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Results for "

phosphorylation metabolism

" in MedChemExpress (MCE) Product Catalog:

59

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1

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7

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1

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3

Isotope-Labeled Compounds

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-Y0445A
    Sodium dichloroacetate
    Maximum Cited Publications
    26 Publications Verification

    		 PDK-1 NKCC PDHK Reactive Oxygen Species (ROS) Apoptosis Cancer
    Sodium dichloroacetate is an orally active pyruvate dehydrogenase kinase (PDK) inhibitor. Sodium dichloroacetate also stimulates pyruvate dehydrogenase (PDH) activity and works as a Na +-K +-2Cl − cotransporter (NKCC) inhibitor. Sodium dichloroacetate prevents the phosphorylation of the E1α subunit of PDC, promoting the entry of pyruvate into the mitochondria for oxidative metabolism, reducing lactate production, and simultaneously increasing the production of reactive oxygen species (ROS). Sodium dichloroacetate inhibits tumor cell proliferation and induces apoptosis. Sodium dichloroacetate is promising for research of cancers .
    Sodium dichloroacetate
  • HY-113596
    Acetyl Coenzyme A trisodium
    4 Publications Verification

    Acetyl-CoA trisodium

    		 Oxidative Phosphorylation Endogenous Metabolite Autophagy Metabolic Disease
    Acetyl-coenzyme A (Acetyl-CoA) trisodium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A trisodium, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A trisodium is also a key precursor of lipid synthesis .
    Acetyl Coenzyme A trisodium
  • HY-N10574
    Queuine
    1 Publications Verification

    		 Bacterial Metabolic Disease Cancer
    Queuine is a selective substrate for tRNA guanine transglycosylase (TGT) and can be incorporated into eukaryotic tRNA. Queuine promotes tRNA modification, affecting mitochondrial function and Warburg metabolic phenotype. If Queuine is deficient, aerobic glycolysis can be enhanced, oxidative phosphorylation can be inhibited, and Warburg metabolism can be promoted, accompanied by increased ammonia and lactate production and increased lactate dehydrogenase activity. Queuine can be used for autoimmune diseases (such as experimental models of multiple sclerosis) and cancer metabolic regulation, and its deficiency is associated with low tRNA modification in tumor cells .
    Queuine
  • HY-W040127
    Peonidin 3-O-glucoside chloride
    1 Publications Verification

    		 Insulin Receptor Metabolic Disease
    Peonidin 3-O-glucoside chloride is an agonist of the free fatty acid receptor FFAR1 and Glucokinase. Peonidin 3-O-glucoside chloride enhances insulin secretion of pancreatic beta cells and increases glucose uptake by liver cells. Peonidin 3-O-glucoside chloride activates FFAR1, promotes the phosphorylation of related proteins in the insulin secretion pathway, and increases the expression of FFAR1. In liver cells, Peonidin 3-O-glucoside chloride activates GK and regulates proteins associated with carbohydrate metabolism. Peonidin 3-O-glucoside chloride can be used in diabetes research .
    Peonidin 3-O-glucoside chloride
  • HY-W012722
    4-Methyl-2-oxopentanoic acid
    1 Publications Verification

    α-Ketoisocaproic acid

    		 Endogenous Metabolite Autophagy mTOR SOD Neurological Disease Metabolic Disease
    4-Methyl-2-oxopentanoic acid (α-Ketoisocaproic acid) is a metabolite of L-leucine and is involved in energy metabolism. 4-Methyl-2-oxopentanoic acid increases endoplasmic reticulum stress, promotes lipid accumulation in preadipocytes and insulin resistance by impairing mTOR and autophagy signaling pathways. 4-Methyl-2-oxopentanoic acid also causes oxidative damage, leading to cognitive deficits, inhibits α-ketoglutarate dehydrogenase activity, acts as an oxidative phosphorylation uncoupler and metabolic inhibitor. 4-Methyl-2-oxopentanoic acid acts as a nutrient signal and stimulates skeletal muscle protein synthesis. 4-Methyl-2-oxopentanoic acid can be used in the study of maple syrup urine disease .
    4-Methyl-2-oxopentanoic acid
  • HY-125848
    Ginsenoside F2

    		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 .
    Ginsenoside F2
  • HY-114293A
    Acetyl coenzyme A trilithium

