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Adezmapimod

产品编号 T1764 CAS 152121-47-6

别名: PB 203580, 4-(4-氟苯基)-2-(4-甲基亚磺酰基苯基)-5-(4-吡啶基)-1H-咪唑, RWJ 64809, SB203580

Adezmapimod (SB 203580) 是一种 p38 MAPK 抑制剂 (IC50=0.3-0.5 μM)，具有选择性和 ATP 竞争性。Adezmapimod 具有自噬和线粒体自噬的激活活性。Adezmapimod 显示出比 PKB、LCK 和 GSK-3β 高 100 倍以上的选择性。

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Adezmapimod, CAS 152121-47-6

规格	价格/CNY	货期
5 mg	￥ 297	现货
10 mg	￥ 488	现货
25 mg	￥ 783	现货
50 mg	￥ 1,160	现货
100 mg	￥ 1,730	现货
200 mg	￥ 2,580	现货
500 mg	￥ 4,270	现货
1 mL * 10 mM (in DMSO)	￥ 348	现货

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其他形式的 Adezmapimod:

SB 203580 hydrochloride
询价

选择批次

纯度: 99.87%

纯度: 99.79%

纯度: 99.59%

纯度: 99.42%

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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	Adezmapimod (SB 203580) is a p38 MAPK inhibitor (IC50=0.3-0.5 μM) that is selective and ATP-competitive. Adezmapimod possesses autophagy and mitochondrial autophagy activating activity. Adezmapimod displays more than 100-fold higher selectivity than PKB, LCK, and GSK-3β.
靶点活性	PKB:3-5 μM (THP-1 cells), p38 MAPK:0.3-0.5 μM (THP-1 cells)
体外活性	方法：人肝癌细胞 HepG2 用 Adezmapimod (0.1-20 μM) 处理 30 min，使用 Western Blot 方法检测靶点蛋白表达水平。结果：Adezmapimod 剂量依赖性地激活 ERK，但不激活 p38 和 JNK。ERK 的最大活化是在 1- 10 μM 之间。[1] 方法：CD4+T 细胞用 Adezmapimod (1-25 μM) 处理 72 h，使用 Flow Cytometry 方法分析 Tregs 的增殖。结果：Adezmapimod 以剂量依赖的方式抑制 TNF 诱导的 Tregs 增殖，抑制率为32.0-73.2%。Adezmapimod 处理也显著降低了培养的 CD4+T 细胞中 Foxp3+ Treg 的比例，抑制率为24.9-47.05%。[2]
体内活性	方法：为检测体内活性，将 Adezmapimod (25 mg/kg in 4% DMSO+30% PEG 300+5% Tween 80+61% ddH2O) 单次腹腔注射给 LPS 处理的 C57BL/6J 小鼠，24 和 72 h 后，处死小鼠。结果：通过 Adezmapimod 的处理，LPS 诱导的 Tregs 上 Ki-67 和 TNFR2 表达的上调被完全消除。在 LPS 处理的小鼠中，Adezmapimod 对 Tregs 增殖扩增的抑制作用可以持续至少 72 h。[2] 方法：检测对子宫内膜异位症 (EM) 发育的影响，将 Adezmapimod (1 μg/mg) 腹腔注射给诱导 EM 的 BALB/c 小鼠，每天一次，持续二十四天。结果：Adezmapimod 降低了小鼠子宫内膜异位病变的重量和大小。与 EM 组相比，Adezmapimod 组腹膜细胞的 IL-1β、TNF-α、MMP-2 和 MMP-9 水平降低。EM 组 p38 MAPK 的磷酸化水平升高，Adezmapimod 下调了磷酸化水平。[3]
激酶实验	Cells were lysed in Buffer A for Western blotting and PKB kinase assays. Kinase assays were performed according to the manufacturer's instructions. Briefly, 4 μg of sheep anti-PKBα was immobilized on 25 μl of protein G-Sepharose overnight (or 1.5 h) and washed in Buffer A (50 mM Tris, pH 7.5, 1 mM EDTA, 1 mMEGTA, 0.5 mM Na3VO4, 0.1% β-mercaptoethanol, 1% Triton X-100, 50 mM sodium fluoride, 5 mM sodium pyrophosphate, 0.1 mM phenylmethylsulfonyl fluoride, 1 μg/ml aprotinin, pepstatin, leupeptin, and 1 μM microcystin). The immobilized anti-PKB was then incubated with 0.5 ml of lysate (from 5 × 10^6 cells) for 1.5 h and washed three times in 0.5 ml of Buffer A supplemented with 0.5 M NaCl, two times in 0.5 ml of Buffer B (50 mM Tris-HCl, pH 7.5, 0.03% (w/v) Brij-35, 0.1 mM EGTA, and 0.1% β-mercaptoethanol), and twice with 100 μl of assay dilution buffer; 5× assay dilution buffer is 100 mM MOPS, pH 7.2, 125 mMβ-glycerophosphate, 25 mM EGTA, 5 mM sodium orthovanadate, 5 mM DTT. To the PKB enzyme immune complex was added 10 μl of assay dilution buffer, 40 μM protein kinase A inhibitor peptide, 100 μM PKB-specific substrate peptide, and 10 μCi of [γ-32P]ATP, all made up in assay dilution buffer. The reaction was incubated for 20 min at room temperature with shaking, then samples were pulse spun, and 40 μl of reaction volume were removed into another tube to which was added 20 μl of 40% trichloroacetic acid to stop the reaction. This was mixed and incubated for 5 min at room temperature, and 40 μl was transferred onto P81 phosphocellulose paper and allowed to bind for 30 s. The P81 pieces were washed three times in 0.75% phosphoric acid then in acetone at room temperature. γ-32P incorporation was then measured by scintillation counting [1].
