2. PI3K/Akt/mTOR Apoptosis Cell Cycle/DNA Damage
  3. PI3K Akt mTOR Apoptosis CDK
  4. PI3Kα-IN-33

PI3Kα-IN-33 is an orally active and selective PI3Kα inhibitor with an IC50 of 9.9 nM. PI3Kα-IN-33 blocks the PI3K/Akt/mTOR signaling pathway. PI3Kα-IN-33 induces apoptosis and triggers G2/M-phase arrest via Cyclin B1 and CDK1 downregulation. PI3Kα-IN-33 can be used for the research of colorectal cancer.

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PI3Kα-IN-33

PI3Kα-IN-33 Chemical Structure

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PI3Kα-IN-33 Related Antibodies

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Description

PI3Kα-IN-33 is an orally active and selective PI3Kα inhibitor with an IC50 of 9.9 nM. PI3Kα-IN-33 blocks the PI3K/Akt/mTOR signaling pathway. PI3Kα-IN-33 induces apoptosis and triggers G2/M-phase arrest via Cyclin B1 and CDK1 downregulation. PI3Kα-IN-33 can be used for the research of colorectal cancer[1].

IC50 & Target[1]

PI3Kα

9.9 nM (IC50)

CDK1/cyclinB1

 

In Vitro

PI3Kα-IN-33 (Compound 8b) forms a stable, high-affinity complex with PI3Kα[1].
PI3Kα-IN-33 (48 h) potently inhibits proliferation of multiple cancer cell lines, with the highest activity against HCT-116 colorectal cancer cells (IC50 = 0.53 μM), and has reduced cytotoxicity toward normal HEK293 cells (IC50 = 7.42 μM)[1].
PI3Kα-IN-33 (2.0 μM; 12 h) effectively inhibits the migratory ability of HCT-116 colorectal cancer cells[1].
PI3Kα-IN-33 (0.5-2.0 μM; 2 weeks) inhibits colony formation of HCT-116 colorectal cancer cells in a concentration-dependent manner[1].
PI3Kα-IN-33 (0.5-2.0 μM; 48 h) induces selective G2/M-phase arrest in HCT-116 colorectal cancer cells at concentrations of 0.5, 1.0, and 2.0 μM[1].
PI3Kα-IN-33 (0.5-2.0 μM; 48 h) at concentrations of 0.5, 1.0, and 2.0 μM causes concentration-dependent downregulation of Cyclin B1 and CDK1 in HCT-116 colorectal cancer cells[1].
PI3Kα-IN-33(0.5-2.0 μM; 48 h) at concentrations of 0.5, 1.0, and 2.0 μM triggers concentration-dependent activation of the mitochondrial apoptotic pathway and induction of DNA double-strand breaks in HCT-116 colorectal cancer cells[1].
PI3Kα-IN-33 (0.5-2.0 μM; 24 h) triggers concentration-dependent mitochondrial membrane potential depolarization in HCT-116 colorectal cancer cells[1].
PI3Kα-IN-33 (0.5-2.0 μM; 48 h) induces concentration-dependent apoptosis in HCT-116 colorectal cancer cells, with 33.3% total apoptosis at 2.0 μM[1].
PI3Kα-IN-33 (1.0-5.0 μM; 48 h) concentration-dependently inhibits the PI3K/Akt/mTOR signaling pathway in HCT-116 colorectal cancer cells[1].
PI3Kα-IN-33 blocks the PI3K-Akt-mTOR axis in HCT-116 colorectal cancer cells, driving transcriptional reprogramming of oncogenic and metabolic pathways including suppressed glycolysis and MTORC1 signaling[1].

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

PI3Kα-IN-33 Related Antibodies

Cell Migration Assay [1]

Cell Line: HCT-116 colorectal cancer cells
Concentration: 2.0 μM
Incubation Time: 12 h
Result: Significantly reduced HCT-116 cell migration compared to the control, with a migration inhibition rate of approximately 75%.

Cell Proliferation Assay[1]

Cell Line: HCT-116 colorectal cancer cells
Concentration: 0.5 μM; 1 μM; 2.0 μM
Incubation Time: 2 weeks
Result: Inhibited HCT-116 colony formation in a concentration-dependent manner.
At 2.0 μM, the number of surviving colonies was reduced to approximately 1 × 103, showing a strong inhibitory effect.

