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Pathways Recommended:	Metabolic Enzyme/Protease

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lipid metabolic disease

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By Targets:	Acyltransferase (1) Akt (6) AMPK (9) Amylin Receptor (2) Androgen Receptor (1) Apolipoprotein (1) Apoptosis (19) ATP-binding cassette (ABC) transporters (1) Autophagy (15) Bcl-2 Family (8) Biochemical Assay Reagents (1) c-Met/HGFR (1) Carnitine Palmitoyltransferase (CPT) (1) Caspase (1) Ceramidase (1) CGRP Receptor (6) Cholinesterase (ChE) (1) Collagen (2) COX (2) Cuproptosis (1) Cytochrome P450 (2) DNA/RNA Synthesis (4) Drug Metabolite (4) ELOVL (1) Endogenous Metabolite (23) Environmental Pollutants (2) ERK (1) Eukaryotic Initiation Factor (eIF) (1) FABP (1) Ferroptosis (9) Fluorescent Dye (1) FXR (2) G protein-coupled Bile Acid Receptor 1 (3) GCGR (2) GLP Receptor (8) GLUT (2) Glutathione Peroxidase (1) Histamine Receptor (4) HMG-CoA Reductase (HMGCR) (5) IKK (1) Influenza Virus (1) Insecticide (1) Insulin Receptor (11) Interleukin Related (8) Isotope-Labeled Compounds (8) JAK (6) JNK (5) Keap1-Nrf2 (1) LDLR (1) Lipase (1) Lipoxygenase (1) mAChR (2) MNK (1) Monoamine Oxidase (1) mTOR (2) Neuropeptide Y Receptor (2) NF-κB (12) NO Synthase (1) Opioid Receptor (1) p38 MAPK (13) PAK (1) Parasite (1) PCSK9 (1) PGC-1α (1) PGE synthase (2) PI3K (6) PPAR (5) Prostaglandin Receptor (1) RAR/RXR (1) Reactive Oxygen Species (ROS) (9) Reference Standards (10) ROR (4) Sirtuin (5) SOD (1) STAT (6) Stearoyl-CoA Desaturase (SCD) (1) TGF-β Receptor (2) TNF Receptor (7) VEGFR (1) Wnt (2) α-synuclein (8) β-catenin (2)
By Research Areas:	Cancer (27) Cardiovascular Disease (18) Endocrinology (5) Infection (6) Inflammation/Immunology (30) Metabolic Disease (55) Neurological Disease (31)
Oligonucleotides:	Phospholipids (1)

Inhibitors & Agonists

Bibliotecas de Screening

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Biochemical Assay Reagents

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Isotope-Labeled Compounds

Oligonucleotides

Cat. No.	Nombre del producto	Target	Áreas de investigación	Chemical Structure

HY-114118

Semaglutide Maximum Cited Publications 35 Publications Verification	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-D1168

Oil Red O 10+ Cited Publications	Environmental Pollutants Fluorescent Dye	Metabolic Disease
Oil Red O is a fat-soluble diazol dye, with a maximum absorption at 518 nm. Oil Red O stains neutral lipids and cholesteryl esters but not biological membranes. Oil Red O can be used for detecting and quantifying hepatic steatosis in mouse liver biopsies. Oil Red O staining efficiently helps to visualize the radical changes that occur in tissues as metabolic disease occurs and progresses .

HY-113402

Gamma-glutamylcysteine 4 Publications Verification γ-Glu-Cys	Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine 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 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 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 .

HY-W001171

3-Hydroxyanthranilic acid 1 Publications Verification	Endogenous Metabolite	Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology Cancer
3-Hydroxyanthranilic acid is a tryptophan metabolite in the kynurenine pathway.3-hydroxyanthranilic acid has anti-inflammatory, neuroprotective, and lipid-lowering effects. 3-hydroxyanthranilic acid can be used for researches of cardiovascular diseases, tumors, and metabolic diseases .

HY-N7075

Inulin 4 Publications Verification	Endogenous Metabolite	Infection Neurological Disease Metabolic Disease Cancer
Inulin is an orally active prebiotic targeting the intestinal microbiota, selectively promoting the proliferation and activity of beneficial bacteria such as bifidobacteria and lactic acid bacteria, and playing a role in regulating the intestinal microecology. The functions of Inulin include: Fermentation by probiotics in the colon to produce short-chain fatty acids (such as butyrate and propionate), lowering the intestinal pH and inhibiting the overgrowth of harmful bacteria; Enhancing the intestinal barrier function and reducing endotoxin translocation; Directly scavenging free radicals (such as superoxide free radicals, hydroxyl free radicals) and activating antioxidant enzymes (SOD, CAT) to reduce oxidative stress. Inulin can also be used in the study of intestinal diseases (constipation, IBD), metabolic syndrome (diabetes, obesity) and liver damage by regulating glucose and lipid metabolism (such as reducing triglycerides, improving insulin sensitivity) and immune response (enhancing NK cell activity, inhibiting inflammatory factors)[1][2][3][4].

