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Key Documents

681629

Sigma-Aldrich

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).

Synonym(s):

W-7, Hydrochloride, N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide, HCl

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About This Item

Empirical Formula (Hill Notation):
C16H21ClN2O2S · xHCl
CAS Number:
61714-27-0
Molecular Weight:
340.87 (free base basis)
MDL number:
MFCD00012559
UNSPSC Code:
12352200

Quality Level

100

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
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.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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
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
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
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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