    Acetyl-CoA trilithium

    		 Oxidative Phosphorylation Endogenous Metabolite Autophagy Cardiovascular Disease Metabolic Disease
    Acetyl-coenzyme A (Acetyl-CoA) trilithium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A trilithium regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A trilithium is also a key precursor of lipid synthesis .
    Acetyl coenzyme A trilithium
  • HY-30216A
    Leucic acid

    α-Hydroxyisocaproic acid

    		 Drug Metabolite Hydroxycarboxylic Acid Receptor (HCAR) AMPK ERK Metabolic Disease Inflammation/Immunology
    Leucic acid (α-Hydroxyisocaproic acid) is an orally active end-product of the microbial metabolism of leucine. Leucic acid can bind to HCAR2, alters AMPK and ERK1/2 phosphorylation status, suppresses lipid synthesis, promotes catabolism, reduces adiposity, enhances lean mass and exercise capacity. Leucic acid suppresses pro-inflammatory cytokine secretion, inflammation-related gene mRNA expression. Leucic acid decreases basal protein synthesis, attenuates myotube atrophy. Leucic acid can be used for the research of obesity .
    Leucic acid
  • HY-107582
    JW480

    		Ser/Thr Protease Calcium Channel PKC Cancer
    JW480 is a selective KIAA1363/AADACL1 inhibitor with oral activity, featuring IC50 values of 12 nM against human KIAA1363, 20 nM against mouse KIAA1363. JW480 blocks lipid deacetylase activity to restrain HAG metabolism and lowers retinyl ester hydrolase function in hepatic stellate cells. JW480 reduces MAGE lipid levels and inhibits migration, invasion, survival and tumor growth of prostate cancer cells. JW480 lowers PKCδ phosphorylation, facilitates HAGP accumulation, diminishes platelet aggregation, dense granule secretion and Ca 2+ flux, delays arterial thrombosis and prolongs tail bleeding time in rats. JW480 can be used for the study of prostate cancer and thrombosis .
    JW480
  • HY-114293
    Acetyl coenzyme A

    Acetyl-CoA

    		 Oxidative Phosphorylation Endogenous Metabolite Autophagy Cardiovascular Disease Metabolic Disease
    Acetyl-coenzyme A (Acetyl-CoA) is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A is also a key precursor of lipid synthesis .
    Acetyl coenzyme A
  • HY-17598
    Rafoxanide
    5+ Cited Publications

    		 Oxidative Phosphorylation Parasite p38 MAPK Raf Apoptosis Infection Cancer
    Rafoxanide is a poent, orally active halogenated salicylaniline agent with antiparasitic activity. Rafoxanide interferes with energy metabolism in trematodes by uncoupling oxidative phosphorylation. Rafoxanide is also found to be a potent inhibitor of the BRAF V600E mutant protein, which is important in colorectal cancer. Rafoxanide can be used for the control of infestation with Hemonchus species or Fasciola species in sheep and cattle as well as Oestrus ovis in sheep. Rafoxanide can also be used for cancer research .
    Rafoxanide
  • HY-N7176
    Kaempferol 3-O-β-D-glucuronide
    4 Publications Verification

    Kaempferol-3-glucuronide; Kaempferol-3-O-glucuronide

    		 Interleukin Related Metabolic Disease Inflammation/Immunology Cancer
    Kaempferol 3-O-β-D-glucuronide (Kaempferol-3-glucuronide) is a metabolite of kaempferol that can be taken orally and has anti-inflammatory properties. Kaempferol 3-O-β-D-glucuronide can activate AKT/GSK3β phosphorylation and improve glucose metabolism .
    Kaempferol 3-O-β-D-glucuronide
  • HY-113596A
    Acetyl coenzyme A lithium
    4 Publications Verification

    Acetyl-CoA lithium

    		 Oxidative Phosphorylation Endogenous Metabolite Autophagy Cardiovascular Disease Metabolic Disease
    Acetyl-coenzyme A (Acetyl-CoA) lithium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A lithium, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A lithium is also a key precursor of lipid synthesis .
    Acetyl coenzyme A lithium
  • HY-153392
    TYA-018

    		Oxidative Phosphorylation HDAC Cardiovascular Disease
    TYA-018 is an orally active, potent and highly selective HDAC6 inhibitor. TYA-018 can protect heart function in mice. TYA-018 also enhances energetics in mice by increasing expression of targets associated with fatty acid metabolism, protein metabolism, and oxidative phosphorylation .
    TYA-018
  • HY-B0831
    Buprofezin
    2 Publications Verification