细胞实验	The luciferase reporter plasmid pIL6luc(-122) and the CAT reporter plasmid p(TRE)5CAT were transfected into TF-1 cell line by means of electroporation. Prior to transfection, cells were cultured for 16?h at a density of 0.5×10^6 cells/ml in the appropriate medium, washed twice and resuspended in RPMI 1640 at a density of 10×10^6 in 200?μl. When transfected with a single plasmid, 25?μg of DNA was added and the mixture was left at room temperature for 15?min. Cotransfections were performed with 15?μg of the reporter plasmid pIL6luc(-122) together with 15?μg of the dominant-negative expression plasmids (pRSV-MKK3(Ala), pcDNA3-MKK6(K82A), pRSV-NΔRaf1, pcDNA3-MKK4(Ala), pcDNA3-Flag-JNK1, or pcDNA3 (empty vector). Cotransfections of pGAL4tkluc (5?μg) with either pGAL4p65 (5?μg) or pGAL4dbd (5?μg) were performed under similar conditions. In addition, cells were cotransfected with 2?μg of a CMV-CAT plasmid, to normalize for transfection efficiency. Electroporation, in 0.4?cm electroporation cuvettes, was performed at 240?V and 960?μF with Gene Pulser electroporator. After electroporation, the cells were replated in RPMI 1640 containing 2% FBS. Six hours after transfection cells were stimulated for 24?h with medium or OA (30?ng/ml) or SB203580 for 30?min prior to OA stimulation. The cells were then harvested and lysed by commercially available luciferase lysis buffer. One-hundred μl of lysis product was added to 100?μl of luciferase assay reagents and luciferase activity was measured with the Anthos Lucy1 luminometer. CAT reporter activity of 100?μl lysis product plus 100?μl CAT dilution buffer was determined with a commercially available CAT Elisa kit [3].
动物实验	In survival studies, C57BL/6J mice weighing 20 g to 30 g were briefly anesthetized with isoflurane and challenged with 0.05 mL of IT normal saline (NS, noninfected controls) or E. coli (15 × 10^9 CFU/kg) as previously described. One hour before NS challenge, mice (n = 24) received either intraperitoneal SB203580 (100 mg/kg in 0.25 mL) or diluent only (placebo). Infected animals received SB203580 in doses of 100, 10, 1, or 0.1 mg/kg or placebo 1 hour before IT E. coli (n = 241); SB203580 100 or 0.1 mg/kg or placebo 1 hour after E. coli (n = 121); or SB203580 100 mg/kg or placebo 12 hours after E. coli (n = 72). All animals received ceftriaxone (100 mg/kg in 0.1 mL, subcutaneously) for 4 days and NS (0.5 mL, subcutaneously) for 1 day beginning 4 hours after challenge. Animals were observed every 2 hours for the initial 48 hours, every 4 hours from 48 hours to 72 hours, every 8 hours from 72 hours to 96 hours, and then twice daily until study completion (168 hours). Sequential weekly experiments with 24 animals each compared either two to three doses of SB203580 versus placebo administered at similar times or similar doses of SB203580 versus placebo at differing treatment times. Study groups in each experiment were of equivalent sample size (i.e., 6 – 8 per group) [5].

