| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Animal experiment: | Adult (appr 4 month) male HF+AF and Ntg mice are administered with BGP-15 (15 mg/kg per day in saline) for 4 weeks by oral gavage or remained untreated (oral gavage with saline or no gavage). Gavage with saline has no effect on morphological or functional parameters in the HF+AF model. Therefore, untreated mice (no gavage) and mice administered saline are combined and referred to as HF+AF control. Echocardiography and ECG studies are performed before and after treatment. |
| 产品描述 | Ki= 57 μM BGP-15 is a PARP inhibitor. As a group of pharmacological inhibitors of the enzyme poly ADP ribose polymerase(PARP), PARP inhibitors are considered a potential treatment for stroke and myocardial infarction. In vitro: Previous study showed that BGP-15 at 200 μM could prevent the imatinib-induced oxidative damages, attenuate the depletion of high-energy phosphates, alter the signaling effect of imatinib by preventing p38 MAP kinase and JNK activation, and also induce the Akt and GSK-3β phosphorylation [1]. In vivo: In-vivo study indicated that BGP-15 improved cardiac function and reduced arrhythmic episodes in two HF and AF mouse models. In these models, BGP-15 was associated with increased phosphorylation of IGF1R. Moreover, cardiac-specific IGF1R transgenic overexpression in mice recapitulated the protection caused by BGP-15. The authors further demonstrated that BGP-15 with IGF1R could provide protection independent of phosphoinositide 3-kinase-Akt and heat-shock protein 70 [2]. Clinical trial: A safety and efficacy of BGP-15 in patients with type 2 diabetes mellitus has been scheduled, however, this study is now terminated due to the funding support withdrawn. (https://clinicaltrials.gov/ct2/show/NCT01069965 term=BGP-15&rank=1) References: |
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