| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 25mg | 电议 |
| 100mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
Cell lines | Rhabdomyosarcoma cell line（RD,SJCRH30 and A204) |
Preparation Method | BYL-719 was dissolved in DMSO,to generate a stock solution (10 mM) which was subsequently diluted with the medium before adding to the cells. Rhabdomyosarcoma cell line were treated with BYL-719, then cell viability was evaluated by MTT assay. |
Reaction Conditions | Rhabdomyosarcoma cell line were treated with BYL-719 (0-20μM) for 72 h. |
Applications | BYL-719 decrease the viability of rhabdomyosarcoma(RMS) cell lines.BYL-719 treatment significantly affected cell proliferation of all the Rhabdomyosarcoma cell lines tested, confirming that PI3Kɑ was one of the isoforms expected to be involved in sustaining RMS cell proliferation. |
Animal models | Wild-type FVB/N mice, c-Met/H1047R mice |
Preparation Method | BYL-719 was administered daily by oral gavage.Treatments were performed for 3 consecutive weeks after moderate tumor burden occurred. |
Dosage form | 25mg/kg/day, oral gavage |
Applications | BYL-719 suppressed HCC angiogenesis in all the mouse models tested. BYL-719-treated mice were alive and in relatively good conditions when harvested after 3 weeks of treatment.Lliver weight in the BYL-719 cohort was lower than that from the vehicle cohort and similar to that of pretreatment tumor burden. |
| 产品描述 | BYL719 (Alpelisib) is a selective PI3Kɑ inhibitor.It induced fewer toxicities and had a more favorable safety profile compared to a pan class I PI3K inhibitor.PI3K/AKT and mTOR pathways regulate several processes involved in cell survival, protein synthesis, cell proliferation and differentiation, metabolism, senescence, motility, and angiogenesis.Results from preclinical studies show that BYL719 inhibits PI3K signaling and prevents AKT phosphorylation in cell lines harboring PIK3CA mutations, and blocks tumor growth in xenograft models[1]. BYL-719 treatment induced G0/G1 cell cycle arrest irrespective of PIK3CA mutational status. Notably, in PIK3CA-mutant cells (AGS and MKN1), sub-G1 fraction remarkably increased (p < 0.05), suggesting increased apoptosis by BYL-719 in these cell lines. BYL-719 in combination with paclitaxel demonstrated synergistic anti-proliferative effects, preferentially in PIK3CA-mutant GC cells, resulting in increased DNA damage response and apoptosis[2]. In mouse xenograft model of PIK3CA-mutant MKN1 GC cells, BYL-719 (25mg/kg/day) combined with paclitaxel (20mg/kg/day) significantly enhanced anti-tumor activity by decreasing Ki-67 expression and increasing TUNEL expression. Moreover, this combination prolonged the survival of tumor-bearing mice during 4 weeks of treatment period without resulting in significant change in body weight[2]. Oral consumption of BYL-719 results in dose-dependent hyperglycemia and hyperinsulinemia. Littermates were block-randomised to receive either the diet containing either 0.3 g/kg BYL-719. Following 6 weeks of treatment higher fed blood glucose and plasma insulin levels were evident in the BYL-719 treated groups, and a trend towards decreased body weight was seen with BYL-719 treatment without a difference in food intake. We have previously shown that p110α inhibitors can prevent weight gain in young (4–5 weeks old) mice during development[3]. BYL-719 reduces obesity and elevates energy expenditure in mice.The most dramatic on-target effect of BYL-719 was hyperglycemia, which in the case of the ob/ob mice was severe due to their diabetic condition.However, it is important to note that in normal lean mice, the glycemia induced by PI3Kɑ inhibition is within physiological range[4]. References: |
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