HY-135425

10,12-Tricosadiynoic acid 5+ Cited Publications	Acyltransferase	Metabolic Disease
10,12-Tricosadiynoic acid is a highly specific, selective, high affinity and orally active acyl-CoA oxidase-1 (ACOX1) inhibitor. 10,12-Tricosadiynoic acid can treat high fat diet- or obesity-induced metabolic diseases by improving mitochondrial lipid and ROS metabolism . 10,12-Tricosadiynoic acid is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

HY-114118B

Semaglutide acetate Maximum Cited Publications 35 Publications Verification	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide acetate is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-114118A

Semaglutide TFA Maximum Cited Publications 35 Publications Verification	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

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 .

HY-N9933

Tauro-β-muricholic acid 4 Publications Verification TβMCA	FXR Apoptosis	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC₅₀=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .

HY-Y1422

Triacylglycerol lipase Alkaline lipase	Environmental Pollutants Lipase	Metabolic Disease
Triacylglycerol lipase is an enzyme catalyzing the hydrolysis of triacylglycerol. Triacylglycerol lipase promotes fat decomposition, providing energy and lipid precursors for cells. Triacylglycerol lipase is used in the research of metabolic diseases such as diabetes and obesity .

HY-113149A

Argininosuccinic acid disodium	Endogenous Metabolite Reactive Oxygen Species (ROS)	Neurological Disease Metabolic Disease Inflammation/Immunology
Argininosuccinic acid disodium is an intermediate metabolite in the urea cycle, and its level is associated with argininosuccinic aciduria. Argininosuccinic acid disodium can induce oxidative stress, leading to lipid and protein oxidation, reduction of glutathione, and decrease in antioxidant enzyme activity. Argininosuccinic acid disodium can be converted into guanidinosuccinic acid, a nitric oxide mimic, under the action of nitric oxide-derived free radicals. Argininosuccinic acid disodium can be used in the research of metabolic diseases, renal failure, nervous system diseases, etc .

HY-P11274A

Zenagamtide sodium Amycretin sodium; NN 9487 sodium	Amylin Receptor Insulin Receptor GCGR	Metabolic Disease
Zenagamtide (Amycretin; NN 9487) sodium is an orally active, blood-brain barrier permeable triple agonist that targets GLP-1, amylin (Amylin Receptor) and calcitonin receptor (Calcitonin Receptor). Zenagamtide sodium is a single peptide consisting of 68 amino acids that can target brain regions regulating food intake, significantly suppress appetite and reduce energy intake. Therefore, Zenagamtide sodium improves body weight, waist circumference, glycated hemoglobin and lipid profile, and also alleviates the histological features of metabolic dysfunction-associated steatotic liver disease (MASLD) and enhances insulin sensitivity. Zenagamtide sodium may cause transient increases in heart rate and fluctuations in serum calcium levels, but it is an important compound for the study of overweight, obesity, insulin resistance and related metabolic diseases .

HY-W015924

2-Hydroxyisobutyric acid	Endogenous Metabolite	Metabolic Disease
2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

HY-P2048

MOTS-c (human) 1 Publications Verification	Apoptosis GLUT AMPK	Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
MOTS-c (human) is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders .

HY-101036

Choline bitartrate 4 Publications Verification	mAChR Endogenous Metabolite	Neurological Disease Cancer
Choline bitartrate is a vitamin-like essential nutrient, can affect diseases such as liver disease, atherosclerosis and neurological disorders . Choline bitartrate is a precursor for the neurotransmitter acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism .

HY-143712

Allolithocholic acid 1 Publications Verification	Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR	Metabolic Disease Inflammation/Immunology Cancer
Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC₅₀ = 2.7 μM) and RORγt inverse agonist (IC₅₀ = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .

HY-114118CP

Semaglutide (crude)	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide (crude) is the crude form of Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances Autophagy, inhibits oxidative stress and Apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-113110

Cysteinylglycine L-Cysteinylglycine; Cys-Gly; H-Cys-Gly-OH	Endogenous Metabolite Reactive Oxygen Species (ROS) DNA/RNA Synthesis	Cardiovascular Disease Cancer
Cysteinylglycine (L-Cysteinylglycine; Cys-Gly) is a dipeptide formed by the peptide bond linkage between cysteine (Cysteine) and glycine (Glycine). Cysteinylglycine is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine reduces ferric iron to ferrous iron, drives the redox cycle of iron, generates reactive oxygen species (ROS), stimulates oxidative reactions, induces lipid peroxidation of human plasma LDL lipoproteins, and causes oxidative damage to DNA bases. Cysteinylglycine can be used as a biomarker to evaluate ischemic heart disease, breast cancer and other conditions .

