444143
MDM2 Antagonist, Nutlin-3, Racemic
The MDM2 Antagonist, Nutlin-3, Racemic, also referenced under CAS 548472-68-0, controls the biological activity of MDM2. This small molecule/inhibitor is primarily used for Cancer applications.
Sinonimo/i:
MDM2 Antagonist, Nutlin-3, Racemic, MDM2 Inhibitor IV
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About This Item
Formula empirica (notazione di Hill):
C30H30Cl2N4O4
Numero CAS:
Peso molecolare:
581.49
Numero MDL:
Codice UNSPSC:
12352200
NACRES:
NA.77
Prodotti consigliati
Livello qualitativo
Saggio
≥98% (TLC and HPLC)
Forma fisica
solid
Produttore/marchio commerciale
Calbiochem®
Condizioni di stoccaggio
OK to freeze
protect from light
Solubilità
DMSO: 25 mg/mL
ethanol: 25 mg/mL
Condizioni di spedizione
wet ice
Temperatura di conservazione
−20°C
InChI
1S/C30H30Cl2N4O4/c1-18(2)40-25-16-23(39-3)12-13-24(25)29-34-27(19-4-8-21(31)9-5-19)28(20-6-10-22(32)11-7-20)36(29)30(38)35-15-14-33-26(37)17-35/h4-13,16,18,27-28H,14-15,17H2,1-3H3,(H,33,37)
BDUHCSBCVGXTJM-UHFFFAOYSA-N
Descrizione generale
A cell-permeable cis-imidazoline compound that acts as a potent and selective MDM2 antagonist (IC50 = 90 nM for Nutlin-3a and 13.6 µM for Nutlin-3b) and displays antitumor properties. Activates p53 pathway by binding MDM2 in the p53-binding pocket and inhibits MDM2-p53 interaction. Shown to suppress tumor growth by induction of apoptosis in several cancer cells with wild-type p53 and in xenografted tumor mice. A 10 mM (1 mg/172 µl) solution of MDM2 Antagonist, Nutlin-3, Racemic (Cat. No. 444151) in DMSO is also available.
A cell-permeable, potent, and selective MDM2 antagonist (IC50 = 90 nM for Nutlin-3a and 13.6 µM for Nutlin-3b) that displays antitumor properties. Activates the p53 pathway by binding MDM2 in the p53-binding pocket and inhibiting the MDM2-p53 interaction. Shown to induce apoptosis in several cancer cell lines with wild-type p53 and in xenografted tumor mice.
Azioni biochim/fisiol
Cell permeable: yes
Primary Target
MDM2
MDM2
Product does not compete with ATP.
Reversible: no
Target IC50: 90 nM for Nutlin-3a and 13.6 µM for Nutlin-3b
Confezionamento
Packaged under inert gas
Attenzione
Toxicity: Harmful (C)
Ricostituzione
Following reconstitution, aliquot, purge with inert gas, and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Altre note
Thompson, T., et al. 2004. J. Biol. Chem.279, 53015.
Vassilev, L.T., et al. 2004. Science303, 844.
Vassilev, L.T., et al. 2004. Science303, 844.
Note legali
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Codice della classe di stoccaggio
11 - Combustible Solids
Classe di pericolosità dell'acqua (WGK)
WGK 3
Punto d’infiammabilità (°F)
Not applicable
Punto d’infiammabilità (°C)
Not applicable
Certificati d'analisi (COA)
Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘Batch’.
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Tyler P Martinez et al.
eNeuro, 11(3) (2024-02-09)
Alzheimer's Disease (AD) is associated with brain accumulation of synaptotoxic amyloid-β (Aβ) peptides produced by the proteolytic processing of amyloid precursor protein (APP). Cognitive impairments associated with AD correlate with dendritic spine and excitatory synapse loss, particularly within the hippocampus.
Thelma Thompson et al.
The Journal of biological chemistry, 279(51), 53015-53022 (2004-10-09)
The p53 tumor suppressor is a key mediator of the cellular response to stress. Phosphorylation induced by multiple stress-activated kinases has been proposed to be essential for p53 stabilization, interaction with transcriptional co-activators, and activation of p53 target genes. However
Lyubomir T Vassilev et al.
Science (New York, N.Y.), 303(5659), 844-848 (2004-01-06)
MDM2 binds the p53 tumor suppressor protein with high affinity and negatively modulates its transcriptional activity and stability. Overexpression of MDM2, found in many human tumors, effectively impairs p53 function. Inhibition of MDM2-p53 interaction can stabilize p53 and may offer
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eLife, 11 (2022-06-14)
Quantification of gene dependency across hundreds of cell lines using genome-scale CRISPR screens has revealed co-essential pathways/modules and critical functions of uncharacterized genes. In contrast to protein-coding genes, robust CRISPR-based loss-of-function screens are lacking for long noncoding RNAs (lncRNAs), which
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