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Bortezomib (Velcade)

Bortezomib is a potent 20S proteasome inhibitor with Ki of 0.6 nM.

Catalog No.S1013
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Bortezomib (Velcade) Chemical Structure
Molecular Weight: 384.24

Validation & Quality Control

Product Citations(53)

Customer Reviews(12)

Quality Control & MSDS

Related Compound Libraries

Bortezomib (Velcade) is available in the following compound libraries:

Cambridge Cancer Compound Library(96-well) Chemical Library (96-well) Chemotherapeutic Agent Library (96-well) FDA Approved Drug Library (96-well) Inhibitor Library (96-well)

Products used with Bortezomib (Velcade) in previous publications

Targets Related Products References Purpose
HDAC inhibitors Vorinostat (SAHA) [1][2][3] The combination of the HDAC inhibitors with the Proteasome inhibitors sharply increases apoptosis in various cancer cell lines and exerts synergistic antiproliferative effects.
ACY-1215 [4]
PCI-24781 [5]
Belinostat [6]
DNA/RNA Synthesis inhibitors Cisplatin [7][8][9] The combination of the Proteasome inhibitor Bortezomib with the DNA/RNA synthesis inhibitors, including Cisplatin and Oxaliplatin, results in synergistic induction of apoptosis, and significant reduction in tumor volume and weight in vivo.
Oxaliplatin [14]
Topoisomerase inhibitors Doxorubicin [10] The combination of the proteasome inhibitor Bortezomib with the topoisomerase inhibitors Doxorubicin and Topotecan causes a significant reduction of tumor growth compared to individual drugs alone.
Topotecan [15]
Proteasome inhibitors MG-132 [16][7][18] Positive Control. Compared to the Proteasome inhibition potency of Bortezomib, MG-132, and Carfilzomib.
Carfilzomib [19]

Product Information

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Product Description

Biological Activity Protocol Chemical Information Customer Reviews Product Citations Tech Support & FAQs

Biological Activity

Description Bortezomib is a potent 20S proteasome inhibitor with Ki of 0.6 nM.
Targets 20S proteasome
IC50 0.6 nM (Ki) [1]
In vitro Bortezomib, a boronic acid dipeptide, is a highly selective, reversible inhibitor of the 26S proteasome which primarily functions in the degradation of mis-folded proteins and is essential for the regulation of the cell cycle. Exposure to Bortezomib has been shown to stabilize p21, p27, and p53, as well as the proapoptotic Bid and Bax proteins, caveolin-1, and inhibitor κB-α, which prevents activation of nuclear factor κB-induced cell survival pathways. Bortezomib also promots the activation of the proapoptotic c-Jun-NH2 terminal kinase, as well as the endoplasmic reticulum stress response. Alteration of the levels of these cellular proteins leads to inhibition of proliferation, migration, and promotion of apoptosis of cancer cells. [2] Bortezomib is shown to penetrate into cells and inhibit proteasome-mediated intracellular proteolysis of long-lived proteins with a concentration that inhibits 50% of the proteolysis of ∼0.1 μM. The average growth inhibition of 50% value for Bortezomib across the entire panel of 60 cancer cell lines derived from multiple human tumors from the US National Cancer Institute (NCI) is 7 nM. Treatment of PC-3 cells with Bortezomib (100 nM) for 8 h results in the accumulation of cells in G2-M, with a corresponding decrease in the number of cells in G1. Bortezomib kills PC-3 cells at 24 and 48 hr with IC50 of 100 and 20 nM, respectively. Bortezomib induces nuclear condensation at 16–24 hr after treatment. Bortezomib treatment leads to PARP cleavage in a time-dependent manner with concentrations as low as 100 nM being effective at 24 hr. [1]
In vivo The anticancer effects of bortezomib as a single agent have been demonstrated in xenograft models of multiple myeloma, adult T-cell leukemia, lung, breast, prostate, pancreatic, head and neck, and colon cancer, and in melanoma. [2] Oral bortezomib 1.0 mg/ kg daily for 18 days causes tumor growth delays, as well as a decrease in the number of metastases in the Lewis lung cancer model. Bortezomib at a single dose of up to 5 mg/kg significantly decreased the surviving fraction of breast tumor cells. Bortezomib 1.0 mg/kg administrated weekly for 4 weeks reduces tumor growth by 60% in murine xenograft models of prostate cancer. 1.0 mg/kg Bortezomib administration for 4 weeks results in a 72% or 84% reduction in pancreatic cancer murine xenografts growth, as well as an increase in tumor cell apoptosis. 1.0 mg/kg Bortezomib treatment results in significant inhibition of human plasmacytoma xenograft growth, increase in tumor cells apoptosis and overall survival, and a decrease in tumor angiogenesis. [3]
Clinical Trials A phase I study of weekly subcutaneous Bortezomib in patients with steroid-refractory or -dependent chronic graft versus host disease is currently in recruiting.
Features