HY-114118S3

Semaglutide-13C6,15N TFA	Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Metabolic Disease
Semaglutide- ¹³C₆, ¹⁵N TFA is the ¹³C- and ¹⁵N-labeled Semaglutide TFA (HY-114118A). Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-113402A

Gamma-glutamylcysteine TFA 4 Publications Verification γ-Glu-Cys TFA	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
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 .

HY-50683

JNJ-38877605 5+ Cited Publications	c-Met/HGFR	Metabolic Disease Cancer
JNJ-38877605 is an orally active ATP-competitive inhibitor of c-Met with an IC₅₀ of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases . JNJ-38877605 inhibits c-Met phosphorylation and regulates lipid accumulation. JNJ-38877605 can be used for tumor and metabolic disease reseach .

HY-N6677

β-Apo-8'-carotenal Apocarotenal	Cytochrome P450 DNA/RNA Synthesis	Metabolic Disease Cancer
β-Apo-8'-carotenal (Apocarotenal), an orally active provitamin A carotenoid. β-Apo-8'-carotenal can induce the expression of CYP1A through the Ah receptor-dependent pathway. β-Apo-8'-carotenal can induce cancer cells DNA strand breaks and lipid peroxidation. β-Apo-8'-carotenal can be used for the researches of cancer and metabolic disease .

HY-N2392

Kukoamine A 1 Publications Verification	Parasite Lipoxygenase Opioid Receptor Apoptosis Autophagy Reactive Oxygen Species (ROS) Interleukin Related TNF Receptor PGE synthase COX	Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Kukoamine A, a spermine alkaloid, is an orally active and brain-penetrant component found in the root barks of Lycium chinense (L. chinense) Miller. Kukoamine A inhibits purified Crithidia fasciculata trypanothione reductase and soybean lipoxygenase, activates μ-opioid receptor. Kukoamine A can inhibt cancer cell proliferation, migration and invasion, cause G0/G1 phase cell cycle arrest and induce apoptosis. Kukoamine A exerts neuroprotective effect and can induce autophagy . Kukoamine A inhibits LPS (HY-D1056)-induced NO, ROS, PGE₂, TNF-α, IL-1β, IL-6 production and COX-2 activity. Kukoamine A reverses palmitic acid-induced insulin resistance, lipid accumulation, and oxidative stress via downregulation of Srebp-1c. Kukoamine A can be used for the research of cancer, infection, inflammation, metabolic and neurological disease, such as glioblastoma and Parkinson's disease .

HY-B1189

Meglutol Dicrotalic acid; 3-Hydroxy-3-methylglutaric acid	HMG-CoA Reductase (HMGCR) Autophagy Endogenous Metabolite	Cardiovascular Disease Metabolic Disease
Meglutol is a lipid-lowering agent. Meglutol can reduces cholesterol, triglycerides, serum β-lipoprotein, and phospholipids, and inhibits the activity of HMG-CoA reductase (a rate-limiting enzyme in cholesterol biosynthesis). Meglutol can induce significant lipid oxidative damage in brain tissue. It is promising for research in the field of cardiovascular diseases and metabolic diseases .

HY-113149

Argininosuccinic acid	Endogenous Metabolite Reactive Oxygen Species (ROS)	Neurological Disease Metabolic Disease Inflammation/Immunology
Argininosuccinic acid is an intermediate metabolite in the urea cycle, and its level is associated with argininosuccinic aciduria. Argininosuccinic acid can induce oxidative stress, leading to lipid and protein oxidation, reduction of glutathione, and decrease in antioxidant enzyme activity. Argininosuccinic acid can be converted into guanidinosuccinic acid, a nitric oxide mimic, under the action of nitric oxide-derived free radicals. Argininosuccinic acid can be used in the research of metabolic diseases, renal failure, nervous system diseases, etc .

HY-P11274

Zenagamtide Amycretin; NN 9487	Amylin Receptor GCGR Insulin Receptor	Metabolic Disease
Zenagamtide (Amycretin; NN 9487) is an orally active, blood-brain barrier permeable triple agonist that targets GLP-1, amylin (Amylin Receptor) and calcitonin receptor (Calcitonin Receptor). Zenagamtide is a single peptide consisting of 68 amino acids that can target brain regions regulating food intake, significantly suppress appetite and reduce energy intake. Therefore, Zenagamtide improves body weight, waist circumference, glycated hemoglobin and lipid profile, and also alleviates the histological features of metabolic dysfunction-associated steatotic liver disease (MASLD) and enhances insulin sensitivity. Zenagamtide may cause transient increases in heart rate and fluctuations in serum calcium levels, but it is an important compound for the study of overweight, obesity, insulin resistance and related metabolic diseases .