别名	PB 203580, 4-(4-氟苯基)-2-(4-甲基亚磺酰基苯基)-5-(4-吡啶基)-1H-咪唑, RWJ 64809, SB203580
分子量	377.43
分子式	C21H16FN3OS
CAS No.	152121-47-6

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

DMSO: 50 mg/mL (132.47 mM)

1eq. HCl: 37.7 mg/mL (100 mM)

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
DMSO / 1eq. HCl	1 mM	2.6495 mL	13.2475 mL	26.495 mL	66.2374 mL
	5 mM	0.5299 mL	2.6495 mL	5.299 mL	13.2475 mL
	10 mM	0.2649 mL	1.3247 mL	2.6495 mL	6.6237 mL
	20 mM	0.1325 mL	0.6624 mL	1.3247 mL	3.3119 mL
	50 mM	0.053 mL	0.2649 mL	0.5299 mL	1.3247 mL
	100 mM	0.0265 mL	0.1325 mL	0.2649 mL	0.6624 mL

计算器

摩尔浓度计算器

稀释计算器

配液计算器

分子量计算器

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浓度

容积

分子量

浓度 (起始)

容积 (起始)

浓度 (终)

容积 (终)

溶液体积

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配液浓度

参考文献

1. Henklova P, et al. SB203580, a pharmacological inhibitor of p38 MAP kinase transduction pathway activates ERK and JNK MAP kinases in primary cultures of human hepatocytes. Eur J Pharmacol. 2008 Sep 28;593(1-3):16-23. 2. He T, et al. The p38 MAPK Inhibitor SB203580 Abrogates Tumor Necrosis Factor-Induced Proliferative Expansion of Mouse CD4+Foxp3+ Regulatory T Cells. Front Immunol. 2018 Jul 9;9:1556. 3. Zhou WD, et al. SB203580, a p38 mitogen-activated protein kinase inhibitor, suppresses the development of endometriosis by down-regulating proinflammatory cytokines and proteolytic factors in a mouse model. Hum Reprod. 2010 Dec;25(12):3110-6. 4. Jin N, et al. The selective p38 mitogen-activated protein kinase inhibitor, SB203580, improves renal disease in MRL/lpr mouse model of systemic lupus. Int Immunopharmacol. 2011 Sep;11(9):1319-26. 5. Su J, et al. SB203580, a p38 inhibitor, improved cardiac function but worsened lung injury and survival during Escherichia coli pneumonia in mice. J Trauma. 2010 Jun;68(6):1317-27. 7. Liu J, Lv L, Gong J, et al. Overexpression of F-box only protein 31 predicts poor prognosis and deregulates p38α- and JNK-mediated apoptosis in esophageal squamous cell carcinoma [J]. International journal of cancer. 2018 Jan 1;142(1):145-155. 8. Zhou B, Yan J, Guo L, et al. Hepatoma cell-intrinsic TLR9 activation induces immune escape through PD-L1 upregulation in hepatocellular carcinoma[J]. Theranostics. 2020, 10(14): 6530. 9. Hu S, Zhu L, Song Y, et al. Radiation-induced abscopal reproductive effect is driven by TNF-α/p38 MAPK/Rac1 axis in Sertoli cells[J]. Theranostics. 2021, 11(12): 5742.

