[4-t-Butylphenyl]-N-(4-imidazol-1-yl phenyl)sulfonamide, Benzenesulfonamide, 4-(1,1-dimethylethyl)-N-[4-(1H-imidazol-1-yl)phenyl]-

Inhibits in vitro phosphorylation of c-Kit. Also inhibits SCF (stem cell factor)-induced c-kit phosphorylation in 501mel human melanoma cells

isck03 is an inhibitor of scf-mediated c-kit activation.the signaling downstream of scf/c-kit plays a key role in the development of various mammalian cells, such as mast cells, melanocytes, primordial germ cells, and hematopoietic progenitor cells.

previous study showed that the pretreatment of 501mel cells with isck03 could dose-dependently inhibit scf-induced c-kit phosphorylation. isck03 could also inhibit the phosphorylation of p44/42 erk mitogen-activated protein kinase that was known to be involved in scf/c-kit downstream signaling. however, isck03 was not able to inhibit hepatocyte growth factor-induced phosphorylation of p44/42 erk proteins [1].

to determine the in vivo efficacy, isck03was orally administered to depilated c57bl/6 mice. results showed that the oral administration of isck03 could induce the dose-dependent depigmentation of newly regrown hair, and this was reversed with cessation of isck03 treatment. in addition, the topical application of isck03 could promote the depigmentation of uv-induced hyperpigmented spots on n brownish guinea pig skin. moreover, the fontana–masson staining analyses showed epidermal melanin was diminished in spots treated with isck03 [1].

[1] y. j. na, h. s. baek, s. m. ahn, et al. [4-t-butylphenyl]-n-(4-imidazol-1-yl phenyl)sulfonamide (isck03) inhibits scf/c-kit signaling in 501mel human melanoma cells and abolishes melanin production in mice and brownish guinea pigs. biochemical pharmacology 74(5), 780-786 (2007).