2. Metabolic Enzyme/Protease Apoptosis Autophagy
  3. Proteasome MMP Apoptosis Autophagy
  4. 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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BSc2118

BSc2118 Chemical Structure

CAS No. : 863924-64-5

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BSc2118 Related Antibodies

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Description

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[1][2].

IC50 & Target[1]

MMP-9

 

In Vitro

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.

BSc2118 Related Antibodies

Cell Cycle Analysis[2]

Cell Line: MM.1S, MM.1R human multiple myeloma (MM) cell lines
Concentration: 100 and 200 nM
Incubation Time: 24 h
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.

Apoptosis Analysis[2]

Cell Line: MM.1S, MM.1R human multiple myeloma (MM) cell lines
Concentration: 100 and 200 nM
Incubation Time: 24 h
Result: Induced apoptosis in a dose-dependent manner, causing a significant increase in Annexin V+ cell population.

Western Blot Analysis[2]

Cell Line: MM.1S, MM.1R (dexamethasone-resistant) human multiple myeloma (MM) cell lines
Concentration: 100 and 200 nM
Incubation Time: 24 h
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.

Western Blot Analysis[2]

Cell Line: MM.1S, MM.1R human multiple myeloma (MM) cell lines
Concentration: 100 and 200 nM
Incubation Time: 24 h
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).

Western Blot Analysis[2]

Cell Line: MM.1S human multiple myeloma (MM) cell line
Concentration: 100 and 200 nM (24 h); 100 nM (3, 12 and 24 h)
Incubation Time: 3, 12 and 24 h
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.

Western Blot Analysis[2]

Cell Line: Human umbilical vein endothelial cells (HUVECs)
Concentration: 100 and 200 nM
Incubation Time: 24 h; 4 h (TNFα/CoCl2 co-treatment)
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.

Real Time qPCR[2]

Cell Line: Human MM bone marrow stromal cells (MM-BMSCs)
Concentration: 100 and 200 nM
Incubation Time: 48 h
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.

Western Blot Analysis[2]

Cell Line: ANBL-6.WT (bortezomib-sensitive), ANBL-6.BR (bortezomib-resistant) human multiple myeloma (MM) cell lines
Concentration: 100 and 200 nM (ANBL-6.WT); 500 nM (ANBL-6.BR)
Incubation Time: 24 h
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.
In Vivo

BSc2118 (10-60 mg/kg; intrastriatal injection; single dose) exerts acute and long-term neuroprotective effects against reperfusion-induced cerebral ischemia in male C57BL/6N mice, and improves long-term neuronal survival, functional recovery, angioneurogenesis and blood-brain barrier stability[1].
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.

Animal Model: C57BL/6N (adult male, reperfusion-induced cerebral ischaemia model)[1]
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)
Administration: intrastriatal injection; single dose
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).
Animal Model: NOD/SCID mice[2]
Dosage: 30 mg/kg
Administration: i.p.; twice a week; 3 weeks
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.
Molecular Weight

533.66

Formula

C28H43N3O7
CAS No.
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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Purity & Documentation
References
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BSc2118 Related Classifications

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  • Do most proteins show cross-species activity?

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Keywords:

BSc2118863924-64-5BSc 2118BSc-2118ProteasomeMMPApoptosisAutophagyMatrix metalloproteinasesmyeloma cellsMM.1S cellsMM.1R cellsHUVECsNOD/SCID miceC57BL/6N mice20S proteasomecerebral ischaemiamultiple myelomaHIF1AInhibitorinhibitorinhibit

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