Protocol(Only for Reference)

Kinase Assay: [4]

Kinetic Methods In a typical kinetic run, 2.00 mL of assay buffer (20 mM HEPES, 0.5 mM EDTA, 0.035% SDS, pH 7.8) and Suc-Leu-Leu-Val-Tyr-AMC in DMSO are added to a 3 mL fluorescence cuvette, and the cuvette is placed in the jacketed cell holder of a fluorescence spectrophotometer. Reaction temperature is maintained at 37℃ by a circulating water bath. After the reaction solution has reached thermal equilibrium (5 minutes), 1 μL−10 μL of the stock enzyme solution is added to the cuvette. Reaction progress is monitored by the increase in fluorescence emission at 440 nm (λex= 380 nm) that accompanies cleavage of AMC from peptide-AMC substrates.

Cell Assay: [5]

Cell lines Human multiple myeloma cells line U266
Concentrations ~10 μM
Incubation Time 2 days
Method The inhibitory effect of Bortezomib on cell growth is assessed by measuring MTT dye absorbance of the cells. Cells from 48-hour cultures are pulsed with 10 μL of 5 mg/mL MTT to each well for the last 4 hour of 48-hour cultures, followed by 100 μL of isopropanol containing 0.04 N HCl. Absorbance is measured at 570 nm using a spectrophotometer.

Animal Study: [3]

Animal Models Human plasmacytoma xenografts RPMI 8226
Formulation Saline
Dosages 1 mg/kg
Administration i.v. twice weekly for 4 weeks, then once weekly
1

References

Chemical Information

Download Bortezomib (Velcade) SDF
Molecular Weight (MW) 384.24
Formula

C19H25BN4O4
CAS No. 179324-69-7
Synonyms MG-341, PS-341
Solubility (25°C)
  • DMSO 77 mg/mL
  • Water <1 mg/mL
  • Ethanol <1 mg/mL
Storage 2 years -20°CPowder
2 weeks4°Cin DMSO
6 months-80°Cin DMSO
Chemical Name
Molarity Calculator Dilution Calculator Molecular Weight Calculator

Research Area

Customer Reviews (12)


Click to enlarge 		Rating
Source PLoS One, 2011, 6(8), e23712.?. Bortezomib (Velcade) purchased from Selleck
Method Western blotting
Cell Lines HEK293 cells
Concentrations 50 μM
Incubation Time 4 h
Results upon proteasome inhibition by Bortezomib an increased amount of around 5–6 fold of biotinylated molecules was detected, both in the absence and presence of US2 and US11.

Click to enlarge 		Rating
Source Carcinogenesis , 2010, 31, 1948–1955. Bortezomib (Velcade) purchased from Selleck
Method Luciferase assay
Cell Lines LNCaP-AI cells, LNCaP cells
Concentrations 20 μM
Incubation Time 24 h
Results EGF significantly stimulates the promoter activity of sPLA2-IIa gene in both LNCaP and LNCaP-AI cells (shown in LNCaP-AI cells), whereas Bortezomib and other inhibitors tested downregulated the promoter activity both at the basal level (shown in LNCaP cells) and in response to EGF stimulation (shown in LNCaP-AI cells).

