454202
8-Methoxymethyl-3-isobutyl-1-methylxanthine
A cell-permeable selective inhibitor of Ca2+-calmodulin-dependent phosphodiesterase (PDE I; IC₅₀ = 4 µM).
别名:
8-Methoxymethyl-3-isobutyl-1-methylxanthine, 8-Methoxymethyl-IBMX
质量水平
方案
≥98% (TLC)
表单
solid
制造商/商品名称
Calbiochem®
储存条件
OK to freeze
颜色
white
溶解性
ethanol: 2 mg/mL
DMSO: 5 mg/mL
运输
ambient
储存温度
10-30°C
SMILES字符串
[nH]1c2c(nc1COC)N(C(=O)N(C2=O)C)CC(C)C
InChI
1S/C12H18N4O3/c1-7(2)5-16-10-9(11(17)15(3)12(16)18)13-8(14-10)6-19-4/h7H,5-6H2,1-4H3,(H,13,14)
InChI key
NBLBCGUCPBXKOV-UHFFFAOYSA-N
相关类别
一般描述
A cell-permeable selective inhibitor of Ca2+-calmodulin-dependent phosphodiesterase (PDE I; IC50 = 4 µM).
A cell-permeable, selective inhibitor of Ca2+-calmodulin-dependent phosphodiesterase (PDE I, IC50 = 4 µM).
生化/生理作用
Cell permeable: yes
Primary Target
PDE 1
PDE 1
Product does not compete with ATP.
Reversible: no
Target IC50: 4 µM against Ca2+-calmodulin-dependent phosphodiesterase (PDE I)
制备说明
Following reconstitution aliquot and freeze at -20°C. Stock solutions are stable for up to 3 months at -20°C.
其他说明
Jackson, E.K., et al. 1997. J. Cardiovasc. Pharmacol. 30, 798.
Ahn, H.S., et al. 1989. Biochem. Pharmacol.38, 3331.
Han, P., et al. 1989. J. Biol. Chem.274, 22337.
Ahn, H.S., et al. 1989. Biochem. Pharmacol.38, 3331.
Han, P., et al. 1989. J. Biol. Chem.274, 22337.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
免责声明
Toxicity: Standard Handling (A)
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
E K Jackson et al.
Journal of cardiovascular pharmacology, 30(6), 798-801 (1998-01-22)
The objective this investigation was to determine the relative importance of type I, III, and IV phosphodiesterases in the regulation of cyclic adenosine monophosphate (cAMP) in the renal circulation. In the first experimental series, four groups of isolated rat kidneys
H S Ahn et al.
Biochemical pharmacology, 38(19), 3331-3339 (1989-10-01)
In this study three forms of cyclic nucleotide phosphodiesterase (PDE) isolated from rabbit aorta were pharmacologically characterized, and the consequence of selective inhibition of calmodulin-stimulated PDE (CaM-PDE) and cGMP specific PDE (cG-PDE) was evaluated using PDE inhibitors. The cG-PDE (F1)
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