Carfilzomib (PR-171)


Carfilzomib (PR-171)化学構造


Carfilzomib (PR-171) is an irreversible proteasome inhibitor with IC50 of <5 nM in ANBL-6 cells, displayed preferential in vitro inhibitory potency against the ChT-L activity in the β5 subunit, but little or no effect on the PGPH and T-L activities.

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  • Validation of activity and specificity of chemical inhibitors of; ATM, ATR, and DNAPK. H460 cells were treated with 1 uM camptothecin (CPT) or 20 ug/ml bleomycin for 1 h in the presence of the indicated inhibitors: DNAPK-i1—NU7026, DNAPK-i2—NU7441. MSH6,

    Sci Transl Med 2014 6(250), 250ra112. Carfilzomib (PR-171) purchased from Selleck.

    MM.1S cells were treated with or without carfilzomib (10 nM) in the presence or absence of TAS-117 (0.5 uM) for 24 h. Whole cell lysates were subjected to western blotting using CHOP, PARP, and GAPDH Abs.The graph represents fold changes of CHOP density relative to GAPDH.

    Cancer Res 2014 74(16), 4458-69. Carfilzomib (PR-171) purchased from Selleck.

  • Transduction at 24 h is indicated as normalized luciferase activity. HeLa cells were cotreated with 1 uM Carfilzomib and 500 vg/cell rAAV2-EGFP, and transduction was analyzed by flow cytometry at 24 h. Bright-field and EGPF fluorescence images at 24 h postransduction of cells visually indicating transduction.

    J Virol 2013 87(23), 13035-41. Carfilzomib (PR-171) purchased from Selleck.




製品説明 Carfilzomib (PR-171) is an irreversible proteasome inhibitor with IC50 of <5 nM in ANBL-6 cells, displayed preferential in vitro inhibitory potency against the ChT-L activity in the β5 subunit, but little or no effect on the PGPH and T-L activities.
Proteasome [1]
(ANBL-6 cells)
5 nM

Carfilzomib inhibits proliferation in a variety of cell lines and patient-derived neoplastic cells, including multiple myeloma, and induced intrinsic and extrinsic apoptotic signaling pathways and activation of c-Jun-N-terminal kinase (JNK). Carfilzomib reveals enhanced anti-MM activity compared with bortezomib, overcome resistance to bortezomib and other agents, and acts synergistically with dexamethasone (Dex). Carfilzomib shoes preferential in vitro inhibitory potency against the ChT-L activity in the β5 subunit, with over 80% inhibition at doses of 10 nM. Short exposure to low-dose Carfilzomib leads to preferential binding specificity for the β5 constitutive 20S proteasome and the β5i immunoproteasome subunits. Measurement of caspase activity in ANBL-6 cells pulsed with Carfilzomib reveals substantial increases in caspase-8, caspase-9, and caspase-3 activity after 8 hours, giving a 3.2-, 3.9- and 6.9-fold increase, respectively, over control cells after 8 hours. In carfilzomib pulse-treated cells, the mitochondrial membrane integrity is decreased to 41% (Q1 + Q2), compared with 75% in vehicle-treated control cells. [1] In another study, Carfilzomib has also shown preclinical effectiveness against hematological and solid malignancies. [2] Carfilzomib directly inhibits osteoclasts formation and bone resorption. [3]

