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Overview
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Background
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.
In vitro: 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].
In vivo: 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].
Clinical trial: Up to now, ISCK03 is still in the preclinical development stage.[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).
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