ISCK03 - CAS 945526-43-2
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
ISCK03, a phenyl-imidazolosulfonamide compound, is a cell-permeable, specific SCF/c-Kitinhibitor (IC50 <<2.5 μM in cell-free kinase assays).
Brife Description:
A cell-permeable inhibitor of SCF-mediated c-kit activation
4-tert-butyl-N-(4-imidazol-1-ylphenyl)benzenesulfonamide; c-Kit Inhibitor II; Stem-Cell Factor/c-Kit Inhibitor; ISCK-03; ISCK 03
DMSO: ≥ 38 mg/mL
Store in a cool and dry place (or refer to the Certificate of Analysis).
Boiling Point:
520.0±60.0 ℃ at 760 Torr
1.20±0.1 g/cm3
Canonical SMILES:
1.[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.
Na YJ;Baek HS;Ahn SM;Shin HJ;Chang IS;Hwang JS Biochem Pharmacol. 2007 Sep 1;74(5):780-6. Epub 2007 Jun 14.
It is well known that c-kit is related to pigmentation as well as to the oncology target protein. The objective of this study was to discover a skin-whitening agent that regulates c-kit activity. We have developed a high-throughput screening system using recombinant human c-kit protein. Approximately 10,000 synthetic compounds were screened for their effect on c-kit activity. Phenyl-imidazole sulfonamide derivatives showed inhibitory activity on c-kit phosphorylation in vitro. The effects of one derivative, [4-t-butylphenyl]-N-(4-imidazol-1-yl phenyl)sulfonamide (ISCK03), on stem-cell factor (SCF)/c-kit cellular signaling in 501mel human melanoma cells were examined further. Pretreatment of 501mel cells with ISCK03 inhibited SCF-induced c-kit phosphorylation dose dependently. ISCK03 also inhibited p44/42 ERK mitogen-activated protein kinase (MAPK) phosphorylation, which is known to be involved in SCF/c-kit downstream signaling. However ISCK03 did not inhibit hepatocyte growth factor (HGF)-induced phosphorylation of p44/42 ERK proteins. To determine the in vivo potency of ISCK03, it was orally administered to depilated C57BL/6 mice. Interestingly, oral administration of ISCK03 induced the dose-dependent depigmentation of newly regrown hair, and this was reversed with cessation of ISCK03 treatment.
2.Comparison of the effects of carbon ion and photon irradiation on the angiogenic response in human lung adenocarcinoma cells.
Kamlah F;Hänze J;Arenz A;Seay U;Hasan D;Juricko J;Bischoff B;Gottschald OR;Fournier C;Taucher-Scholz G;Scholz M;Seeger W;Engenhart-Cabillic R;Rose F Int J Radiat Oncol Biol Phys. 2011 Aug 1;80(5):1541-9. doi: 10.1016/j.ijrobp.2011.03.033. Epub 2011 May 27.
PURPOSE: ;Radiotherapy resistance is a commonly encountered problem in cancer treatment. In this regard, stabilization of endothelial cells and release of angiogenic factors by cancer cells contribute to this problem. In this study, we used human lung adenocarcinoma (A549) cells to compare the effects of carbon ion and X-ray irradiation on the cells' angiogenic response.;METHODS AND MATERIALS: ;A549 cells were irradiated with biologically equivalent doses for cell survival of either carbon ions (linear energy transfer, 170 keV/μm; energy of 9.8 MeV/u on target) or X-rays and injected with basement membrane matrix into BALB/c nu/nu mice to generate a plug, allowing quantification of angiogenesis by blood vessel enumeration. The expression of angiogenic factors (VEGF, PlGF, SDF-1, and SCF) was assessed at the mRNA and secreted protein levels by using real-time reverse transcription-PCR and enzyme-linked immunosorbent assay. Signal transduction mediated by stem cell factor (SCF) was assessed by phosphorylation of its receptor c-Kit. For inhibition of SCF/c-Kit signaling, a specific SCF/c-Kit inhibitor (ISCK03) was used.;RESULTS: ;Irradiation of A549 cells with X-rays (6 Gy) but not carbon ions (2 Gy) resulted in a significant increase in blood vessel density (control, 20.
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