Click to enlarge 		Rating
Source Development, 2011, 138, 2903-2908. Bortezomib (Velcade) purchased from Selleck
Method Immunofluorescence
Cell Lines wild-type oocytes, Fmn2-/-oocytes
Concentrations 0.1 μM
Incubation Time 90 min
Results Endogenous Fmn2, localized in the cortex of prophase I oocytes, disappeared at NEBD, reappeared later and was enriched in the cortex opposite the spindle. Fmn2 -/-oocytes lacked cortical Fmn2 staining, suggesting that the staining is specific. Cortical localization was maintained at NEBD in wild-type oocytes treated with the proteasome inhibitor, Bortezomib, indicating that Fmn2 is degraded at NEBD.

Click to enlarge 		Rating
Source J Virol, 2010, 84, 9439–9451. Bortezomib (Velcade) purchased from Selleck
Method Proteasome activity assay, Standard plaque assay
Cell Lines A549 cells
Concentrations 10-100 nM
Incubation Time 1 h
Results As expected bortezomib treatment resulted in a block of viral replication of the avian influenzavirus strain A/FPV/Bratislava/79 (H7N7; FPV) in a concentration-dependent manner. While concentrations of 10 nM had no antiviral effect, 50 nM led to a significant titer reduction of up to 3 orders of magnitude (Fig.A). The highest concentration used (100 nM) led to a titer reduction of up to 4 orders of magnitude.These results were also confirmed in a virus growth kinetics study in infected cells that received a single dose of 50nM bortezomib. Virus titers were reduced at every time point analyzed (Fig.C).Since bortezomib is a proteasome inhibitor, we investigated whether the antiviral concentrations of bortezomib may have an inhibitory effect on the 26S proteasome in A549 cells. A concentration-dependent inhibition of the proteasome was observed in FPV-infected A549 cells at 24 h p.i. (Fig. B).

Click to enlarge 		Rating
Source J Virol, 2010, 84, 9439–9451. Bortezomib (Velcade) purchased from Selleck
Method Standard plaque assay, Western blot
Cell Lines A549 cells
Concentrations 50 nM
Incubation Time 1-10 h
Results A strong antiviral activity of bortezomib was observed upon addition of the compound up to 2 h p.i. At time points of 4 h p.i. and later, a dramatic decrease in the antiviral efficacy was observed. This indicates that the event in the viral life cycle that is affected by bortezomib occurs within the first 4 h. Since this correlates with the strong onset of viral gene and protein expression, we analyzed whether viral protein accumu-lation is affected by bortezomib. Indeed, we observed a strong reduction in viral matrix protein (M1) and PB1 polymerase synthesis in FPV- and PR8-infected cells at 5 h and 8 h p.i.

Click to enlarge 		Rating
Source J Virol, 2010, 84, 9439–9451. Bortezomib (Velcade) purchased from Selleck
Method Western blot
Cell Lines A549 cells
Concentrations 50 nM
Incubation Time 1/6/24 h
Results After a 6-h treatment with 50 nM bortezomib, activation of JNK was detected as evidenced by phosphorylation of the kinase at Thr183 and Tyr185 (lane 4). This was even enhanced upon a 24-h treatment (lane 6). Downstream substrates of JNK are the AP-1 transcription factors c-Jun and ATF-2, which are activated by JNK-mediated phosphorylation at Ser63 and Thr71, respectively. Consistent with JNK activation, we also found c-Jun and ATF-2 were phosphorylated and activated( lane 6), leading to the conclusion that, besides NF-κB, the JNK/c-Jun/ATF-2 pathway is also activated in A549 upon bortezomib treatment.

