| Bortezomib (PS-341) Proteasome Inhibitor |
Sample solution is provided at 25 µL, 10mM.
- 1.Xinchun Li, Li Zhong, et al. "Phosphorylation of IRS4 by CK1γ2 promotes its degradation by CHIP through the ubiquitin/lysosome pathway." Theranostics, 2018, Vol. 8, Issue13.
- 2.Yuancai Xiang, Josefin Halin, et al."Topovectorial mechanisms control the juxtamembrane proteolytic processing of Nrf1 to remove its N-terminal polypeptides during maturation of the CNC-bZIP factor." bioRxiv.2018. March 27.
- 3.Liew PL, Huang RL, et al. "Distinct methylation profile of mucinous ovarian carcinoma reveals susceptibility to proteasome inhibitors." Int J Cancer. 2018 Feb 16. PMID:29451304
- 4.Yuancai Xiang, et al."Molecular mechanisms controlling the multistage post-translational processing of endogenous Nrf1/TCF11 proteins to yield distinct proteoforms within the coupled positive and negative feedback circuits."bioRxiv.2018. April 12.
- 5. Farris TR, Zhu B, et al. "Ehrlichia chaffeensis TRP32 Nucleomodulin Function and Localization Is Regulated by NEDD4L-Mediated Ubiquitination." Front Cell Infect Microbiol. 2018 Jan 11;7:534. PMID:29376035
- 6. Mañas A, Chen W, et al. "BaxΔ2 sensitizes colorectal cancer cells to proteasome inhibitor-induced cell death." Biochem Biophys Res Commun.2018 Jan 29;496(1):18-24. PMID:29291406
- 7. An H, Harper JW. "Systematic analysis of ribophagy in human cells reveals bystander flux during selective autophagy." Nat Cell Biol. 2017 Dec 11. PMID:29230017
- 8. Chun H, Catterton T, et al. "Organ-specific regulation of ATP7A abundance is coordinated with systemic copper homeostasis." Sci Rep. 2017 Sep 20;7(1):12001. PMID:28931909
- 9. Tian C, Yuan Z, et al. "Inhibition of glycolysis by a novel EGFR/HER2 inhibitor KU004 suppresses the growth of HER2+ cancer." Exp Cell Res. 2017 May 19. pii: S0014-4827(17)30297-5. PMID:28532652
- 10. Lai, Tsung-Hsuan, et al. "Gold Nanoparticles Compromise TNF-α-Induced Endothelial Cell Adhesion Molecule Expression Through NF-κB and Protein Degradation Pathways and Reduce Neointima Formation in a Rat Carotid Balloon Injury Model." Journal of Biomedical Nanotechnology 12.12 (2016): 2185-2201.
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- 13. Lee BH, Lu Y, et al. "USP14 deubiquitinates proteasome-bound substrates that are ubiquitinated at multiple sites." Nature. 2016 Apr 21;532(7599):398-401 PMID:27074503
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| Description | Bortezomib (PS-341) is a potent inhibitor of 20S proteasome with Ki of 0.6 nM. | |||||
| Targets | 20S proteasome | |||||
| IC50 | 0.6 nM (Ki) | |||||
| Cell experiment [1]: | |
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Cell lines |
Canine malignant melanoma cell lines (CMM-1, CMM-2, ChMC, KMeC, LMeC, OMJ, OMS, OMK, and NML |
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Preparation method |
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months. |
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Reaction Conditions |
72h; IC50=3.5~5.6 nM (nine kinds of cells) |
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Applications |
Bortezomib potently suppressed the growth in 21 drugs, while other compounds had no or minimal effect on cell growth. We thus focused on bortezomib and examined its growth inhibitory properties against nine canine malignant melanoma cell lines (CMM-1, CMM-2, ChMC, KMeC, LMeC, OMJ, OMS, OMK, and NML). Bortezomib inhibited the growth of all cell lines with calculated IC50 values of 3.5~5.6 nM. |
| Animal experiment [1]: | |
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Animal models |
Nude athymic mice |
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Dosage form |
0.8 mg/kg; intravenous injection |
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Applications |
The in vivo growth inhibitory activity of bortezomib against CMM-1 cells was evaluated using a xenograft mouse model. Bortezomib significantly suppressed the growth of tumours after Day 4 of treatment (P < 0.01, control vs. bortezomib). Tumours from the bortezomib-treated mice showed a significant decrease in mitotic index compared to controls (P<0.01). Similarly, the Ki67 index was significantly decreased in tumours excised from the bortezomib-treated mice when compared to controls (P < 0.01). |
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Other notes |
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
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References: [1] Ito K, Kobayashi M, Kuroki S, et al. The proteasome inhibitor bortezomib inhibits the growth of canine malignant melanoma cells in vitro and in vivo[J]. The Veterinary Journal, 2013, 198(3): 577-582. | |
Bortezomib (PS-341) Dilution Calculator
Bortezomib (PS-341) Molarity Calculator
| Cas No. | 179324-69-7 | SDF | Download SDF |
| Synonyms | Bortezomib,PS-341,LDP-341,MLM341,MG-341,NSC-681239 | ||
| Chemical Name | [(1R)-3-methyl-1-[[(2S)-3-phenyl-2-(pyrazine-2-carbonylamino)propanoyl]amino]butyl]boronic acid | ||
| Canonical SMILES | B(C(CC(C)C)NC(=O)C(CC1=CC=CC=C1)NC(=O)C2=NC=CN=C2)(O)O | ||
| Formula | C19H25BN4O4 | M.Wt | 384.24 |
| Solubility | >19.2mg/mL in DMSO | Storage | Store at -20°C |
| Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
Abstract
Bortezomib, a proteasome inhibitor with anti-pancreatic cancer activity, was assessed for its role in ceramide production.
Abstract
The resistance to bortezomib, a 20S proteasome inhibitor, in MM cell lines is correlated with mitochondrial activities and could be eliminated through regulation of mitochondrial genes.
Abstract
Bortezomib, a proteasome inhibitor with modes anti-malignant glioma activity, was reviewed in terms of its effects and disadvantages.
Abstract
Instead of synergistically killing multiple myeloma cells, bortezomib inhibited the replication and spread of VSV in vitro through suppressing NF-KB activation resulting in diminished anti-tumor activity and increased VSV response. However, the combination of those two drugs exhibited synergistic effects in vivo to reduce tumor burden in two syngeneic, immunocompetent myeloma models.
Abstract
The treatment of bortezomib combined with idarubicin was well tolerated in older AML patients with the maximum tolerated dose of 1.2 mg/m(2) and 10 mg/m(2) respectively.
Bortezomib (originally codenamed PS-341) is the first therapeutic proteasome inhibitor to the tested in humans. It is approved in the U.S. for treating relapsed multiple myeloma and mantle cell lymphoma. [1] The drug is an N-protected dipeptide and can be written as Pyz-Phe-boroLeu, which stands for pyrazinoic acid, phenylalanine and Leucine with a boronic acid instead of a carboxylic acid. Peptides are written N-terminus to C-terminus, and this convention is used here even though the "C-terminus" is a boronic acid instead of a carboxylic acid. While multiple mechanisms are likely to be involved, proteasome inhibition may prevent degradation of pro-apoptotic factors, permitting activation of programmed cell death in neoplastic cells dependent upon suppression of pro-apoptotic pathways. Recently, it was found that bortezomib caused a rapid and dramatic change in the levels of intracellular peptides that are produced by the proteasome. [2] Some intracellular peptides have been shown to be biologically active, and so the effect of bortezomib on the levels of intracellular peptides may contribute to the biological and/or side effects of the drug.
A potent (Ki = 0.6 nM), specific and reversible proteasome inhibitor. It inhibits cell proliferation of H460 cells (Human non-small cell lung cancer cell lines) with an IC₅₀ of 0.1 µM.
References:
1. Takimoto CH, Calvo E. "Principles of Oncologic Pharmacotherapy" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.
2. Gelman JS, Sironi J, Berezniuk I, Dasgupta S, Castro LM, Gozzo FC, Ferro ES, Fricker LD (2013). "Alterations of the intracellular peptidome in response to the proteasome inhibitor bortezomib". In Gartel, Andrei L. PLoS One 8 (8): e53263.