BI 2536 

BI 2536 (GMP) is BI 2536 (HY-50698) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. BI 2536 is a dual PLK1 and BRD4 inhibitor with IC₅₀s of 0.83 and 25 nM, respectively^[1]. BI-2536 suppresses IFNB (encoding IFN-β) gene transcription^[4].

超过从 10 nM 开始的 100 倍浓度范围，BI 2536 (GMP) 导致 HeLa 细胞以 4N DNA 含量积累，表明 G2 期或有丝分裂中的细胞周期阻滞。除了 HeLa 细胞外，BI 2536 (GMP) 还能有效抑制一组 32 种人类癌细胞系的增殖，这些细胞系代表不同的器官衍生 (包括乳腺癌、结肠癌、肺癌、胰腺癌和前列腺癌、黑色素瘤和造血系统癌) 和多种多样的肿瘤抑制基因或癌基因突变的模式 (包括 RB1、TP53、PTEN 和KRAS 状态)。该细胞组的半数最大有效浓度 (EC₅₀) 值范围为 2-25 nM，而浓度为 100 nM 的 BI 2536 (GMP) 通常足以诱导完全的有丝分裂停滞。指数生长的 hTERT-RPE1、人脐静脉内皮细胞 (HUVEC) 和正常大鼠肾 (NRK) 细胞的增殖在 12-31 nM 的 EC₅₀ 值范围内被阻断，表明与将未转化的细胞循环至 BI 2536 (GMP)^[3]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

BI 2536 (GMP) (40-50 mg/kg，iv) 在免疫缺陷的 nu/nu 小鼠中阻止人类癌症异种移植物的生长。每周一次或两次静脉注射 40-50 mg/kg BI 2536 (GMP) 的连续周期被发现在不同的异种移植模型中非常有效，例如 HCT 116 结肠癌完全抑制肿瘤，每周两次时间表 (处理与每周一次处理的对照 (T/C) 值为 0.3%，T/C 值为 16%；根据临床体征和没有重大体重变化来判断，这两种方案都具有良好的耐受性^[3]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

521.65

C₂₈H₃₉N₇O₃

755038-02-9

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Malik N, et al. Suppression of IFN β gene transcription by inhibitors of bromodomain and extra-terminal (BET) family members. Biochem J. 2015 Jun 15;468(3):363-72.  [Content Brief]

  [2]. Chen L, et al. BRD4 Structure-Activity Relationships of Dual PLK1 Kinase/BRD4 Bromodomain Inhibitor BI-2536. ACS Med Chem Lett. 2015 May 18;6(7):764-9.  [Content Brief]

  [3]. Steegmaier M, et al. BI 2536, a Potent and Selective Inhibitor of Polo-like Kinase 1, Inhibits Tumor Growth In Vivo. Current Biology (2007), 17(4), 316-322.  [Content Brief]

  [4]. Lénárt P, et al. The Small-Molecule Inhibitor BI 2536 Reveals Novel Insights into Mitotic Roles of Polo-like Kinase 1. Curr Biol. 2007 Feb 20;17(4):304-15.  [Content Brief]