方法：为检测对中性粒细胞哮喘小鼠模型的影响，将 Paquinimod (0.1-25 mg/kg) 饮用水口服给药给 OVA/CFA 致敏和激发的 C57BL/6 小鼠，每天一次，持续十七天。_x000D_ 结果：Paquinimod 可能通过下调 IL-17、IFN-γ 和 IL-1β，有效抑制中性粒细胞哮喘小鼠模型中的中性粒细胞炎症和重塑。[1]_x000D_ 方法：为检测抗炎活性，将 Paquinimod (25 mg/kg) 饮用水口服给药给 NOD 炎症性纤维化 (N-IF) 小鼠，每天一次，持续 4-10 周。_x000D_ 结果：使在疾病发作后开始治疗，对 N-IF 小鼠的治疗也能显著减少炎症并导致纤维化消退。疾病表型的减少与促进疾病的转基因 NKT-II 细胞及其 2-型细胞因子表达谱的数量和活化的系统性减少有关。[2]

H2O:< 1 mg/mL (insoluble);10% DMSO+40% PEG300+5% Tween 80+45% Saline:12.5 mg/mL (35.67 mM);DMSO:123 mg/mL (351.02 mM)

Two OA mouse models differing in level of synovial activation were treated prophylactic with paquinimod. Synovial thickening, osteophyte size and cartilage damage were measured histologically, using an arbitrary score, adapted Pritzker OARSI score or imaging software, respectively. Human OA synovia were stimulated with S100A9, with or without paquinimod[1].Seven weeks old female B6.Cg-Fbn1(Tsk)/J (Tsk-1) mice were treated with vehicle or paquinimod at the dose of 5 or 25mg/kg/day in the drinking water for 8 weeks. The effect of paquinimod on the level of skin fibrosis and on different subpopulations within the myeloid cell compartment in skin biopsies were evaluated by using histology, immunohistochemisty, a hydroxyproline assay and real-time PCR. Furthermore, the level of IgG in serum from treated animals was also analysed. The statistical analyses were performed using Mann-Whitney nonparametric two tailed rank test[1].