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Description: Alpelisib (formerly also known as BLY719; trade name: Piqray) is a novel, potent, newly approved, orally bioavailable phosphatidylinositol 3-kinase (PI3K) inhibitor with antineoplastic activity. As of May 2019, it has been approved by FDA as the first PI3K inhibitor to treat postmenopausal women, and men, with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative, PIK3CA-mutated, advanced or metastatic breast cancer (as detected by an FDA-approved test) following progression on or after an endocrine-based regimen. PI3K inhibitor BYL719 specifically inhibits PIK3 in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents. Clinical data suggests a disable safety profile with manageable side effects for BYL719.
References: Bioorg Med Chem Lett. 2013 Jul 1;23(13):3741-8; Nature. 2018 Jun;558(7711):540-546.; Cancer Lett. 2018 Oct 10;440-441:54-63.
Product Catalog 2023
Guide to Product Handling
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
Cell Assay: Multiple myeloma cells (OPM1, OPM2, RPMI8226, U266, MM1s,MM1R) and NCI-H9290. BYL719 prominently decreases the activation of the PI3K signaling proteins (pAKT, pS6R, and pGSK), this effect are also observed in slico that BYL719 decreases the expression of the PI3K signaling proteins in a dose-dependent manner. Furthermore, BYL719 dose-dependently triggers G1 arrest and induces apoptosis in MM cells. BYL719 inhibits the proliferation of breast cancer cell lines harboring PIK3CA mutations, correlating with inhibition of various downstream signaling components of the PI3K/Akt pathway.
Lot#: V011401,Purity ≥98%
COA
MSDS
NMR
Lot#: V011402,Purity ≥98%
Lot#: V011403,Purity ≥98%
Lot#: V011404,Purity ≥98%
PK/PD/efficacy relationship of NVP-BYL719 in PI3Kα-dependent tumor mouse models in vivo. Mol Cancer Ther. 2014 May;13(5):1117-29.
Determination of NVP-BYL719 safety profile compared with pan-class I PI3K inhibitors. Mol Cancer Ther. 2014 May;13(5):1117-29.
PTEN mutation and PIK3CA amplification/copy number modulate response to NVP-BYL719. Mol Cancer Ther. 2014 May;13(5):1117-29.
A, genetic alterations in PIK3CA predict NVP-BYL719 in vivo efficacy. B, PDX models carrying a PIK3CA mutation and/or amplification were established by implanting surgical tumor tissues from treatment-naïve cancer patients into athymic mice. Mol Cancer Ther. 2014 May;13(5):1117-29.
PIK3CA mutation is the top positive predictor for NVP-BYL719 sensitivity. A, NVP-BYL719 sensitivity profile. Scatter plot showing Amax (%) by EC50 values expressed in μmol/L of NVP-BYL719 in cell viability assays assessed on 474 cancer cell lines. Mol Cancer Ther. 2014 May;13(5):1117-29.
Identification of selectivity index of small molecule inhibitors for PIK3CA mutant versus PIK3CA wild-type (WT) cell line populations across ∼1,000 different compounds. Mol Cancer Ther. 2014 May;13(5):1117-29.