2. PI3K/Akt/mTOR Apoptosis
  3. PI3K Apoptosis
  4. Alpelisib

Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome.

Para uso exclusivo en investigación. No vendemos a pacientes.

Alpelisib

Alpelisib Estructura química

No. CAS : 1217486-61-7

Tamaño Stock
50 mg   Obtener un presupuesto  
100 mg   Obtener un presupuesto  
250 mg   Obtener un presupuesto  

* Seleccione Cantidad antes de agregar artículos.

This product is a controlled substance and not for sale in your territory.

Alpelisib Related Antibodies

Top Publications Citing Use of Products

Ver todos los productos específicos de isoformas PI3K:

Ver todas las isoformas
PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

  • Actividad biológica

  • Pureza y Documentación

  • Referencias

  • Revisión del cliente

Descripciòn

Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome[1][2][3][4].

IC50 & Target

IC50: 5 nM (p110α), 250 nM (p110γ), 290 nM (p110δ), 1200 nM (p110β)[1]
In Vitro

Alpelisib GMP (0-5 μM; 14 d) significantly inhibits the clonal growth of MCF-7 and T47D breast cancer cells in 2D colony formation assays[1].
Alpelisib GMP (5 μM; 5 d) reduces the mammosphere formation efficiency of MCF-7 and T47D breast cancer stem cell-like (BCSC-like) cells in a dose-dependent manner[1].
Alpelisib GMP (0-10 μM; 10 d) significantly reduces the spheroid diameter of MCF-7 and T47D breast cancer stem cell-like (BCSC-like) cells in 3D culture systems, and inhibits their stem cell properties and drug resistance[1].
Alpelisib GMP (1 μM; 24 h) significantly reduces the protein levels of the stem cell markers Nanog, Sox2, and OCT3/4 in MCF-7 and T47D breast cancer stem-like cells (BCSC-like cells)[1].
Alpelisib (10 μM; 10 d) inhibits adipogenesis, thereby attenuating adipocyte differentiation of primary LipPD1 lipoma cells in 2D culture systems and reducing the volume of 3D LipPD1 lipospheres[2].
Combination treatment with Alpelisib GMP (10 μM; 4 d) and a 1 μM SGK3 inhibitor (VPS34-IN1 (HY-12795) or SGK3-IN) produces enhanced antiproliferative activity in Alpelisib GMP-resistant MCF7R and T47DR breast cancer cells, with a synergistic effect observed for the Alpelisib+SGK3-IN combination[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Alpelisib Related Antibodies

Cell Viability Assay[1]

Cell Line: human MCF-7 breast cancer monolayer cells, MCF-7 breast cancer stem cell (BCSC)-enriched mammosphere cells, human T47D breast cancer monolayer cells, T47D BCSC-enriched mammosphere cells
Concentration: Serial dilutions
Incubation Time: 96 h
Result: Inhibited cell viability in a dose-dependent manner.
Achieved an IC50 of 0.225 μM in MCF-7 monolayer cells.
Achieved an IC50 of 0.453 μM in MCF-7 BCSC-enriched mammosphere cells.
Achieved an IC50 of 3.055 μM in T47D monolayer cells.
Achieved an IC50 of 5.105 μM in T47D BCSC-enriched mammosphere cells.

Cell Proliferation Assay[2]

Cell Line: LipPD1, LipPD2, LipPD3 primary lipoma cells
Concentration: 1-100 µM
Incubation Time: 24-144 h
Result: Attenuated growth of all three lipoma cell cultures alone and in combination with rapamycin.
Maintained stable cell count for 6 days in LipPD1 cells treated with 100 µM.
Exhibited IC50 values for 72 h Hoechst assays of 15.91 µM (LipPD1), 10.06 µM (LipPD2), and 15.79 µM (LipPD3).
Reduced the fraction of Ki-67 positive LipPD1 cells in a concentration-dependent manner: to 0.75 fold (1 µM, p=0.074), 0.55 fold (10 µM, p=0.018), and 0.22 fold (100 µM, p=0.017).

Apoptosis Analysis[2]

Cell Line: LipPD1, LipPD2, LipPD3, Lip3, Lip4 primary lipoma cells
Concentration: 50 µM
Incubation Time: 24, 72 h
Result: Observed no cell death after 72 h 50 µM treatment in LipPD1 and Lip3 cells.
Detected a slight reduction in viable cells in Lip4 cells.
Detected no additional LDH release in LipPD1, LipPD2, or LipPD3 cells after 24 h or 72 h 50 µM treatment, indicating no induction of cell death.

