| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | Spleen cells of BALB/c mice |
Preparation Method | Spleen cells of BALB/c mice (1 × 107/ml) were incubated in RPMI1640 medium supplemented with 0.5% BSA or 10% FCS in the presence or absence of 100 µM CPYPP. 1 or 5 hr of incubation at 37°C. |
Reaction Conditions | 100µM for 1 hour or 5 hours |
Applications | CPYPP was nontoxic when applied to spleen cells at 100 µM . |
Animal models | male C57BL/6J mice |
Preparation Method | Mice were randomized into four groups (n = 6): the saline + vehicle group, LPS + vehicle group, saline + CPYPP group, and LPS + CPYPP group. ALI was induced by intraperitoneal (i.p.) injection of LPS (10 mg/kg) body weight; The mice in the LPS + vehicle and LPS + CPYPP groups received CPYPP (250 mg/kg) or an equivalent volume of vehicle via i.p. injection 10 min after LPS administration. The mice in the saline + vehicle and saline + CPYPP groups received CPYPP (250 mg/kg) or an equivalent volume of vehicle via i.p. injection 10 min after saline administration. |
Dosage form | Intraperitoneal injection, 250 mg/kg |
Applications | CPYPP-treated mice had decreased lung injury scores compared with vehicle-treated mice. Furthermore, CPYPP-treated mice exhibited significantly decreased MPO activity and W/D ratios, which indicated decreased pulmonary edema. |
| 产品描述 | CPYPP bound to DOCK2 DHR-2 domain (DOCK2DHR-2) in a reversible manner and inhibited its catalytic activity[1]. CPYPP inhibited the guanine nucleotide exchange factor (GEF) activity of DOCK2DHR-2 for Rac1 in a dose-dependent manner, with a half-maximal inhibitory concentration (IC50) of 22.8 ± 2.4 μM. This inhibitory activity was independent on length of preincubation time, ranging from 2 min to 30 min. In addition, CPYPP was nontoxic when applied to spleen cells or thymoma cells (BW5147α-β-) at 100 μM for 3 hr or 3 days, respectively[1]. Pre-treatment of human neutrophils with CPYPP, a small molecule inhibitor of the DHR-2 domain of DOCK proteins and thus of the Rac GEF activity of human DOCK2 and DOCK5, significantly impaired neutrophil chemotaxis and ROS production[2]. CPYPP effectively decreased the secretion and gene expression of TNF-α, IL-1β and IL-6 in the lungs, suggested effects of DOCK2 on endotoxemia-induced inflammatory responses in mice. CPYPP remarkably inhibited the infiltration of total cells, macrophages and neutrophils into the bronchoalveolar lavage fluid[3]. A reseach found out that a joint usage of both CPYPP and C25-140 revealed a better consequence compared to monotherapy against hepatic I/R injury[4]. References: |
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