420323
KT5720
InSolution, ≥95%
别名:
InSolution KT5720, PKA Inhibitor VII
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关于此项目
经验公式（希尔记法）:
C32H31N3O5
化学文摘社编号:
分子量:
537.61
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
产品名称
KT5720, InSolution, ≥95%
SMILES string
[n]21c3c4[n](c6c(c4c7c(c3c8c2cccc8)CNC7=O)cccc6)[C@H]5O[C@@]1([C@](C5)(O)C(=O)OCCCCCC)C
InChI
1S/C32H31N3O5/c1-3-4-5-10-15-39-30(37)32(38)16-23-34-21-13-8-6-11-18(21)25-26-20(17-33-29(26)36)24-19-12-7-9-14-22(19)35(28(24)27(25)34)31(32,2)40-23/h6-9,11-14,23,38H,3-5,10,15-17H2,1-2H3,(H,33,36)/t23-,31+,32+/m0/s1
InChI key
ZHEHVZXPFVXKEY-RUAOOFDTSA-N
assay
≥95% (HPLC)
form
liquid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
solubility
DMSO: soluble
shipped in
wet ice
storage temp.
−20°C
Quality Level
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Biochem/physiol Actions
Cell permeable: yes
Product competes with ATP.
Reversible: yes
Target Ki: 56 nM against protein kinase A
Disclaimer
Toxicity: Irritant (B)
Other Notes
Simpson, C.S., and Morris, B.J. 1995. Neurosci.68, 97.
Cabell, L, and Audesirk, G. 1993. Int. J. Dev. Neurosci.11, 357.
Gadbois, D.M., et al. 1992. Proc. Natl. Acad. Sci. USA89, 8626.
Kase, H., et al. 1987. Biochem. Biophys. Res. Commun.142, 436.
Cabell, L, and Audesirk, G. 1993. Int. J. Dev. Neurosci.11, 357.
Gadbois, D.M., et al. 1992. Proc. Natl. Acad. Sci. USA89, 8626.
Kase, H., et al. 1987. Biochem. Biophys. Res. Commun.142, 436.
Packaging
Packaged under inert gas
Physical form
A 2 mM (50 µg/47 µl) solution of KT 5720 (Cat. No. 420320) in DMSO.
Preparation Note
Following the initial thaw, aliquot and freeze (20°C).
存储类别
10 - Combustible liquids
wgk
WGK 1
flash_point_f
188.6 °F - (refers to pure substance)
flash_point_c
87 °C - (refers to pure substance)
Ilse Delint-Ramirez et al.
Molecular cell, 82(20), 3794-3809 (2022-10-08)
Neuronal activity induces topoisomerase IIβ (Top2B) to generate DNA double-strand breaks (DSBs) within the promoters of neuronal early response genes (ERGs) and facilitate their transcription, and yet, the mechanisms that control Top2B-mediated DSB formation are unknown. Here, we report that
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