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It has been reported that BIBR 1532 inhibited the reverse transcriptase of telomerase, hTERT, and shortened the length of the telomerase to suppress human cancer cell proliferation [1]. In pre-B acute lymphoblastic leukemia cells, BIBR1532 suppressed c-Myc and hTERT expression in a concentration-dependent manner to inhibit telomerase activity, and high doses of BIBR1532 could induce apoptosis by elevating p73, Bax/Bcl-2 and caspase-3 activation [2]. In NB4 leukemic cells, combined treatments with BIBR 1532 and arsenic trioxide suppressed cell proliferative capacity and inhibited telomerase activity probably via transcriptional suppression of c-Myc and hTERT. [4]

References:

[1]. Damm, K.; Hemmann, U.; Garin-Chesa, P.; Hauel, N.; Kauffman, I.; Priepke, H.; Niestroj, C.; Daiber, C.; Enenkel, B.; Guilliard, B.; Lauritsch, I.; Muller, E.; Pascolo, E.; Sauter, G.; Pantic, M.; Martens, U. M.; Wenz, C.; Linger, J.; Kraut, N.; Rettig, W. J.;Schnapp, A. A highly selective telomerase inhibitor limiting human cancer cell proliferation. EMBO J. 2001, 20, 6958?6968.

[2]. Bashash D1, Ghaffari SH, Mirzaee R, Alimoghaddam K, Ghavamzadeh A. Telomerase inhibition by non-nucleosidic compound BIBR1532 causes rapid cell death in pre-B acute lymphoblastic leukemia cells. Leuk Lymphoma. 2013 Mar;54[4]:561-8. doi: 10.3109/10428194.2012.704034. Epub 2012 Sep 28.

[3]. Bashash D1, Ghaffari SH, Zaker F, Kazerani M, Hezave K, Hassani S, Rostami M, Alimoghaddam K, Ghavamzadeh A. Anticancer Agents Med Chem. 2013 Sep;13(7):1115-25. BIBR 1532 increases arsenic trioxide-mediated apoptosis in acute promyelocytic leukemia cells: therapeutic potential for APL.

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