96 Well Format Sample Storage Tube With Screw Cap and Optional 2D Barcode

Protease Inhibitor Library

A unique collection of 53 protease inhibitors

规格 价格  
预溶于DMSO
100uL/well (10mM solution) RMB 14447.16
2x100uL/well (10mM solution) RMB 22702.68
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产品详情

产品描述及优势

    • A unique collection of 53 small molecule inhibitors used for chemical genomics, high-throughput screening (HTS), and high content screening (HCS).
    • Bioactivity and safety confirmed by preclinical research and clinical trials.
    • Targets proteasome, HCV Protease, DPP-4, Caspase, MMP, Gamma-secretase, Beta Amyloid.
    • Structurally diverse, medicinally active, and cell permeable.
    • Rich documentation with structure, IC50, and customer reviews.
    • NMR and HPLC validated to ensure high purity.

产品详细信息

配制: A unique collection of 53 protease inhibitors supplied as pre-dissolved DMSO solutions
96-孔板: 96 Well Format Sample Storage Tube With Screw Cap and Optional 2D Barcode
稳定性:
1年 -20°C 溶于DMSO
2年 -80°C 溶于DMSO
发货: 蓝冰物流
包装: 惰性气体

化合物库组成成份

Chemical Library Composition

客户使用Selleck产品的实验数据 (10)

AS-605240 Review
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数据来源 Sci Transl Med,2015, 6(250), 250ra112. Bortezomib (PS-341) purchased from Selleck
方法 Western blots
细胞系 Primary myoblasts
浓度 10, 50 uM
处理时间 24 h
结果 To demonstrate the biological functionality of the salvaged missense mutated dysferlin protein, we performed membrane resealing experiments on primary myoblasts derived from percutaneous muscle biopsies taken from patient 2. Bortezomib treatment of primary myoblasts increased dysferlin expression in a dose-dependent manner, and bortezomib-treated myoblasts regained their capability to reseal laser-induced plasma membrane injuries.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Sci Transl Med 2014, 6(250), 250ra112. Carfilzomib (PR-171) purchased from Selleck
方法 Western blot
细胞系 Primary myoblasts
浓度 5, 10 nM
处理时间 24 h
结果 To demonstrate that treatment with proteasome inhibitors other than bortezomib can also salvage missense mutated dysferlin, we treated primary myoblasts from patient 2 with either the irreversible proteasome inhibitor carfilzomib, which is the biologically active, hydrolyzed form of the investigational, reversible proteasome inhibitor ixazomib (MLN9708) being developed for oral application. It found that treatment with carfilzomib resulted in a dose-dependent increase in dysferlin expression.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Sci Transl Med 2014, 6(250), 250ra112. Ixazomib (MLN2238) purchased from Selleck
方法 Western blot
细胞系 Primary myoblasts
浓度 25, 50 nM
处理时间 24 h
结果 To demonstrate that treatment with proteasome inhibitors other than bortezomib can also salvage missense mutated dysferlin, we treated primary myoblasts from patient 2 with MLN2238, which is the biologically active, hydrolyzed form of the investigational. MLN2238 was reported to have less neuropathic side effects as compared to bortezomib. It found that treatment with either of these newer-generation proteasome inhibitors resulted in a dose-dependent increase in dysferlin expression.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 J Clin Invest 2014, 124(9), 3757-66. Bortezomib (PS-341) purchased from Selleck
方法 Fluorescence
细胞系 Primary myoblasts
浓度 2 mg/kg
处理时间 2 weeks
结果 To examine this further, it determined whether inhibition of the proteasome with bortezomib blocked proplatelet formation in murine megakaryocytes. Similar responses were observed in human megakaryocytes, and removal of bortezomib from the incubation media restored proplatelet formation.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Blood 2012, 119, 4686-97. Ritonavir purchased from Selleck
方法 annexin V/DAPI staining
细胞系 Primary myeloma cells
浓度 20 uM
处理时间 24 h
结果 A range of cell death induction is seen in patient samples after incubation with a concentration of ritonavir (20 μM).
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Blood 2012, 119, 4686-97. Ritonavir purchased from Selleck
方法 Western blot
细胞系 KMS11 and L363 cells
浓度 1-50 uM
处理时间 17, 72 h
结果 As shown in Figure A through D, ritonavir treatment elicits dose-dependent abrogation of both glucose transport and proliferation in KMS11 and L363 cells.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Cancer Res 2014, 74(16), 4458-69. Carfilzomib (PR-171) purchased from Selleck
方法 Western blot
细胞系 MM.1S cells
浓度 10 nM
处理时间 24 h
结果 CHOP expression was induced by carfilzomib indicating ER stress, which was enhanced by TAS-117 and associated with enhanced PARP cleavage.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Mol Biol Evol 2014, 31(6), 1546-53. Danoprevir (ITMN-191) purchased from Selleck
方法 Western blot
细胞系
浓度 20 uM
处理时间 3 h
结果 Using site-directed mutagenesis, we introduced the A156T substitution in the dominant NS3 protease variant of each individual. The catalytic efficiency of the 56 wild-type and 56 mutated proteases was assayed via MAVS cleavage using a bacteriophage λ genetic screen. The enzymatic activities of variant proteases were evaluated by engineering the MAVS cleavage site into the λ cI repressor. The enzymatic activity was related to the activity of a protease variant carrying the lethal substitution S139A. The S139 residue is part of the catalytic triad of the enzyme. As it have previously demonstrated, the expression of the HCV NS3 protease resulted in cleavage of the lambda cI repressor with MAVS cleavage site. Expression of an NS3 protease that included a substitution in catalytic residue S139 completely abolished the cleavage of lambda cI repressor.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Oncogene 2014, 10.1038/onc.2014.319. DAPT (GSI-IX) purchased from Selleck
方法 Western blot
细胞系 Notch1 ΔE cells
浓度 10 uM
处理时间 3 days
结果 Indeed, depleted SUMO1 were observed in NOTCH1 cells compared with control MCF10A cells. Western blotting showing increased unconjugated SUMO1 levels in Notch1 ΔE cells treated with 10 uM DAPT for 3 days.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Stem Cells 2014, 32(1), 301-12. DAPT (GSI-IX) purchased from Selleck
方法 Western blot
细胞系 Glioma tumor-initiating cells
浓度 5-50 uM
处理时间 48 h
结果 This cleavage can release the NICD, and released NICD translocates into the nucleus and binds CBF-1 to activate Notch targeting genes, such as the Hes genes, to antagonize the activity of proneural genes like Mash1, Math, NeuroD, and Neurogenins. As shown in Figure , DAPT, BMS-708163 inhibited expression of NICD, Hes1, Hes3, and Hes5 in a time- and dose-dependent manner.

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