444152
MDM2 Antagonist IV, Nutlin-3a
The MDM2 Antagonist IV, Nutlin-3a, also referenced under CAS 675576-98-4, controls the biological activity of MDM2. This small molecule/inhibitor is primarily used for Cancer applications.
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别名:
MDM2 Antagonist IV, Nutlin-3a, (-)-4-(4,5- bis-(4-Chlorophenyl)-2-(2-isopropoxy-4-methoxyphenyl)-4,5-dihydroimidazole-1-carbonyl)piperazine-2-one, (-)-4-(4,5-bis-(4-Chlorophenyl)-2-(2-isopropoxy-4-methoxyphenyl)-4,5-dihydroimidazole-1-carbonyl)piperazine-2-one
经验公式（希尔记法）:
C30H30Cl2N4O4
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质量水平
检测方案
≥98% (HPLC)
形式
powder
制造商/商品名称
Calbiochem®
储存条件
OK to freeze
protect from light
颜色
white
溶解性
DMSO: 100 mg/mL
运输
ambient
储存温度
−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)/t27-,28+/m0/s1
InChI key
BDUHCSBCVGXTJM-WUFINQPMSA-N
一般描述
A cell-permeable and highly potent active enantiomer of Nutlin-3 (Cat. No. 444143) that binds to the p53-binding pocket and blocks the interaction of p53 and MDM2 (IC50 = 90 nM). Exhibits over 150-fold greater affinity for MDM2 than its less active enantiomer, Nutlin-3b. Induces p53 mediated apoptosis by both transcription-dependent and independent mechanisms. Shown to greatly potentiate the cytotoxic effects of chemotherapeutic agents and reduce tumor burden in vivo. Also shown to overcome ATM-mediated resistance to fludarabine in chronic lymphocyte leukemia. Cells treated with Nutlin-3a permanently lose their ability to proliferate and enter into a pattern of permanent senescence. Mouse embryonic fibroblasts with p53+/+MEFs show significantly reduced reprogramming capabilities following Nutlin-3a treatment.
包装
Packaged under inert gas
警告
Toxicity: Standard Handling (A)
重悬
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
其他说明
Ohnstad, H.O., et al. 2011. BMC Cancer11, 211.
Shen, H. and Maki, C.G., 2010. J. Biol. Chem.285, 23105.
Kawamura, T., et al. 2009. Nature460, 1140.
Kojima, K., et al. 2006. Blood108, 993.
Laurie, N.A., et al. 2006. Nature444, 61.
Tovar, C., et al. 2006. Proc. Natl. Acad. Sci. USA103, 1888.
Vassilev, L.T. 2006. Trends Mol Med.13, 23.
Thompson, T., et al. 2004. J. Biol. Chem.279, 53015.
Vassilev, L.T., et al. 2004. Science303, 844.
Shen, H. and Maki, C.G., 2010. J. Biol. Chem.285, 23105.
Kawamura, T., et al. 2009. Nature460, 1140.
Kojima, K., et al. 2006. Blood108, 993.
Laurie, N.A., et al. 2006. Nature444, 61.
Tovar, C., et al. 2006. Proc. Natl. Acad. Sci. USA103, 1888.
Vassilev, L.T. 2006. Trends Mol Med.13, 23.
Thompson, T., et al. 2004. J. Biol. Chem.279, 53015.
Vassilev, L.T., et al. 2004. Science303, 844.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Nikia A Laurie et al.
Nature, 444(7115), 61-66 (2006-11-03)
Most human tumours have genetic mutations in their Rb and p53 pathways, but retinoblastoma is thought to be an exception. Studies suggest that retinoblastomas, which initiate with mutations in the gene retinoblastoma 1 (RB1), bypass the p53 pathway because they
Lyubomir T Vassilev
Trends in molecular medicine, 13(1), 23-31 (2006-11-28)
The tumor suppressor p53 is a powerful antitumoral molecule frequently inactivated by mutations or deletions in cancer. However, half of all human tumors express wild-type p53, and its activation by antagonizing its negative regulator murine double minute 2 (MDM2) might
Christian Tovar et al.
Proceedings of the National Academy of Sciences of the United States of America, 103(6), 1888-1893 (2006-01-31)
The p53 tumor suppressor retains its wild-type conformation and transcriptional activity in half of all human tumors, and its activation may offer a therapeutic benefit. However, p53 function could be compromised by defective signaling in the p53 pathway. Using a
Kensuke Kojima et al.
Blood, 108(3), 993-1000 (2006-03-18)
Although TP53 mutations are rare in B-cell chronic lymphocytic leukemia (CLL), Mdm2 overexpression has been reported as an alternative cause of p53 dysfunction. We investigated the potential therapeutic use of nongenotoxic p53 activation by a small-molecule antagonist of Mdm2, Nutlin-3a
Hege O Ohnstad et al.
BMC cancer, 11, 211:1-21111 (2011-06-01)
Frequent failure and severe side effects of current sarcoma therapy warrants new therapeutic approaches. The small-molecule MDM2 antagonist Nutlin-3a activates the p53 pathway and efficiently induces apoptosis in tumours with amplified MDM2 gene and overexpression of MDM2 protein. However, the
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