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CaMKII-IN-1 Sale

(Synonyms: 3-氯-2-甲基-N-[5,6,7,8-四氢-2-[(2-苯基乙基)氨基]-6-(苯基甲基)吡啶并[4,3-D]嘧啶-4-基]苯磺酰胺) 目录号 : GC35601

CaMKII-IN-1是CaMKII高效选择性抑制剂,IC50值为63nM,对CaMKIV, MLCK, p38a, Akt1,和PKC几乎无作用。

CaMKII-IN-1 Chemical Structure

Cas No.:1208123-85-6

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥3,798.00
现货
2mg
¥2,100.00
现货
5mg
¥3,150.00
现货
10mg
¥4,500.00
现货
50mg
¥13,500.00
现货
100mg
¥18,900.00
现货
200mg 待询 待询
500mg 待询 待询

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

CaMKII-IN-1 is a potent and highly selective CaMKII inhibitor with IC50 of 63 nM; significantly high selectivity against CaMKIV, MLCK, p38a, Akt1, and PKC.IC50 value: 63 nMTarget: CaMKII

[1]. Asano S, et al. 5,6,7,8-Tetrahydropyrido[4,3-d]pyrimidines as novel class of potent and highly selective CaMKII inhibitors. Bioorg Med Chem Lett. 2010 Nov 15;20(22):6696-8.

Chemical Properties

Cas No. 1208123-85-6 SDF
别名 3-氯-2-甲基-N-[5,6,7,8-四氢-2-[(2-苯基乙基)氨基]-6-(苯基甲基)吡啶并[4,3-D]嘧啶-4-基]苯磺酰胺
Canonical SMILES O=S(C1=CC=CC(Cl)=C1C)(NC2=C(CN(CC3=CC=CC=C3)CC4)C4=NC(NCCC5=CC=CC=C5)=N2)=O
分子式 C29H30ClN5O2S 分子量 548.1
溶解度 DMSO: ≥ 54 mg/mL (98.52 mM) 储存条件 Store at -20°C
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1 mM 1.8245 mL 9.1224 mL 18.2448 mL
5 mM 0.3649 mL 1.8245 mL 3.649 mL
10 mM 0.1824 mL 0.9122 mL 1.8245 mL
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Research Update

Chronic Intermittent Hypoxia Regulates CaMKII-Dependent MAPK Signaling to Promote the Initiation of Abdominal Aortic Aneurysm

Oxid Med Cell Longev 2021 Dec 21;2021:2502324.PMID:34970414DOI:PMC8714336

Obstructive sleep apnea (OSA) is highly prevalent in patients with abdominal aortic aneurysm (AAA). However, the effects of OSA on AAA initiation in a murine model of sleep apnea have not been completely studied. In this paper, Apoe-/- C57BL/6 mice infused with angiotensin II (Ang II) were placed in chronic intermittent hypoxia (CIH) condition for inducing OSA-related AAA. CIH significantly promoted the incidence of AAA and inhibited the survival of mice. By performing ultrasonography and elastic Van Gieson staining, CIH was found to be effective in promoting aortic dilation and elastin degradation. Immunohistochemical and zymography results show that CIH upregulated the expression and activity of MMP2 and MMP9 and upregulated MCP1 expression while downregulating α-SMA expression. Also, CIH exposure promoted ROS generation, apoptosis, and mitochondria damage in vascular smooth muscle cells (VSMCs), which were measured by ROS assay, TUNEL staining, and transmission electron microscopy. The result of RNA sequencing of mouse aortas displayed that 232 mRNAs were differently expressed between Ang II and Ang II+CIH groups, and CaMKII-dependent p38/Jnk was confirmed as one downstream signaling of CIH. CaMKII-IN-1, an inhibitor of CaMKII, eliminated the effects of CIH on the loss of primary VSMCs. To conclude, a mouse model of OSA-related AAA, which contains the phenotypes of both AAA and OSA, was established in this study. We suggested CIH as a risk factor of AAA initiation through CaMKII-dependent MAPK signaling.