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PZ0115

Sigma-Aldrich

CP-31398 dihydrochloride hydrate

≥98% (HPLC)

Sinónimos:

N′-[2-[2-(4-Methoxyphenyl)ethenyl]-4-quinazolinyl]-N,N-dimethyl-1,3-propanediamine dihydrochloride hydrate

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About This Item

Fórmula empírica (notación de Hill):
C22H26N4O·2HCl · xH2O
Peso molecular:
435.39 (anhydrous basis)
MDL number:
MFCD17215956
UNSPSC Code:
12352200
PubChem Substance ID:
329823707
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

storage condition

desiccated

color

yellow

solubility

H2O: ≥20 mg/mL

storage temp.

2-8°C

SMILES string

O.Cl.Cl.COc1ccc(cc1)\C=C\c2nc(NCCCN(C)C)c3ccccc3n2

InChI

1S/C22H26N4O.2ClH.H2O/c1-26(2)16-6-15-23-22-19-7-4-5-8-20(19)24-21(25-22)14-11-17-9-12-18(27-3)13-10-17;;;/h4-5,7-14H,6,15-16H2,1-3H3,(H,23,24,25);2*1H;1H2/b14-11+;;;

InChI key

JXIVIAMOMIONKY-UWCBQFGESA-N

Gene Information

human ... TP53(7157)
mouse ... TP53(22059)
rat ... TP53(24842)

Application

CP-31398 dihydrochloride hydrate has been used as a p53 stabilizer:
  • to evaluate its effects on the upregulation of miRNA in human neuroblastoma cells
  • to study its effects on arsenic trioxide (ATO) stabilization of p53 folding
  • to study its effects on regulation of miR-34 in PC12 cells

Biochem/physiol Actions

CP-31398 is a styryl quinazoline that functions in preserving the activity of p53 as a tumor suppressor and transcription factor. The DNA-binding activity and apoptosis functionality of the p53 are restored by CP-31398. CP-31398 exhibits therapeutic effects against liver, skin, pancreatic, and colon cancers.
CP-31398 dihyrochloride hydrate is a p53 stabilizer; apoptosis inducer.

Features and Benefits

This compound is a featured product for Apoptosis research. Click here to discover more featured Apoptosis products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.

pictograms

Exclamation mark
GHS07

signalword

Warning

Hazard Classifications

Acute Tox. 4 Oral - Aquatic Chronic 4 - Eye Irrit. 2 - Skin Irrit. 2

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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William D Johnson et al.
Toxicology, 289(2-3), 141-150 (2011-08-26)
CP-31398 (N'-[2-[2-(4-methoxyphenyl)ethenyl]-4-quinazolinyl]-N,N-dimethyl-1,3-propanediamine dihydrochloride) is a styrylquinazoline that stabilizes the DNA binding conformation of p53, thereby maintaining the activity of p53 as a transcription factor and tumor suppressor. In consideration of the potential use of p53 stabilizers for cancer prevention and
Abhishek Jauhari et al.
Molecular neurobiology, 54(7), 4986-4995 (2016-08-16)
MicroRNAs (miRNAs) are generated by endonuclease activity of Dicer, which also helps in loading of miRNAs to their target sequences. SH-SY5Y, a human neuroblastoma and a cellular model of neurodevelopment, consistently expresses genes related to neurodegenerative disorders at different biological
Abhishek Jauhari et al.
Molecular neurobiology, 55(2), 936-945 (2017-01-14)
Differentiation of neural stem cells (NSC's) to mature and functional neurons requires coordinated expression of mRNA, microRNAs (miRNAs) and regulatory proteins. Our earlier unbiased miRNA profiling studies have identified miR-200, miR-34 and miR-221/222 as maximally up-regulated miRNA families in differentiating
Ling Liu et al.
International journal of oncology, 54(3), 942-954 (2019-01-11)
Endometrial cancer (EC) is one of the most common malignancies of the female reproductive system, and metastasis is a major cause of mortality. In this study, we aimed to explore the role of CP‑31398 in the migration, invasion and apoptosis
Shuo Chen et al.
Cancer cell, 39(2), 225-239 (2020-12-29)
TP53 is the most frequently mutated gene in cancer, yet these mutations remain therapeutically non-actionable. Major challenges in drugging p53 mutations include heterogeneous mechanisms of inactivation and the absence of broadly applicable allosteric sites. Here we report the identification of

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