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SCH772984

产品编号 T6066 CAS 942183-80-4

SCH772984 是高选择性和 ATP 竞争性ERK 抑制剂，对 ERK1 和 ERK2 的IC50分别为 4 和 1 nM。它在含有 BRAF 或 RAS 突变的 MAPK 抑制剂初治和 MAPK 抑制剂耐药细胞中具有抗肿瘤活性。

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SCH772984, CAS 942183-80-4

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其他形式的 SCH772984:

SCH772984 HCl
询价

选择批次

纯度: 98.75%

纯度: 98.45%

纯度: 98.01%

纯度: 98%

纯度: 97.65%

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生物活性

化学信息

存储 & 溶解度

参考文献

相关产品

产品描述	SCH 772984 is a potent inhibitor of ERK1/ERK2 (IC50: 4/1 nM) and has only weak inhibitory for other 300 tested kinases.
靶点活性	ERK2:1 nM (cell free), ERK1:4 nM (cell free)
体外活性	SCH772984 potently inhibited ERK1 and ERK2 activity (IC50s: 4/1 nmol/L). SCH772984 is highly selective, with only seven kinases of 300 tested showing more than 50% inhibition at a concentration of 1 μmol/L. Treatment of the BRAFV600E-mutant human melanoma cell line LOXIMV1 (LOX) with SCH772984 resulted in a dose-dependent inhibition of phosphorylation of the ERK substrate p90 ribosomal S6 kinase. SCH772984 also inhibited phosphorylation of residues in the activation loop of ERK itself [1]. In a panel of 121 human tumor cell lines, SCH772984 showed EC50 values less than 500 nmol/L in approximately 88% and 49% of BRAF-mutant or RAS-mutant tumor lines, respectively [2].
体内活性	Treatment of BRAF-mutant LOX melanoma xenografts with SCH772984 (50 mg/kg twice daily) led to 98% tumor regression. Dose-dependent antitumor activity was also observed in the KRAS-mutant pancreatic MiaPaCa model, with 36% regression at 50 mg/kg twice daily [1].
激酶实验	SCH772984 was tested in 8-point dilution curves in duplicate against purified ERK1 or ERK2. The enzyme was added to the reaction plate and incubated with the compound before adding a solution of substrate peptide and ATP. Fourteen microliters of diluted enzyme (0.3 ng active ERK2 per reaction) was added to each well of a 384-well plate. The plates were gently shaken to mix the reagents and incubated for 45 minutes at room temperature. The reaction was stopped with 60 μL of IMAP Binding Solution (1:2,200 dilutions of IMAP beads in 1× binding buffer). The plates were incubated at room temperature for an additional 0.5 hours to allow complete binding of phosphopeptides to the IMAP beads. Plates were read on the LJL Analyst [1].
细胞实验	For resistant cell line creation, cells were grown in Dulbecco's modified Eagle medium with 10% heat-inactivated FBS media and increasing concentrations of inhibitor (PLX4032, 0.1–10 μmol/L; GSK1120212, 0.01–1 μmol/L) over approximately 4 to 8 months until resistant cells acquired growth properties similar to na?ve parental cells (at their top drug concentrations). For combination resistance, cells were incubated as above but with alternative dose escalation until a top concentration was acquired (PLX4032 10 μmol/L and GSK1120212 1 μmol/L). Stocks and dilutions of PLX4032, GSK1120212, and SCH772984 were made in DMSO solvent. Cell proliferation experiments were carried out in a 96-well format (six replicates), and cells were plated at a density of 4,000 cells per well. At 24 hours after cell seeding, cells were treated with DMSO or a 9-point IC50 dilution (0.001–10 μmol/L) at a final concentration of 1% DMSO for all concentrations. Viability was assayed 5 days after dosing using the ViaLight luminescence kit following the manufacturer's recommendations (n = 6, mean ± SE). For the cell line panel viability assay, cells were treated with SCH772984 for 4 days and assayed by the CellTiterGlo luminescent cell viability assay. For IncuCyte analysis, cells were plated as above in 96-well plates, and image-based cell confluence data were collected every 2 hours during live growth. For engineered resistant lines, cells were infected with lentivirus produced from lentiORF constructs expressing either RFP, KRASG13D, BRAFV600E, truncated BRAFV600E lacking exons 2–8 (Δ2-8), MEK1P124L, MEK1F129L, or constitutively active MEK1DD (S218D+S222D). Cells were selected in blasticidin (20 μg/mL) and used for ViaLight assays as described above [1].
动物实验	Nude mice were injected subcutaneously with specific cell lines, grown to approximately 100 mm^3, randomized to treatment groups (10 mice/group), and treated intraperitoneally with either SCH772984 or vehicle according to the dosing schedule indicated in the figure legends. Tumor length (L), width (W), and height (H) were measured during and after the treatment periods by a caliper twice weekly on each mouse and then used to calculate tumor volume using the formula (L × W × H)/2. Animal body weights were measured on the same days twice weekly. Data were expressed as mean ± SEM. Upon completion of the experiment, vehicle- and SCH772984-treated tumor biopsies were processed for Western blot analysis [1].