    		 Environmental Pollutants Reactive Oxygen Species (ROS) Oxidative Phosphorylation Others
    Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .
    Buprofezin
  • HY-137899
    Dephospho-CoA
    1 Publications Verification

    		 Endogenous Metabolite Metabolic Disease Cancer
    Dephospho-CoA is a key intermediate in the biosynthesis of coenzyme A (CoA), which is catalyzed to form CoA by GTP-dependent Dephospho-CoA kinase (DPCK). Dephospho-CoA completes the final synthetic step of CoA via phosphorylation and participates in energy metabolism and cellular signal transduction. Dephospho-CoA can be used in studies involving cancer (e.g., regulation of cell proliferation) and metabolic diseases (e.g., mitochondrial dysfunction) .
    Dephospho-CoA
  • HY-114293S
    Acetyl coenzyme A-13C2 lithium

    Acetyl-CoA-13C2 lithium

    		 Isotope-Labeled Compounds Endogenous Metabolite Autophagy Oxidative Phosphorylation Metabolic Disease
    Acetyl coenzyme A- 13C2 lithium is the 13C-labeled Acetyl coenzyme A (HY-114293). Acetyl-coenzyme A (Acetyl-CoA) is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A is also a key precursor of lipid synthesis .
    Acetyl coenzyme A-13C2 lithium
  • HY-119725
    Tetradifon

    		Environmental Pollutants Insecticide Infection
    Tetradifon is a broad-spectrum organochlorine insecticide and an inhibitor of the mitochondrial oligomycin sensitivity conferring protein (OSCP), which can be used to control a variety of mites. Tetradifon inhibits energy-related activities such as ADP-stimulated respiration, DNP and Mg 2+-stimulated ATPase, with an IC50 of 4.5-27 nmoL/mg mitochondrial protein. Tetradifon exerts oligomycin-like activity by inhibiting the oxidative phosphorylation process, inducing oxidative stress and interfering with bone metabolism. Tetradifon is currently mainly used in the research of mitochondrial function regulation, bone remodeling mechanism and nephrotoxicity of environmental pollutants .
    Tetradifon
  • HY-N0412
    Sesamoside

    		PERK JNK TNF Receptor Interleukin Related Neurological Disease Inflammation/Immunology
    Sesamoside is an orally active anti-inflammatory, anti-hypoxic and analgesic agent. Sesamoside inhibits the phosphorylation of ERK and JNK, downregulates NLRP3 expression, restricts the nuclear localization of P65, regulates AKR1B1 expression, and reduces the expression of TRPV1 gene in the spinal cord. Sesamoside reduces the production of TNF-α, IL-6, IL-1β, iNOS and NO, restores cellular metabolism and organ function, and alleviates cold and mechanical hyperalgesia. Sesamoside can be used in research related to septic shock, high-altitude pulmonary edema and neuropathic pain .
    Sesamoside
  • HY-114557
    NSC 90469

    3,5-Diiodo-L-thyronine

    		 JNK NF-κB Sirtuin PGC-1α COX TGF-β Receptor Collagen Metabolic Disease Inflammation/Immunology Endocrinology
    NSC 90469 (3,5-Diiodo-L-thyronine) is an orally active thyroid hormone derivative. NSC 90469 inhibits JNK phosphorylation and NF-κB acetylation, blocks SIRT1 protein expression, induces elevated PGC-1α levels, and stimulates COX activity. NSC 90469 enhances UCP1-mediated thermogenesis, increases hepatic Dio1 activity, inhibits TSH levels and hypothalamic-pituitary-thyroid axis function, enhances lipid metabolism, and regulates energy metabolism via the mitochondrial pathway. NSC 90469 prevents blood glucose reduction, reduces urinary albumin excretion, inhibits renal matrix expansion, decreases TGF-β1 expression, and reduces renal fibronectin and type Ⅳ collagen deposition. NSC 90469 also increases energy expenditure and prevents diet-induced overweight. NSC 90469 can be used in studies related to diabetic nephropathy, hypothyroidism, non-alcoholic fatty liver disease, and diet-induced obesity .
    NSC 90469
  • HY-129099A
    N-Desmethyltamoxifen hydrochloride

    		PKC Estrogen Receptor/ERR Drug Metabolite Endogenous Metabolite Cancer
    N-Desmethyltamoxifen hydrochloride is the major metabolite of tamoxifen in humans. N-Desmethyltamoxifen, a poor antiestrogen, is a ten-fold more potent protein kinase C (PKC) inhibitor than Tamoxifen. N-Desmethyltamoxifen hydrochloride is also a potent regulator of ceramide metabolism in human AML cells, limiting ceramide glycosylation, hydrolysis, and sphingosine phosphorylation .
    N-Desmethyltamoxifen hydrochloride
  • HY-156193
    PF-07208254

