Pomalidomide

TNF-α:13 nM (PBMCs)

方法: 为评估在脑缺血中的潜在价值，将 Pomalidomide (50 mg/kg，1% carboxy methyl cellulose) 腹腔注射给长期过度表达 TNF-α 表面活性蛋白 (SP)-C 启动子的转基因小鼠 (SP-C/TNF-α 小鼠)，每天一次，持续 21 天。 结果: Pomalidomide 显著降低血清 TNF-α 和 IL-5水平。[3]

方法: 多发性骨髓瘤细胞 RPMI8226 和 OPM2 用 Pomalidomide (0.01-50 μM) 处理 48 h，使用 MTT assay 检测细胞活力。 结果: Pomalidomide 在 48 h 显著降低 RPMI8226 和 OPM2 细胞的细胞活力，IC50 值分别为 8 μM 和 10 μM。[1] 方法: 多发性骨髓瘤细胞 H929、U266 和 MM.1s 用 Pomalidomide (0.05-1 μM) 和 ACY-241 (3 μM) 处理 4 天，使用 Flow cytometry 检测细胞凋亡。 结果: 当两种药物联合治疗时，相对于任何一种单一药物，细胞凋亡显著增加。[2]

Ethanol:< 1 mg/mL (insoluble or slightly soluble); DMSO:50 mg/mL (182.99 mM); H2O:< 1 mg/mL (insoluble or slightly soluble)

In vitro effects of either CC-5013 or CC-4047 as single agent or in combination with rituximab were evaluated by flow cytometric analysis. Lymphoma cell lines (1 × 10^6 cells) were exposed to either CC-5013 (5 μg/mL), CC-4047 (5 μg/mL), or vehicle control (DMRIE-C, 0.01%) alone or in combination with rituximab at a final concentration of 10 μg/mL. Following a period of incubation of 24 or 48 hours, apoptosis was assessed by staining-treated cells with FITC-labeled Annexin V and propidium iodine. All samples were analyzed by multicolor flow cytometric analysis using a fluorescence-activated cell sorter/FACStar Plus flow cytometer. Cells were scored as apoptotic if they were Annexin V–positive and propidium iodine–negative/positive (early and late apoptosis, respectively) [2].

These studies were carried out using a disseminated lymphoma-bearing SCID mouse xenograft model. Raji cells were harvested from confluent cultures and only suspensions with >90% viable cells were used for animal inoculation. Subsequently, on day 0, SCID mice received 1 ×10^6 Raji cells via i.v. Untreated SCID mice inoculated by i.v. injection develop symptomatic central nervous system, pulmonary, and liver metastasis that result in death from massive tumor burden and central nervous system involvement after 17 to 21 days after inoculation. A second lymphoma mouse model was used to address the significance of NK cell expansion in the biological interactions observed between rituximab and IMiDs. The second mouse lymphoma xenograft consisted of SCID mice depleted of NK cells bearing Raji cells implanted via tail vein injection as described above [2].