Click to enlarge 		Rating
Source J Biol Chem, 2010, 285, 41074-41086. Bortezomib (Velcade) purchased from Selleck
Method Real Time PCR
Cell Lines HepAD38 cells
Concentrations 2-50 nM
Incubation Time 18 h
Results An inhibitory effect of proteasome inhibition by bortezomib on HBV replication can be observed in cell culture.Therefore, proteasome activation seems to be a valuable strategy of the infected cells to reduce the stress resulting from misfolded proteins.

Click to enlarge 		Rating
Source J Virol, 2011, 85, 2781–2792. Bortezomib (Velcade) purchased from Selleck
Method Western blot
Cell Lines MA104 cells
Concentrations 0.1-10 μM
Incubation Time 1/7 h
Results Proteasome inhibitors which have different inhibition mechanisms, such as bortezomib and lactacystin, had a strong effect on virus replication in parallel with an increase in p53 accumulation.

Click to enlarge 		Rating
Source J Virol, 2011, 85, 2781–2792. Bortezomib (Velcade) purchased from Selleck
Method Western blot
Cell Lines MA104 cells
Concentrations 10 μM
Incubation Time 5-10 h
Results Further kinetic experiments were performed to better define the time window within the viral replication cycle in which proteasome activity was required. For this, cells were infected for 1 h and treated with MG132 or bortezomib for 4h at different times postinfection (Fig. A). As shown in Fig. B, a more clear arrest on viral protein accumulation was observed when bortezomib or MG132 was added at relatively earlier time points. Indeed, when inhibitors were added at 5 h p.i. or later, the effect was much reduced, suggesting that once the infection was well established with a robust accumulation of viroplasms, the requirement for proteasome activity was less significant.

Click to enlarge 		Rating
Source J Virol, 2011, 85, 2781–2792. Bortezomib (Velcade) purchased from Selleck
Method Immunofluorescence
Cell Lines NSP5-EGFP cells
Concentrations 10 μM
Incubation Time 2-8 h
Results Both MG132 and bortezomib induced a significant arrest on the formation of viroplasms, which appeared in reduced number and with smaller size with respect to those in control cells, particularly when added at time points between 1 h and 5 h p.i.

Click to enlarge 		Rating
Source J Virol, 2011, 85, 2781–2792. Bortezomib (Velcade) purchased from Selleck
Method Quantification of viroplasms
Cell Lines NSP5-EGFP cells, MA104 cells
Concentrations 10 μM
Incubation Time 4 h
Results The number of viroplasms per cell in cells treated for 4 h with MG132 or bortezomib was almost the same as that found in cells fixed at the beginning of each treatment, strongly suggesting that inhibition of proteasome activity affected the assembly of new viroplasms and their growth.

Click to enlarge 		Rating
Source Carcinogenesis, 2010, 31, 1948–1955. Bortezomib (Velcade) purchased from Selleck
Method ELISA
Cell Lines LNCaP-AI cells
Concentrations 20 μM
Incubation Time 24 h
Results Bortezomib, Lapatinib, and LY294002 significantly inhibited sPLA2-IIa secretion, whereas Erlotinib, Gefitinib and CI-1033 had a moderate effect in LNCaP-AI cells.

Product Citations (53)

  • Small molecule-mediated TGF-β type II receptor degradation promotes cardiomyogenesis in embryonic stem cells. [Willems E, et al. Cell Stem Cell 2012;11(2):242-52]

    PubMed: 22862949

  • Increased apoptosis induction in hepatocellular carcinoma by a novel tumor-targeted TRAIL fusion protein combined with bortezomib. [Wahl K, et al. Hepatology 2013;57(2):625-36]

    PubMed: 22991197

  • Blockade of XBP1 splicing by inhibition of IRE1α is a promising therapeutic option in multiple myeloma. [Mimura N, et al. Blood 2012;119(24):5772-81]

    PubMed: 22538852

  • CBS9106 is a novel reversible oral CRM1 inhibitor with CRM1 degrading activity. [Sakakibara K, et al. Blood 2011;118(14):3922-31]

