KDM5A-IN-1
目录号 : GC32842
KDM5A-IN-1是组蛋白去甲基化酶抑制剂。
Cas No.:1905481-36-8
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
KDM5A-IN-1 is an inhibitor histone demethylases. Target: Histone Demethylase
[1]. Kwong Wah LAI, et al. Pyrrolidine amide compounds as histone demethylase inhibitors. PCT Int. Appl. (2016), WO 2016057924 A1 20160414.
| Cas No. | 1905481-36-8 | SDF | |
| Canonical SMILES | O=C(C1CC1)N[C@@H]2CCN(C(C3=CC(C(C)C)=NN3)=O)C2 | ||
| 分子式 | C15H22N4O2 | 分子量 | 290.36 |
| 溶解度 | DMSO : ≥ 50 mg/mL (172.20 mM) | 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 | 3.444 mL | 17.22 mL | 34.44 mL |
| 5 mM | 0.6888 mL | 3.444 mL | 6.888 mL |
| 10 mM | 0.3444 mL | 1.722 mL | 3.444 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。
The therapeutic effect of dexmedetomidine on protection from renal failure via inhibiting KDM5A in lipopolysaccharide-induced sepsis of mice
Life Sci 2019 Dec 15;239:116868.PMID:31682847DOI:10.1016/j.lfs.2019.116868
Background: Sepsis is an inflammatory response undergoing the complicate pathophysiological changes for host defense against pathogens. Previous studies suggested that dexmedetomidine (DEX) was served to controlling the over-reactive inflammatory effects to protect from the sepsis-induced organ failure via modulating histone methylation. However, the genome-wide changes of histone methylations upon DEX for sepsis treatment were poorly explored. Materials and methods: The acute kidney injury (AKI) mouse model were induced by lipopolysaccharide (LPS). DEX and KDM5 (H3K4 demethylases) inhibitors were used to add additionally. H3K4me3 antibody was used to conduct the ChIP-seq assay in renal cortex tissues. Results: We observed that the overall H3K4me3 levels were obviously declined in AKI group compared to the normal control. We further observed that the therapeutic effect of DEX was basically equal with CPI-455 and KDM5A-IN-1 but better than PBIT. The overall H3K4me3 level was reduced in AKI group compared to DEX (p = 0.008), and KDM5A-IN-1 groups (p = 0.022). The H3K4me3 enrichment of the multiple genes associated with inflammatory cytokines such as TNF-α, NOS2 and CCL2 increased in AKI model, but decreased upon DEX or KDM5A-IN-1 treatment. Consistently, transcription and protein levels of genes such as TLR4, MYD88, MTA1, PTGS2, CASP3 associated with NF-κB signaling pathway were all compromising after treated with DEX or KDM5A-IN-1 groups compared to AKI group. Conclusion: Taken together, our data determined that DEX could attenuate AKI through KDM5A inhibition in sepsis.