p38 MAPK Inhibitor
(Synonyms: p38 MAP Kinase Inhibitor, p38 Mitogen-activated Protein Kinase Inhibitor) 目录号 : GC44530
A potent inhibitor of p38 MAP kinase
Cas No.:219138-24-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
p38 MAPK inhibitor is a potent inhibitor of p38 MAP kinase (IC50 = 35 nM). It inhibits senescence induced by the oncogene RAS.
| Cas No. | 219138-24-6 | SDF | |
| 别名 | p38 MAP Kinase Inhibitor, p38 Mitogen-activated Protein Kinase Inhibitor | ||
| Canonical SMILES | FC1=CC=C(C2=C(C3=CC=NC=C3)NN(C4=CC=C(Cl)C=C4)C2=O)C=C1 | ||
| 分子式 | C20H13ClFN3O | 分子量 | 365.8 |
| 溶解度 | DMF: 5 mg/ml,DMSO: 5 mg/ml,DMSO:PBS(pH7.2) (1:1): 0.5 mg/ml,Ethanol: 0.3 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.7337 mL | 13.6687 mL | 27.3373 mL |
| 5 mM | 0.5467 mL | 2.7337 mL | 5.4675 mL |
| 10 mM | 0.2734 mL | 1.3669 mL | 2.7337 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
p38 MAPK Inhibitor, CBS3830 limits vascular remodelling in arterialised vein grafts
Heart Lung Circ 2013 Sep;22(9):751-8.PMID:23523564DOI:10.1016/j.hlc.2013.02.006.
Objective: Following bypass surgery vein grafts undergo a remodelling process that can lead to restenosis and ultimately vein graft failure. Signalling through mitogen activated protein kinases (MAPKs) is a key mechanism involved in vein graft failure. Here, we investigated whether CBS3830 (c-a-i-r biosciences GmbH, Tübingen, Germany), a new highly selectively inhibitor of p38 MAPK, has a significant effect on inhibiting intimal, medial and adventitial hyperplasia. Methods: Sixty specific pathogen free Sprague Dawley male rats were randomly divided into three groups. The control group with a reversed right jugular vein, which is common to carotid artery interposition graft, was compared with sham-operated, and CBS3830 treated animals. Intimal, medial and adventitia morphometric examinations and expression of proliferating cell nuclear antigen (PCNA) were analysed after one, two and four weeks for vein grafts. Results: Intimal, medial and adventitia thickening in CBS3830 group were significantly lower than in the control group at each time point. Moreover, CBS3830 significantly reduced the phosphorylation of p38 MAPK and PCNA expression compared to the control. Conclusion: On the basis of the present work, intima, media and adventitia of saphenous vein grafts undergo vascular remodelling after surgery. The new, highly selective p38 MAPK Inhibitor, CBS3830, ameliorates intimal, medial, and adventitial remodelling by varying degrees.
Administration of SB239063, a potent p38 MAPK Inhibitor, alleviates acute lung injury induced by intestinal ischemia reperfusion in rats associated with AQP4 downregulation
Int Immunopharmacol 2016 Sep;38:54-60.PMID:27236300DOI:10.1016/j.intimp.2016.03.036.
Acute lung injury (ALI), induced by intestinal ischemia reperfusion (II/R) injury, is characterized by pulmonary edema and inflammation. Aquaporin 4 (AQP4), has been pointed out recently involving in edema development. Previous studies have shown that p38 mitogen activated protein kinase (MAPK) activation resulted in lung inflammation, while p38 MAPK Inhibitor can alleviate the pathology injury of lung tissue. However, the regulated mechanism of p38 MAPK in ALI induced by II/R is unclear. In this study, we established II/R rats' model by clamping the superior mesenteric artery (SMA) and coeliac artery (CA) for 40min and subsequent reperfusion for 16h, 24h, 48h. Subsequently, SB239063, a specific inhibitor of the activity of p38 MAPK, was injected (10mg/kg) intraperitoneally 60min before the operation. The severity of ALI was determined by histology analysis (HE staining and ALI scoring) and lung edema (lung wet/dry weight ratio) assessment. Western blot (WB) was applied to detect the expression level of AQP4 and phosphorylated (P)-p38 MAPK, and the localization of AQP4 was detected by immunofluorescent staining (IF). We found that AQP4 could express in the lung tissue. II/R could significantly induce lung injury, confirmed by lung injury scores and lung wet/dry weight ratios. The level of P-p38 MAPK and AQP4 were largely up-regulated in lung tissues. Moreover, inhibition of p38 MAPK activity could effectively down-regulate AQP4 expression and diminish the severity of II/R-induced ALI. These novel findings suggest that inhibition of p38 MAPK function should be a potential strategy for the prevention or treatment of ALI, by targeting AQP4 in future clinic trial.