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MM.1S MmO4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{[3R|AuOTByIH7N MX20PEBp NFHDWlRKSzVywrC9xsAyOCCwTR?= MmT5NlU{OTJ3NEO=
NCI-H929  MljBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXT5U4NUOC1zMECgcm0> M4LE[lQ5KGh? MXrJR|UxKD4EoEG0JI5O MYmyOVMyOjV2Mx?=
SUDHL16  MXzBdI9xfG:|aYOgRZN{e2G7 M1;4VlIvPeLCk{OuOUBvVQ>? NXPxR5gxPDhiaB?= NEHWfI9mdmijbnPld{B1cGViY3XscEBl\WG2aDDjc{11emWjdH3lcpQhf2m2aDDBR3kyOjF3 Mn\LNlUzOzl7M{W=
U2932 M1;UWmFxd3C2b4Ppd{BCe3O|YYm= MofXNk426oDVMz61JI5O M372bVQ5KGh? MU\lcohidmOnczD0bIUh[2WubDDk[YF1cCClbz30doVifG2nboSge4l1cCCDQ2mxNlE2 NF3UVZczPTJ|OUmzOS=>
P-UMSCC-1 NVjsN24zT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnPmTWM2OD1zMT6yJI5O NX60T3dlOjR7MUWwN|k>
R-UMSCC-1 NFTDc|RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3z5NGlEPTB;MkK5OEBvVQ>? MmTvNlQ6OTVyM{m=
P-Cal33 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MorwTWM2OD1zNz6zJI5O Ml7mNlQ6OTVyM{m=
R-Cal33 NU\UfIJxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXm0[5d1UUN3ME2xNVEzKG6P NWH3cYpxOjR7MUWwN|k>
Jurkat MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4i4flEuOTGwTR?= M4mzVlQ5KGh? NXXJU5UxcW6qaXLpeJMhfGinIHPlcIwheHKxbHnm[ZJifGmxbjDjc{11emWjdH3lcpQhf2m2aDD2c5Jqdm:|dHH0 MlPoNlQ5ODFzMki=
Jurkat M2KyZ2Fxd3C2b4Ppd{BCe3O|YYm= MYW4JI5O MnjDNlQwPDhiaB?= M3rkfolv\HWlZYOgZZBweHSxc3nzMEBk[XOyYYPlJIFkfGm4YYTpc44tKGGwZDDQRXJRKGOuZXH2ZYdmKGOxLYTy[YF1dWWwdDD3bZRpKH[xcnnuc5N1[XR? NEe1PXAzPDhyMUGyPC=>
UMSCC-22A MkG2RZBweHSxc3nzJGF{e3OjeR?= MWWyNFAhdk1? NH\vfIkzPCCq NXX5[WpjcW6mdXPlJJRp\SClZXzsJIFxd3C2b4Ppd{Bkdy22cnXheI1mdnRid3n0bEBQVlhiMEmxNi=> MUOyNlkzQThyMx?=
UMSCC-22B Mm[4RZBweHSxc3nzJGF{e3OjeR?= NHTBNY4zODBibl2= NV;1[2U4OjRiaB?= MWLpcoR2[2VidHjlJINmdGxiYYDvdJRwe2m|IHPvMZRz\WG2bXXueEB4cXSqIF;OXEAxQTF{ NIDa[oIzOjl{OUiwNy=>
1483 MX7BdI9xfG:|aYOgRZN{e2G7 MWeyNFAhdk1? NVPRWZBuOjRiaB?= MXPpcoR2[2VidHjlJINmdGxiYYDvdJRwe2m|IHPvMZRz\WG2bXXueEB4cXSqIF;OXEAxQTF{ MYmyNlkzQThyMx?=
UMSCC-1 NWq1SppPSXCxcITvd4l{KEG|c4PhfS=> M13E[FIxOCCwTR?= NYP4V4RbOjRiaB?= MYLpcoR2[2VidHjlJINmdGxiYYDvdJRwe2m|IHPvMZRz\WG2bXXueEB4cXSqIF;OXEAxQTF{ MlzXNlI6Ojl6MEO=
UMSCC-22A NY\ZeIRLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGq0SnVKSzVyPUO4MlchyrFiMT6wJI5O NV36WY1uOjJ7Mkm4NFM>
UMSCC-22B M4jQT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3rTbGlEPTB;M{CuO{DDuSB7LkOgcm0> MXWyNlkzQThyMx?=
1483 NEfMOXNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUTVdZZ2UUN3ME21NE42KMLzIEGxMlkhdk1? MXOyNlkzQThyMx?=
Cal33 NXf1ZWhiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkfRTWM2OD12OT6zJOKyKDhwOTDuUS=> NYDrPHpSOjJ7Mkm4NFM>
PCI-15A NGX3T3NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU\peY96UUN3ME23NE41KMLzIEKyMlYhdk1? M4jTW|IzQTJ7OECz
PCI-15B MlPiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFTuPGpKSzVyPUO5MlUhyrFiMUGuNEBvVQ>? NELDXYQzOjl{OUiwNy=>
OSC-19 NVPqUI1wT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlfaTWM2OD1zOD6zJOKyKDRwMjDuUS=> MmK4NlI6Ojl6MEO=
SUDHL16 NVH5WWlzSXCxcITvd4l{KEG|c4PhfS=> MX6yMlAuPC5yIH7N Ml;3OFghcA>? MUPpcoR2[2W|IHPlcIwh\GWjdHigZ48ufHKnYYTt[Y51KHerdHigc4JifG:lbHH4 M4niOlIzPDFzOEm5
SUDHL16 M4\mU2Z2dmO2aX;uJGF{e2G7 MljhNk42KG6P NITvNVQzPCCq MXzhZ5RqfmG2ZYOgTm5MNCCrbnHjeIl3[XSnczDBT3QtKHWyLYLl[5Vt[XSnczDOc5hiNCCjbnSgbY5lfWOnczFOt2gzSS6[IHPvMZRz\WG2bXXueEB4cXSqIH;iZZRw[2yjeB?= NFzXe5czOjRzMUi5PS=>
Granta NEHoNHlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2[3XVAuPCCwTR?= MUi0PEBp NULSd5RXcW6mdXPlJINmdGxiZHXheIgh[29vdILlZZRu\W62IIfpeIghUEGGQ1nz MVWyNVc2ODJ{NB?=
SUDHL16 NFrkbJNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{T4WFEuPCCwTR?= M3T3e|M3KGh? NGX0dWRqdmS3Y3WgZ4VtdCCmZXH0bEBkdy22cnXheI1mdnRid3n0bEBJSUSFSYO= MkP6NlAzOzN7N{O=


体内試験 Carfilzomib moderately reduces tumor growth in an in vivo xenograft model. Carfilzomib effectively decreases multiple myeloma cell viability following continual or transient treatment mimicking. Carfilzomib increases trabecular bone volume, decreases bone resorption and enhances bone formation in non-tumor bearing mice. [3]


