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Product name : BIBR1532
Item : CR1818
Price : 200mg, $745; 500mg, $1185
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CAS : 321674-73-1
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Details:
 Chemical Information
M.Wt 331.36 Storage Please store the product under the recommended conditions in the Certificate of Analysis.
Formula C21H17NO3
CAS No 321674-73-1
Solubility

DMSO 100 mg/mL Ethanol



Biological Activity of BIBR 1532

 

BIBR 1532 is a potent, selective, non-competitive telomerase inhibitor with IC50 of 100 nM.
IC50 Value: 100 nM
Target: Telomerase
BIBR 1532 is a selective telomerase inhibitor (IC50 values are 93, > 100000 and > 100000 nM for human telomerase, human RNA polymerase I and human RNA polymerase II + III respectively). Studies indicate that BIBR 1532 inhibits the reverse transcriptase of telomerase, hTERT, and shortens the length of the telomere. In addition, reports indicate that BIBR 1532 has the ability to stop cell proliferation in lung cancer cell studies after 120 days. BIBR 1532 causes telomere shortening in exponentially growing NCI-H460 lung carcinoma cells and eventual growth arrest.

 

[1]. El-Daly H, Kull M, Zimmermann S et al. Selective cytotoxicity and telomere damage in leukemia cells using the telomerase inhibitor BIBR1532. Blood. 2005 Feb 15;105(4):1742-9.

[2]. Mueller S, Hartmann U, Mayer F et al. Targeting telomerase activity by BIBR1532 as a therapeutic approach in germ cell tumors. Invest New Drugs. 2007 Dec;25(6):519-24.

[3]. El Daly H, Martens UM. Telomerase inhibition and telomere targeting in hematopoietic cancer cell lines with small non-nucleosidic synthetic compounds (BIBR1532). Methods Mol Biol. 2007;405:47-60.

[4]. Parsch D, Brassat U, Brümmendorf TH, Fellenberg J. Consequences of telomerase inhibition by BIBR1532 on proliferation and chemosensitivity of chondrosarcoma cell lines. Cancer Invest. 2008 Jul;26(6):590-6.

[5]. Bashash D, Ghaffari SH, Zaker F et al. Direct short-term cytotoxic effects of BIBR 1532 on acute promyelocytic leukemia cells through induction of p21 coupled with downregulation of c-Myc and hTERT transcription. Cancer Invest. 2012 Jan;30(1):57-64.


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