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Pathways Recommended: PI3K/Akt/mTOR
Results for "

PI3K/AKT-IN-3

" in MedChemExpress (MCE) Product Catalog:

20

Inhibitors & Agonists

1

Peptides

7

Natural
Products

2

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N2515
    Ginsenoside Rk1
    5+ Cited Publications

    NF-κB PI3K JAK Apoptosis Inflammation/Immunology Cancer
    Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures . Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB . Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis . Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway .
    Ginsenoside Rk1
  • HY-B1203

    9α-Fludrocortisone; 9α-Fluorcortisol

    Mineralocorticoid Receptor Glucocorticoid Receptor Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Fludrocortisone (9α-Fludrocortisone) is an orally active mineralocorticoid and glucocorticoid receptor agonist. Fludrocortisone suppresses pro-inflammatory cytokine expression, reduces CCL2, IL-6, IL-8 levels, upregulates mineralocorticoid receptor (MR) expression, induces PI3K/Akt, GSK-3β, CREB, ERK1/2, mTOR phosphorylation, blocks Tau hyperphosphorylation, prevents apoptosis, promotes survival and proliferation, enhances renal sodium and water transport, increases plasma volume and blood pressure, reduces plasma potassium and renin activity, stimulates erythropoietin expression, modulates uterine receptivity genes, and reverses PP242-induced MUC1 upregulation. Fludrocortisone can be used for the research of congenital adrenal hyperplasia, postural hypotension, and adrenal insufficiency [3] .
    Fludrocortisone
  • HY-N0721
    Neoandrographolide
    1 Publications Verification

    Neoandrographiside

    ERK p38 MAPK JNK NF-κB PI3K PPAR GSK-3 CaMK NO Synthase Reactive Oxygen Species (ROS) Apoptosis Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Neoandrographolide is a diterpenoid compound isolated from Andrographis paniculata. Neoandrographolide inhibits osteoclasts differentiation and bone resorption through inhibition of MAPK/NF-κB/PI3K/AKT/GSK3β/PPAR/CAMK signaling pathway. Neoandrographolide inhibits apoptosis in rat embryonic ventricular cardiomyocytes. Neoandrographolide inhibits iNOS and the generation of ROS, activates eNOS, exhibiting anti-inflammatory and hypolipidemic activity [3] .
    Neoandrographolide
  • HY-125848

    Apoptosis AMPK PPAR p38 MAPK PI3K Akt GSK-3 Reactive Oxygen Species (ROS) SOD Caspase Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota . Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma [3] .
    Ginsenoside F2
  • HY-P6292

    PACAP Receptor PKA ERK PI3K Akt GSK-3 Neurological Disease Cancer
    KS-133 is a bicyclic peptide with VIPR2 antagonistic activity that can cross the blood-brain barrier. KS-133 selectively blocks VIPR2-mediated Gq/Ca, Gs/cAMP, cAMP/PKA/ERK and PI3K/AKT/GSK3β signaling pathways. KS-133 inhibits VIPR2 agonist-induced CREB phosphorylation in the prefrontal cortex of mice. KS-133 shifts the polarization direction of macrophages toward M1. KS-133 attenuates cancer cell proliferation and reduces the cell cycle distribution level at the S-M phase. KS-133 exerts antitumor effects in a mouse model of colorectal cancer. KS-133 reverses cognitive decline in mouse models of psychiatric disorders. KS-133 can be used for research related to schizophrenia, colorectal cancer and breast cancer [3] .
    KS-133
  • HY-N7363

    (-)-Isolongifolene

    Environmental Pollutants Apoptosis Neurological Disease Inflammation/Immunology Cancer
    Isolongifolene ((-)-Isolongifolene) is a tricyclic sesquiterpene isolated from Murraya koenigii. Isolongifolene attenuates Rotenone-induced oxidative stress, mitochondrial dysfunction and apoptosis through the regulation of PI3K/AKT/GSK-3β signaling pathways. Isolongifolene has antioxidant, anti-inflammatory, anticancer and neuroprotective properties .
    Isolongifolene
  • HY-N3542