    PubMed: 21841164

  • Preclinical activity, pharmacodynamic, and pharmacokinetic properties of a selective HDAC6 inhibitor, ACY-1215, in combination with bortezomib in multiple myeloma. [Santo L, et al. Blood 2012;119(11):2579-89]

    PubMed: 22262760

  • Anti-KIT monoclonal antibody inhibits imatinib-resistant gastrointestinal stromal tumor growth. [Edris B, et al. Proc Natl Acad Sci U S A 2013;ahead of print]

    PubMed: 23382202

  • Dual inhibition of canonical and noncanonical NF-κB pathways demonstrates significant antitumor activities in multiple myeloma. [Fabre C, et al. Clin Cancer Res 2012;18(17), 4669-4681]

    PubMed: 22806876

  • In vitro and in vivo selective antitumor activity of a novel orally bioavailable proteasome inhibitor MLN9708 against multiple myeloma cells. [Chauhan D, et al. Clin Cancer Res 2011;17(16):5311-21]

    PubMed: 21724551

  • Symmetry breaking in mouse oocytes requires transient F-actin meshwork destabilization. [Azoury J, et al. Development 2011;138(14), 2903-2908]

    PubMed: 21653611

  • Noncompetitive Modulation of the Proteasome by Imidazoline Scaffolds Overcomes Bortezomib Resistance and Delays MM Tumor Growth in Vivo. [Lansdell TA, et al. ACS Chem Biol 2013;8(3):578-87]

    PubMed: 23198928

  • MDM2 inhibitor nutlin-3a induces apoptosis and senescence in cutaneous T-cell lymphoma: role of p53. [Manfe V, et al. J Invest Dermatol 2012;132(5), 1487-1496]

    PubMed: 22377766

  • Controlling murine and rat chronic pain through A3 adenosine receptor activation. [Chen Z, et al. FASEB J 2012;26(5):1855-65]

    PubMed: 22345405

  • SARS-CoV replication is severely impaired by MG132 due to proteasome-independent inhibition of m-calpain. [Schneider M, et al. J Virol 2012;86(18):10112-22]

    PubMed: 22787216

  • Severe Acute Respiratory Syndrome Coronavirus Replication Is Severely Impaired by MG132 due to Proteasome-Independent Inhibition of M-Calpain. [Schneider M, et al. J Virol 2012;86(18):10112-22]

    PubMed: 22787216

  • The cellular ataxia telangiectasia-mutated kinase promotes epstein-barr virus lytic reactivation in response to multiple different types of lytic reactivation-inducing stimuli. [Hagemeier SR, et al. J Virol 2012;86(24):13360-70]

    PubMed: 23015717

  • Secretory phospholipase A2-IIa is involved in prostate cancer progression and may potentially serve as a biomarker for prostate cancer. [Dong Z, et al. Carcinogenesis 2010;31(11), 1948-1955]

    PubMed: 20837598

  • Chalcone-based small-molecule inhibitors attenuate malignant phenotype via targeting deubiquitinating enzymes. [Issaenko OA, et al. Cell Cycle 2012;11(9):1804-17]

    PubMed: 22510564

  • Superior antitumoral activity of dimerized targeted single-chain TRAIL fusion proteins under retention of tumor selectivity. [Siegemund M, et al. Cell Death Dis 2012;3:e295]

    PubMed: 22495350

  • Sangivamycin-Like Molecule 6 (SLM6) exhibits potent anti-multiple myeloma activity through inhibition of cyclin-dependent kinase-9 (CDK9). [Dolloff NG, et al. Mol Cancer Ther 2012;11(11):2321-30]

    PubMed: 22964485

  • Drug resistance to inhibitors of the human double minute-2 E3 ligase is mediated by point mutations of p53, but can be overcome with the p53 targeting agent RITA. [Jones RJ, et al. Mol Cancer Ther 2012;11(10):2243-53]

