NSC 207895抑制MDMX，IC50为2.5 μM，促进p53稳定/激活和DNA损伤，也调节MDM2（E3连接酶）。NSC-207895 decreases both the MDMX mRNA and protein in MCF-7 cells. NSC-207895 induces expression of p53 as well as well-characterized p53-target gene, p21 and MDM2, in a dose-dependent manner in MCF-7 cells. NSC-207895 extends the half-life of p53 from 20 to 30 minutes to more than 3 hours as revealed by cycloheximide chase assays in MCF-7 cells. NSC-207895 also activates p53 and induces p21 and MDM2 expression in LNCaP prostate and A549 lung cancer cells. NSC-207895 increases the mRNA levels of proapoptotic genes including PUMA, BAX, and PIG3 in a dose-dependent manner in MCF-7 cells. NSC-207895 results in a significant increase in the numbers of sub-G0/G1 cells as well as G2 arrest. NSC-207895 also results in more than 40% of cells dying via apoptosis and decreases cell viability in A549 and LNCaP cells. NSC-207895 inhibits biosynthesis of nucleic acids and proteins in L1210 cells. NSC-207895 interacts with DNA repair to activate the DNA damage repair pathway in three species (S. cerevisiae, S. pombe and H. sapiens). NSC-207895 acts as cytotoxic agent in the G/R-luc astrocytoma cell line with GI50 of 117 nM.NSC 207895 (XI-006) 抑制MDMX，IC50为2.5 μM，促进p53稳定/激活和DNA损伤，也调节MDM2（E3连接酶）。

Target	Value
p53
MDMX	2.5 μM

NSC-207895减少MCF-7细胞中MDMX mRNA和蛋白质。NSC-207895剂量依赖性诱导MCF-7细胞中p53，以及充分表征的p53-靶基因，p21 和 MDM2的表达。在MCF-7细胞中的环己酰亚胺追踪试验表明，NSC-207895将p53的半衰期从20-30分钟延长到3小时以上。 在LNCaP 前列腺癌和A549肺癌细胞中，NSC-207895也会活化p53，并诱导p21 和MDM2表达。在MCF-7细胞中，NSC-207895剂量依赖性增加促凋亡基因，包括PUMA，BAX，和PIG3的mRNA水平。在A549和LNCaP 细胞中，NSC-207895也会导致超过40%的细胞死亡，并降低细胞活性。 NSC-207895抑制L1210细胞中核酸和蛋白质的合成。 在三个物种(S. cerevisiae，S. pombe 和 H. sapiens)中，NSC-207895与DNA修复相互作用以激活DNA损伤修复通路。 NSC-207895在G/R-luc星形细胞瘤细胞系中是一种细胞毒性剂，GI50 为117 nM。