HY-W355700

1-Oleoyl-2-hydroxy-sn-glycero-3-phosphoethanolamine	Drug Metabolite	Infection
1-oleoyl-sn-glycero-3-phosphoethanolamine (LysoPE 18:1) is a lysophosphatidylethanolamine molecule involved in phospholipid metabolism, targeting cell membrane receptors (such as G protein-coupled receptors) to regulate cell signaling pathways. 1-oleoyl-sn-glycero-3-phosphoethanolamine may activate mitogen-activated protein kinase (MAPK) signaling, promote cell migration, regulate inflammatory responses and lipid metabolism, and has both pro-inflammatory and anti-inflammatory activities. 1-oleoyl-sn-glycero-3-phosphoethanolamine is mainly used in the screening of biomarkers for metabolic diseases (such as non-alcoholic fatty liver disease and obesity), as well as the study of the mechanism of lysophospholipids in cell membrane homeostasis and signal transduction .

HY-160912

ELOVL6-IN-5	ELOVL	Metabolic Disease
ELOVL6-IN-5 is an orally active and selective elongase enzyme of long-chain fatty acid family 6 (ELOVL6) inhibitor with IC₅₀values of 85 nM and 38 nM for human and mouse ELOVL6, respectively. ELOVL6-IN-5 shows >60-fold selectivity over other ELOVL family enzymes (ELOVL1, 2, 3, 5) and no effect on other lipid synthesis enzymes like ACC1, ACC2. ELOVL6-IN-5 reduces hepatic fatty acid composition ratio of C18 to C16 in diet-induced obesity (DIO) and KKAy mice. ELOVL6 inhibition by ELOVL6-IN-5 does not improve insulin resistance. ELOVL6-IN-5 can be used for the research of metabolic disease .

HY-114118S1

Semaglutide-d8 tetraTFA	Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide-d₈ tetraTFA is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-114118S

Semaglutide-d8	Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide-d₈ is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-P1723

Spexin 2 Publications Verification Neuropeptide Q	Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy	Cardiovascular Disease Neurological Disease
Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .

HY-126359

1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine SLPC; 18:0-18:2 PC	Endogenous Metabolite	Cardiovascular Disease Metabolic Disease
1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine (SLPC; 18:0-18:2 PC) is an endogenous phospholipid marker molecule in the glycerophospholipid metabolic pathway. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine is a core component of the phospholipid bilayer of biological membranes and a key responsive lipid for radiation injury and cardiometabolic diseases. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine constitutes the phospholipid bilayers of cell membranes and high-density lipoprotein (HDL), and regulates the core activity of lipoprotein functional homeostasis. The content of 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine in mouse serum shows a significant dose-dependent decrease with increasing ionizing radiation dose, and its level in human HDL also decreases significantly in metabolic syndrome. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine can serve as a biological dosimeter marker for ionizing radiation injury, and is used for rapid and accurate assessment of radiation absorbed dose in exposed individuals. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine can also act as a lipidomics research target for cardiometabolic diseases such as lipid metabolic syndrome and early-onset coronary heart disease .

HY-N0899

Wilforine	JAK STAT Wnt β-catenin	Inflammation/Immunology Cancer
Wilforine is an orally active JAK-STAT pathway inhibitor with immunomodulatory effects and the ability to inhibit osteoclast fusion. Wilforine disrupts lipid raft integrity, reprograms cholesterol and glycosphingolipid metabolic pathways, regulates NF-κB and the complement system, and modulates the expression of various interleukins. Wilforine also inhibits the Wnt11/β-catenin signaling pathway and suppresses the proliferation of fibroblast-like synoviocytes. Wilforine can serve as a quality and pharmacokinetic marker for Tripterygium glycoside tablets, and can be applied to research on related diseases such as rheumatoid arthritis, inflammatory osteolysis, and SAPHO syndrome .

HY-P2048A

MOTS-c(human) acetate 1 Publications Verification	AMPK GLUT	Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
MOTS-c (human) acetate is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) acetate inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) acetate has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders .

HY-120657

9-PAHSA	CGRP Receptor NF-κB	Neurological Disease Metabolic Disease Inflammation/Immunology
9-PAHSA is an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

HY-W012865

Tartronic acid	Carnitine Palmitoyltransferase (CPT) Endogenous Metabolite FABP PPAR	Metabolic Disease
Tartronic acid, a dicarboxylic acid derive, is an inhibitor of the transformation of carbohydrates into fat under fat-deficient diet conditions. Tartronic acid promotes 3T3-L1 adipocyte differentiation by increasing the protein expression of FABP-4, PPARγ and SREBP-1. Tartronic acid promotes de novo lipogenesis and inhibits CPT-1β by upregulating acetyl-CoA and malonyl-CoA. Tartronic acid promotes weight gain and induces adipocyte hypertrophy in epididymal white adipose tissue and lipid accumulation in the livers of high-fat diet induced obese mice. Tartronic acid can be used for lipid metabolic disease research .

HY-N4124

Poricoic acid B	NO Synthase TNF Receptor Interleukin Related	Metabolic Disease Inflammation/Immunology
Poricoic acid B is a triterpenoid compound that can be isolated from Poria cocos. Poricoic acid B inhibits intracellular lipid accumulation and reduces the levels of hepatocyte injury markers. Poricoic acid B inhibits the production of NO, TNF-α, IL-1β and IL-6, thereby exerting anti-inflammatory activity. Poricoic acid B can be used in the research of metabolic dysfunction-associated fatty liver disease and inflammatory diseases ^[3].

HY-142026

Vitisin A (+)-Vitisin A	Caspase ERK NF-κB Influenza Virus PAK LDLR PPAR PCSK9 Androgen Receptor Keap1-Nrf2 Monoamine Oxidase Cholinesterase (ChE) IKK Wnt β-catenin Reactive Oxygen Species (ROS) Apoptosis Cuproptosis	Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC₅₀ values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases .

HY-106281

Bemfivastatin PPD 10558	HMG-CoA Reductase (HMGCR)	Metabolic Disease
Bemfivastatin (PPD 10558) is an orally active HMG-CoA Reductase (HMGCR) inhibitor. Bemfivastatin enhances the activity of liver extraction and reduces blood lipid levels. Bemfivastatin can be used for research of metabolic disease, such as hypercholesterolemia .

HY-163436

F44-A13	FXR Cytochrome P450 RAR/RXR PPAR ROR	Metabolic Disease
F44-A13 is an orally active and highly selective farnesoid X receptor (FXR) antagonist with an IC₅₀ value of 1.1 μM. F44-A13 can optimize cholesterol metabolism and reduce its activity by inducing CYP7A1 expression. F44-A13 reduces levels of cholesterol, triglycerides, and low-density lipoprotein cholesterol (LDL-C) in mouse models. F44-A13 can be used in the study of metabolic diseases associated with lipid disorders .

HY-N15841

C25 Ceramide (d18:1/25:0)	Ceramidase	Others
C25 Ceramide (d18:1/25:0) is an endogenous ultra-long-chain ceramide that antagonizes the detrimental effects of long-chain ceramides on insulin sensitivity. C25 Ceramide (d18:1/25:0) is specifically enriched in oxidative skeletal muscle fibers, where it serves dual roles in providing structural support to cell membranes and regulating cellular signaling. By participating in the regulation of lipid homeostasis within muscle fibers, C25 Ceramide (d18:1/25:0) helps maintain normal insulin signaling. C25 Ceramide (d18:1/25:0) is primarily utilized in research concerning metabolic diseases—particularly in mechanistic studies investigating the muscle fiber type-specific aspects of insulin resistance .

HY-101036R

Choline bitartrate (Standard)	Reference Standards mAChR Endogenous Metabolite	Neurological Disease Cancer
Choline (bitartrate) (Standard) is the analytical standard of Choline (bitartrate). This product is intended for research and analytical applications. Choline bitartrate is a vitamin-like essential nutrient, can affect diseases such as liver disease, atherosclerosis and neurological disorders . Choline bitartrate is a precursor for the neurotransmitter acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism .

HY-113402R

Gamma-glutamylcysteine (Standard) γ-Glu-Cys (Standard)	Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Inflammation/Immunology
Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine 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 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 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.

HY-W015924R

2-Hydroxyisobutyric acid (Standard)	Reference Standards Endogenous Metabolite	Metabolic Disease
2-Hydroxyisobutyric acid (Standard) is the analytical standard of 2-Hydroxyisobutyric acid. This product is intended for research and analytical applications. 2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

HY-170509

Ferroptosis-IN-17	Ferroptosis Glutathione Peroxidase	Cardiovascular Disease Neurological Disease Cancer
Ferroptosis-IN-17 (Compound 18) is a ferroptosis (Ferroptosis) inhibitor with an EC₅₀ value of 0.57 μM. Ferroptosis-IN-17 reduces intracellular ferrous ion accumulation, lipid peroxidation, and effectively restores the levels of glutathione (GSH) and glutathione peroxidase 4 (GPX4). Ferroptosis-IN-17 shows good solubility and significant metabolic stability in rat plasma. Ferroptosis-IN-17 is promising for research in tumor suppression, neurodegenerative diseases, and cardiovascular diseases .