文献引用

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11. Li Z J, Hou Y J, Hao G P, et al. CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells. Journal of Cell Communication and Signaling. 2020: 1-11. 12. Lyu L, Hu Y, Yin S, et al. Autophagy inhibition enhances anti‐pituitary adenoma effect of tetrandrine. Phytotherapy Research. 2021, 35(7): 4007-4021. 13. Zhang H, Wei Q, Gao Z, et al. G protein-coupled receptor 30 mediates meiosis resumption and gap junction communications downregulation in goat cumulus-oocyte complexes by 17β-estradio. Journal of Steroid Biochemistry and Molecular Biology. 2019, 187: 58-67 14. Hu S, Zhu L, Song Y, et al. Radiation-induced abscopal reproductive effect is driven by TNF-α/p38 MAPK/Rac1 axis in Sertoli cells. Theranostics. 2021 Mar 31;11(12):5742-5758. doi: 10.7150/thno.56853. eCollection 2021. 15. Zhou B, Yan J, Guo L, et al. Hepatoma cell-intrinsic TLR9 activation induces immune escape through PD-L1 upregulation in hepatocellular carcinoma. Theranostics. 2020, 10(14): 6530. 16. Li Z J, Hou Y J, Hao G P, et al. CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells. Journal of Cell Communication and Signaling. 2020: 1-11. 17. Cen W J, Feng Y, Li S S, et al. Iron overload induces G1 phase arrest and autophagy in murine preosteoblast cells. Journal of cellular physiology. 2018, 233(9): 6779-6789. 18. Tang J, Yao C, Liu Y, et al. Arsenic trioxide induces expression of BCL-2 expression via NF-κB and p38 MAPK signaling pathways in BEAS-2B cells during apoptosis. Ecotoxicology and Environmental Safety. 2021, 222: 112531. 19. Wang D, Wang H, Yan Y, et al.Coating 3D-printed bioceramics with histatin promotes adhesion and osteogenesis of stem cells.Tissue Engineering.2023 (ja). 20. Du T, Yan Z, Zhu S, et al. QKI deficiency leads to osteoporosis by promoting RANKL-inducedosteoclastogenesis and disrupting bone metabolism. Cell Death and Disease. 2020 21. Wen Y, Peng D, Li C, et al. A new polysaccharide isolated from Morchella importuna fruiting bodies and its immunoregulatory mechanism. International Journal of Biological Macromolecules. 2019, 137: 8-19. 22. Yuan J, Yao C, Tang J, et al. Enhanced GRP78 protein expression via the IRE1α/ASK1/p38 MAPK pathway during As2O3-induced endoplasmic reticulum stress in BEAS-2B cells. Toxicology. 2021, 462: 152962. 23. Hu Q, Du H, Ma G, et al. Purification, identification and functional characterization of an immunomodulatory protein from Pleurotus eryngii. Food & Function. 2018, 9(7): 3764-3775 24. Zhu N, Xiang Y, Zhao X, et al. Thymoquinone suppresses platelet‐derived growth factor‐BB–induced vascular smooth muscle cell proliferation, migration and neointimal formation. Journal of Cellular and Molecular Medicine. 2019 25. 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. Journal of neuroinflammation. 2020, 17(1): 1-17. 26. Liu Y, Tang J, Yuan J, et al. Arsenite-induced downregulation of occludin in mouse lungs and BEAS-2B cells via the ROS/ERK/ELK1/MLCK and ROS/p38 MAPK signaling pathways. Toxicology Letters. 2020, 332: 146-154 27. Da Q, Yan Z, Li Z, et al. TAK1 is involved in sodium L-lactate-stimulated p38 signaling and promotes apoptosis. Molecular and Cellular Biochemistry. 2020: 1-10 28. Lu D, Zhang H, Zhang Y, et al. Secreted MbovP0145 Promotes IL-8 Expression through Its Interactive β-Actin and MAPK Activation and Contributes to Neutrophil Migration. Pathogens. 2021, 10(12): 1628. 29. Zhao M, Zheng Z, Yin Z, et al.DEL-1 deficiency aggravates pressure overload-induced heart failure by promoting neutrophil infiltration and neutrophil extracellular traps formation.Biochemical Pharmacology.2023: 115912. 30. Cui S, Suo N, Yang Y, et al.The aminosteroid U73122 promotes oligodendrocytes generation and myelin formation.Acta Pharmacologica Sinica.2023: 1-12. 31. Zhang X, Wang J, Wang M, et al.IFN-β Pretreatment Alleviates Allogeneic Renal Tubular Epithelial Cell–Induced NK Cell Responses via the IRF7/HLA-E/NKG2A Axis.The Journal of Immunology.2023 32. Ni L, Zhu X, Zhao Q, et al.Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways.Neoplasia.2024, 51: 100991.

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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

剂量

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+

计算重置

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。

技术支持

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

Adezmapimod 152121-47-6 Autophagy MAPK Mitophagy p38 MAPK Inhibitor PKBα PB 203580 inhibit 4-(4-氟苯基)-2-(4-甲基亚磺酰基苯基)-5-(4-吡啶基)-1H-咪唑 SAPK2a GSK3β RWJ 64809 Mitochondrial Autophagy SB-203580 PB-203580 SB203580 SB 203580 RWJ64809 PB203580 LCK SAPK2b RWJ-64809 ATP-competitive inhibitor

我们的所有产品和服务仅用于科学研究，不能被用于人体，我们也不向个人提供产品和服务。

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Adezmapimod

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参考文献

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剂量换算

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