Carfilzomib (PR-171)

Catalog No.S2853

Carfilzomib (PR-171) Chemical Structure

Molecular Weight(MW): 719.91

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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Cited by 40 Publications

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Biological Activity

Description 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.
Targets
Proteasome [1]
(ANBL-6 cells)
5 nM
In vitro

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 Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
MM.1S MkfFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M364eVAuOTByIH7N MXy0PEBp NXvOTnB{UUN3MNMgQeKhOTBibl2= NXHnPIFNOjV|MUK1OFM>
NCI-H929  M4TXbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHX3XIExNTFyMDDuUS=> MYC0PEBp MkDUTWM2OCB;wrCxOEBvVQ>? NVfUSYp2OjV|MUK1OFM>
SUDHL16  MmPqRZBweHSxc3nzJGF{e3OjeR?= NFT6[|IzNjYkgKOzMlUhdk1? NUTCXoVtPDhiaB?= M{[2fYVvcGGwY3XzJJRp\SClZXzsJIRm[XSqIHPvMZRz\WG2bXXueEB4cXSqIFHDXVEzOTV? M320blI2OjN7OUO1
SUDHL14 MnTDRZBweHSxc3nzJGF{e3OjeR?= M4\EPVIvPeLCk{OuOUBvVQ>? NH7DZ2E1QCCq NWnvUWxD\W6qYX7j[ZMhfGinIHPlcIwh\GWjdHigZ48ufHKnYYTt[Y51KHerdHigRWN[OTJzNR?= M{nYeFI2OjN7OUO1
U2932 MmLtRZBweHSxc3nzJGF{e3OjeR?= M3O3NVIvPeLCk{OuOUBvVQ>? MmDFOFghcA>? MWnlcohidmOnczD0bIUh[2WubDDk[YF1cCClbz30doVifG2nboSge4l1cCCDQ2mxNlE2 NVT0TVhzOjV{M{m5N|U>
P-UMSCC-1 M{Ttd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2rDOGlEPTB;MUGuNkBvVQ>? MViyOFkyPTB|OR?=
R-UMSCC-1 MmfwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlvyTWM2OD1{Mkm0JI5O MUGyOFkyPTB|OR?=
P-Cal33 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYDJR|UxRTF5LkOgcm0> NHzo[JgzPDlzNUCzPS=>
R-Cal33 Mo\5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3ntcGlEPTB;MUGxNkBvVQ>? MoHzNlQ6OTVyM{m=
Jurkat MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVixMVEydk1? NXrHOmdOPDhiaB?= NF63c5pqdmirYnn0d{B1cGViY3XscEBxem:uaX\ldoF1cW:wIHPvMZRz\WG2bXXueEB4cXSqII\vdolvd3O2YYS= NGf4SYwzPDhyMUGyPC=>
Jurkat NU\RcVdKSXCxcITvd4l{KEG|c4PhfS=> MY[4JI5O MX:yOE81QCCq NFTHe2lqdmS3Y3XzJIFxd3C2b4Ppd{wh[2G|cHHz[UBi[3SrdnH0bY9vNCCjbnSgVGFTWCClbHXheoFo\SClbz30doVifG2nboSge4l1cCC4b4Lpco9{fGG2 M1n4fFI1QDBzMUK4
UMSCC-22A NG\UN|ZCeG:ydH;zbZMhSXO|c3H5 MVOyNFAhdk1? M2C1flI1KGh? Ml;JbY5lfWOnIITo[UBk\WyuIHHwc5B1d3OrczDjc{11emWjdH3lcpQhf2m2aDDPUnghODlzMh?= MX[yNlkzQThyMx?=