    		PDHK Cardiovascular Disease Metabolic Disease
    PF-07208254 is a selective, orally active allosteric inhibitor of branched-chain ketoacid dehydrogenase kinase (BDK) (IC50=110 nM, Ki=54 nM, KD=84 nM). PF-07208254 inhibits BDK-mediated BCKDH phosphorylation and enhances the catabolism of branched-chain amino acids (BCAAs) and branched-chain keto acids (BCKAs) by binding to the allosteric pocket of BDK, reducing BDK binding to BCKDH-E2 and promoting BDK degradation. PF-07208254 inhibits BDK activity in human skeletal muscle cells (IC50=540 nM) and has activity to improve cardiac function and metabolism. PF-07208254 can be used in the study of cardiometabolic diseases (e.g., heart failure, type 2 diabetes) .
    PF-07208254
  • HY-149987
    LY3522348

    KHK-IN-3

    		 Ketohexokinase Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    KHK-IN-3 (Example 1) is a ketohexokinase (KHK) inhibitor. KHK-IN-3 can be used in the study of kidney disease, nonalcoholic steatohepatitis (NASH), diabetes and heart failure. KHK is a rate-limiting enzyme and fructokinase involved in fructose metabolism. KHK catalyzes the phosphorylation of fructose to fructose-1-phosphate (FIP) at the expense of ATP. The lack of feedback inhibition of fructose metabolism triggers the accumulation of downstream intermediates such as lipogenesis, gluconeogenesis, and oxidative phosphorylation .
    LY3522348
  • HY-114293S5
    Acetyl coenzyme A-d3

    Acetyl-CoA-d3

    		 Isotope-Labeled Compounds Oxidative Phosphorylation Endogenous Metabolite Autophagy Cardiovascular Disease Metabolic Disease
    Acetyl coenzyme A-d3 (Acetyl-CoA-d3) is the deuterium labeled Acetyl coenzyme A (HY-114293). Acetyl-coenzyme A (Acetyl-CoA) is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A is also a key precursor of lipid synthesis .
    Acetyl coenzyme A-d3
  • HY-N10574A
    Queuine dihydrochloride
    1 Publications Verification

    		 Others Metabolic Disease Cancer
    Queuine dihydrochloride is a selective substrate for tRNA guanine transglycosylase (TGT) and can be incorporated into eukaryotic tRNA. Queuine dihydrochloride promotes tRNA modification, affecting mitochondrial function and Warburg metabolic phenotype. If Queuine dihydrochloride is deficient, aerobic glycolysis can be enhanced, oxidative phosphorylation can be inhibited, and Warburg metabolism can be promoted, accompanied by increased ammonia and lactate production and increased lactate dehydrogenase activity. Queuine dihydrochloride can be used for autoimmune diseases (such as experimental models of multiple sclerosis) and cancer metabolic regulation, and its deficiency is associated with low tRNA modification in tumor cells .
    Queuine dihydrochloride
  • HY-155063
    TRAP1-IN-1

    		HSP Mitochondrial Metabolism Cancer
    TRAP1-IN-1 (compound 35) is a potent and selective inhibitor of TRAP1，a mitochondrial isoform of Hsp90. TRAP1-IN-1 has >250-fold TRAP1 selectivity over Grp94，and disrupts TRAP1 tetramer stability，induces TRAP1 client protein degradation. TRAP1-IN-1 also inhibits mitochondrial complex I of oxidative phosphorylation OXPHOS，disrupts the mitochondrial membrane potential，and enhances glycolysis metabolism .
    TRAP1-IN-1
  • HY-P1844A
    Chemerin-9 (149-157) TFA
    4 Publications Verification

    		 Chemerin Receptor Akt ERK Reactive Oxygen Species (ROS) Amyloid-β Inflammation/Immunology
    Chemerin-9 (149-157) TFA is a potent agonist of chemokine-like receptor 1 (CMKLR1) . Chemerin-9 (149-157) TFA has anti-inflammatory activity. Chemerin-9 (149-157) TFA stimulates phosphorylation of Akt and ERK as well as ROS production. Chemerin-9 (149-157) TFA ameliorates Aβ1-42-induced memory impairmen. Chemerin-9 (149-157) TFA regulates immune responses, adipocyte differentiation, and glucose metabolism .
    Chemerin-9 (149-157) TFA
  • HY-N10423
    Cubebin