+ 展開

Enzyme-linked immunosorbent assay for subunit profiling of carfilzomib:

ANBL-6 cells (2 × 106/well) are plated in 96-well plates and treated with Carfilzomib doses from 0.001 to 10 μM for 1 hour. Cells are then lysed (20 mM Tris-HCl, 0.5 mM EDTA), and cleared lysates are transferred to polymerase chain reaction (PCR) plates. A standard curve is generated using untreated ANBL-6 cell lysates starting at a concentration of 6 μg protein/μL. The active site probe [biotin-(CH2)4-Leu-Leu-Leu-epoxyketone; 20 μM] is added and incubated at room temperature for 1 hour. Cell lysates are then denatured by adding 1% sodium dodecyl sulfate (SDS) and heating to 100°C, followed by mixing with 20 μL per well streptavidin-sepharose high-performance beads in a 96-well multiscreen DV plate and incubated for 1 hour. These beads are then washed with enzyme-linked immunosorbent assay (ELISA) buffer (PBS, 1% bovine serum albumin, and 0.1% Tween-20), and incubated overnight at 4°C on a plate shaker with antibodies to proteasome subunits. Antibodies used included mouse monoclonal anti-β1, anti-β2, anti-β1i, and anti-β5i, goat polyclonal anti-β2i, and rabbit polyclonal anti-β5 (affinity-purified antiserum against KLH-CWIRVSSDNVADLHDKYS peptide). The beads are washed and incubated for 2 hours with horseradish peroxidase-conjugated secondary goat antirabbit, goat antimouse or rabbit antigoat antibodies. After washing, the beads are developed using the supersignal ELISA picochemiluminescence substrate. Luminescent detection is performed. Raw luminescence is converted to μg/mL by comparison with the standard curve and expressed as the % inhibition relative to vehicle control. Curve fits are generated using the following nonsigmoidal dose-response equation: Y = Bottom + (Top-Bottom)/(1 + 10̂((LogEC50 − X) × HillSlope)), where X is the logarithm of concentration, Y is the % inhibition, and EC50 is the dose showing 50% effect.
細胞試験: [1]
+ 展開
  • 細胞株: WST-1, ANBL-6 cells
  • 濃度: 100 nM
  • 反応時間: 1 hour
  • 実験の流れ: WST-1 is used to determine the effects of proteasome inhibitor Carfilzomib on cell proliferation. The inhibition of proliferation is calculated in relation to parallel control cells that receives vehicle alone. A linear spline function is used to interpolate the median inhibitory concentration (IC50) using XLfit 4 software. The degree of resistance (DOR) is calculated using the formula: DOR = IC50(resistant cells)/IC50(sensitive cells). ANBL-6 cells pulsed with 100 nM carfilzomib are washed and suspended in PBS containing 5 μg/mL of JC-1, which exhibits potential-dependent accumulation in mitochondria. Analysis of the mitochondrial membrane potential-dependent color shift from 525 to 590 nm is carried out on a FacScan, and the data are analyzed with CellQuest software.
+ 展開
  • 動物モデル: Beige-nude-XID mice
  • 製剤: 10% sulfobutylether β-cyclodextrin in 10 mmol/L citrate buffer pH 3.5,
  • 投薬量: 2.0 mg/kg
  • 投与方法: i.v.

溶解度 (25°C)

体外 DMSO 50 mg/mL (69.45 mM)
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます:
2% DMSO+30% PEG 300+2%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 719.91


CAS No. 868540-17-4
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
NCT02802163 Not yet recruiting Multiple Myeloma H. Lee Moffitt Cancer Center and Research Institute|Novartis|Amgen April 30, 2017 Phase 1|Phase 2
NCT01402284 Active, not recruiting Multiple Myeloma National Cancer Institute (NCI)|Celgene|Onyx Therapeutics, Inc.|National Institutes of Health Clinical Center (CC) July 21, 2011 Phase 2
NCT03031730 Not yet recruiting Hypercalcemia|Plasmacytoma|Recurrent Plasma Cell Myeloma|Refractory Plasma Cell Myeloma National Cancer Institute (NCI) October 2017 Phase 1
NCT03029234 Not yet recruiting Relapsed and Refractory Multiple Myeloma Amgen|Onyx Therapeutics, Inc. February 2017 Phase 3
NCT02891811 Not yet recruiting Multiple Myeloma Arbeitsgemeinschaft medikamentoese Tumortherapie|Amgen January 2017 Phase 2
NCT03004287 Not yet recruiting Multiple Myeloma University of Arkansas|Janssen, LP January 2017 Phase 2



Handling Instructions


  • * 必須


  • 質問1:

    How should I prepare solution of Carfilzomib for ongoing in vivo study?

  • 回答:

    This compound can be dissolved in 2% DMSO/30% PEG 300/dd H2O at 10 mg/ml as a suspension, and can be dissolved in 2% DMSO/ castor oil at 10 mg/ml as a clear solution.


Proteasome Inhibitors with Unique Features


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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