Until now, information is still limited about the transmission and Compound Library pathogenicity associated with this novel avian influenza H7N9 virus. Currently, the NA inhibitors Oseltamivir and Zanamivir are the front-line therapeutic options against this novel H7N9 influenza virus, which contains an S31N mutation in its M2 protein and thus confers resistance to the M2 ion channel blockers. However, recent studies have reported that H7N9 isolates with the R292K mutation are resistant to Zanamivir, Peramivir and Oseltamivir. Two of 14 patients infected with the novel H7N9 influenza virus possessing an R292K NA mutation had a poor clinical outcome. Therefore, discovering novel antiviral targets and drug candidates is urgently expected. HA-mediated virus-host membrane fusion is a prerequisite for the viral life cycle and is a promising antiviral target. Based on the HA-dependent membrane fusion model, we designed a cholesterol-conjugated peptide, named P155-185-chol, which is derived from the amino acid 155-185 region of H7N9 HA2. P155-185-chol demonstrated H7N9pp-specific inhibition of infection and exhibited significant inhibitory effects against H7N9 virus. In summary, our study demonstrated that the established H7N9-pseudotyped particle system can largely mimic the entry properties of the H7N9 virus, thus providing a relatively safe experimental system for studying the entry of H7N9 virus and for high-throughput screening of entry inhibitors, such as small molecules, peptides or antibodies. A potent anti-H7N9 peptide was successfully identified in this study. When used in combination with neuraminidase 
inhibitors, P155-185-chol showed additive and significant inhibitory effects against H7N9. By virtue of its distinct mechanisms of inhibition, P155-185-chol may be further optimized to improve its activity, highlighting a potential therapeutic candidate for H7N9 infections that can be used in combination with other anti-flu drugs. Obesity is a high risk factor for the development of many human pathologies, including insulin resistance, type 2 diabetes, hyperlipidemia, hypertension, cardiovascular disease, and cancer. Mounting evidence RWJ 64809 suggests that obesity is a multi-factorial disorder caused by a variety of genetic and endocrine abnormalities, some medicines, a low metabolic rate, nutritional and environmental factors, as well as imbalance of energy homeostasis. A number of studies have demonstrated that adipose tissue plays a critical role in the regulation of energy metabolism by secreting adipokines. However, there is strong evidence suggesting that abnormal expansion/accumulation of adipose tissue, which is largely associated with excessive adipocyte differentiation, increased numbers and lipid contents of fat cells, are closely linked to the development of obesity. Thus, any compound that inhibits excessive adipocyte differentiation and/or adipocyte hyperplasia/hypertrophy may have preventive and/or therapeutic potential against obesity and obesity-related disease. Research has accumulated to indicate that the differentiation of preadipocyte into adipocyte is controlled by a complex network of a variety of cellular proteins, including transcription factors, cell cycle-related proteins, adipocyte-specific genes, lipogenic enzymes, and signaling proteins. 3T3-L1 is a well-established murine preadipocyte cell line and has widely been used for understanding the molecular regulation of adipocyte differentiation and for screening potential anti-obesity drugs or agents. Interestingly, recent studies have shown that a number of polyphenolic natural products inhibit adipogenesis and have anti-proliferative and/or proapoptotic effects on 3T3-L1 adipocytes at high concentrations.