The p38 MAPK Inhibitor, SB203580, inhibits cell invasion by Neospora caninum
Parasitol Res 2017 Feb;116(2):813-819.PMID:28039498DOI:10.1007/s00436-016-5346-1.
The Apicomplexan parasite Neospora caninum is an obligate intracellular parasitic protozoan. It can cause severe diseases in a number of animals throughout the world. Infection with N. caninum leads to abortions in pregnant animals and neuromuscular disorders of newborns which cause great economic losses to animal husbandry. However, the mechanism of cell invasion by N. caninum is still unclear. This paper aims to investigate the impact of SB203580, a p38 MAPK Inhibitor, on host cell invasion by N. caninum. The results suggested the presence of putative p38 MAPK homologues in N. caninum, and incubation of N. caninum with SB203580 markedly reduced the tachyzoite motility and microneme exocytosis (NcMIC2, 3, and 6). Furthermore, treatment or pretreatment of MDBK cells with SB203580 effectively reduced cell invasion by N. caninum. Therefore, SB203580 affected both, parasites and host cells, resulting in inhibition of cell invasion by N. caninum.
Vandetanib combined with a p38 MAPK Inhibitor synergistically reduces glioblastoma cell survival
Med Oncol 2013;30(3):638.PMID:23783486DOI:10.1007/s12032-013-0638-0.
The survival for patients with high-grade glioma is poor, and only a limited number of patients respond to the therapy. The aim of this study was to analyze the significance of using p38 MAPK phosphorylation as a prognostic marker in high-grade glioma patients and as a therapeutic target in combination chemotherapy with vandetanib. p38 MAPK phosphorylation was analyzed with immunohistochemistry in 90 high-grade glioma patients. Correlation between p38 MAPK phosphorylation and overall survival was analyzed with Mann-Whitney U test analysis. The effects on survival of glioblastoma cells of combining vandetanib with the p38 MAPK Inhibitor SB 203580 were analyzed in vitro with the median-effect method with the fluorometric microculture cytotoxicity assay. Two patients had phosphorylated p38 MAPK in both the cytoplasm and nucleus, and these two presented with worse survival than patients with no detectable p38 MAPK phosphorylation or phosphorylated p38 MAPK only in the nucleus. This was true for both high-grade glioma patients (WHO grade III and IV, n = 90, difference in median survival: 6.1 months, 95 % CI [0.20, 23], p = 0.039) and for the subgroup with glioblastoma patients (WHO grade IV, n = 70, difference in median survival: 6.1 months, 95 % CI [0.066, 23], p = 0.043). The combination of vandetanib and the p38 MAPK Inhibitor SB 203580 had synergistic effects on cell survival for glioblastoma-derived cells in vitro. In conclusion, p38 MAPK phosphorylation may be a prognostic marker for high-grade glioma patients, and vandetanib combined with a p38 MAPK Inhibitor may be useful combination chemotherapy for glioma patients.
Inhibition of p38 MAPK in the brain through nasal administration of p38 inhibitor loaded in chitosan nanocapsules
Nanomedicine (Lond) 2019 Sep;14(18):2409-2422.PMID:31456488DOI:10.2217/nnm-2018-0496.
Aim: To determine whether a p38 MAPK Inhibitor incorporated into nanoemulsion-based chitosan nanocapsules can reduce the activity of this kinase in the brain through their nasal administration in mice. Materials & methods: We selected the p38 MAPK Inhibitor PH797804, an ATP-competitive inhibitor of p38α encapsulated in nanoemulsion-based chitosan nanocapsules. Biological effect was evaluated in microglial and neuronal cells in vitro and in ex vivo and in vivo systems, in a mouse model of Alzheimer's disease. Results: Encapsulated inhibitor retains enzymatic inhibitory activity and tissue penetration capacity in vitro, ex vivo and in vivo. Conclusion: Nasal administration of chitosan nanocapsules can be an effective approach for brain-restricted reduction of p38 MAPK activity, thus reducing the side effects of systemic administration.