UMSCC-22B M1HJfmFxd3C2b4Ppd{BCe3O|YYm= MlHGNlAxKG6P MmTzNlQhcA>? MULpcoR2[2VidHjlJINmdGxiYYDvdJRwe2m|IHPvMZRz\WG2bXXueEB4cXSqIF;OXEAxQTF{ Ml\ENlI6Ojl6MEO=
1483 M3;ERWFxd3C2b4Ppd{BCe3O|YYm= NHTU[pQzODBibl2= NFLOepEzPCCq M{m0WIlv\HWlZTD0bIUh[2WubDDhdI9xfG:|aYOgZ48ufHKnYYTt[Y51KHerdHigU25ZKDB7MUK= MUCyNlkzQThyMx?=
UMSCC-1 Ml:1RZBweHSxc3nzJGF{e3OjeR?= NWHSb4JIOjByIH7N NYjQNVRPOjRiaB?= NFuyPYJqdmS3Y3WgeIhmKGOnbHygZZBweHSxc3nzJINwNXS{ZXH0cYVvfCC5aYToJG9PYCByOUGy NWi5RmROOjJ7Mkm4NFM>
UMSCC-22A NXLrZ|NNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn;GTWM2OD1|OD63JOKyKDFwMDDuUS=> MkPGNlI6Ojl6MEO=
UMSCC-22B M3nnPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEP6W2JKSzVyPUOwMlchyrFiOT6zJI5O NHvxRXEzOjl{OUiwNy=>
1483 NVXVbpRZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1u0RWlEPTB;NUCuOUDDuSBzMT65JI5O Mn[yNlI6Ojl6MEO=
UMSCC-1 MlvXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWHPbm03UUN3ME2zOE43KMLzIEKuOkBvVQ>? M4jLdlIzQTJ7OECz
Cal33 M4j3eWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWDUSotDUUN3ME20PU4{KMLzIEiuPUBvVQ>? MW[yNlkzQThyMx?=
PCI-15A NUG2PW17T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MknOTWM2OD15MD60JOKyKDJ{Lk[gcm0> MXqyNlkzQThyMx?=
PCI-15B MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUS4XoUzUUN3ME2zPU42KMLzIEGxMlAhdk1? Mo\lNlI6Ojl6MEO=
OSC-19 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MonxTWM2OD1zOD6zJOKyKDRwMjDuUS=> MnnHNlI6Ojl6MEO=
SUDHL16 NUTSUmRXSXCxcITvd4l{KEG|c4PhfS=> MkHFNk4xNTRwMDDuUS=> M4nCeFQ5KGh? NWPzR2p3cW6mdXPld{Bk\WyuIHTlZZRpKGOxLYTy[YF1dWWwdDD3bZRpKG:kYYTvZ4xigA>? MmP1NlI1OTF6OUm=
SUDHL16 NIf2[W1HfW6ldHnvckBCe3OjeR?= NW\YOVlnOi53IH7N MnXlNlQhcA>? M4fpV4FkfGm4YYTld{BLVktuIHnuZYN1cX[jdHXzJGFMXCxidYCtdoVofWyjdHXzJG5wgGFuIHHu[EBqdmS3Y3XzJO6{UDKDLmigZ48ufHKnYYTt[Y51KHerdHigc4JifG:lbHH4 NVWzTmlqOjJ2MUG4PVk>
Granta MlPQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYW4U2RXOC12IH7N NEezenE1QCCq NFX3dWtqdmS3Y3WgZ4VtdCCmZXH0bEBkdy22cnXheI1mdnRid3n0bEBJSUSFSYO= MlXVNlE4PTB{MkS=
SUDHL16 MojLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnTyNU01KG6P MWezOkBp NEKxR4JqdmS3Y3WgZ4VtdCCmZXH0bEBkdy22cnXheI1mdnRid3n0bEBJSUSFSYO= NEfiW|EzODJ|M{m3Ny=>