    (-)-Cubebin

    		 Cholinesterase (ChE) Bacterial Fungal Parasite p38 MAPK Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Cubebin ((-)-Cubebin), a dibenzyl butyrolactone lignan, is an orally active AChE inhibitor. Cubebin binds to active sites of NF-κB, TNF-α, and TGF-β1 via hydrogen and hydrophobic interactions, obstructing critical residues to inhibit pro-inflammatory or renal fibrosis-related activity. Cubebin enhances p38 MAPK phosphorylation to increase tyrosinase gene expression, stimulating melanogenesis via elevated tyrosinase activity, expression, and mRNA levels. Cubebin reduces oxidative stress via enhanced endogenous antioxidant enzyme activity and inhibited lipid peroxidation, regulates lipid metabolism, improves glycemic control, and exerts renoprotective effects via reduced renal dysfunction markers and improved renal architecture. Cubebin shows antimicrobial activity. Cubebin exerts larvicidal activity against Angiostrongylus cantonensis larvae, with no cytotoxicity toward monkey or human cell lines or Caenorhabditis elegans. Cubebin can be used for the research of diabetic nephropathy, melanoma, colon adenocarcinoma, neuroangiostrongyliasis, Alzheimer’s disease (AD) and depression .
    Cubebin
  • HY-168049
    ZLY06

    		PPAR Akt Metabolic Disease
    ZLY06 is an orally active dual agonist of peroxisome proliferator-activated receptor (PPAR) δ and γ (PPAR δ: EC50=341 nM; PPAR γ: EC50=237 nM). ZLY06 induces hepatic lipid accumulation by inhibiting the phosphorylation of AKT1, mediating the upregulation of CD36. In addition, ZLY06 significantly improves glucose and lipid metabolism without increasing body weight, and alleviates fatty liver by promoting β-oxidation of fatty acids and inhibiting hepatic lipogenesis .
    ZLY06
  • HY-E70121
    Succinyl-CoA synthetase

    		Endogenous Metabolite Mitochondrial Metabolism Neurological Disease Metabolic Disease Inflammation/Immunology
    Succinyl-CoA synthetase is a mitochondrial matrix enzyme and catalyst. Succinyl-CoA synthetase supports TCA, ketone and heme metabolism and is activated by mitochondrial phosphate. Succinyl-CoA synthetase distributes broadly across mammalian tissues with distinct substrate-related biochemical features. Succinyl-CoA synthetase gains structural stability after phosphorylation and relies on SUCLG1-encoded subunit for activity. Succinyl-CoA synthetase malfunction links to metabolic and neurological disorders. Succinyl-CoA synthetase serves as a research tool for mitochondrial hepatoencephalomyopathy .
    Succinyl-CoA synthetase
  • HY-161767
    JWJ-01-306

    		Molecular Glues Oxidative Phosphorylation Ras Cancer
    JWJ-01-306 is a CRBN-recruiting ZBTB11 Molecular Glues degrader. JWJ-01-306 degrades ZBTB11 and reprograms cellular metabolism, thereby reducing the level of Oxidative Phosphorylation and the activity of the tricarboxylic acid cycle. JWJ-01-306 enhances the response of organoids to K-Ras inhibition. JWJ-01-306 inhibits the proliferation of pancreatic ductal adenocarcinoma cells and melanoma cells. JWJ-01-306 can be used in studies related to pancreatic ductal adenocarcinoma and melanoma .
    JWJ-01-306
  • HY-N11709
    Theasaponin E1

