AMPK Activator

Mogroside I E1 is a triterpenoid glycoside and a nonsugar sweetener. Mogrosides are sweeter than sucrose. Mogrosides exhibit antioxidant, antidiabetic and anticancer activities.

Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide. Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.

Ginkgolide C (Standard) is the analytical standard of Ginkgolide C. This product is intended for research and analytical applications. Ginkgolide C is a flavone isolated from Ginkgo biloba leaves, possessing multiple biological functions, such as decreasing platelet aggregation and ameliorating Alzheimer disease.

Procyanidin C2 (Procyanidine C2) is a lipid metabolism regulator and antioxidant with free radical scavenging activity. Procyanidin C2 down-regulates ACC, SREBP-1c, FAS, SCD-1 and PPARγ. Procyanidin C2 increases the level of phosphorylated AMPKα and inhibits the level of phosphorylated mTOR. Procyanidin C2 reduces lipid accumulation, alleviates oxidative stress, enhances fatty acid oxidation and improves mitochondrial function. Procyanidin C2 can be used in the research of non-alcoholic fatty liver disease.

AICAR (phosphate) (Standard) is the analytical standard of AICAR (phosphate). This product is intended for research and analytical applications. AICAR phosphate (Acadesine phosphate) is an adenosine analog and a AMPK activator. AICAR phosphate regulates the glucose and lipid metabolism, and inhibits proinflammatory cytokines and iNOS production. AICAR phosphate is also an autophagy, YAP and mitophagy inhibitor.

(+)-Magnoflorine (α-Magnoflorine) is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine also has significant antifungal activity.

IQZ23 inhibits adipocyte differentiation via AMPK pathway activation. IQZ23 exerts a high efficacy in decreasing the triglyceride level (EC₅₀=0.033 μM) in 3T3-L1 adipocytes. IQZ23 could be used for the research of obesity and related metabolic disorders.

Buformin (1-Butylbiguanide), a potent AMPK activator, acts as an orally active biguanide antidiabetic agent. Buformin decreases hepatic gluconeogenesis and lowers blood glucose production in vivo. Buformin also has anti-cancer activities and is applied in cancer study (such as, cervical cancer and breast cancer, et al).

PDIC-DPC is a HMGA1 inhibitor and lung-targeting agent. PDIC-DPC upregulates STING expression and enhances STING-mediated immune signaling. PDIC-DPC inhibits the TGFβ-Smad pathway and activates AMPK. PDIC-DPC forms nanocomplexes with fibrinogen β chain and vitronectin, and achieves lung-specific accumulation by binding to pulmonary endothelial receptors. PDIC-DPC reverses established pulmonary fibrosis, reduces collagen deposition, restores alveolar structure, improves pulmonary function, and inhibits in situ ESCC growth. PDIC-DPC can be used for the research of esophageal squamous cell carcinoma and idiopathic pulmonary fibrosis.

Mito-Esculetin (Mito-Esc) is an orally active mitochondria-targeted derivative of Esculetin (HY-N0284). Mito-Esculetin inhibits LPS-induced phosphorylation of STAT3 Tyr-705, partially reverses LPS-mediated depletion of SIRT3, and enhances the AMPK-SIRT1 signaling axis. Mito-Esculetin inhibits PAI-1 activity, regulates miRNA, and induces phosphorylation of IRS and AKT. Mito-Esculetin suppresses oxidant-induced endothelial dysfunction, Ang-II (HY-13948)- and high glucose-induced atherosclerotic plaque formation, Palmitate (HY-N0830)-induced insulin resistance, as well as high glucose-mediated endothelial cell senescence and inflammatory responses. Mito-Esculetin reduces body weight and non-esterified fatty acid (NEFA) levels. Mito-Esculetin can be used in research related to acute coronary syndrome, type 2 diabetes, and hyperglycemia-induced atherosclerosis.

Buformin-d₉ (hydrochloride) is the deuterium labeled Buformin. Buformin (1-Butylbiguanide), a potent AMPK activator, acts as an orally active biguanide antidiabetic agent. Buformin decreases hepatic gluconeogenesis and lowers blood glucose production in vivo. Buformin also has anti-cancer activities and is applied in cancer study (such as, cervical cancer and breast cancer, et al).

AMPK/mTOR modulator-1, Ginsenoside derivative, is an orally active mTOR inhibitor and AMPK activator. AMPK/mTOR modulator-1 activates AMPK signaling with a K_d of 4.759 μM. AMPK/mTOR modulator-1 promotes M1-like tumor-associated macrophage polarization while suppressing M2-like polarization. AMPK/mTOR modulator-1 can enhance glycolysis. AMPK/mTOR modulator-1 significantly inhibits tumor progression and shows anti-inflammation activity. AMPK/mTOR modulator-1 can be used for the research of colorectal cancer.

