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Results for "

Akt+Activators

" in MedChemExpress (MCE) Product Catalog:

16

Inhibitors & Agonists

2

Inhibitory Antibodies

4

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-18749
    SC79
    Maximum Cited Publications
    308 Publications Verification

    		 Akt Neurological Disease Inflammation/Immunology Cancer
    SC79, a unique specific and BBB permeable Akt activator, activates Akt in the cytosol and inhibits Akt membrane translocation. SC79 specifically binds to the PH domain of Akt .
    SC79
  • HY-18676
    OSU-T315
    10+ Cited Publications

    		 Integrin Autophagy Apoptosis Cancer
    OSU-T315 (ILK-IN-1) is a small Integrin-linked kinase (ILK) inhibitor with an IC50 of 0.6 μM, inhibiting PI3K/AKT signaling by dephosphorylation of AKT-Ser473 and other ILK targets (GSK-3β and myosin light chain) . OSU-T315 abrogates AKT activation by impeding AKT localization in lipid rafts and triggers caspase-dependent apoptosis in an ILK-independent manner . OSU-T315 causes cell death through apoptosis and autophagy .
    OSU-T315
  • HY-N12060
    Ginkgo biloba extract

    		Bcl-2 Family Caspase Apoptosis Autophagy Reactive Oxygen Species (ROS) Akt JNK ERK Cardiovascular Disease Neurological Disease
    Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves . Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy) . Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis .
    Ginkgo biloba extract
  • HY-P99274
    Xentuzumab
    1 Publications Verification

    BI 836845; Anti-Human IGF1 and IGF2 Recombinant Antibody

    		 IGF-1R Cancer
    Xentuzumab (Anti-Human IGF1 and IGF2 Recombinant Antibody; BI836845) is a recombinant a human monoclonal antibody that targets IGF ligands IGF1 and IGF2. Xentuzumab inhibits both of IGF1 and IGF2 growth-promoting signalling and suppresses AKT activation .
    Xentuzumab
  • HY-101985
    BV02
    3 Publications Verification

    		 Bacterial PARP Caspase Apoptosis Autophagy Akt Infection Neurological Disease Inflammation/Immunology
    BV02 is a 14-3-3 inhibitor and an antibacterial agent. BV02 enhances the cleavage of PARP and caspase-3. BV02 induces Apoptosis, Autophagy, and enhances Akt activation. BV02 has anti-B. melitensis infection and epilepsy-promoting effects. BV02 can also be used in colitis research.
    BV02
  • HY-N2283
    Deltonin
    1 Publications Verification

    		 ERK Akt Endogenous Metabolite Cancer
    Deltonin, a steroidal saponin, isolated from Dioscorea zingiberensis, has antitumor activity; Deltonin inhibits ERK1/2 and AKT activation.
    Deltonin
  • HY-18676B
    ILK-IN-2

    OSU-T315 analog

    		 Integrin Autophagy Apoptosis Caspase PDHK Cancer
    ILK-IN-2 (OSU-T315 analog) is an oral PDK2 inhibitor and also an ILK inhibitor, with an IC50 of 0.6 μM. ILK-IN-2 induces cell autophagy and apoptosis, showing anti-tumor activity. ILK-IN-2 directly abolishes AKT activation by preventing AKT from translocating to lipid rafts, triggering Caspase-dependent apoptosis in chronic lymphocytic leukemia (CLL) and extending the lifespan in TCL1 mouse models .
    ILK-IN-2
  • HY-107586
    Demethylasterriquinone B1

    DAQ B1; L-783281; Dimethylasterriquinone

    		 Insulin Receptor Akt NO Synthase NADPH Oxidase JAK STAT FOXO DNA/RNA Synthesis ERK Flavivirus Cardiovascular Disease Infection Metabolic Disease Inflammation/Immunology
    Demethylasterriquinone B1 (DAQ B1; L-783281) is an orally active insulin receptor (insulin receptor) agonist and AKT activator. By activating AKT, Demethylasterriquinone B1 upregulates the expression and activity of eNOS to increase NO production, while downregulating the expression of the NADPH oxidase subunit p22phox to reduce oxidative stress and improve vascular endothelial dysfunction in hypertensive rats. Demethylasterriquinone B1 combind with an AKT inhibitor targets the insulin signaling pathway to activate two antiviral pathways, RNA interference and JAK/STAT, in mosquitoes, thereby reducing Zika virus infection .
    Demethylasterriquinone B1
  • HY-19820A
    NSC45586 sodium
    1 Publications Verification