Cell Cycle Analysis[1]

Cell Line: HCT-116 colorectal cancer cells
Concentration: 0.5 μM; 1 μM; 2.0 μM
Incubation Time: 48 h
Result: Selectively induced G2/M-phase arrest in HCT-116 cells, increasing the G2/M population from 14.2% (control) to 23.4% at 0.5 μM, while G0/G1 and S-phase fractions remained largely unchanged.

Western Blot Analysis[1]

Cell Line: HCT-116 colorectal cancer cells
Concentration: 0.5 μM; 1 μM; 2.0 μM
Incubation Time: 48 h
Result: Induced concentration-dependent downregulation of Cyclin B1 and CDK1 protein levels, supporting blockade of the G2/M transition.\nInduced concentration-dependent increases in the Bax/Bcl-2 ratio, upregulation of cleaved caspase-9 and cleaved caspase-3, and increased levels of γ-H2AX (a marker of DNA double-strand breaks).

Apoptosis Analysis[1]

Cell Line: HCT-116 colorectal cancer cells
Concentration: 0.5 μM; 1 μM; 2.0 μM
Incubation Time: 48 h
Result: Induced apoptosis in a concentration-dependent manner, with total apoptotic cell percentages increasing to 21.66% (0.5 μM), 29.6% (1.0 μM), and 33.3% (2.0 μM).

Western Blot Analysis[1]

Cell Line: HCT-116 colorectal cancer cells
Concentration: 1 μM; 2 μM; 5 μM
Incubation Time: 48 h
Result: Inhibited phosphorylation of PI3K, Akt, p70S6K, and 4EBP1 in a concentration-dependent manner.
At 2.0 μM, it exhibited strong inhibitory effects on p-PI3K, p-p70S6K, and p-Akt phosphorylation.
Parmacokinetics
Species Dose Route AUC0-t AUC0-∞ MRT0-t MRT0-∞ T1/2 CL Vd Cmax Tmax F
Rat[1] 10 mg/kg i.v. 23078 μg/L·h 23119 μg/L·h 2.41 h 2.45 h 2.95 h 0.22 L/h/kg 0.94 L/kg 13600 μg/L / /
Rat[1] 5 mg/kg p.o. 16453 μg/L·h 16418 μg/L·h 5.89 h 5.92 h 2.31 h 0.61 L/h/kg 2.04 L/kg 2666.62 μg/L 1 h 35.6 %
In Vivo

PI3Kα-IN-33 (Compound 8b) (5–10 mg/kg; i.v. or i.g.; single dose) exhibits favorable pharmacokinetic properties, with an oral bioavailability of 35.6%[1].

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

Animal Model: Sprague-Dawley (SD) rats (male and female)[1]
Dosage: 5 mg/kg; 10 mg/kg
Administration: i.v. or i.g.; single dose
Result: Exhibited an AUC0-t of 23078 μg/L·h, an AUC0-∞ of 23119 μg/L·h, a MRT0-t of 2.41 h, a MRT0-∞ of 2.45 h, a t1/2 of 2.95 h, a CL of 0.22 L/h·kg, a Vd of 0.94 L/kg, and a Cmax of 13600.39 μg/L at 5 mg/kg i.v.
Exhibited an AUC0-t of 16453 μg/L·h, an AUC0-∞ of 16481 μg/L·h, a MRT0-t of 5.89 h, a MRT0-∞ of 5.92 h, a t1/2 of 2.31 h, a CL of 0.61 L/h·kg, a Vd of 2.04 L/kg, a Cmax of 2666.62 μg/L, a tmax of 1 h, and a F of 35.6% at 10 mg/kg i.g.
Molecular Weight

377.40

Formula

C20H19N5O3
SMILES

NC1=NC2=CC(C3=CC=C(N=CC(N4CCOCC4CO)=N5)C5=C3)=CC=C2O1
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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PI3Kα-IN-33 Related Classifications

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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:

PI3Kα-IN-33PI3KAktmTORApoptosisCDKPhosphoinositide 3-kinasePKBProtein kinase BMammalian target of RapamycinCyclin dependent kinaseHCT-116 colorectal cancer cellsPI3KγPI3KδPI3K/Akt/mTOR signaling pathwayCDK1PI3KαHEK293 cellsCyclin B1PI3Kβmitochondrial apoptotic pathwayInhibitorinhibitorinhibit

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