681629
W-7, Hydrochloride
A cell-permeable and reversible calmodulin antagonist that inhibits myosin light chain kinase (IC₅₀ = 51 µM) and Ca2+-calmodulin-dependent phosphodiesterase (IC₅₀ = 28 µM).
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Synonym(s):
W-7, Hydrochloride, N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide, HCl
Empirical Formula (Hill Notation):
C16H21ClN2O2S · xHCl
CAS Number:
Molecular Weight:
340.87 (free base basis)
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
Recommended Products
Quality Level
Assay
≥98% (TLC)
form
crystalline solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
desiccated (hygroscopic)
protect from light
color
off-white
solubility
DMSO: 5 mg/mL
DMF: soluble
warm ethanol: soluble
shipped in
ambient
storage temp.
2-8°C
InChI
1S/C16H21ClN2O2S.ClH/c17-15-9-5-8-14-13(15)7-6-10-16(14)22(20,21)19-12-4-2-1-3-11-18;/h5-10,19H,1-4,11-12,18H2;1H
InChI key
OMMOSRLIFSCDBL-UHFFFAOYSA-N
General description
A cell-permeable and reversible calmodulin antagonist that inhibits Ca2+-calmodulin-dependent phosphodiesterase (IC50 = 28 µM) and myosin light chain kinase (IC50 = 51 µM).
A cell-permeable and reversible calmodulin antagonist that inhibits myosin light chain kinase (IC50 = 51 µM) and Ca2+-calmodulin-dependent phosphodiesterase (IC50 = 28 µM).
Biochem/physiol Actions
Cell permeable: yes
Primary Target
Myosin light chain kinase
Myosin light chain kinase
Product does not compete with ATP.
Reversible: yes
Target IC50: 51 µM inhibiting myosin light chain kinase; 28 µM inhibiting Ca2+-calmodulin-dependent phosphodiesterase
Warning
Toxicity: Standard Handling (A)
Other Notes
Caulfield, M.P., et al. 1991. Neurosci. Lett.125, 57.
Asano, M. 1989. J. Pharmacol. Exp. Ther.251, 764.
Itoh, H., and Hidaka, H. 1984. J. Biochem.96, 1721.
Tanaka, T., et al. 1983. Pharmacol.26, 249.
Hidaka, H. 1981. Proc. Natl. Acad. Sci. USA 78, 4354.
Asano, M. 1989. J. Pharmacol. Exp. Ther.251, 764.
Itoh, H., and Hidaka, H. 1984. J. Biochem.96, 1721.
Tanaka, T., et al. 1983. Pharmacol.26, 249.
Hidaka, H. 1981. Proc. Natl. Acad. Sci. USA 78, 4354.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Shuhang Dai et al.
Biochimica et biophysica acta. Molecular cell research, 1869(7), 119252-119252 (2022-03-11)
Engagement of epidermal growth factor (EGF) with its receptor (EGFR) produces a broad range of cancer phenotypes. The overriding aim of this study was to understand EGFR signaling and its regulation by the Ca2+/calmodulin (CaM) dependent protein kinase kinase 2
Manao Kinoshita et al.
EBioMedicine, 32, 72-83 (2018-06-12)
Although psychotropic drugs act on neurons and glial cells, how glia respond, and whether glial responses are involved in therapeutic effects are poorly understood. Here, we show that fluoxetine (FLX), an anti-depressant, mediates its anti-depressive effect by increasing the gliotransmission
Susumin Yang et al.
Cell death & disease, 14(6), 391-391 (2023-07-01)
Phagocytosis of apoptotic cells, called efferocytosis, requires calcium inside and outside of phagocytes. Due to its necessity, calcium flux is sophisticatedly modulated, and the level of intracellular calcium in phagocytes is ultimately elevated during efferocytosis. However, the role of elevated
Estelle R Simo-Cheyou et al.
Journal of cellular physiology, 232(12), 3496-3509 (2017-01-21)
An upregulation of Egr-1 expression has been reported in models of atherosclerosis and intimal hyperplasia and, various vasoactive peptides and growth promoting stimuli have been shown to induce the expression of Egr-1 in vascular smooth muscle cells (VSMC). Angiotensin-II (Ang-II)
Konstantin E Komolov et al.
Molecular cell, 81(2), 323-339 (2020-12-16)
The phosphorylation of G protein-coupled receptors (GPCRs) by GPCR kinases (GRKs) facilitates arrestin binding and receptor desensitization. Although this process can be regulated by Ca2+-binding proteins such as calmodulin (CaM) and recoverin, the molecular mechanisms are poorly understood. Here, we
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