产品说明书

CP-31398 2HCl

Print
Chemical Structure| 1217195-61-3 同义名 : CP 31,398 (hydrochloride);CP-31398 Dihydrochloride
CAS号 : 1217195-61-3
货号 : A675515
分子式 : C22H28Cl2N4O
纯度 : 98%
分子量 : 435.39
MDL号 : MFCD11519956
存储条件:

粉末 Inert atmosphere,Room Temperature

液体 -20°C:3-6个月-80°C:12个月

溶解度 :

DMSO: 190 mg/mL(436.39 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

动物实验配方:
生物活性
描述 The tumor suppressor p53 plays various functional roles in the cell by regulating multiple regulatory signals that ensure adequate temporal and spatial responses to cellular stress. p53 is usually kept inactive due to ubiquitination by a number of E3 ubiquitin ligases that target p53 for proteasomal degradation[3].CP-31398, a styrylquinazoline, emerges from a screen for therapeutic agents that restore the wild-type DNA-binding conformation of mutant p53 to suppress tumors in vivo.CC cells treated with CP-31398 or treated with sh-PAX2 inhibited proliferation, invasion, and migration but promoted apoptosis with decreased PAX2 expression. The EMT process in CC cells was also reversed after treatment with CP-31398 or sh-PAX2. Moreover, the tumor formation experiment in nude mice revealed the inhibitory activity of CP-31398 in CC tumor in nude mice by suppressing PAX2[4].CP-31398 induced growth retardation but the cytotoxic effects were irrelevant to p53 genotype. CP-31398 influenced expression of p53 and the downstream molecules in a cell-dependent manner, but constantly increased p21 expression at the transcriptional level with decreased YY1 expression[5].The EC cells treated with CP‑31398 or siRNA against MDM2 exhibited an increased apoptosis and a suppressed migration and invasion, corresponding to an increased expression of p53, p21, Bad, Bax, Cyt‑c and caspase‑3, as well as to a decreased expression of Bcl‑2, Cox‑2, MMP‑2 and MMP‑9[6].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.30mL

0.46mL

0.23mL

11.48mL

2.30mL

1.15mL

22.97mL

4.59mL

2.30mL

参考文献

[1]Fujiwara T, Morimoto K. A compound CP-31398 suppresses excitotoxicity-induced neurodegeneration. Biochem Biophys Res Commun. 2013 Oct 25;440(3):359-63.

[2]Johnson WD, Muzzio M, et al. Subchronic oral toxicity and metabolite profiling of the p53 stabilizing agent, CP-31398, in rats and dogs. Toxicology. 2011 Nov 18;289(2-3):141-50.

[3] Chuck C-K Chao. Mechanisms of p53 degradation. Clin Chim Acta. 2015 Jan 1;438:139-47.

[4]Ling Liu,et al. CP-31398 inhibits the progression of cervical cancer through reversing the epithelial mesenchymal transition via the downregulation of PAX2s. J Cell Physiol. 2019 Mar;234(3):2929-2942.

[5]Boya Zhong,et al. A p53-stabilizing agent, CP-31398, induces p21 expression with increased G2/M phase through the YY1 transcription factor in esophageal carcinoma defective of the p53 pathway. Am J Cancer Res. 2019 Jan 1;9(1):79-93. eCollection 2019.

[6] Ling Liu,et al. CP‑31398 attenuates endometrial cancer cell invasion, metastasis and resistance to apoptosis by downregulating MDM2 expression. Int J Oncol. 2019 Mar;54(3):942-954.