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

Target Selective Inhibitor Library

605 target selective inhibitors

规格 价格  
预溶于DMSO
100uL/well (10mM solution) RMB 74920.68
2x100uL/well (10mM solution) RMB 138001.81
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产品详情

产品描述及优势

     

    • A unique collection of validated bioactive compounds covering over 174 targets

    • Each compound was selected based on its ability to principally interact with a single target, leading to minimal off-target activity

    • Selectivity is at least 100-fold higher relative to non-primary target(s)

    •Targets cover a wide variety of signaling pathways, including PI3K/Akt, MAPK, PTK, JAK, apoptosis, and others!

    • This unique tool is ideal for studying mechanisms of action or for target screening

    • Compounds are structurally diverse, biologically active, and cell permeable

    • Selleck provides rich supporting documentation which includes compound structure, IC50, and customer reviews

    • Compounds are NMR and HPLC validated to ensure our customers receive high purity compounds

产品详细信息

配制:
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 Nature,2015, 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck
方法 Animal studies
细胞系 A375 tumours
浓度 10 mg/kg
处理时间 4, 5 days
结果 Although vemurafenib treatment decreased the volume of sensitive tumours (A375 alone)(b), Green fluorescent protein (GFP) staining confirmed increased numbers of resistant cells in regressing tumours, and EdU or BrdU staining confirmed their increased proliferation rate compared to the vehicletreated controls (c). Tumours comprising only resistant cells showed no growth difference when treated with vehicle or vemurafenib (d), indicating that the growth advantage of resistant cells in regressing tumours was not caused by direct effects of vemurafenib on cancer or stromal cells. In line with these findings, A375R cells co-implanted with other vemurafenib-sensitive melanoma cell lines (Colo800, LOX and UACC62) also showed an up toeightfold growthincreasecompared to vehicle-treated control groups (e). Local growth acceleration of resistant cells in the regressing subcutaneous tumours resulted in higher lung metastatic burden (f).
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Nature 2015, 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck
方法 Immunofluorescence staining
细胞系 A375/A375R tumours
浓度 0.1-1 uM
处理时间 5 days
结果 This analysis highlighted FRA1 (also known FOSL1), a member of the AP1 transcription factor complex and effector of the ERK pathway27, as one of the putative upstream regulators of the TIS .FRA1 was downregulated in all drug-sensitive cells, but not in resistan cells, treated with vemurafenib, crizotinib and erlotinib (c, d).
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Nature 2015, 517(7534), 391-5. PD0325901 purchased from Selleck
方法 Western blot
细胞系 Metabolic
浓度 10 mg/kg
处理时间 5 days
结果 PD0325901 caused a decrease in PPARc phosphorylation at S112 and S273, confirming the established role of ERKs in regulating S112 and strongly suggesting a new role in regulating S273 (refs 22-24).
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Nature 2010, 468, 968-972. Selumetinib (AZD6244) purchased from Selleck
方法 Immunoblotting
细胞系 A375 cells
浓度 1 μM
处理时间
结果 Ectopic COT expression in A375 and SKMEL28 cells also conferred decreased sensitivity to the MEK inhibitors CI-1040 and AZD6244, suggesting that COT expression alone was sufficient to induce this phenotype. In the setting of ectopic COT expression, exposure to AZD6244 or CI-1040 in combination with PLX470 (1 μM each) reduced cell growth and pERK expression more effectively than did single-agent PLX4720, even at concentrations of 10 μM.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Nature 2010, 468, 973-977. Selumetinib (AZD6244) purchased from Selleck
方法 Survival Assay
细胞系 isogenic cell
浓度 0.01-10 μM
处理时间 72 h
结果 The growth of M249 R4 and Pt55 R was sensitive to MEK inhibition in the presence of PLX4032
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Science 2011, 331, 912-916. PD184352 (CI-1040) purchased from Selleck
方法 Immunohistochemistry
细胞系 Hand2d/d mice
浓度
处理时间 24h
结果 The epithelia of vehicle-treated horn showed prominent expression of p-FRS2 and p-ERK1/2(Fig.A,a and c). However, the levels of both p -FRS2 and p -ERK1/2 were reduced in the epithelia of PD173074-treated horn on day 4 of pregnancy (Fig. A, b and d). We also observed a marked decline in the proliferative activity of Hand2-null uterine epithelia, as indicated by decreased Ki-67 staining (Fig. A, e and f) . In parallel experiments, administration of PD184352, an inhibitor of the ERK1/2 pathway, to uterine horns of Hand2 d/d mice suppressed the level of pERK1/2 (Fig.B, a and b) , as well as luminal epithelial proliferation ( Fig. B, c and d).The ERK1/2-dependent phosphorylation of epithelial ERα at Ser118 is critical for the transcriptional activation of ERα. Administration of either PD173074 (Fig. C, a to d) or PD184352 (Fig. C, e to h) to Hand2-null uterine horns blocked the phosphorylation of epithelial ERα at Ser118 and the expression of Muc -1.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Cell 2010, 142, 444–455. VX-680 (Tozasertib, MK-0457) purchased from Selleck
方法 Immunofluorescence Microscopy
细胞系 HeLa cells
浓度
处理时间
结果 Inhibition of Aurora kinases with VX-680 sharply reduced kinetochore-localized pT422 signal (Figure G). When normalized to the total level of CENP-E at the kinetochore (which is also reduced in VX-680 treated cells (Ditchfield et al. 2003)), a > 90% reduction in T422 phosphorylation was seen following VX-680 treatment ( Figure H).
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Cancer Cell 2013, 24, 766-76. MK-2206 2HCl purchased from Selleck
方法 analysis of luciferase activity
细胞系 immunodeficient NOG mice
浓度 10 mg kg-1
处理时间 3 days
结果 In this experiment, animalstreated with dexamethasone or MK2206 showed progressivetumor growth similar to that observed in vehicle-treated controls,while mice treated with MK2206 plus dexamethasone had significant antitumor responses.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Cancer Cell 2012, 21(2), 155-67. Everolimus (RAD001) purchased from Selleck
方法 Western blotting
细胞系 MP tumor cells
浓度 1, 5 uM
处理时间 3 h
结果 To confirm that these compounds were acting on the PI3K/mTOR pathway, it performed western blotting to analyze phosphorylation of critical proteins in the pathway. As shown in figure, MP tumor cells showed substantial amounts of phospho-AKT and phospho-S6 in the absence of inhibitors (DMSO lanes). RAD-001 inhibited S6 phosphorylation but did not affect phospho-AKT. In contrast with RAD-001, treatment with BEZ-235 or BKM-120 inhibited phosphorylation of both AKT and S6.
Axitinib and PF2341066(Crizotinib) Reviews
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数据来源 Cancer Cell 2010, 18, 641–654. BI 2536 purchased from Selleck
方法 Immunohistochemical analysis
细胞系 SCID mice
浓度
处理时间
结果 Control tumors grow exponentially, whereas genetic ablation of Cdc20 results in complete tumor regression in about 10 days. In comparison, treatment with taxol, vincristine, and BI2536 only induces partial responses ( Figure C). In agreement with the data observed in vitro, immunohistochemical analysis of samples taken 3 days after the first treatment indicates lack of proliferation (as measured by BrdU incorporation) and massive apoptosis in Cdc20 null cells, whereas all other samples maintain significant levels of proliferation and reduced apoptotic markers ( Figure D)

Selleck产品在文献中的引用 (32)

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