    PubMed: 22933706

  • The clinically approved proteasome inhibitor PS-341 efficiently blocks influenza A virus and vesicular stomatitis virus propagation by establishing an antiviral state. [Dudek SE, et al. J Virol 2010;84(18), 9439-9451]

    PubMed: 20592098

  • Rotavirus replication requires a functional proteasome for effective assembly of viroplasms. [Contin R, et al. J Virol 2011;85(6), 2781-2792]

    PubMed: 21228236

  • Halofuginone inhibits multiple myeloma growth in vitro and in vivo and enhances cytotoxicity of conventional and novel agents. [Leiba M, et al. Br J Haematol 2012;157(6):718-31]

    PubMed: 22533681

  • Down-regulation of mitogen-inducible gene 6, a negative regulator of EGFR, enhances resistance to MEK inhibition in KRAS mutant cancer cells. [Yoon YK, et al. Cancer Lett 2012;316(1), 77-84]

    PubMed: 22082529

  • Preclinical evaluation of a novel SIRT1 modulator SRT1720 in multiple myeloma cells. [Chauhan D, et al. Brit J Haematol 2011;155(5), 588-598]

    PubMed: 21950728

  • Pathological adaptive responses of Schwann cells to endoplasmic reticulum stress in bortezomib‐induced peripheral neuropathy. [Shin YK, et al. Glia 2010;58(16):1961-76]

    PubMed: 20830808

  • Proteasomal inhibition restores biological function of mis-sense mutated dysferlin in patient-derived muscle cells. [Azakir BA, et al. J Biol Chem 2012;287(13):10344-54]

    PubMed: 22318734

  • Proteasome-dependent activation of mammalian target of rapamycin complex 1 (mTORC1) is essential for autophagy suppression and muscle remodeling following denervation. [Quy PN, et al. J Biol Chem 2012;288(2), 1125-1134]

    PubMed: 23209294

  • Deubiquitinases regulate the activity of caspase-1 and IL-1β secretion via assembly of the inflammasome. [Lopez-Castejon G, et al. J Biol Chem 2012;288(4), 2721-2733]

    PubMed: 23209292

  • BaxΔ2 is a novel bax isoform unique to microsatellite unstable tumors. [Haferkamp B, et al. J Biol Chem 2012;287(41):34722-9]

    PubMed: 22910913

  • Hepatitis B virus induces expression of antioxidant response element-regulated genes by activation of Nrf2. [Schaedler S, et al. J Biol Chem 2010;285(52):41074-86]

    PubMed: 20956535

  • Inhibition of p53 DNA binding function by the MDM2 protein acidic domain. [Cross B, et al. J Biol Chem 2011;286(18):16018-29]

    PubMed: 21454483

  • JAK/STAT3 pathway inhibition blocks skeletal muscle wasting downstream of IL-6 and in experimental cancer cachexia. [Bonetto A, et al. Am J Physiol Endocrinol Metab 2012;303(3):E410-21]

    PubMed: 22669242

  • Tolerance to Nitroglycerin Through Proteasomal Downregulation of Aldehyde Dehydrogenase-2 in a Genetic Mouse Model of Ascorbate Deficiency. [Wölkart G, et al. Br J Pharmacol 2012;ahead of print]

    PubMed: 23194305

  • miR-122 regulates p53/Akt signalling and the chemotherapy-induced apoptosis in cutaneous T-cell lymphoma. [Manfe V, et al. PLoS One 2012;7(1), e29541]

    PubMed: 22235305

  • Efficient detection of proteins retro-translocated from the ER to the cytosol by in vivo biotinylation. [Petris G, et al. PLoS One 2011;6(8):e23712]

    PubMed: 21887304

  • Proteasome Inhibition Is Partially Effective in Attenuating Pre-Existing Immunity against Recombinant Adeno-Associated Viral Vectors. [Karman J, et al. PLoS One 2012;7(4):e34684]