Western Blot Analysis[2]

Cell Line: LipPD1 primary lipoma cells
Concentration: 10-100 µM
Incubation Time: 24, 48 h
Result: Reduced AKT activation (phospho-Thr 308) in 50 µM treated cells.
Reduced mTOR activation (phospho-Ser 2448) in 10 µM and 50 µM treated cells.
Significantly reduced phosphorylation of S6 (phospho-Ser 235/236) for all tested concentrations.
Reduced the fraction of pS6 positive LipPD1 cells to 0.57 fold (10 µM) and 0.01 fold (100 µM).

Cell Differentiation Assay[2]

Cell Line: LipPD1 primary lipoma cells
Concentration: 10 µM
Incubation Time: 10 days
Result: Reduced lipid accumulation in 2D culture, with the fraction of adipocytes decreasing from 54.8% to 29.9%.
Downregulated mRNA expression of differentiation markers: PPARγ to 0.55 fold, adiponectin to 0.54 fold, aP2 to 0.54 fold, and FASN to 0.58 fold.
Reduced 3D spheroid size to 0.78 fold after 4 days and 0.79 fold after 10 days, with significant differences from day 4 onward, while control spheroid size increased to 1.25 fold after 10 days.
In Vivo

Alpelisib GMP (50 mg/kg; i.p.; daily) exerts partial antitumor activity against alpelisib-resistant MCF7R breast cancer xenografts, with maximum efficacy achieved when combined with SGK3 knockdown[3].
Alpelisib GMP (50 mg/kg; i.p.; daily) exerts partial antitumor activity against alpelisib-resistant T47DR breast cancer xenografts, with maximum efficacy achieved when combined with SGK3 knockdown[3].
Alpelisib GMP (25 mg/kg; p.o.; daily; 4 weeks) significantly inhibits tumor growth, reduces tumor cell proliferation, and increases tumor cell apoptosis in a PIK3CA-mutant gastric cancer xenograft model with 100% survival of treated mice over 4 weeks[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c nude (6-week-old female)[3]
Dosage: 50 mg/kg
Administration: i.p.; daily
Result: Exerted partial inhibition of MCF7R xenograft tumor growth.
Achieved maximum tumor growth inhibition when combined with SGK3 knockdown, with significantly reduced final tumor volumes and weights compared to vehicle control or SGK3 knockdown alone.\nExerted partial inhibition of T47DR xenograft tumor growth.
Achieved maximum tumor growth inhibition when combined with SGK3 knockdown, with significantly reduced final tumor volumes and weights compared to vehicle control or SGK3 knockdown alone.
Animal Model: Balb/c athymic nude mice (female, 5 weeks old, 26-28 g, subcutaneous xenograft of luciferase-expressing PIK3CA-mutant MKN1 human gastric cancer cells)[4]
Dosage: 25 mg/kg
Administration: p.o.; daily; 4 weeks
Result: Significantly retarded tumor growth compared to the control group.
Decreased Ki-67 expression (proliferation marker).
Increased TUNEL expression (apoptosis marker).
Maintained stable body weight over the 4-week period.
Achieved 100% survival of treated mice over the 4-week period.
Peso molecular

441.47

Fòrmula

C19H22F3N5O2S
No. CAS
SMILES

CC(N=C(S1)NC(N2CCC[C@H]2C(N)=O)=O)=C1C3=CC(C(C)(C(F)(F)F)C)=NC=C3
Envío

Room temperature in continental US; may vary elsewhere.
Almacenamiento

Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.

Alpelisib Related Classifications

  • Calculadora de molaridad

  • Calculadora de dilución

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Alpelisib (GMP)1217486-61-7PI3KApoptosisPhosphoinositide 3-kinaseNotch signalingT47Dgastric cancerMCF-7PI3K/AKT/mTOR signalingMAPK/ERK signalingJAK-STAT signalingbreast cancerPI3KαPTEN Hamartoma Tumor Syndrome-related lipomaInhibitorinhibitorinhibit

Productos vistos recientemente:

Consulta en línea

Your information is safe with us. * Required Fields.

Nombre del producto

  

Requested Quantity *

Nombre del solicitante *

 

Saludo

Direcciòn del E-mail *

 

Número de teléfono *

Department

 

Nombre de la Organizaciòn *

City

Provincia

Country or Region *

      

Observaciones

Consulta para venta a granel

Inquiry Information

Nombre del producto:
Alpelisib
Cat. No.:
HY-15244G
Cantidad:
MCE Japan Authorized Agent:

Revisión del cliente

Thank You for Your Feedback!

Request for HNMR Report

Please fill out this form to request the QC report. We will send it to your Email address shortly.

Your information is safe with us. * Required Fields.

Nombre del producto

  

Lot #

Nombre del solicitante *

 

Direcciòn del E-mail *

Número de teléfono

 

Department *

Nombre de la Organizaciòn *

 

Country or Region *

Observaciones

SAFETY DATA SHEET (SDS)

Request for HNMR Report

We have received your request and will respond to you as soon as possible.