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
pERK / ERK / pSTAT5 / STAT5 / pPI3K / PI3K; 

PubMed: 24590311     


Western blot analysis for activated (phosphorylated) ERK, Stat5 and PI3K signaling pathways following exposure to carfilzomib, total levels of ERK, Stat5 and PI3K were used as a loading control.

caspase-9 / caspase-8; 

PubMed: 24590311     


Western blot analysis for activated (cleaved) caspase-8 and caspase-9 following exposure to carfilzomib.

c-PARP / PARP / caspase-3; 

PubMed: 22929803     


UMSCC-22A, UMSCC-22B, 1483 and UMSCC-1 cells were treated for 24 hours with 0.1% DMSO, or 200 nmol/L carfilzomib or ONX 0912, followed by immunoblotting with anti-PARP, anti-caspase-3, or anti-β-actin. Shown are full-length PARP, cleaved PARP (c-PARP), and the cleaved, active subunits of caspase-3. Similar results were obtained in 3 independent experiments.

Bcl-2 / Bcl-Xl / Mcl-1 / Bik / Bim / Bax / Bak; 

PubMed: 22929803     


UMSCC-22A, UMSCC-22B, 1483 and UMSCC-1 cells were treated for 24 hours with 0.1% DMSO, or 100 nmol/L carfilzomib or ONX 0912, followed by immunoblotting for the indicated proteins. In the case of Bik immunoblotting, cells were treated with 200 nmol/L carfilzomib or ONX 0912 to more clearly demonstrate Bik upregulation in 1483 and UMSCC-1 cells. Blots shown are representative of 3 independent experiments. 

Atg5 / Atg12 / Beclin-1 / LC3-II; 

PubMed: 22929803     


HNSCC cells were treated for 24 hours with 100 nmol/L carfilzomib or ONX 0912, or with 0.1% DMSO. Immunoblots were probed for Beclin-1, Atg5/12 conjugate, LC3-II, or β-actin. Representative blots from 3 independent experiments are shown. 

Noxa / Bik / Puma / Mcl-1; 

PubMed: 25548100     


SW620 cells were treated with the indicated dosage for 48 h. Expression of Noxa, Bik and/or Puma, c-myc and Mcl-1 proteins was then analyzed by immunoblotting. Tubulin served as control for protein loading. 

EGFR / HER2 / ER alpha / p-Akt(Ser473) / Akt / p-ERK / ERK / p53; 

PubMed: 29069787     


T47D and MCF7 cells were cultured with the indicated carfilzomib concentrations for 32 or 36 hours, respectively. Western blots of protein lysates were probed with the indicated antibodies. β-actin served as loading control.

BDP1 / HER2(Tyr1248) / HER2(Tyr1221/Tyr1222) / PARP1 / caspase-7 / p53 Mut; 

PubMed: 29069787     


BT474 cells were cultured in the presence of the indicated carfilzomib concentrations for 32 hours. Western blots of protein lysates were probed with the indicated antibodies.

HLA class I; 

PubMed: 26323098     


Immunofluorescence analysis was performed to confirm the consequence that down-regulation of HLA class I was in a dose- and time-dependent manner.

24590311 22929803 25548100 29069787 26323098
Growth inhibition assay
Cell viability; 

PubMed: 27655642     


Cytotoxic effects of carfilzomib on breast cancer cells in MTT assays. Seven human breast cancer cell lines, MCF7, T-47D, MDA-MB-361, HCC1954, MDA-MB-468, MDA-MB-231, and BT-549 were treated with carfilzomib at 0, 0.001 μM, 0.01 μM, 0.05 μM, 0.1 μM, 1 μM, 10 μM, or 50 μM for 72 h, then subjected to MTT assays. The absorbance of each well was measured at 540 nm and plotted for the cell viability curve. IC50 values of carfilzomib in breast cancer cell lines were listed.

27655642
In vivo 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]

Protocol

Kinase Assay:[1]
+ Expand

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.
Cell Research:[1]
+ Expand
  • Cell lines: WST-1, ANBL-6 cells
  • Concentrations: 100 nM
  • Incubation Time: 1 hour
  • Method: 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.
    (Only for Reference)
Animal Research:[4]
+ Expand
  • Animal Models: Beige-nude-XID mice
  • Formulation: 10% sulfobutylether β-cyclodextrin in 10 mmol/L citrate buffer pH 3.5,
  • Dosages: 2.0 mg/kg
  • Administration: i.v.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 50 mg/mL (69.45 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2%Tween 80+ddH2O
For best results, use promptly after mixing. 		1mg/mL

* 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 Information

Molecular Weight 719.91
Formula

C40H57N5O7
CAS No. 868540-17-4
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03673826 Recruiting Drug: Carfilzomib|Drug: Dexamethasone|Drug: Lenalidomide Smouldering Myeloma Stichting Hemato-Oncologie voor Volwassenen Nederland November 19 2018 Phase 2
NCT03336073 Recruiting Drug: Carfilzomib|Drug: Dexamethasone|Drug: cyclophosphamide Multiple Myeloma PETHEMA Foundation December 18 2017 Phase 2
NCT03091127 Recruiting -- Multiple Myeloma Amgen March 14 2017 --

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Frequently Asked Questions

  • Question 1:

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

  • Answer:

    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.