    PubMed: 22514654

  • Expression of the Ubiquitin Proteasome System in Neonatal Rat Gonocytes and Spermatogonia: Role in Gonocyte Differentiation. [Manku G, et al. Biol Reprod 2012;87(2):44]

    PubMed: 22592496

  • Eeyarestatin causes cervical cancer cell sensitization to bortezomib treatment by augmenting ER stress and CHOP expression. [Brem GJ, et al. Gynecol Oncol 2013;128(2):383-90]

    PubMed: 23107612

  • Proteasome inhibition reduces proliferation, collagen expression, and inflammatory cytokine production in nasal mucosa and polyp fibroblasts. [Pujols L, et al. J Pharmacol Exp Ther 2012;343(1):184-97]

    PubMed: 22787116

  • Novel cell-and tissue-based assays for detecting misfolded and aggregated protein accumulation within aggresomes and inclusion bodies. [Shen D, et al. Cell Biochem Biophys 2011;60(3):173-85]

    PubMed: 21132543

  • The Raf/MEK/extracellular signal-regulated kinase 1/2 pathway can mediate growth inhibitory and differentiation signaling via androgen receptor downregulation in prostate cancer cells. [Hong SK, et al. Exp Cell Res 2011;317(18), 2671-2682]

    PubMed: 21871886

  • Secretory phospholipase A2-IIa is a target gene of the HER/HER2-elicited pathway and a potential plasma biomarker for poor prognosis of prostate cancer. [Oleksowicz L, et al. Prostate 2012;72(10):1140-9]

    PubMed: 22127954

  • Polysaccharide-gold nanoparticles as anticancer drugs carriers. [Venkatpurwar V, et al. Int J Pharm 2011;409(1-2):314-20]

    PubMed: 21376108

  • The downregulation of Mcl-1 via USP9X inhibition sensitizes solid tumors to Bcl-xl inhibition. [Peddaboina C, et al. BMC Cancer 2012;12, 541]

    PubMed: 23171055

  • The use of a reversible proteasome inhibitor in a model of reduced-size orthotopic liver transplantation in rats. [Padrissa-Altés S, et al. Exp Mol Pathol 2012;93(1), 99-110]

    PubMed: 22475623

  • NFκB pathway is down-regulated by 1α,25(OH)(2)-vitamin D(3) in endothelial cells transformed by Kaposi sarcoma-associated herpes virus G protein coupled receptor. [Gonzalez-Pardo V, et al. Steroids 2012;77(11):1025-32]

    PubMed: 22683670

  • HSPA2 overexpression protects V79 fibroblasts against bortezomib-induced apoptosis. [Filipczak PT, et al. Biochem Cell Biol 2012;90(2):224-31]

    PubMed: 22397456

  • The use of a reversible proteasome inhibitor in a model of reduced-size orthotopic liver transplantation in rats. [Padrissa-Altés S, et al. Exp Mol Pathol 2012;93(1):99-110]

    PubMed: 22475623

  • Differential action of 3-hydroxyanthranilic acid on viability and activation of stimulated lymphocytes. [Piscianz E, et al. Int Immunopharmacol 2011;11(12):2242-5]

    PubMed: 21979495

  • A 1536-Well Quantitative High-Throughput Screen to Identify Compounds Targeting Cancer Stem Cells. [Mathews LA, et al. J Biomol Screen 2012;17(9), 1231-1242.]

    PubMed: 22927676

  • Agents That Stabilize Mutated von Hippel–Lindau (VHL) Protein Results of a High-Throughput Screen to Identify Compounds That Modulate VHL Proteostasis. [Ding Z, et al. J Biomol Screen 2012;17(5):572-80]

    PubMed: 22357874

  • Comparative Gene Expression Profiling of Benign and Malignant Lesions Reveals Candidate Therapeutic Compounds for Leiomyosarcoma. [Edris B, et al. Sarcoma 2012;2012:805614]

    PubMed: 22919280

Tech Support & FAQs

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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