to enlarge
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).

Click to enlarge
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.

Product Use Citation (29)

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.

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

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

* Indicates a Required Field

Related BTK Products

  • RN486

    RN486 is a potent and selective BTK inhibitor with IC50 of 4 nM.

  • LFM-A13

    LFM-A13 is a specific Bruton's tyrosine kinase (BTK) inhibitor with IC50 of 2.5 μM, >100-fold selectivity over other protein kinases including JAK1, JAK2, HCK, EGFR,and IRK.

  • ONO-4059

    ONO-4059 is a highly potent and selective oral BTK inhibitor with IC50 of 23.9 nM. Phase 1.

  • CGI1746

    CGI1746 is a potent and highly selective small-molecule inhibitor of the Btk with IC50 of 1.9 nM.

  • CC-292 (AVL-292)

    CC-292 (AVL-292) is a covalent, orally active, and highly selective BTK inhibitor with IC50 of <0.5 nM, displaying at least 1400-fold selectivity over the other kinases assayed. Phase 1.

  • CNX-774

    CNX-774 is an irreversible, orally active, and highly selective BTK inhibitor with IC50 of <1 nM.

  • Dasatinib

    Dasatinib is a novel, potent and multi-targeted inhibitor that targets Abl, Src and c-Kit, with IC50 of <1 nM, 0.8 nM and 79 nM in cell-free assays, respectively.

  • Saracatinib (AZD0530)

    Saracatinib (AZD0530) is a potent Src inhibitor with IC50 of 2.7 nM in cell-free assays, and potent to c-Yes, Fyn, Lyn, Blk, Fgr and Lck; less active for Abl and EGFR (L858R and L861Q). Phase 2/3.

    Features:The 1st Src inhibitor to show inhibition of the Src pathway in human tumor tissue.

  • Imatinib Mesylate (STI571)

    Imatinib Mesylate (STI571) is an orally bioavailability mesylate salt of Imatinib, which is a multi-target inhibitor of v-Abl, c-Kit and PDGFR with IC50 of 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively.

  • BGJ398 (NVP-BGJ398)

    BGJ398 (NVP-BGJ398) is a potent and selective FGFR inhibitor for FGFR1/2/3 with IC50 of 0.9 nM/1.4 nM/1 nM in cell-free assays, >40-fold selective for FGFR versus FGFR4 and VEGFR2, and little activity to Abl, Fyn, Kit, Lck, Lyn and Yes. Phase 2.

Recently Viewed Items

Tags: buy Ibrutinib (PCI-32765) | Ibrutinib (PCI-32765) ic50 | Ibrutinib (PCI-32765) price | Ibrutinib (PCI-32765) cost | Ibrutinib (PCI-32765) solubility dmso | Ibrutinib (PCI-32765) purchase | Ibrutinib (PCI-32765) manufacturer | Ibrutinib (PCI-32765) research buy | Ibrutinib (PCI-32765) order | Ibrutinib (PCI-32765) mouse | Ibrutinib (PCI-32765) chemical structure | Ibrutinib (PCI-32765) mw | Ibrutinib (PCI-32765) molecular weight | Ibrutinib (PCI-32765) datasheet | Ibrutinib (PCI-32765) supplier | Ibrutinib (PCI-32765) in vitro | Ibrutinib (PCI-32765) cell line | Ibrutinib (PCI-32765) concentration | Ibrutinib (PCI-32765) nmr
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Contact Us