KG-501

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

CREB-CBP 相互作用的小分子拮抗剂，通过 CREB 抑制细胞基因的 cAMP 依赖性激活。

A small-molecule antagonist of CREB-CBP interaction, inhibits the cAMP-dependent activation of cellular genes via CREB; disruptes phospho (Ser-133) CREB binding to CBP KIX domain with Ki of 90 uM, similar Ki for binding of phospho (Ser-133) CREB protein to p300; also interferes with the Myb-KIX interaction in vitro and inhibits Myb activity in vivo.

KG-501, which directly targets the KIX domain of CBP, results in a disrupted CREB-CBP complex, inhibits CREB-target gene induction, and inhibits IL-1β-mediated angiogenic activity in NSCLC. KG-501 disrupts phospho (Ser-133) CREB binding to KIX with a Ki of ~90 μM, using concentrations of CREB that are within the linear range of the binding assay. Treatment of HEK293T cells with KG-501 also blocks induction of endogenous CREB target genes (NR4A2, αCG, c-fos, and RGS2) by forskolin, indicating that KG-501 likely exerts a general effect on CREB activity. KG-501 can also inhibit NF-κB transcription activity because NF-κB also uses CBP as a cofactor to regulate gene expression. The migration of HUVECs induced by CM from A549 cells treated with IL-1β plus 10 μM of KG-501 is significantly lower than that induced by CM from A549 cells treated with IL-1β alone. At 10 μM, KG-501 suppresses the expression of all of the IL-1β–induced CXC chemokine genes except CXCL8. For the protein level, KG-501 significantly suppresses IL-1β–induced CXCL5 protein secretion. Similar effects of KG-501 are also observed in the H1734 cell line.

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Naphthol AS-E phosphate

Nuclear Receptor/Transcription Factor

CREB/CBP

CREB/CBP

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18228-17-6

377.72

C17H13ClNO5P

>98% (HPLC)

DMSO : 6 mg/mL 15.88 mM; H2O : < 0.1 mg/mL

O=C(C1=C(OP(O)(O)=O)C=C2C=CC=CC2=C1)NC3=CC=C(Cl)C=C3

2-Naphthanilide, 4'-chloro-3-hydroxy-, phosphate (6CI,7CI)

(-20℃)

With Ice Pack

≥ 2 years