HY-178192

mTORC1-IN-3	mTOR Autophagy	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
mTORC1-IN-3 is a potent and selective mTORC1 inhibitor with an IC₅₀ of 26.38 μM . mTORC1-IN-3 selectively inhibits the phosphorylation of mTORC1 substrates and does not without affect the phosphorylation of mTORC2 substrate. mTORC1-IN-3 can reduce cellular lipid accumulation and induce autophagy. mTORC1-IN-3 can be used for the researches of cancer, immunology, metabolic and neurological disease, such as diabetes and Alzheimer’s disease .

HY-113110A

Cysteinylglycine TFA L-Cysteinylglycine TFA; Cys-Gly TFA; H-Cys-Gly-OH TFA	Endogenous Metabolite Reactive Oxygen Species (ROS) DNA/RNA Synthesis	Cardiovascular Disease Cancer
Cysteinylglycine (L-Cysteinylglycine; Cys-Gly) TFA is a dipeptide formed by the peptide bond connection of cysteine and glycine. Cysteinylglycine TFA is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine TFA can reduce trivalent iron to divalent iron, driving the redox cycle of iron, generating reactive oxygen species (ROS), stimulating oxidative reactions, inducing lipid peroxidation in human plasma LDL lipoproteins, and causing oxidative damage to DNA base. Cysteinylglycine TFA can be used as a biomarker to assess ischemic heart disease and breast cancer, etc ^[1][2][3][4].

HY-P5081

Endotrophin (Mus musculus)	TGF-β Receptor Collagen	Inflammation/Immunology
Endotrophin (Mus musculus) is an adipokine, a cleavage fragment derived from Collagen VI, whose levels are elevated in adipose tissue and breast tumors of obese mice. Endotrophin (Mus musculus) activates the TGF-β signaling pathway and reduces the expression of hormone-sensitive lipase. Endotrophin (Mus musculus) induces adipogenesis, lipid accumulation, fibrosis, inflammation, angiogenesis, adipose tissue expansion, epithelial-mesenchymal transition, and insulin resistance; it also induces Cisplatin (HY-17394) resistance in cancer cells. Endotrophin (Mus musculus) can be used in research related to metabolic diseases such as obesity and type 2 diabetes, as well as cancers such as breast cancer .

HY-W770410

9-PAHSA-13C4	Isotope-Labeled Compounds CGRP Receptor NF-κB	Others
9-PAHSA- ¹³C₄ is ¹³C-labeled 9-PAHSA. 9-PAHSAis an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSAsignificantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSAinduces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSAregulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSAdoes not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSAcan be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

Cat. No.	Nombre del producto

HY-L146

Metabolic Enzyme Compound Library

4,169 compounds

Metabolism is the set of life-sustaining chemical reactions in organisms that maintain cell homeostasis. Metabolic pathways are enzyme-mediated biochemical reactions that lead to biosynthesis (anabolism) or breakdown (catabolism) of molecules including glucose metabolism, lipid metabolism and amino acid or protein metabolism within a cell or tissue. As catalysts, enzymes are crucial to metabolism as they allow a reaction to proceed more rapidly and tregulate the rate of a metabolic reaction. Due to the importance of metabolic balance in the organism, the abnormal function of metabolic enzymes often leads to the occurrence of a variety of metabolic diseases, such as diabetes, obesity, cardiovascular disease, etc.

MCE designs a unique collection of 4,169 metabolic enzymes related small molecules, which is an important tool for studying the metabolic activities of organisms and developing drugs for metabolic diseases.

HY-L091

Lipid Metabolism Compound Library

978 compounds

Lipids are a fundamental class of organic molecules implicated in a wide range of biological processes, and based on this can be broadly classified into five categories: fatty acids, triacylglycerols (TAGs), phospholipids, sterol lipids and sphingolipids. Lipids play a crucial role in different metabolic pathways and cellular functions. Lipid metabolism is an important physiological process that is related to nutrient adjustment, hormone regulation, and homeostasis. Lipid metabolism dysregulation is associated with many diseases such as obesity, liver disease, aging and inflammation.

MCE offers a unique collection of 978 compounds related to lipid metabolism, which target relevant targets in the process of lipid metabolism, such as ATGL, MAGL, FAAH, acetyl-Coa Carboxylase, FASN, etc. MCE lipid metabolism compound library is a useful tool for research lipid metabolism and drug discovery of diseases related to lipid metabolism.