    		 Akt Ser/Thr Protease Apoptosis MMP Cardiovascular Disease Neurological Disease Inflammation/Immunology
    NSC45586 sodium is an inhibitor of PHLPP. NSC45586 sodium targets the PP2C phosphatase domains of PHLPP1 and PHLPP2, blocks the phosphatase activity of PHLPP, increases the expression level of FOXO1 in the nucleus, and reduces the protein expression of PHLPP1. NSC45586 sodium activates the AKT survival signaling pathway, enhances IGF-1-induced AKT activation, and inhibits the phosphorylation of AKT/ERK under basal conditions. NSC45586 sodium reduces staurosporine-induced neuronal death, preserves notochord cell morphology and KRT19 expression, inhibits cell apoptosis (apoptosis), improves the viability and proliferation of nucleus pulposus cells, upregulates the expression of ACAN/SOX9, and downregulates the expression of MMP13. NSC45586 sodium binds tightly to bovine serum albumin (bovine serum albumin), and exerts a more significant effect on nucleus pulposus in male individuals. NSC45586 sodium can be used in studies related to global cerebral ischemia and intervertebral disc degeneration .
    NSC45586 sodium
  • HY-N0430
    Coptisine

    Coptisin

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine
  • HY-N0430A
    Coptisine Sulfate
    5 Publications Verification

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine Sulfate
  • HY-177760
    PrCP-7414

    		Carboxypeptidase Apoptosis Akt Cancer
    PrCP-7414 is a prolyl carboxypeptidase (PRCP) inhibitor. PrCP-7414 blocks PRCP-mediated activation of the IGF1R/HER3 signaling pathway and subsequent AKT activation. PrCP-7414 exhibits pro-apoptotic, anti-tumor and synergistic cytotoxic activities, and inhibits the proliferation and survival of triple-negative breast cancer cells. PrCP-7414 can be used for the research of breast cancer .
    PrCP-7414
  • HY-U00458
    K-80003
    1 Publications Verification

    TX-803

    		 Akt Cancer
    K-80003 is a potent inhibitor of tRXRα-dependent Akt activation and cancer cell growth.
    K-80003
  • HY-P990805
    Anti-Human/Mouse GRP78 Antibody (C38)

    		HSP Metabolic Disease Cancer
    Anti-Human/Mouse GRP78 Antibody (C38) is a kind of mouse IgG2b antibody inhibitor, targeting to GRP78. Anti-Human/Mouse GRP78 Antibody (C38) inhibits RhoA, ROCK and AKT activation. Anti-Human/Mouse GRP78 Antibody (C38) can be used for the researches of cancer and metabolic disease, such as melanoma and diabetes .
    Anti-Human/Mouse GRP78 Antibody (C38)
  • HY-16469
    SR 13668

    		Akt Cancer
    SR13668 is a potent indole analog derived from indole-3-carbinol (I3C), known for its natural anticancer properties but limited by poor metabolic characteristics. Developed to enhance I3C's anticancer efficacy, SR13668 effectively inhibits growth factor-stimulated Akt activation. It demonstrates strong oral anticancer activity across different cancer types in preclinical studies, showing promise in clinical development due to its favorable safety profile and potent therapeutic effects .
    SR 13668
  • HY-101985R
    BV02 (Standard)

    		Reference Standards Bacterial PARP Caspase Apoptosis Autophagy Akt Infection Neurological Disease Inflammation/Immunology
    BV02 (Standard) is the analytical standard of BV02 (HY-101985). This product is intended for research and analytical applications. BV02 is a 14-3-3 inhibitor and an antibacterial agent. BV02 enhances the cleavage of PARP and caspase-3. BV02 induces Apoptosis, Autophagy, and enhances Akt activation. BV02 has anti-B. melitensis infection and epilepsy-promoting effects. BV02 can also be used in colitis research.
    BV02 (Standard)

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