    		Apoptosis VEGFR ATM/ATR PTEN Akt mTOR HIF/HIF Prolyl-Hydroxylase NF-κB Notch Cholinesterase (ChE) Amyloid-β γ-secretase Ferroptosis Fungal Infection Neurological Disease Metabolic Disease Cancer
    Theasaponin E1 is an orally effective tea saponin. Theasaponin E1 inhibits the proliferation of cancer cells by activating apoptosis. Theasaponin E1 inhibits angiogenesis in ovarian cancer cells and HUVECs by reducing the expression of VEGF. Theasaponin E1 upregulates the phosphorylation level of ATM protein and the expression level of PTEN protein in cancer cells, decreases the phosphorylation levels of Akt, mTOR, p70S6K and 4E-BP1 proteins, downregulates the expression of HIF-1α and NF-κB, and reduces the protein expression of Notch ligands Dll4 and Jagged1. Theasaponin E1 exerts neuroprotective effects by inhibiting the activity of acetylcholinesterase, activating α-secretase and neprilysin, reducing the concentration of Aβ, and inhibiting the activities of β-secretase and γ-secretase. Theasaponin E1 exhibits toxic effects on cancer cells and quinone reductase-inducing activity, and inhibits tumor growth in vivo. Theasaponin E1 induces ferroptosis in Pomacea canaliculata by synergistically disrupting cholesterol homeostasis and sphingolipid metabolism. Theasaponin E1 possesses anti-biofilm activity against Candida albicans. Theasaponin E1 can be used in the research of ovarian cancer, obesity, Alzheimer's disease and fungal infections .
    Theasaponin E1
  • HY-129099
    N-Desmethyltamoxifen

    		PKC Estrogen Receptor/ERR Drug Metabolite Endogenous Metabolite Cancer
    N-Desmethyltamoxifen is the major metabolite of tamoxifen in humans. N-Desmethyltamoxifen, a poor antiestrogen, is a ten-fold more potent protein kinase C (PKC) inhibitor than Tamoxifen. N-Desmethyltamoxifen is also a potent regulator of ceramide metabolism in human AML cells, limiting ceramide glycosylation, hydrolysis, and sphingosine phosphorylation .
    N-Desmethyltamoxifen
  • HY-N11262
    Sudachitin

    		Phosphodiesterase (PDE) Sirtuin PGC-1α p38 MAPK HSP TNF Receptor NO Synthase Apoptosis Metabolic Disease Inflammation/Immunology
    Sudachitin is an orally active compound that potently inhibits mouse PDE1C and human PDE4B, with IC50 values of 5.0 μM and 15.0 μM, respectively. Sudachitin upregulates Sirt1 and PGC‑1α expression in skeletal muscle to regulate energy metabolism and promote mitochondrial biogenesis. Sudachitin improves lipid metabolism, glucose tolerance, insulin sensitivity, energy expenditure, and fatty acid β‑oxidation. Sudachitin activates p38MAPK signaling, induces HSP27 phosphorylation and caspase‑dependent apoptosis, and blocks EGF‑driven keratinocyte migration and proliferation. Sudachitin suppresses LPS‑induced TNF‑α, NO, and iNOS expression in macrophages and shows potent anti‑inflammatory activity. Sudachitin can be used for the research of metabolic syndrome, type 2 diabetes, and psoriasis. .
    Sudachitin
  • HY-P1844
    Chemerin-9 (149-157)
    4 Publications Verification

    		 Chemerin Receptor Akt ERK Reactive Oxygen Species (ROS) Amyloid-β Inflammation/Immunology
    Chemerin-9 (149-157) is a potent agonist of chemokine-like receptor 1 (CMKLR1) . Chemerin-9 (149-157) has anti-inflammatory activity. Chemerin-9 (149-157) stimulates phosphorylation of Akt and ERK as well as ROS production. Chemerin-9 (149-157) ameliorates Aβ1-42-induced memory impairmen. Chemerin-9 (149-157) regulates immune responses, adipocyte differentiation, and glucose metabolism .
    Chemerin-9 (149-157)
  • HY-P11358
    IRW

    		Angiotensin-converting Enzyme (ACE) Acetyl-CoA Carboxylase Mitochondrial Metabolism Inflammation/Immunology
    IRW is an orally active tripeptide produced from egg white with angiotensin converting enzyme (ACE) inhibitory properties. IRW can prevent high-fat diet (HFD)-induced Non-alcoholic fatty liver disease (NAFLD) by modulating hepatic lipid metabolism and increasing mitochondrial content. IRW decreases hepatic triglyceride content and lipid droplet size. IRW increases the hepatic mitochondrial complexes and citrate synthase activity, phosphorylation of 5’-AMP-activated protein kinase and microsomal triglyceride transfer protein abundance. IRW increases phosphorylated acetyl CoA carboxylase and mitochondrial complexes, IRW can be used for the research of inflammation .
    IRW
  • HY-B0831S
    Buprofezin-d6

    		Oxidative Phosphorylation Reactive Oxygen Species (ROS) Metabolic Disease
    Buprofezin-d6 is the deuterium labeled Buprofezin. Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .
    Buprofezin-d6
  • HY-P3444
    CD31