    Glycosidase Cancer
    Carpachromene is a potent α-glucosidase enzyme inhibitor. Carpachromene ameliorates insulin resistance in HepG2 cells via modulating IR/IRS1/PI3k/Akt/GSK3/FoxO1 pathway .
    Carpachromene
  • HY-161816

    Apoptosis Autophagy PI3K Akt Cancer
    PI3K/AKT-IN-3 (compound 8C) can induce autophagy and apoptosis by inhibiting the PI3K/AKT signaling pathway. PI3K/AKT-IN-3 can be used in cancer research .
    PI3K/AKT-IN-3
  • HY-126049

    (S)-(-)-Oxiracetam; (S)-ISF2522

    Apoptosis Neurological Disease
    (S)-oxiracetam (S-ORC) is an inhibitor targeting apoptosis. S-ORC reduces brain infarct size and lessens neurological dysfunction in middle cerebral artery occlusion/reperfusion (MCAO/R) models. S-ORC prevents neuronal apoptosis via activating PI3K/Akt/GSK3β signaling pathway via α7 nAChR after ischemic stroke. S-ORC can prevent neuronal death after ischemic stroke .
    (S)-Oxiracetam
  • HY-N0721R

    Neoandrographiside (Standard)

    Reference Standards ERK p38 MAPK JNK NF-κB PI3K PPAR GSK-3 NO Synthase Reactive Oxygen Species (ROS) Apoptosis Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Neoandrographolide (Standard) is the analytical standard of Neoandrographolide. This product is intended for research and analytical applications. Neoandrographolide is a diterpenoid compound isolated from Andrographis paniculata. Neoandrographolide inhibits osteoclasts differentiation and bone resorption through inhibition of MAPK/NF-κB/PI3K/AKT/GSK3β/PPAR/CAMK signaling pathway. Neoandrographolide inhibits apoptosis in rat embryonic ventricular cardiomyocytes. Neoandrographolide inhibits iNOS and the generation of ROS, activates eNOS, exhibiting anti-inflammatory and hypolipidemic activity [3] .
    Neoandrographolide (Standard)
  • HY-158017

    PI3K Cancer
    WXM-1-170 (compound 10) is a Indisulam (HY-13650) derivative,and inhibits the migration of gastric cancer cells. WXM-1-170 attenuates PI3K/AKT/GSK-3β/β-catenin signaling pathway .
    WXM-1-170
  • HY-161362

    PI3K Cancer
    SR-3-65 (compound 6) is a Indisulam (HY-13650) derivative,and inhibits the migration of gastric cancer cells. SR-3-65 attenuates PI3K/AKT/GSK-3β/β-catenin signaling pathway .
    SR-3-65
  • HY-173005

    PI3K Akt GSK-3 Apoptosis Cardiovascular Disease
    JZ19 reduces the LDH and ROS levels, and exhibits antioxidant activity against oxygen-glucose deprivation (OGD)-induced cardiomyocyte injury. JZ19 reverses Isoproterenol (HY-B0468)-induced cardiomyocyte hypertrophy and apoptosis through PI3K-AKT-GSK3β signaling pathway. JZ19 alleviates Isoproterenol (HY-B0468)-induced heart failure in mouse models .
    JZ19
  • 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
  • HY-116604A

    PD 139530 hydrochloride

    PI3K Akt Cancer
    RLX (PD 139530) hydrochloride is the hydrochloride of RLX (HY-116604). RLX 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 hydrochloride
  • HY-N2515R

    Reference Standards NF-κB PI3K JAK Apoptosis Inflammation/Immunology Cancer
    Ginsenoside Rk1 (Standard) is the analytical standard of Ginsenoside Rk1. This product is intended for research and analytical applications. Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures . Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB . Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis . Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway .
    Ginsenoside Rk1 (Standard)
  • HY-B1203S

    9α-Fludrocortisone-d5; 9α-Fluorcortisol-d5

    Isotope-Labeled Compounds Mineralocorticoid Receptor Glucocorticoid Receptor Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    Fludrocortisone-d5 (9α-Fludrocortisone-d5) is the deuterium labeled Fludrocortisone (HY-B1203). Fludrocortisone is an orally active mineralocorticoid and glucocorticoid receptor agonist. Fludrocortisone suppresses pro-inflammatory cytokine expression, reduces CCL2, IL-6, IL-8 levels, upregulates mineralocorticoid receptor (MR) expression, induces PI3K/Akt, GSK-3β, CREB, ERK1/2, mTOR phosphorylation, blocks Tau hyperphosphorylation, prevents apoptosis, promotes survival and proliferation, enhances renal sodium and water transport, increases plasma volume and blood pressure, reduces plasma potassium and renin activity, stimulates erythropoietin expression, modulates uterine receptivity genes, and reverses PP242-induced MUC1 upregulation. Fludrocortisone can be used for the research of congenital adrenal hyperplasia, postural hypotension, and adrenal insufficiency.
    Fludrocortisone-d5
  • HY-B1203R

    9α-Fludrocortisone (Standard); 9α-Fluorcortisol (Standard)

    Reference Standards Mineralocorticoid Receptor Glucocorticoid Receptor Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    Fludrocortisone (Standard) (9α-Fludrocortisone (Standard)) is the analytical standard of Fludrocortisone (HY-B1203). This product is intended for research and analytical applications. Fludrocortisone is an orally active mineralocorticoid and glucocorticoid receptor agonist. Fludrocortisone suppresses pro-inflammatory cytokine expression, reduces CCL2, IL-6, IL-8 levels, upregulates mineralocorticoid receptor (MR) expression, induces PI3K/Akt, GSK-3β, CREB, ERK1/2, mTOR phosphorylation, blocks Tau hyperphosphorylation, prevents apoptosis, promotes survival and proliferation, enhances renal sodium and water transport, increases plasma volume and blood pressure, reduces plasma potassium and renin activity, stimulates erythropoietin expression, modulates uterine receptivity genes, and reverses PP242-induced MUC1 upregulation. Fludrocortisone can be used for the research of congenital adrenal hyperplasia, postural hypotension, and adrenal insufficiency.
    Fludrocortisone (Standard)
  • HY-B1203S1

    9α-Fludrocortisone-d2; 9α-Fluorcortisol-d2

    Isotope-Labeled Compounds Mineralocorticoid Receptor Glucocorticoid Receptor Apoptosis Metabolic Disease Inflammation/Immunology Cancer
    Fludrocortisone-d2 (9α-Fludrocortisone-d2) is the deuterium labeled Fludrocortisone (HY-B1203). Fludrocortisone is an orally active mineralocorticoid and glucocorticoid receptor agonist. Fludrocortisone suppresses pro-inflammatory cytokine expression, reduces CCL2, IL-6, IL-8 levels, upregulates mineralocorticoid receptor (MR) expression, induces PI3K/Akt, GSK-3β, CREB, ERK1/2, mTOR phosphorylation, blocks Tau hyperphosphorylation, prevents apoptosis, promotes survival and proliferation, enhances renal sodium and water transport, increases plasma volume and blood pressure, reduces plasma potassium and renin activity, stimulates erythropoietin expression, modulates uterine receptivity genes, and reverses PP242-induced MUC1 upregulation. Fludrocortisone can be used for the research of congenital adrenal hyperplasia, postural hypotension, and adrenal insufficiency.
    Fludrocortisone-d2
  • HY-177149

    Drug Derivative Neurological Disease
    Allantoin ascorbate is a complexe of Allantoin (HY-N0543). Allantoin is a skin conditioning agent that promotes healthy skin, stimulates new and healthy tissue growth. Allantoin enhances cognitive functions by the mediation of PI3K-Akt-GSK-3β signal pathway. Allantoin ascorbate is slao a skin conditioning agent .
    Allantoin ascorbate

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