BIBR 1532是端粒酶一个新型的选择性抑制剂，IC50值为93 nM[1]。

据报道，BIBR 1532抑制端粒酶和hTERT的逆转录酶，缩短端粒酶的长度来抑制人类癌细胞增殖[1]。在前-B急性淋巴白血病细胞中，BIBR 1532以浓度依赖的方式抑制c-Myc和hTERT表达来抑制端粒酶活性，高剂量的BIBR 1532可通过提升p73、Bax/Bcl-2和Caspase-3活性而诱导细胞凋亡[2]。在NB4白血病细胞中，可通过c-Myc和hTERT的转录抑制，结合BIBR 1532和三氧化二砷抑制细胞增殖能力和端粒酶活性[3]。

参考文献：
[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, 69586968.
[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.