    PECAM-1

    		 SHP2 Bacterial Metabolic Disease Inflammation/Immunology
    CD31 (PECAM-1) is platelet endothelial cell adhesion molecule-1, serves as the endothelial cell-specific receptor of clostridium perfringens b-Toxin (CPB). CD31 is also an ER-MP12 antigen, acts as a linker between mechanical stress, metabolism and inflammation. CD31 peptide is able to sustain phosphorylation of the CD31 ITIM686 and of SHP2 and to inhibit TCR-induced T-cell activation - .
    CD31
  • HY-179557
    iMQT_020

    		Glutathione Peroxidase Reactive Oxygen Species (ROS) Apoptosis Ferroptosis PD-1/PD-L1 Cancer
    iMQT_020 is a selective allosteric SLC1A5_var inhibitor. iMQT_020 disrupts the trimeric assembly of SLC1A5_var, causing metabolic crisis in cancer cells and selectively suppressing their growth. iMQT_020 reduces glutamine anaplerosis and oxidative phosphorylation, resulting in a broad disruption of cancer metabolism. iMQT_020 reduces GSH levels and increases cellular ROS and mitochondrial ROS. iMQT_020 induces apoptosis and ferroptosis. iMQT_020 can epigenetically upregulate PD-L1 expression. iMQT_020 can be used for the study of pancreatic cancer, lung cancer, and colon cancer .
    iMQT_020
  • HY-122949
    Momordicine I
    2 Publications Verification

    		 Apoptosis Autophagy DGK Mitochondrial Metabolism NO Synthase PI3K Akt Interleukin Related Src AMPK mTOR NF-κB c-Met/HGFR STAT Keap1-Nrf2 Reactive Oxygen Species (ROS) Oxidative Phosphorylation Endogenous Metabolite Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    Momordicine I is a cucurbitane-type triterpenoids. Momordicine I suppresses glioma growth by promoting apoptosis and impairing mitochondrial oxidative phosphorylation. Momordicine I inhibits glycolysis, lipid metabolism, induces autophagy in HNC cells to suppress head and neck cancer growth. Momordicine I alleviates isoproterenol-induced cardiomyocyte hypertrophy through suppression of PLA2G6 and DGK-ζ. Momordicine I exerts its cardiovascular benefits by upregulating nitric oxide, inhibiting the activity of angiotensin-converting enzyme (ACE), activating the PI3K/Akt pathway, reducing oxidative stress and inflammation. Momordicine I inhibits AKT1, IL-6, and SRC, suggesting its potential application in type 2 diabetes .
    Momordicine I
  • HY-18284
    AS1938909

    		Akt GLUT Phosphatase Others
    AS1938909 is a compound that inhibits SHIP2 activity. It can selectively inhibit SHIP2, increase Akt phosphorylation, and regulate glucose metabolism. Its effect is related to upregulating GLUT1 gene expression.
    AS1938909
  • HY-170838
    PDHK1-IN-1

    		PDHK Cancer
    PDHK1-IN-1 (compound 17) is a selective inhibitor of PDHK1 (IC50=1.5 μM) with anticancer activity. PDHK1 negatively regulates the pyruvate dehydrogenase complex (PDC), limiting the tricarboxylic acid (TCA) cycle and oxidative phosphorylation. Overexpression of PDHK1 can shift the metabolism towards an increased glycolysis dependence (Warburg effect). PDHK1-IN-1 can inhibit the phosphorylation of the PDC E1α Ser232 recognition site of PDHK1 and the phosphorylation of Ser293 .
    PDHK1-IN-1
  • HY-154973
    AMPK activator 11

    		Oxidative Phosphorylation Mitochondrial Metabolism AMPK Metabolic Disease Cancer
    AMPK activator 11 is an AMP-activated protein kinase (AMPK) activator with nanomolelevel antiproliferation activities against several CRCs. AMPK activator 11 selectively inhibits the RKO xenograft growth along by activating AMPK and upregulating oxidative phosphorylation (OXPHOS) ( mitochondrial metabolism ) and can be used for anti-tumor and metabolic disease research .
    AMPK activator 11
  • HY-178958
    PPAR agonist 7

    		PPAR Adenosine Receptor Fatty Acid Synthase (FASN) Endogenous Metabolite Metabolic Disease Inflammation/Immunology Endocrinology
    PPAR agonist 7 is an orally active pan-PPAR agonist, demonstrating potent activation of all three subtypes, PPARα (EC50 = 1.51 μM), PPARδ (EC50 = 1.11 μM), and PPARγ (EC50 = 3.14 μM). PPAR agonist 7 significantly enhances glucose uptake in adipocytes while exhibiting minimal adipogenic activity. PPAR agonist 7 can suppress PPARγ Ser273 phosphorylation in white adipose tissue and upregulate insulin-sensitizing genes. PPAR agonist 7 does not cause weight gain or fluid retention in high-fat diet (HFD)/ Streptozotocin (HY-13753) (STZ)-induced type 2 diabetes mellitus (T2DM) models. PPAR agonist 7 has selective modulation of PPAR signaling pathways without activation of adipogenic gene programs. PPAR agonist 7 can be used for the study of diabetes .
    PPAR agonist 7
  • HY-W037817
    Dimethyl L-glutamate

    Dimethyl glutamate

    		 Potassium Channel Bacterial Infection Metabolic Disease
    Dimethyl L-glutamate (Dimethyl glutamate), a membrane-permeable analog of Glutamate, can stimulate insulin release induced by Glucose. Dimethyl L-glutamate suppresses the KATP channel activities. Dimethyl L-glutamate inhibits E. gracilis growth and causes abnormal cell division. Dimethyl L-glutamate can be used in the research of diabetes, glucose transport, phosphorylation, and further metabolism .
    Dimethyl L-glutamate
  • HY-136855
    MitoPBN

    		Sirtuin AMPK PGC-1α Apoptosis Reactive Oxygen Species (ROS) Metabolic Disease
    MitoPBN is a AMPK/SIRT3/PGC-1α axis modulator, reactive oxygen species scavenger and mitochondrial function enhancer. MitoPBN increases the phosphorylation level of AMPK, restores SIRT3 expression and reverses the down-regulation of PGC-1α, thereby promoting mitochondrial biogenesis. MitoPBN regulates glucose metabolism, reduces blood glucose by inhibiting hepatic gluconeogenesis and increasing hepatic glucose uptake, while scavenging mitochondrial superoxide anion/hydrogen peroxide, maintaining membrane potential and increasing ATP production. MitoPBN also reduces cell apoptosis, improves sperm motility, survival rate and membrane integrity, but may induce reductive stress in cryopreserved sperm at high concentrations. MitoPBN is widely applicable to research related to diabetes and type 2 diabetes .
    MitoPBN
  • HY-129099AR
    N-Desmethyltamoxifen hydrochloride (Standard)

    		Reference Standards PKC Estrogen Receptor/ERR Drug Metabolite Endogenous Metabolite Cancer
    N-Desmethyltamoxifen (hydrochloride) (Standard) is the analytical standard of N-Desmethyltamoxifen (hydrochloride). This product is intended for research and analytical applications. N-Desmethyltamoxifen hydrochloride is the major metabolite of tamoxifen in humans. N-Desmethyltamoxifen, a poor antiestrogen, is a ten-fold more potent protein kinase C (PKC) inhibitor than Tamoxifen. N-Desmethyltamoxifen hydrochloride is also a potent regulator of ceramide metabolism in human AML cells, limiting ceramide glycosylation, hydrolysis, and sphingosine phosphorylation[1][2][3].
    N-Desmethyltamoxifen hydrochloride (Standard)
  • HY-145306
    DX3-234

    		Oxidative Phosphorylation Mitochondrial Metabolism Cancer
    DX3-234 is an oxidative phosphorylation (OXPHOS) inhibitor. DX3-234 shows significant tumor suppression in the Pan02 syngeneic model of pancreatic cancer .
    DX3-234
  • HY-E70262
    Acetoyl-CoA triammonium

    		Oxidative Phosphorylation Endogenous Metabolite Metabolic Disease
    Acetoyl-CoA (triammonium) is a triammonium derivative of Acetoyl-CoA (HY-114293), Acetyl-CoA is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A is also a key precursor of lipid synthesis .
    Acetoyl-CoA triammonium
  • HY-B0831R
    Buprofezin (Standard)

    		Oxidative Phosphorylation Reference Standards Reactive Oxygen Species (ROS) Others
    Buprofezin (Standard) is the analytical standard of Buprofezin. This product is intended for research and analytical applications. Buprofezin is a broad-spectrum insecticide and chitin synthesis inhibitor that targets developmental stage coleopteran pests.Buprofezin promotes the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Buprofezin also promotes the production of reactive oxygen species (ROS) by inhibiting cytochrome c oxidase .
    Buprofezin (Standard)

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