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Proteasome Signaling Pathway Map

Proteasome Inhibitors with Unique Features

  • Pan Proteasome Inhibitor

    Ixazomib (MLN2238) : β5 site, IC50=3.4 nM; β1 site, IC50=31 nM; β2 site, IC50=3500 nM.

  • Most Potent Proteasome Inhibitor

    Bortezomib (PS-341) : 20S proteasome, Ki of 0.6 nM.

  • Newest Proteasome Inhibitor

    Oprozomib (ONX 0912) : Orally bioavailable inhibitor for CT-L activity of 20S proteasome β5/LMP7 with IC50 of 36 nM/82 nM.

Related Proteasome Products

  • VR23 New

    VR23 is a potent proteasome inhibitor with IC50 of 1 nM, 50-100 nM, and 3 μM for trypsin-like proteasomes, chymotrypsin-like proteasomes, and caspase-like proteasomes, respectively.

  • Calpeptin New

    Calpeptin is a potent, cell-permeable calpain inhibitor with ID50 of 52 nM, 34 nM, 138 nM, and 40 nM for Calpain I (porcine erythrocytes), Calpain II (porcine kidney), Papainb, and Calpain I (human platelets), respectively.

  • Marimastat (BB-2516) New

    Marimastat (BB-2516) is a broad spectrum matrix metalloprotease (MMP) inhibitor for MMP-9, MMP-1, MMP-2, MMP-14 and MMP-7 with IC50 of 3 nM, 5 nM, 6 nM, 9 nM and 13 nM, respectively. Phase 3.

  • MG-132

    MG132 is a potent cell-permeable proteasome and calpain inhibitor with IC50s of 0.1 and 1.2 μM for the inhibition of proteasome and calpain, respectively.

  • Bortezomib (PS-341)

    Bortezomib (PS-341) is a potent 20S proteasome inhibitor with Ki of 0.6 nM. It exhibits favorable selectivity towards tumor cells over normal cells.

  • Ixazomib (MLN2238)

    MLN2238 inhibits the chymotrypsin-like proteolytic (β5) site of the 20S proteasome with IC50 and Ki of 3.4 nM and 0.93 nM in cell-free assays, respectively, also inhibits the caspase-like (β1) and trypsin-like (β2) proteolytic sites, with IC50 of 31 and 3500 nM. Phase 3.

    Features:A first-in-class proteasome inhibitor that has improved pharmacokinetics (PK), pharmacodynamics(PD), and antitumor activity in preclinical studies.

  • Ixazomib Citrate (MLN9708)

    Ixazomib Citrate (MLN9708) immediately hydrolyzed to MLN2238, the biologically active form, on exposure to aqueous solutions or plasma. MLN2238 inhibits the chymotrypsin-like proteolytic (β5) site of the 20S proteasome with IC50/Ki of 3.4 nM/0.93 nM in cell-free assays, less potent to β1 and little activity to β2. Phase 3.

    Features:The 1st oral proteasome inhibitor in early stage clinical trials for Multiple Myeloma.

  • Celastrol

    Celastrol is a potent proteasome inhibitor for the chymotrypsin-like activity of a purified 20S proteasome with IC50 of 2.5 μM.

    Features:A potent antioxidant and anti-inflammatory drug.

  • Oprozomib (ONX 0912)

    Oprozomib (ONX 0912) is an orally bioavailable inhibitor for CT-L activity of 20S proteasome β5/LMP7 with IC50 of 36 nM/82 nM. Phase 1/2.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID