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

BSc2118 是一种 20S 蛋白酶体抑制剂，其 IC50 约为 50 nM。BSc2118 可诱导骨髓瘤细胞发生 G2/M 期细胞周期阻滞和凋亡 (apoptosis)，抑制细胞保护性自噬 (autophagy)，并抑制肿瘤血管生成。BSc2118 可降低 MMP9 活性，促进血管神经生成，并减轻重组组织型纤溶酶原激活剂诱导的脑毒性。BSc2118 可用于脑缺血和多发性骨髓瘤相关研究。

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BSc2118

BSc2118 Chemical Structure

CAS No. : 863924-64-5

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BSc2118 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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

 

体外研究
(In Vitro)

BSc2118 (0-2000 nM; 48 h) 可呈剂量依赖性地强效降低 MM.1S、MM.1R、RPMI-8226、U266 和 NCI-H929 人多发性骨髓瘤细胞系的细胞活力，在 MM.1S、MM.1R 和 RPMI-8226 细胞中的 IC50 值分别为 121.4 nM、116.8 nM 和 313.7 nM[2]。
BSc2118 (100-200 nM; 24 h) 诱导人多发性骨髓瘤细胞系 MM.1S 发生 G2/M 期细胞周期阻滞[2]。
BSc2118 (100-200 nM; 24 h) 诱导 MM.1S 和 MM.1R 人多发性骨髓瘤细胞呈剂量依赖性凋亡[2]。
BSc2118 (100-200 nM; 24 h) 可上调 MM.1S 人多发性骨髓瘤细胞中 p53 和 p21 的蛋白水平[2]。
BSc2118 (100-200 nM; 24 h) 可通过切割 caspase-9、caspase-8、caspase-3 和 PARP，在 MM.1S 和 MM.1R 人多发性骨髓瘤细胞中激活凋亡信号级联反应[2]。
BSc2118 (100-200 nM; 3-24 h) 可强效且持续地抑制 MM.1S 人多发性骨髓瘤细胞中的 CT-L 蛋白酶体活性[2]。
BSc2118 (100-200 nM; 3-24 h) 诱导人多发性骨髓瘤细胞 MM.1S 中泛素化蛋白的积累[2]。
BSc2118 (200 nM; 30 h) 可抑制人脐静脉内皮细胞 (HUVECs) 的毛细血管样管形成[2]。
BSc2118 (100-200 nM; 24 h) 可上调人脐静脉内皮细胞 (HUVECs) 中 PHD2 蛋白水平，同时下调 HIF1α 和 VE-cadherin 蛋白水平[2]。
BSc2118 (100-200 nM; 48 h) 可呈剂量依赖性下调人 MM-BMSCs 中 IL-6、VEGFA 和 bFGF 血管生成细胞因子基因的表达[2]。
BSc2118 (100-500 nM; 24 h) 不会诱导自噬标志物 Beclin-1 或 LC3b 的上调，反而会在Bortezomib (HY-10227) 敏感型 ANBL-6.WT 和 Bortezomib 耐药型 ANBL-6.BR 人多发性骨髓瘤细胞中轻度降低 LC3b 水平[2]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

BSc2118 相关抗体:

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.
体内研究
(In Vivo)

BSc2118 (10-60 mg/kg；纹状体内注射；单剂量) 可对雄性 C57BL/6N 小鼠的再灌注诱导性脑缺血产生急性及长期神经保护作用，并改善长期神经元存活、功能恢复、血管神经发生及血脑屏障稳定性[1]。
BSc2118 (30 mg/kg；腹腔注射；每周 2 次；持续 3 周) 可在多发性骨髓瘤 NOD/SCID 小鼠模型中使肿瘤体积缩小 61.5%，抑制肿瘤血管生成并降低基础自噬水平，且未观察到血液学毒性[2]。

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.
分子量

533.66

Formula

C28H43N3O7
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

BSc2118 相关分类

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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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