Ibrutinib (PCI-32765)


Ibrutinib (PCI-32765)化学構造


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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  • BTK C481S and C481T variants show resistance to ibrutinib. (a and b) COS-7 cells were transfected with wild-type BTK or the two variants. Thirty-six hours post transfection, the cells were serum starved and treated with ibrutinib overnight followed by activation with serum and pervanadate for 5 min at room temperature. The cell lysates were immunoblotted for pY223 BTK and pY753 PLCγ2.

    Leukemia, 2017, 31(1):177-185. Ibrutinib (PCI-32765) purchased from Selleck.

    Identification of Btk as a potent kinase for WIP tyrosine phosphorylation. Total protein lysates were prepared from THP-1 cells that were stably transfected with wild-type WIP-EGFP and treated with PCI-32765 at the concentration specified on the blots for 2h before pervanadate treatment for 30 min. In all cases WIP-EGFP was immunoprecipitated from cell lysates using anti-EGFP antibody and membranes subsequently blotted with the pY (4G10) antibody, EGFP antibody and β-Tubulin.

    J Cell Sci 2015 128(2), 251-65. Ibrutinib (PCI-32765) purchased from Selleck.

  • Phosphorylation of ERK1/2 and AKT, but not BTK, was inhibited in sensitive but not resistant MCL cells. Western blotting of BTK phosphorylation. Mantle cell lymphoma (MCL) cells were treated with indicated doses of ibrutinib, cell lysates were collected at 1 or 4 h, and subjected to Western blotting analysis using phosphorylated BTK (p-BTK) (Y223) and total BTK (t-BTK) antibodies.

    Br J Haematol 2014 166(6), 849-61. Ibrutinib (PCI-32765) purchased from Selleck.

    Effect of Ibrutinib on CLEC-2-mediated platelet activation and signaling in humans. Washed human platelets were incubated with Ibrutinib (5 nM) for 5 min followed by stimulation with convulxin (100 ng/ml) or rhodocytin (30 nM) under stirred conditions. Platelet proteins were separated by SDS-PAGE, Western-blotted, and probed for phospho Syk (Tyr525/526) and PLCγ2 (Tyr759). β-actin was used as a lane loading control.

    J Biol Chem 2015 290(18), 11557-68. Ibrutinib (PCI-32765) purchased from Selleck.

  • BTK is expressed by malignant plasma cells and ibrutinib induces cytotoxicity in MM patient cells. (A) BTK mRNA and protein expression in control B-cells and MM patient cells and MM cell lines as measured by real-time PCR and Western blotting. (B) MM cells (n = 11) were treated with two doses of ibrutinib (1 and 10 μM), bortezomib (10 and 20 nM) and lenalidomide (1 and 10 μM) for 48 h and then assessed for cell death/proliferation by Cell Titer GLO assay. (C and D) MM cell lines were analysed for cell death in response to ibrutinib (1 and 10 μM), bortezomib (10 and 20 nM) and lenalidomide.

    Cell Signal 2013 25, 106-12. Ibrutinib (PCI-32765) purchased from Selleck.

    Ibrutinib induces increased cytotoxicity in combination with lenalidomide and bortezomib in MM patient cells. (A) MM patient cells were treated wit h various combinations of ibrutinib (1 and 10 μM), bortezomib (10 and 20 nM) and lenalidomide (1 and 10 μM) for 48 h and then assessed for cell death/proliferation by Cell Titer GLO assay. (B) MM cell lines were analysed for cell death in response to various combinations of ibrutinib (1 and 10μM), bortezomib (10 and 20 nM) and lenalidomide. (C) RPMI8226 cells were analysed for cell death in response to ibrutinib (1 and 10μM), bortezomib (20 nM) and lenalidomide (10μM) and combinations thereof, and then analysed for apoptosis using annexin-V/propidium iodide staining and flow cytometry. (D) Primary human monocytes were treated with two doses of ibrutinib (1 and 10 μM) and then in combination with bortezomib (20 nM) and lenalidomide (10 μM) for 48 h and then assessed for cell death/proliferation by Cell Titer GLO assay.

    Cell Signal 2013 25, 106-12. Ibrutinib (PCI-32765) purchased from Selleck.

