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Alpelisib

产品编号 T1921 CAS 1217486-61-7

别名: BYL-719

Alpelisib 是一种选择性的，有效的，具有口服活性的PI3Kα抑制剂，具有抗肿瘤活性。它对 PIK3CA 突变癌具有靶向性。它抑制 p110α (IC50:5 nM)、p110γ (IC50:250 nM)、p110δ (IC50:290 nM)、p110β (IC50:1200 nM)。

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Alpelisib, CAS 1217486-61-7

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纯度: 99.62%

纯度: 99.25%

纯度: 99.07%

纯度: 98%

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生物活性

化学信息

存储 & 溶解度

参考文献

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产品描述

Alpelisib is an orally bioavailable PI3Kα inhibitor (IC50: 5 nM in a cell-free assay) with potential antineoplastic activity and minimal effect on PI3Kβ/γ/δ.

靶点活性

p110α:5 nM (cell free), p110γ:250 nM (cell free)

体外活性

In biochemical assays, Alpelisib (NVP-BYL719) inhibits wild-type PI3Kα (IC50: 4.6 nmol/L) more potently than the PI3Kδ (IC50: 290 nmol/L) and PI3Kγ (IC50: 250 nmol/L) isoforms and shows significantly reduced activity against PI3Kβ (IC50: 1,156 nmol/L). Here, in addition, we show that NVP-BYL719 potently inhibits the 2 most common PIK3CA somatic mutations (H1047R, E545K; IC50～4 nmol/L). NVP-BYL719 potently inhibited Akt phosphorylation in cells transformed with PI3Kα (IC50: 74 ± 15 nmol/L) and showed significantly reduced inhibitory activity in PI3Kβ or PI3Kδ isoforms transformed cells (≥15-fold compared with PI3Kα) [1]. After 72 hr of treatment, BYL719 significantly inhibited the cell growth of all osteosarcoma cell lines tested in a dose-dependent manner with an IC50 ranging from 6 to 15 mM and with the IC90 from 24 to 42 mM at 72 hr [2].

CellLine:	HSA cells
Concentration:	20μM
IncubationTime:	8h
Result:	Only the Re21 cells recovered almost completely from the wound after 8 h; the JuA1 and JuB4 cells exhibited a significantly delayed wound healing ability.

CellLine:	HK2 cells
Concentration:	10μM
IncubationTime:	16h
Result:	Alpelisib reduced the actin baskets in OCRL KO HK2 cells in a dose-responsive fashion.

体内活性

NVP-BYL719 (12.5, 25, or 50 mg/kg, p.o.) treatment was associated with dose and time-dependent inhibition of the PI3K/Akt pathway, which notably paralleled time-dependent drug exposure in tumor and plasma. Rat1-myr-p110α tumor-bearing nude mice were treated orally every day with the compound for up to 8 consecutive days. Treatments of 12.5, 25, and 50 mg/kg were well tolerated and resulted in a dose-dependent and statistically significant antitumor effect [1]. BYL719 significantly reduced tumor volumes in a dose-dependent manner compared to a vehicle group (p < 0.01 and p < 0.001, respectively for 12.5 and 50 mg/kg BYL719) [2].

Animal Model:	Eight-week-old male Sprague–Dawley rats weighing 250–300 g
Dosage:	1 and 10mg/kg
Administration:	Intravenous; 8h
Result:	The plasma levels of alpelisib declined in a multi-exponential manner, with a t1/2 of 147–297 min. The dose-normalized AUC of alpelisib was significantly different between the doses; the values were 87.3 ± 21.3 and 134 ± 25 μg·min/mL for 1 and 10 mg/kg

Animal Model:	OcrlY/− mice
Dosage:	50mg/kg
Administration:	Oral gavage for 6 weeks
Result:	Reducted in growth rate relative.

细胞实验

To evaluate the isoform-specific potency of NVP-BYL719 in a cell-based system, an N-terminally myristoylated form of each PI3K class IA isoform was expressed in Rat1 fibroblasts. The retroviral expression plasmid pBabePuro containing human p110α, p110β, and p110δ with an N-terminal myristoylation (myr) signal followed by an HA-tag were generated. Successfully infected Rat1 cells were selected in medium containing 4 μg/mL of puromycin, expanded and characterized for expression of the p110 isoforms. Transgenic expression of the myristoylated protein was confirmed by increased levels of phosphorylated Akt [1].