OSU-53 is an orally active AMPK activator and mTOR inhibitor, with an IC₅₀ of 0.3 μM for AMPK, an EC₅₀ of 2-5 μM for AMPK, and an IC₅₀ of 8.23 μM for mTOR. OSU-53 inhibits the Akt signaling pathway, directly activates AMPK by binding to its autoinhibitory domain, reduces IKKβ-mediated phosphorylation of Foxo3a, blocks Akt-mediated phosphorylation of MDM2, and promotes the nuclear localization and stabilization of Foxo3a, while directly inhibiting mTOR. OSU-53 inhibits epithelial-mesenchymal transition (EMT), induces epithelial phenotype, suppresses invasion and metastasis, induces autophagy, inhibits the activation of ERK and Akt, reduces the secretion of nitric oxide and proinflammatory cytokines, and inhibits the migration of MDSC; at high doses, it induces MDSC apoptosis, attenuates the immunosuppressive effect of MDSC, reduces MDSC levels, and blocks incision-induced mechanical hyperalgesia. OSU-53 can be used in studies related to breast cancer, prostate cancer, thyroid cancer, melanoma and postoperative pain.

AMPK activator 10 is an orally active, potent AMPK activator with EC₁₅₀ of 44.3 nM by cell-ELISA. AMPK activator 10 increases the phosphorylation levels of ACC. AMPK activator 10 exhibits a glucose lowering effect.

AMPK activator 2 (compound 7a), a fluorine-containing proguanil derivative, up-regulates AMPK signal pathway and downregulates mTOR/4EBP1/p70S6K. AMPK activator 2 inhibits proliferation and migration of human cancer cell lines (UMUC3, T24, A549).

(2R)-Kazinol B is a prenylated flavane enantiomer found in the stem and root barks of Daphne giraldii, and it is also an isomer of Kazinol B (HY-N3426). (2R)-Kazinol B exerts selective cytotoxicity against liver cancer cells, induces apoptosis via both intrinsic and extrinsic pathways, and triggers protective autophagy through AMPK activation. (2R)-Kazinol B can be used in the research of liver cancer.

Dimethoxycurcumin-d₆ (DiMC-d₆; CHC 004-d₆; Di-O-methylcurcumin-d₆) is the deuterated-labeled Dimethoxycurcumin (HY-100977). Dimethoxycurcumin (DiMC) is a curcuminoid compound found in Curcuma longa. Dimethoxycurcumin is also an orally active thioredoxin reductase inhibitor (IC₅₀ = 5.4 μM) and androgen receptor antagonist. Dimethoxycurcumin inhibits thioredoxin reductase, leading to oxidized thioredoxin accumulation, ROS production, DNA damage, glutathione depletion, mitochondrial membrane potential decrease, ATP depletion, S phase arrest, and apoptosis. Dimethoxycurcumin inhibits NF-κB, NADPH oxidase subunits, ATP synthase subunits, CDK4, cyclin-D1, FASN, ACC, and the IRS2-PI3K-Akt pathway, while activating AMPK, ERK, and JNK. Dimethoxycurcumin can be used for research on cancer, arsenic-induced hepatotoxicity, and tuberculosis.

NFAT-133 is an aromatic polyketide with immunosuppressive and antidiabetic activity. NFAT-133 activates the AMPK pathway, promoting glucose uptake in L6 muscle fibers, thereby resisting diabetes. NFAT-133 inhibits the transcriptional activity of activated T-cell nuclear factor (NFAT), thereby suppressing the expression of IL-2 and the proliferation of T cells, demonstrating an immunosuppressive effect. NFAT-133 does not exhibit antibacterial activity or cytotoxicity, but it can weaken the production of NO in RAW264.7 cells induced by Lipopolysaccharide (LPS) (HY-D1056).

FuBIG is an iminoguanidine derivative with neuroprotective effects. FuBIGL inhibits L-LDH activation and reduces lactate production. FuBIGL exerts protective effects on inflammatory nerve cells, upregulates the expressions of AMPK, pAMPK and FOXO3, and activates the AMPK pathway in cells. FuBIG exerts anti-inflammatory effects by reducing pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) and increasing the anti-inflammatory cytokine IL-10. FuBIG maintains mitochondrial membrane potential, alleviates mitochondrial dysfunction, reduces ROS production, and relieves oxidative stress. FuBIG upregulates Bcl-2, downregulates Bax and Caspase-3, and inhibits cell apoptosis (apoptosis). FuBIG improves metabolic disorders in diabetic mice, decreases the levels of LDL-C, ALT and AST, and increases HDL-C level simultaneously. FuBIG can be used in the research of diabetic neuroinflammation.

Phenformin-d₅ (Phenethylbiguanide-d₅) hydrochloride is the deuterium labeled Phenformin hydrochloride. Phenformin hydrochloride is an orally active biguanide hypoglycemic agent. Phenformin hydrochloride inhibits mitochondrial respiratory chain complex I, leading to an increased AMP/ATP ratio, activation of AMPK, and subsequent inhibition of the mTOR pathway, thereby suppressing cell proliferation, inducing apoptosis and autophagy. Phenformin hydrochloride inhibits cancer stem cells (CSCs) and possesses potent antitumor potential.