Carfilzomib (PR-171) 化学構造
分子量: 719.91



Quality Control & MSDS


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製品説明 Carfilzomib (PR-171) is a proteasome inhibitor with IC50 less than 5 nM.
ターゲット Proteasome
IC50 5 nM [1]
In vitro試験 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 Data
Cell LinesAssay TypeConcentrationIncubation TimeFormulationActivity DescriptionPMID
MM.1S NYDvZ|NQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mnf0NE0yODBibl2= NF7weos1QCCq MlTzTWM2OMLiPdMgNVAhdk1? MnuxNlU{OTJ3NEO=
NCI-H929  Mm\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NILLRZIxNTFyMDDuUS=> Mnq3OFghcA>? MnroTWM2OCB;wrCxOEBvVQ>? NV\We4U{OjV|MUK1OFM>
SUDHL16  M4D6OGFxd3C2b4Ppd{BCe3O|YYm= M1m4blIvPeLCk{OuOUBvVQ>? NULReYNpPDhiaB?= NGTScmVmdmijbnPld{B1cGViY3XscEBl\WG2aDDjc{11emWjdH3lcpQhf2m2aDDBR3kyOjF3 MXyyOVI{QTl|NR?=
SUDHL14 M2ThUmFxd3C2b4Ppd{BCe3O|YYm= MXKyMlXjiJN|LkWgcm0> M3HwTVQ5KGh? NUHFWGZM\W6qYX7j[ZMhfGinIHPlcIwh\GWjdHigZ48ufHKnYYTt[Y51KHerdHigRWN[OTJzNR?= MVSyOVI{QTl|NR?=
U2932 NXLGSJFwSXCxcITvd4l{KEG|c4PhfS=> M{jqeVIvPeLCk{OuOUBvVQ>? MYG0PEBp MVjlcohidmOnczD0bIUh[2WubDDk[YF1cCClbz30doVifG2nboSge4l1cCCDQ2mxNlE2 NYOxdnlMOjV{M{m5N|U>
P-UMSCC-1 NH\OVlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWfJR|UxRTFzLkKgcm0> MWmyOFkyPTB|OR?=
R-UMSCC-1 M{fqWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUP3eGRtUUN3ME2yNlk1KG6P NV3QR4dFOjR7MUWwN|k>
P-Cal33 NGD3T2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1v4eGlEPTB;MUeuN{BvVQ>? MXSyOFkyPTB|OR?=
R-Cal33 Ml25S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmLHTWM2OD1zMUGyJI5O MkLKNlQ6OTVyM{m=
Jurkat NG\SNWZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWH4VoppOS1zMX7N NYHqeGhDPDhiaB?= NVPs[|lYcW6qaXLpeJMhfGinIHPlcIwheHKxbHnm[ZJifGmxbjDjc{11emWjdH3lcpQhf2m2aDD2c5Jqdm:|dHH0 MmCxNlQ5ODFzMki=
Jurkat MV7BdI9xfG:|aYOgRZN{e2G7 NUfjOmx6QCCwTR?= NH7mdWMzPC92ODDo MnfibY5lfWOnczDhdI9xfG:|aYOsJINie3Cjc3WgZYN1cX[jdHnvckwh[W6mIGDBVnAh[2ynYY\h[4Uh[29vdILlZZRu\W62IIfpeIghfm:{aX7vd5RifA>? MnzJNlQ5ODFzMki=
UMSCC-22B MnnURZBweHSxc3nzJGF{e3OjeR?= NGLV[GIzODBibl2= M4PzcVI1KGh? MYHpcoR2[2VidHjlJINmdGxiYYDvdJRwe2m|IHPvMZRz\WG2bXXueEB4cXSqIF;OXEAxQTF{ Mn7MNlI6Ojl6MEO=
1483 MlfHRZBweHSxc3nzJGF{e3OjeR?= NHXPVZYzODBibl2= M4joc|I1KGh? NX7jVIVscW6mdXPlJJRp\SClZXzsJIFxd3C2b4Ppd{Bkdy22cnXheI1mdnRid3n0bEBQVlhiMEmxNi=> MWKyNlkzQThyMx?=
UMSCC-1 NFi4W2tCeG:ydH;zbZMhSXO|c3H5 MWiyNFAhdk1? MnjrNlQhcA>? MWLpcoR2[2VidHjlJINmdGxiYYDvdJRwe2m|IHPvMZRz\WG2bXXueEB4cXSqIF;OXEAxQTF{ M{nrOFIzQTJ7OECz
UMSCC-22A MlfhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYDJR|UxRTN6LkegxtEhOS5yIH7N MlnPNlI6Ojl6MEO=
UMSCC-22B MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVO0VGk2UUN3ME2zNE44KMLzIEmuN{BvVQ>? NVvoSItKOjJ7Mkm4NFM>
1483 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlL3TWM2OD13MD61JOKyKDFzLkmgcm0> MWSyNlkzQThyMx?=
UMSCC-1 NG\2PZJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTN2Lk[gxtEhOi54IH7N NV3ybpZ2OjJ7Mkm4NFM>
Cal33 MkOwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlPlTWM2OD12OT6zJOKyKDhwOTDuUS=> M3:wbVIzQTJ7OECz
PCI-15A NGfxcGlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4jNXmlEPTB;N{CuOEDDuSB{Mj62JI5O M2fuOlIzQTJ7OECz
PCI-15B M4fnbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnL5TWM2OD1|OT61JOKyKDFzLkCgcm0> MkHINlI6Ojl6MEO=
OSC-19 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYnJR|UxRTF6LkOgxtEhPC5{IH7N NUfSdWlZOjJ7Mkm4NFM>
SUDHL16 NHL6bJpHfW6ldHnvckBCe3OjeR?= M4HlVlIvPSCwTR?= Mk\sNlQhcA>? NV7yZ49L[WO2aY\heIV{KEqQSzygbY5i[3SrdnH0[ZMhSUuWLDD1dE1z\We3bHH0[ZMhVm:6YTygZY5lKGmwZIXj[ZMh|rOKMlGuXEBkdy22cnXheI1mdnRid3n0bEBw[mG2b3PsZZg> NFGwcVIzOjRzMUi5PS=>
Granta MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3vFeVAuPCCwTR?= M1jUb|Q5KGh? MUnpcoR2[2ViY3XscEBl\WG2aDDjc{11emWjdH3lcpQhf2m2aDDIRWREUXN? NWnEbnozOjF5NUCyNlQ>
SUDHL16 NXr4ZnpGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV3YPWx1OS12IH7N MXKzOkBp NHzrSVNqdmS3Y3WgZ4VtdCCmZXH0bEBkdy22cnXheI1mdnRid3n0bEBJSUSFSYO= MWeyNFI{Ozl5Mx?=

