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Restrict the search for
m cidofovir
to a specific field?
Status:
Other
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
ML-9 is a selective inhibitor of MYLK and CaMK that acts by delaying MYLK phosphorylation through binding at or near the ATP binding site. This naphthalenesulfonamide derivative has been shown to inhibit insulin-stimulated 2-deoxyglucose transport (IC50 = 27 μM), PP-1 activation in adipocytes, PKA, Akt1 (PKB) and Rsk (S6 kinase). ML-9 was also observed to disrupt microfilament bundles with accompanying decrease in P32 incorporation in rat astrocytes. Carbachol illicited cationic currents were inhibitied with ML-9 (IC50 = 7.8 uM) in HEK293 cells. ML-9 has also demonstrated to inhibit natural killer cell lytic acitivity by regulating microfilament contraction as well as catecholamine secretion in intact and permeabilized chromaffin cells. In addition, agonist-induced Ca2+ entry into endothelial cells was completely abolished in the presence of ML-9. ML-9 was found to be a new type of vascular relaxant. ML-9 produced the relaxation of vascular strips contracted by high K+. The relaxation induced by this
compound was not affected by treatment with adrenergic and
cholinergic blocking agents. Thus, the ML-9-induced relaxation
is not due to a block of membrane receptor-associated
mechanisms; rather it has an effect on more basic and common
events in smooth muscle contraction. Moreover, ML-9
inhibited the Ca2+-induced contraction in chemically skinned
vascular smooth muscle cells, suggesting that ML-9 is not a
“calcium channel blocker.”