  • Ibrutinib downregulates anti-apoptotic proteins and induces caspase mediated apoptosis in MM cells. (A) FLIPL , survivin and Bcl- xL mRNA expression was determined in MM patient cells and MM cell lines treated with ibrutinib (10 μM) and bortezomib (20 nM) both alone and in combination. (B) FLIPL protein expression was measured by Western blotting in extracts from RPMI8226 cells treated with ibrutinib (10μM) and bortezomib (20 nM) both alone and in combination for 8 hours. (C) The MM cell line RPMI8226 was treated with the pan caspase inhibitor zVAD-fmk (10 μM) before treatment with ibrutinib (10 μM) and borte zomib (20 nM) both alone and in combination for 48 h and then assessed for cell death/prolife ration by Cell Titer GLO assay.

    Cell Signal 2013 25, 106-12. Ibrutinib (PCI-32765) purchased from Selleck.

    Cell lines were exposed to 0, 50 and 150 mM Ibrutinib for 4 h. The level of phosphorylated ERK1/2 (p-ERK1/2) was reduced in TCF3-rearranged MHH-CALL3 compared with non-TCF3-rearranged Nalm6 and MHH-CALL4 cell lines. b-Actin served as a loading control. P-ERK/b-actin: ratio of the intensities. See Supplementary Materials and methods document for more information.

    Blood Cancer J 2014 4, e181. Ibrutinib (PCI-32765) purchased from Selleck.




製品説明 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.
BTK [1]
(Cell-free assay)
BLK [1]
(Cell-free assay)
Bmx [1]
(Cell-free assay)
CSK [1]
(Cell-free assay)
FGR [1]
(Cell-free assay)
0.5 nM 0.5 nM 0.8 nM 2.3 nM 2.3 nM

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]

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Sf9 cells MWTGeY5kfGmxbjDhd5NigQ>? NXnKXXhiOSCq M13VOGlvcGmkaYTpc44hd2ZiaIXtZY4h\nWubD3s[Y5ofGhiQmTLJIV5eHKnc4Pl[EBqdiCVZkmgZ4VtdHNidYPpcochTkGPLWPyZ5Rq\GVicHXweIll\SCjczDzeYJ{fHKjdHWgZYZ1\XJiNkCgcYlveyCkeTDUVk1HWkWWIFHzd4F697zOIFnDOVA:OC53IH7NMi=> MY[yNVk2QDV2Nx?=
human Pfeiffer cells NXnO[pluTnWwY4Tpc44h[XO|YYm= M{\MWVczKGh? NIjYVIVEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBR\mWrZn\ldkBk\WyuczDhd5Nme3OnZDDhd{Boem:5dHigbY5pcWKrdHnvckBi\nSncjC3NkBpenNiYomgR4VtdFSrdHXyMWdtdyCudX3pcoV{[2WwdDDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2yJI5ONg>? NVnxcWlZOjR7MUWyPVE>
human Ramos cells Moj4SpVv[3Srb36gZZN{[Xl? Ml6yNUBp M1;ZV2lvcGmkaYTpc44hd2ZiQoTrJIlvKGi3bXHuJHJidW:|IHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhWEyFLXfhcY1iOiCyaH;zdIhwenmuYYTpc44h[XRiVInyNVIyPyCjZoTldkAyKGi{IHL5JHdme3Sncn6gZoxwfCCjbnHsfZNqeyxiSVO1NF0yPCCwTT6= NV;XTXVJOjR7MUWyPVE>
Sf9 cells NIjjTHlHfW6ldHnvckBie3OjeR?= NVnK[WxzOSCq Moe0TY5pcWKrdHnvckBw\iCOWV6tRUBmgHC{ZYPz[YQhcW5iU3[5JINmdGy|IHHmeIVzKDZyIH3pcpMh[nliVGKtSnJGXCCDc4PhfUwhUUN3ME2wMlIh|ryPLh?= MX:yNVk2QDV2Nx?=
human DOHH2 cells MVLDfZRwfG:6aXRCpIF{e2G7 NHTJNoI4OiCq M2TmUGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGRQUEh{IHPlcIx{KGG|c3Xzd4VlKGG|IHfyc5d1cCCrbnjpZol1cW:wIHHmeIVzKDd{IHjyd{BjgSCFZXzsWIl1\XJvR3zvJIx2dWmwZYPj[Y51KGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR|UxRTBwNEGg{txONg>? NF7Xe4EzPDlzNUK5NS=>
human SU-DHL6 cells NWXabHh4S3m2b4TvfIlkyqCjc4PhfS=> M1zkOVczKGh? NF;pNodEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUXS2GSFy2JINmdGy|IHHzd4V{e2WmIHHzJIdzd3e2aDDpcohq[mm2aX;uJIFnfGW{IEeyJIhzeyCkeTDD[YxtXGm2ZYKtS4xwKGy3bXnu[ZNk\W62IHPlcIwhfmmjYnnsbZR6KGG|c3H5MEBKSzVyPUCuOVgh|ryPLh?= NY\1fGZjOjR7MUWyPVE>
human WSU-NHL cells NXfvPVl3S3m2b4TvfIlkyqCjc4PhfS=> NEHWdZY4OiCq NX\iO3BCS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hX1OXLV7IUEBk\WyuczDhd5Nme3OnZDDhd{Boem:5dHigbY5pcWKrdHnvckBi\nSncjC3NkBpenNiYomgR4VtdFSrdHXyMWdtdyCudX3pcoV{[2WwdDDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlA6KM7:TR?= NWj2cZF7OjR7MUWyPVE>
human Rec1 cells NEfWVIlHfW6ldHnvckBie3OjeR?= NHTLbJYzNjVizszN MnW3OkBp NXryTIdbUW6qaXLpeIlwdiCxZjDMfY4heGixc4Doc5J6dGG2aX;uJIlvKGi3bXHuJHJm[zFiY3XscJMh[XRiMj61JJVOKGmwY4XiZZRm\CCob4KgOkBpenNiYomgW4V{fGW{bjDicI91fGmwZzDt[ZRpd2R? NHvqUGozPTJ{Mki3Oy=>


