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PZ0115

Sigma-Aldrich

CP-31398 dihydrochloride hydrate

≥98% (HPLC)

Sinônimo(s):

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 (Notação de Hill):
C22H26N4O·2HCl · xH2O
Peso molecular:
435.39 (anhydrous basis)
Número MDL:
MFCD17215956
Código UNSPSC:
12352200
ID de substância PubChem:
329823707
NACRES:
NA.77

Ensaio

≥98% (HPLC)

condição de armazenamento

desiccated

cor

yellow

solubilidade

H2O: ≥20 mg/mL

temperatura de armazenamento

2-8°C

cadeia de caracteres SMILES

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+;;;

chave InChI

JXIVIAMOMIONKY-UWCBQFGESA-N

Informações sobre genes

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

Aplicação

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

Ações bioquímicas/fisiológicas

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.

Características e benefícios

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.

Pictogramas

Exclamation mark
GHS07

Palavra indicadora

Warning

Frases de perigo

H302,H315,H319,H413

Classificações de perigo

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

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “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
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
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
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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