... Click to View More Cell Line Experimental Data

In vivo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]
臨床試験 Carfilzomib has entered in a Phase II clinical trial in the treatment of multiple myeloma.

プロトコル (参考用のみ)

キナーゼアッセイ: [1]

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.

細胞アッセイ: [1]

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.

動物実験: [4]

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.

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 Carfilzomib (PR-171) SDF
分子量 719.91


CAS No. 868540-17-4
保管 2年-20℃
6月-80℃in solvent
別名 N/A
溶解度 (25°C) * In vitro DMSO 50 mg/mL (69.45 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 L-Phenylalaninamide, (αS)-α-[[2-(4-morpholinyl)acetyl]amino]benzenebutanoyl-L-leucyl-N-[(1S)-3-methyl-1-[[(2R)-2-methyl-2-oxiranyl]carbonyl]butyl]-

カスタマーフィードバック (3)

Click to enlarge
Source Sci Transl Med, 2014, 6(250), 250ra112. Carfilzomib (PR-171) purchased from Selleck
Method Western blot
Cell Lines Primary myoblasts
Concentrations 5, 10 nM
Incubation Time 24 h
Results To demonstrate that treatment with proteasome inhibitors other than bortezomib can also salvage missense mutated dysferlin, we treated primary myoblasts from patient 2 with either the irreversible proteasome inhibitor carfilzomib, which is the biologically active, hydrolyzed form of the investigational, reversible proteasome inhibitor ixazomib (MLN9708) being developed for oral application. It found that treatment with carfilzomib resulted in a dose-dependent increase in dysferlin expression.

Click to enlarge
Source Cancer Res, 2014, 74(16), 4458-69. Carfilzomib (PR-171) purchased from Selleck
Method Western blot
Cell Lines MM.1S cells
Concentrations 10 nM
Incubation Time 24 h
Results CHOP expression was induced by carfilzomib indicating ER stress, which was enhanced by TAS-117 and associated with enhanced PARP cleavage.

Click to enlarge
Source J Virol, 2013, 87(23), 13035-41. Carfilzomib (PR-171) purchased from Selleck
Method Flow cytometry
Cell Lines HeLa cells
Concentrations 1 uM
Incubation Time 24 h
Results The Carfilzomib enhanced the fluorescence of Hela cells, obviously.

文献中の引用 (15)



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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID