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.”

N-(Fluorenyl-9-methoxycarbonyl)leucine (NPC 15199) is an organic compound that demonstrates antiinflammatory effects. NPC 15199 and other N-(9-fluorenylmethoxycarbonyl)-protected amino acids are demonstrated to block recruitment of neutrophils into inflammatory lesions and to inhibit T-cell activation in vitro, and are classified as leumedins. N-(Fluorenyl-9-methoxycarbonyl)leucine is described to act as a chemically distinct ligand and modulator of PPARγ (peroxisome proliferator-activated receptor γ). N-(Fluorenyl-9-methoxycarbonyl)leucine is demonstrated to increase intracellular Ca2+ and to mobilize Ca2+ stores in human bladder female transitional cancer (BFTC) cells.