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Pathways Recommended: PI3K/Akt/mTOR
Results for "

AKT/FoxO3a

" in MedChemExpress (MCE) Product Catalog:

6

Inhibitors & Agonists

3

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-16558
    Butein
    5 Publications Verification

    2’,3,4,4’-tetrahydroxy Chalcone

    EGFR Autophagy Apoptosis Phosphodiesterase (PDE) Cancer
    Butein is a cAMP-specific PDE inhibitor with an IC50 of 10.4 μM for PDE4 . Butein is a specific protein tyrosine kinase inhibitor with IC50s of 16 and 65 μM for EGFR and p60 c-src in HepG2 cells . Butein sensitizes HeLa cells to Cisplatin through AKT and ERK/p38 MAPK pathways by targeting FoxO3a . Butein is a SIRT1 activator (STAC).
    Butein
  • HY-15186
    Ipatasertib
    Maximum Cited Publications
    54 Publications Verification

    GDC-0068; RG7440

    Organoid Akt Apoptosis Cancer
    Ipatasertib (GDC-0068) is an orally active, highly selective and ATP-competitive pan-Akt inhibitor with IC50 values of 5, 18, 8 nM for Akt1/2/3, respectively. Ipatasertib synchronously activates FoxO3a and NF-κB through inhibition of Akt leading to p53-independent activation of PUMA. Ipatasertib also induces apoptosis in cancer cells and inhibits tumor growth in xenograft mouse models .
    Ipatasertib
  • HY-N2255
    Crebanine
    3 Publications Verification

    Akt Apoptosis NF-κB Reactive Oxygen Species (ROS) p38 MAPK ERK Interleukin Related TNF Receptor NO Synthase nAChR Bacterial Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Crebanine is an isoquinoline-like alkaloid that can be derived from Stephania. Crebanine is an antagonist of the α7-nAChR with an IC50 of 19.1 μM. Crebanine suppresses the proliferation, migration, and invasion of cancer cells, triggers reactive oxygen species (ROS) burst, and promotes apoptosis. Crebanine inhibits the AKT/FoxO3a, NF-κB and MAPK signaling pathways. Crebanine attenuates NOX2 hyperactivation, exhibits antioxidant properties by reducing reactive oxygen species and peroxidation. Crebanine inhibits voltage-dependent Na + current in guinea-pig ventricular myocytes. Crebanine has high inhibitory activity against gram-positive animal pathogenic bacteria. Crebanine ameliorates ischemia-reperfusion brain damage in middle cerebral artery occlusion and reperfusion (MCAO/R) rats. Crebanine significantly improves Scopolamine (HY-N0296)-induced cognitive deficits in ICR mice. Crebanine can be used for the study of hepatocellular carcinoma (HCC), cerebral ischemia and Alzheimer's disease .
    Crebanine
  • HY-16558R

    2’,3,4,4’-tetrahydroxy Chalcone (Standard)

    Reference Standards EGFR Autophagy Apoptosis Phosphodiesterase (PDE) Cancer
    Butein (Standard) is the analytical standard of Butein. This product is intended for research and analytical applications. Butein is a cAMP-specific PDE inhibitor with an IC50 of 10.4 μM for PDE4 . Butein is a specific protein tyrosine kinase inhibitor with IC50s of 16 and 65 μM for EGFR and p60c-src in HepG2 cells . Butein sensitizes HeLa cells to Cisplatin through AKT and ERK/p38 MAPK pathways by targeting FoxO3a . Butein is a SIRT1 activator (STAC).
    Butein (Standard)
  • HY-15186C

    GDC-0068 tosylate; RG7440 tosylate

    Organoid Akt Apoptosis Cancer
    Ipatasertib (GDC-0068) tosylate is an orally active, highly selective and ATP-competitive pan-Akt inhibitor with IC50 values of 5, 18, 8 nM for Akt1/2/3, respectively. Ipatasertib tosylate synchronously activates FoxO3a and NF-κB through inhibition of Akt leading to p53-independent activation of PUMA. Ipatasertib tosylate also induces apoptosis in cancer cells and inhibits tumor growth in xenograft mouse models .
    Ipatasertib tosylate
  • HY-116604

    PD 139530

    PI3K Akt Cancer
    RLX (PD 139530) is a PI3K/Akt/FoxO3a signaling inhibitor, possessing significant therapeutic potential in experimental colon cancer. RLX can effectively modulate the tumor microenvironment, enhancing the efficacy of cancer immunotherapy. RLX demonstrates the ability to improve the retention time of therapeutic agents within the tumor microenvironment by utilizing advanced nanoparticle delivery systems. RLX can be integrated with various treatment modalities, such as chemotherapy and radiotherapy, to enhance overall tumor therapy effectiveness. RLX highlights the necessity for further research into the tumor microenvironment’s dynamics to develop more tailored treatment approaches for diverse tumor types.
    RLX

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