化合物与蛋白结合的复合物	Structure of human haspin (GSG2) in complex with SCH772984 revealing the first type-I binding mode
分子量	587.67
分子式	C33H33N9O2
CAS No.	942183-80-4

存储

　|　Powder: -20°C for 3 years | In solvent: -80°C for 2 years

溶解度

H2O: <1 mg/mL

Ethanol: <1 mg/mL

DMSO: 51 mg/mL(86.8 mM)

( < 1 mg/mL refers to the product slightly soluble or insoluble )

参考文献

1. Morris EJ, et al. Discovery of a novel ERK inhibitor with activity in models of acquired resistance to BRAF and MEK inhibitors. Cancer Discov. 2013 Jul;3(7):742-50. 2. Chaikuad A, et al. A unique inhibitor binding site in ERK1/2 is associated with slow binding kinetics. Nat Chem Biol. 2014 Oct;10(10):853-60. 3. Jiang S, Wang Z, Zhu T, et al. The Downregulation of EIF3a Contributes to Vemurafenib Resistance in Melanoma By Activating ERK Via PPP2R1B[J]. 2021 4. Lang J Y, Wang X, Xie Q, et al. Targeting KRAS-mutant stomach/colorectal tumours by disrupting the ERK2-p53 complex[J]. bioRxiv. 2020 5. Chang G, Xiao W, Xu Z, et al. Pterostilbene Induces Cell Apoptosis and Cell Cycle Arrest in T-Cell Leukemia/Lymphoma by Suppressing the ERK1/2 Pathway[J]. BioMed Research International. 2017;2017:9872073 6. Zhang B, Zhao J, Wang Z, et al. DL0410 attenuates oxidative stress and neuroinflammation via BDNF/TrkB/ERK/CREB and Nrf2/HO-1 activation[J]. International Immunopharmacology. 2020, 86: 106729. 7. Bin Y F, Ma N, Lu Y X, et al. Erythromycin reverses cigarette smoke extract-induced corticosteroid insensitivity by inhibition of the JNK/c-Jun pathway[J]. Free Radical Biology and Medicine. 2020, 152: 494-503. 8. Xie D, Ge X, Ma Y, et al. Clemastine improves hypomyelination in rats with hypoxic–ischemic brain injury by reducing microglia-derived IL-1β via P38 signaling pathway[J]. Journal of neuroinflammation. 2020, 17(1): 1-17. 9. Zhao Z, Xue F, Gu Y, et al. Crosstalk between the muscular estrogen receptor α and BDNF/TrkB signaling alleviates metabolic syndrome via 7, 8-dihydroxyflavone in female mice[J]. Molecular Metabolism. 2020: 101149. 10. Caiola E, Iezzi A, Tomanelli M, et al. LKB1 deficiency renders non-small-cell lung cancer cells sensitive to ERK inhibitors.: ERK inhibitors in LKB1 mutated NSCLC[J]. Journal of Thoracic Oncology. 2019.

文献引用

1. Wang X, Xie Q, Ji Y, et al.Targeting KRAS-mutant stomach/colorectal tumors by disrupting the ERK2-p53 complex.Cell Reports.2023, 42(1): 111972. 2. Lai J, Li Y, Ran M, et al.Xanthotoxin, a novel inducer of platelet formation, promotes thrombocytopoiesis via IL-1R1 and MEK/ERK signaling.Biomedicine & Pharmacotherapy.2023, 163: 114811. 3. Li M, Wang Z, Fu S, et al.Taurine reduction of injury from neutrophil infiltration ameliorates Streptococcus uberis-induced mastitis.International Immunopharmacology.2023, 124: 111028. 4. Jiang S, Wang Z, Zhu T, et al. The Downregulation of EIF3a Contributes to Vemurafenib Resistance in Melanoma By Activating ERK Via PPP2R1B. Frontiers in Pharmacology. 2021: 2242. 5. Zhang B, Zhao J, Wang Z, et al. DL0410 attenuates oxidative stress and neuroinflammation via BDNF/TrkB/ERK/CREB and Nrf2/HO-1 activation. International Immunopharmacology. 2020, 86: 106729. 6. Zhao Z, Xue F, Gu Y, et al. Crosstalk between the muscular estrogen receptor α and BDNF/TrkB signaling alleviates metabolic syndrome via 7, 8-dihydroxyflavone in female mice. Molecular Metabolism. 2020: 101149. 7. Caiola E, Iezzi A, Tomanelli M, et al. LKB1 Deficiency Renders NSCLC Cells Sensitive to ERK Inhibitors. Journal of Thoracic Oncology. 2020, 15(3): 360-370 8. Caiola E, Iezzi A, Tomanelli M, et al. LKB1 deficiency renders non-small-cell lung cancer cells sensitive to ERK inhibitors.: ERK inhibitors in LKB1 mutated NSCLC. Journal of Thoracic Oncology. 2019 9. Chang Y W, Wang C C, Yin C F, et al. Quantitative phosphoproteomics reveals ectopic ATP synthase on mesenchymal stem cells to promote tumor progression via ERK/c-Fos pathway activation. Molecular & Cellular Proteomics. 2022, 21(6) 10. Yang J, Wang X, Fan Y, et al. Tropoelastin improves adhesion and migration of intra-articular injected infrapatellar fat pad MSCs and reduces osteoarthritis progression. Bioactive Materials. 2021

剂量换算

对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

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mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

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计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

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您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

SCH772984 942183-80-4 MAPK ERK MEK Extracellular signal regulated kinases Inhibitor SCH 772984 SCH-772984 inhibit inhibitor

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SCH772984

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