动物实验

All in life experimentation and efficacy studies were conducted as described previously. Tumor xenografts were grown subcutaneously or orthotopically in nude mice or nude Rowett rats (Hsd: RH-Fox1rnu) by injection of 3 × 10^6 to 1 × 10^7 cells or implantation of tumor fragments of approximately 50 mg. Tumor-bearing animals mice were treated with either vehicle control, NVP-BYL719, or NVP-BKM120 (p.o., every day) at the doses indicated [1].

别名	BYL-719
分子量	441.47
分子式	C19H22F3N5O2S
CAS No.	1217486-61-7

存储

Powder: -20°C for 3 years | In solvent: -80°C for 2 years

溶解度

DMSO: 82 mg/mL (185.7 mM)

Ethanol: 2 mg/mL (4.53 mM)

( < 1 mg/mL refers to the product slightly soluble or insoluble )

参考文献

1. Fritsch C, et al. Characterization of the novel and specific PI3Kα inhibitor NVP-BYL719 and development of the patient stratification strategy for clinical trials. Mol Cancer Ther. 2014 May;13(5):1117-29. 2. Gobin B, et al. BYL719, a new α-specific PI3K inhibitor: single administration and in combination with conventional chemotherapy for the treatment of osteosarcoma. Int J Cancer. 2015 Feb 15;136(4):784-96. 3. Young CD, et al. Conditional loss of ErbB3 delays mammary gland hyperplasia induced by mutant PIK3CA without affecting mammary tumor latency, gene expression, or signaling. Cancer Res. 2013 Jul 1;73(13):4075-85. 4. Elkabets M, et al. mTORC1 inhibition is required for sensitivity to PI3K p110α inhibitors in PIK3CA-mutant breast cancer. Sci Transl Med. 2013 Jul 31;5(196):196ra99. 5. Yang T, Xu R, Su Q, et al. Chelerythrine hydrochloride inhibits proliferation and induces mitochondrial apoptosis in cervical cancer cells via PI3K/BAD signaling pathway[J]. Toxicology in Vitro. 2020, 68: 104965. 6. Liao W, Wang Z, Han Y, et al. Design, synthesis and biological activity of novel 2, 3, 4, 5-tetra-substituted thiophene derivatives as PI3Kα inhibitors with potent antitumor activity[J]. European Journal of Medicinal Chemistry. 2020: 112309.

文献引用

1. Liao W, Wang Z, Han Y, et al. Design, synthesis and biological activity of novel 2,3,4,5-tetra-substituted thiophene derivatives as PI3Kα inhibitors with potent antitumor activity. European Journal of Medicinal Chemistry. 2020, 197: 112309 2. Yang T, Xu R, Su Q, et al. Chelerythrine hydrochloride inhibits proliferation and induces mitochondrial apoptosis in cervical cancer cells via PI3K/BAD signaling pathway. Toxicology in Vitro. 2020, 68: 104965. 3. Chen R, Wang Z, Sima L, et al.Design, synthesis and evaluation of 2, 6, 8-substituted Imidazopyridine derivatives as potent PI3K α inhibitors.Journal of Enzyme Inhibition and Medicinal Chemistry.2023, 38(1): 2155638.

剂量换算

对于不同动物的给药剂量换算，您也可以参考 更多...

体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

第一步：请输入动物实验的基本信息

剂量

mg/kg

每只动物体重

给药体积

μL

动物数量

第二步：请输入动物体内配方组成，不同的产品配方组成不同，如有配方需求，可先联系我们提供正确的体内配方。

% DMSO+

% +

% Tween 80+

% ddH₂O

%DMSO+

计算重置

计算结果如下:

工作液浓度: mg/ml;

母液配置方法: mg 药物溶于 μL DMSO (母液浓度为 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 μL DMSO 主液，加入 μL PEG300，混匀澄清，再加 μL Tween 80，混匀澄清，再加 μL ddH₂O, 混匀澄清。

备注:

要按顺序从左向右依次添加助溶剂。可配合物理方法，如涡流、超声波或热水浴使之帮助溶解。

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技术支持

您可能有的问题的答案可以在抑制剂处理说明中找到，包括如何准备库存溶液，如何存储产品，以及基于细胞的分析和动物实验需要特别注意的问题。

Keywords

Alpelisib 1217486-61-7 PI3K/Akt/mTOR signaling PI3K Inhibitor Phosphoinositide 3-kinase inhibit phosphorylation p110α cancer BYL 719 BYL-719 antineoplastic AKT metastasis mutant BYL719 PIK3CA breast inhibitor

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Alpelisib

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