HY-L228

Lipid Metabolite Compound Library

145 compounds

Lipids are important energy storage substances in the human body. They are involved in the regulation of cell structure and function, as well as signaling pathways and gene expression. Abnormal lipid levels in tissues or their dysregulation can lead to various diseases. These include obesity, type 2 diabetes, non-alcoholic fatty liver disease, neurodegenerative diseases, infections, and cancer. Therefore, maintaining normal levels of lipid metabolism is critical to overall health.

One of the key features of cancer is aberrant lipid metabolism. This includes alterations in lipid uptake, lipid desaturation, neolipogenesis, lipid droplets, and fatty acid oxidation in cancer cells. These changes all contribute to cellular survival in an ever-changing microenvironment. They do this by modulating feed-forward oncogenic signals and key oncogenic functions. Additionally, they affect oxidative stress, other types of stress, immune responses, and intercellular communication. Alterations in lipid metabolism have a strong impact on the properties of cancer stem cells. This includes aspects such as self-renewal, differentiation, invasion, metastasis, drug sensitivity, and resistance. Furthermore, these alterations also modulate T cell responses.

MCE can offer 145 metabolites of lipid metabolism pathways, which can be used for drug screening in cancer, immune-based diseases, metabolic diseases, and other diseases.

HY-L208

Bile Acids Library

61 compounds

Bile acids are a class of amphiphilic molecules derived from the metabolic breakdown of cholesterol, primarily synthesized in the liver, and play a crucial role in the intestines. Based on their structural characteristics, bile acids are mainly divided into two categories: free bile acids (including Cholic acid, Deoxycholic acid, Chenodeoxycholic acid) and conjugated bile acids (including Glycocholic acid, Glycochenodeoxycholic acid, Taurocholic acid, etc.). Bile acids play a significant role in the pathophysiological research of liver and gastrointestinal diseases and are closely associated with the occurrence of metabolic diseases such as obesity, type II diabetes, non-alcoholic fatty liver disease, and atherosclerosis. Bile acids maintain metabolic balance within the body by regulating sugar metabolism, lipid metabolism, and amino acid metabolism, and they influence the activity of metabolism-related enzymes and transporters. In addition, Bile acids can also be used to construct a bile acid metabolism research platform, which helps to delve into the metabolic pathways and dynamic changes of bile acids in living organisms and aids in identifying new biomarkers for certain diseases.

MCE included 61 bile acids, including Cholic acid, Deoxycholic acid, Glycocholic acid, etc., which are effective tools for the study of liver and gallbladder diseases.

HY-L043

Lipid Compound Library

1,266 compounds

Lipids are a diverse and ubiquitous group of compounds which have many key biological functions, such as acting as structural components of cell membranes, serving as energy storage sources and participating in signaling pathways. Several studies suggest that bioactive lipids have effects on the treatment of some mental illnesses and metabolic syndrome. For example, DHA and EPA are important for monoaminergic neurotransmission, brain development and synaptic functioning, and are also correlated with a reduced risk of cancer and cardiovascular disease in clinical and animal studies.

MCE supplies a unique collection of 1,266 lipid and lipid derivative related compounds including triglycerides, phospholipids, sphingolipids, steroids and their structural analogues or derivatives. MCE lipid compound library can be used for research in bioactive lipids, and high throughput screening (HTS) and high content screening (HCS).

HY-L123

Human Metabolite Library

6,717 compounds

Human metabolism is an integral part of cellular function that reflects individual differences in health, disease, diet, and lifestyle. Many health conditions such as obesity, diabetes, hypertension, heart disease, and cancer are associated with abnormal metabolic states. In the pathological state of the human body, metabolic pathways are significantly altered, resulting in aberrant levels of intermediates or end-products that can be viewed as potential diagnostic biomarkers or even therapeutic targets. Therefore, detection, identification and quantification of human metabolites are very important for drug metabolism research in drug development.

MCE offers a unique collection of 6,717 human metabolites, including endogenous metabolites and exogenous metabolites, covering multiple structure types, such as lipids, amino acids, nucleic acids, carbohydrates, organic acids, biogenic amines, vitamins,. MCE Human Metabolites Library is a helpful tool for studying the relationship between diseases and metabolism.

HY-L199

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

4,703 compounds

Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide and is the primary liver manifestation of metabolic syndrome. The growth of NAFLD has coincided with the obesity epidemic. NAFLD is composed of excess lipid accumulation in the liver, causing steatotoxicity, and shows a wide range of histopathological abnormalities. NAFLD may progress from simple steatosis to Non-alcoholic steatohepatitis (NASH) with or without fibrosis (NASH), and eventually to cirrhosis and hepatocellular carcinoma. To date, very few drugs have been approved for marketing specifically for the treatment of NAFLD, so increased efforts to develop NAFLD drugs are necessary.

