Ibrutinib (PCI-32765) 化学構造
分子量: 440.5



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製品説明 Ibrutinib (PCI-32765)は、0.5nMのIC50による有力で非常に選択的なブラットンのチロシン・キナーゼ(Btk)阻害剤です。



0.5 nM [1]

In vitro試験 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試験 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]
臨床試験 Ibrutinib is currently in Phase II clinical trials in patients with Chronic Lymphocytic Leukemia (CLL) or Small Lymphocytic Lymphoma (SLL). Combination of Ibrutinib and Rituximab is currently in Phase II clinical trials in patients with High-Risk Chronic

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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.



細胞株 Chronic lymphocytic leukemia (CLL) cells
濃度 0.01-100 μM
反応時間 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.



動物モデル MRL-Fas(lpr) lupus model and collagen-induced arthritis model.
製剤 Ibrutinib is dissolved in DMSO.
投薬量 ≤50 mg/kg
投与方法 Administered via p.o.

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

SpeciesMouseRatRabbitGuinea pigHamsterDogMonkeyBaboon
Weight (kg)
Body Surface Area (m2)0.0070.0250.
Km factor361285201220
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)



Download Ibrutinib (PCI-32765) SDF
分子量 440.5


CAS No. 936563-96-1
保管 2年-20℃
6月-80℃in solvent
別名 N/A
溶解度 (25°C) * In vitro DMSO 88 mg/mL (199.77 mM)
<1 mg/mL (<1 mM)
エタノール <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.
化学名 (R)-1-(3-(4-amino-3-(4-phenoxyphenyl)-1H-pyrazolo[3,4-d]pyrimidin-1-yl)piperidin-1-yl)prop-2-en-1-one

カスタマーフィードバック (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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID