BSc2118
BSc2118 is a 20S proteasome inhibitor with an IC50 of approximately 50 nM. BSc2118 induces G2/M phase cell cycle arrest and apoptosis in myeloma cells, inhibits cytoprotective autophagy, and suppresses tumor angiogenesis. BSc2118 reduces MMP9 activity, promotes angioneurogenesis, and alleviates recombinant tissue-type plasminogen activator-induced cerebral toxicity. BSc2118 is applicable to studies related to cerebral ischemia and multiple myeloma.
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- CAS No.: 863924-64-5
- Formule: C28H43N3O7
- Masse moléculaire:533.66
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Stockage:
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Activité biologique
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Chemical Information
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Activité biologique
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MMP-9 |
BSc2118 (0-2000 nM; 48 h) potently reduces the cell viability of human multiple myeloma cell lines MM.1S, MM.1R, RPMI-8226, U266 and NCI-H929 in a dose-dependent manner, with IC50 values of 121.4 nM, 116.8 nM and 313.7 nM in MM.1S, MM.1R and RPMI-8226 cells, respectively[2].
BSc2118 (100-200 nM; 24 h) induces G2/M cell cycle arrest in the human multiple myeloma cell line MM.1S[2].
BSc2118 (100-200 nM; 24 h) induces dose-dependent apoptosis in MM.1S and MM.1R human multiple myeloma cells[2].
BSc2118 (100-200 nM; 24 h) upregulates the protein levels of p53 and p21 in MM.1S human multiple myeloma cells[2].
BSc2118 (100-200 nM; 24 h) activates the apoptotic signaling cascade in MM.1S and MM.1R human multiple myeloma cells by cleaving caspase-9, caspase-8, caspase-3 and PARP[2].
BSc2118 (100-200 nM; 3-24 h) potently and persistently inhibits CT-L proteasome activity in MM.1S human multiple myeloma cells[2].
BSc2118 (100-200 nM; 3-24 h) induces the accumulation of ubiquitinated proteins in human multiple myeloma cells MM.1S[2].
BSc2118 (200 nM; 30 h) inhibits capillary-like tube formation in human umbilical vein endothelial cells (HUVECs)[2].
BSc2118 (100-200 nM; 24 h) upregulates the protein level of PHD2 and downregulates the protein levels of HIF1α and VE-cadherin in human umbilical vein endothelial cells (HUVECs)[2].
BSc2118 (100-200 nM; 48 h) downregulates the expression of angiogenic cytokine genes including IL-6, VEGFA and bFGF in human MM-BMSCs in a dose-dependent manner[2].
BSc2118 (100-500 nM; 24 h) does not induce upregulation of the autophagy markers Beclin-1 or LC3b; instead, it slightly reduces LC3b levels in both Bortezomib (HY-10227)-sensitive ANBL-6.WT and Bortezomib-resistant ANBL-6.BR human multiple myeloma cells[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MM.1S, MM.1R human multiple myeloma (MM) cell lines
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Concentration:100 and 200 nM
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Incubation Time:24 h
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Result:Caused marked G2/M-phase arrest in MM.1S cells.
Reduced BrdU-positive cell numbers, inhibiting cell cycle progression through the G1-S transition.
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Cell Line:MM.1S, MM.1R human multiple myeloma (MM) cell lines
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Concentration:100 and 200 nM
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Incubation Time:24 h
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Result:Induced apoptosis in a dose-dependent manner, causing a significant increase in Annexin V+ cell population.
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Cell Line:MM.1S, MM.1R (dexamethasone-resistant) human multiple myeloma (MM) cell lines
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Concentration:100 and 200 nM
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Incubation Time:24 h
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Result:Increased p53 protein levels in MM.1S cells by 1.32-fold at 100 nM and 1.81-fold at 200 nM.
Increased p21 protein levels in MM.1S cells by 1.57-fold at 100 nM and 2.20-fold at 200 nM.
Showed no increase in p53 or p21 protein levels in MM.1R cells.
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Cell Line:MM.1S, MM.1R human multiple myeloma (MM) cell lines
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Concentration:100 and 200 nM
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Incubation Time:24 h
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Result:Induced cleavage of caspase-9, caspase-8, caspase-3, and PARP in both MM.1S and MM.1R cells.
Achieved cleaved/full-length ratios in MM.1S cells of 1.23 (caspase-9, 100 nM), 1.47 (caspase-9, 200 nM), 4.67 (caspase-8, 100 nM), 12.35 (caspase-8, 200 nM), 1.18 (caspase-3, 100 nM), 5.00 (caspase-3, 200 nM), 3.25 (PARP, 100 nM), and 16.3 (PARP, 200 nM).
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Cell Line:MM.1S human multiple myeloma (MM) cell line
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Concentration:100 and 200 nM (24 h); 100 nM (3, 12 and 24 h)
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Incubation Time:3, 12 and 24 h
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Result:Increased ubiquitinated protein levels in MM.1S cells by 1.25-fold at 100 nM for 24 h, 1.38-fold at 200 nM for 24 h, 1.14-fold at 100 nM for 3 h, 1.14-fold at 100 nM for 12 h, and 1.23-fold at 100 nM for 24 h relative to control.
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Cell Line:Human umbilical vein endothelial cells (HUVECs)
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Concentration:100 and 200 nM
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Incubation Time:24 h; 4 h (TNFα/CoCl2 co-treatment)
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Result:Increased PHD2 protein levels in HUVECs by 2.95-fold at 100 nM and 1.88-fold at 200 nM under normoxia, 2.11-fold at 100 nM and 1.02-fold at 200 nM with TNFα, and 1.56-fold at 100 nM and 1.35-fold at 200 nM with CoCl2.
Decreased HIF1α expression to 0.90-fold at 100 nM and 0.78-fold at 200 nM under normoxia, 0.79-fold at 100 nM and 0.66-fold at 200 nM with TNFα, and 0.95-fold at 100 nM and 0.89-fold at 200 nM with CoCl2.
Decreased VE-cadherin expression to 0.69-fold at 100 nM and 0.43-fold at 200 nM under normoxia, 0.41-fold at 100 nM and 0.23-fold at 200 nM with TNFα, and 0.29-fold at 100 nM and 0.36-fold at 200 nM with CoCl2.
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Cell Line:Human MM bone marrow stromal cells (MM-BMSCs)
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Concentration:100 and 200 nM
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Incubation Time:48 h
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Result:Reduced IL-6 gene expression to ~0.7-fold at 100 nM and ~0.2-fold at 200 nM relative to control.
Reduced VEGFA gene expression to ~0.8-fold at 100 nM and ~0.5-fold at 200 nM relative to control.
Reduced bFGF gene expression to ~1.6-fold at 100 nM and ~0.9-fold at 200 nM relative to control.
Inhibited gene expression in a dose-dependent manner.
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Cell Line:ANBL-6.WT (bortezomib-sensitive), ANBL-6.BR (bortezomib-resistant) human multiple myeloma (MM) cell lines
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Concentration:100 and 200 nM (ANBL-6.WT); 500 nM (ANBL-6.BR)
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Incubation Time:24 h
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Result:Reduced Beclin-1 levels in ANBL-6.WT cells to 0.97-fold at 100 nM and 0.68-fold at 200 nM relative to control.
Reduced LC3b levels in ANBL-6.WT cells to 0.79-fold at 100 nM and 0.82-fold at 200 nM relative to control.
Reduced Beclin-1 levels in ANBL-6.BR cells to 0.82-fold at 500 nM relative to control.
Reduced LC3b levels in ANBL-6.BR cells to 0.37-fold at 500 nM relative to control.
Failed to up-regulate Beclin-1 or LC3b in either cell line.
BSc2118 (30 mg/kg; i.p.; twice weekly for 3 consecutive weeks) reduces tumor volume by 61.5% in a multiple myeloma NOD/SCID mouse model, inhibits tumor angiogenesis and decreases basal autophagy levels, with no hematological toxicity observed[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6N (adult male, reperfusion-induced cerebral ischaemia model)[1]
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Dosage:10 mg/kg (12h pre-stroke); 30 mg/kg (12h pre-stroke, 6h post-stroke, 12h post-stroke); 60 mg/kg (12h pre-stroke)
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Administration:intrastriatal injection; single dose
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Result:Induced long-term neuroprotection (lasting up to 3 months), significantly reduce the volume of cerebral infarction, and improve motor coordination and cognitive deficits.
Inhibited the proteasomal degradation of the transcription factor hypoxia-inducible factor 1α (HIF1A), resulting in a significant accumulation of its protein level.
Enhanced post-ischemic angiogenesis and neurogenesis, accompanied by an increase in the levels of pro-angiogenic and neurotrophic factors (such as erythropoietin, brain-derived neurotrophic factor, and vascular endothelial growth factor).
Reduced the secondary brain injury, bleeding and disruption of the blood-brain barrier caused by the thrombolytic drug recombinant tissue-type plasminogen activator (rt-PA).
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Animal Model:NOD/SCID mice[2]
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Dosage:30 mg/kg
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Administration:i.p.; twice a week; 3 weeks
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Result:Reduced tumor volume by 61.5% compared to vehicle control.
Reduced density of CD31-positive blood vessels (microvessel density) in tumor tissues.
Decreased number of endothelial cells and surrounding pericytes.
Diminished basal levels of autophagy markers Beclin-1 and LC3b in tumor tissues.
Showed no hematologic toxicity (unchanged serum hemoglobin, white blood cell counts, and platelet counts) relative to the control group.
Chemical Information
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CAS No. 863924-64-5
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Masse moléculaire 533.66
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Formule C28H43N3O7
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SMILES
CC(C[C@H](NC(OCC1=CC=CC=C1)=O)C(N[C@@H](CC(OC(C)(C)C)=O)C(N[C@@H](CC(C)C)C=O)=O)=O)C
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Doeppner TR, et al. The novel proteasome inhibitor BSc2118 protects against cerebral ischaemia through HIF1A accumulation and enhanced angioneurogenesis. Brain. 2012;135(Pt 11):3282-3297. [Content Brief]
[2]. Zang M, et al. Anti-tumor activity of the proteasome inhibitor BSc2118 against human multiple myeloma. Cancer Lett. 2015;366(2):173-181. [Content Brief]
Calculators
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BSc2118 Related Classifications
HY-123255 Related Classifications
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