体内試験 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]




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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.


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  • 細胞株: Chronic lymphocytic leukemia (CLL) cells
  • 濃度: 0.01-100 μM
  • 反応時間: 48 hours
  • 実験の流れ:

    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.



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  • 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.

溶解度 (25°C)

体外 DMSO 88 mg/mL (199.77 mM)
Ethanol 45 mg/mL (102.15 mM)
Water Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます:
5% DMSO+30% PEG 300+5% Tween 80+ddH2O

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。


分子量 440.5


CAS No. 936563-96-1
別名 N/A





マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)


  • マス




貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積


この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1



  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):




チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2


マス 濃度 ボリューム 分子量


NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02575300 Recruiting Carcinoid Tumors|Pancreatic NET H. Lee Moffitt Cancer Center and Research Institute|Pharmacyclics LLC. October 9, 2015 Phase 2
NCT02973399 Recruiting Cancer Esanex Inc. February 7, 2017 Phase 1
NCT02756897 Recruiting Leukemia|Chronic Lymphocytic Leukemia|Small Lymphocytic Lymphoma M.D. Anderson Cancer Center|AbbVie July 7, 2016 Phase 2
NCT03021460 Recruiting Metastatic Melanoma|Stage III Skin Melanoma|Stage IIIA Skin Melanoma|Stage IIIB Skin Melanoma|Stage IIIC Skin Melanoma|Stage IV Skin Melanoma Mayo Clinic|National Cancer Institute (NCI) January 31, 2017 Phase 2
NCT02514083 Recruiting CLL (Chronic Lymphocytic Leukemia)|SLL (Small Lymphocytic Lymphoma) National Heart, Lung, and Blood Institute (NHLBI)|National Institutes of Health Clinical Center (CC) July 28, 2015 Phase 2
NCT03053440 Recruiting Waldenströms Macroglobulinemia BeiGene January 25, 2017 Phase 3



Handling Instructions


  • * 必須


  • 質問1:

    How to reconstitute the compound S2680 for in vivo studies?

  • 回答:

    For in vivo study, we suggest to use 5% DMSO+30% PEG 300+5% Tween 80+ddH2O up to 10mg/ml.


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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID