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.
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
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About This Item
价格与库存信息目前不能提供
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品質等級
化驗
≥98% (HPLC)
形狀
powder
製造商／商標名
Calbiochem®
儲存條件
OK to freeze
protect from light
顏色
white
溶解度
DMSO: 100 mg/mL
運輸包裝
ambient
儲存溫度
−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 密鑰
BDUHCSBCVGXTJM-WUFINQPMSA-N
一般說明
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.
包裝
Packaged under inert gas
警告
Toxicity: Standard Handling (A)
重構
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
其他說明
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.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°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
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
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
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
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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