MCE designs a unique collection of 4,703 small molecules with definite or potential anti-NAFLD activity, which is an important tool for studying the pathological mechanism of NAFLD and developing drugs for NAFLD.

HY-L253

Fungal-Sourced Compound Library

88 compounds

For thousands of years, natural products have always been an important source for drug discovery. Fungi, due to their unique and diverse secondary metabolic capabilities, have become a valuable resource for natural active molecules. Since the discovery of penicillin, natural products derived from fungi have demonstrated significant application value in areas such as anti-infection, anti-tumor, immune regulation, and metabolic disease research. A large number of clinical drugs, such as antibiotics, immunosuppressants, and lipid-lowering drugs, are derived from fungal metabolites or their structurally optimized derivatives.

MCE fungal-derived compound library contains 88 structurally diverse and bioactive fungal natural products and their derivatives. It can be widely applied in various research fields such as antibacterial, anti-tumor, anti-inflammatory, immune regulation, epigenetics, and cell signaling pathways, providing high-quality tools for natural product drug development and high-throughput screening.

Cat. No.	Nombre del producto	Type

HY-D1168

Oil Red O 10+ Cited Publications	Fluorescent Dyes
Oil Red O is a fat-soluble diazol dye, with a maximum absorption at 518 nm. Oil Red O stains neutral lipids and cholesteryl esters but not biological membranes. Oil Red O can be used for detecting and quantifying hepatic steatosis in mouse liver biopsies. Oil Red O staining efficiently helps to visualize the radical changes that occur in tissues as metabolic disease occurs and progresses .

Cat. No.	Nombre del producto	Type

HY-131306B

2-Hexadecenoic acid

Gaidic acid

Biochemical Assay Reagents

2-Hexadecenoic acid is a natural unsaturated fatty acid. It is ubiquitously present in various animal and plant tissues, especially adipose tissue and certain vegetable oils, such as macadamia nut oil. 2-Hexadecenoic acid has unique chemical properties that make it an important component of cell membranes and storage lipids, and participates in various metabolic processes such as lipid metabolism and inflammation. It's also been linked to potential health benefits, including improved insulin sensitivity and a lower risk of heart disease.

Cat. No.	Nombre del producto	Target	Research Area

HY-114118

Semaglutide Maximum Cited Publications 35 Publications Verification	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-114118B

Semaglutide acetate Maximum Cited Publications 35 Publications Verification	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide acetate is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-114118A

Semaglutide TFA Maximum Cited Publications 35 Publications Verification	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-P11274A

Zenagamtide sodium Amycretin sodium; NN 9487 sodium	Amylin Receptor Insulin Receptor GCGR	Metabolic Disease
Zenagamtide (Amycretin; NN 9487) sodium is an orally active, blood-brain barrier permeable triple agonist that targets GLP-1, amylin (Amylin Receptor) and calcitonin receptor (Calcitonin Receptor). Zenagamtide sodium is a single peptide consisting of 68 amino acids that can target brain regions regulating food intake, significantly suppress appetite and reduce energy intake. Therefore, Zenagamtide sodium improves body weight, waist circumference, glycated hemoglobin and lipid profile, and also alleviates the histological features of metabolic dysfunction-associated steatotic liver disease (MASLD) and enhances insulin sensitivity. Zenagamtide sodium may cause transient increases in heart rate and fluctuations in serum calcium levels, but it is an important compound for the study of overweight, obesity, insulin resistance and related metabolic diseases .

HY-P2048

MOTS-c (human) 1 Publications Verification	Apoptosis GLUT AMPK	Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
MOTS-c (human) is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders .

HY-114118CP

Semaglutide (crude)	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide (crude) is the crude form of Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances Autophagy, inhibits oxidative stress and Apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-113110

Cysteinylglycine L-Cysteinylglycine; Cys-Gly; H-Cys-Gly-OH	Endogenous Metabolite Reactive Oxygen Species (ROS) DNA/RNA Synthesis	Cardiovascular Disease Cancer
Cysteinylglycine (L-Cysteinylglycine; Cys-Gly) is a dipeptide formed by the peptide bond linkage between cysteine (Cysteine) and glycine (Glycine). Cysteinylglycine is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine reduces ferric iron to ferrous iron, drives the redox cycle of iron, generates reactive oxygen species (ROS), stimulates oxidative reactions, induces lipid peroxidation of human plasma LDL lipoproteins, and causes oxidative damage to DNA bases. Cysteinylglycine can be used as a biomarker to evaluate ischemic heart disease, breast cancer and other conditions .

HY-113402A

Gamma-glutamylcysteine TFA 4 Publications Verification γ-Glu-Cys TFA	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
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 .

HY-P11274

Zenagamtide Amycretin; NN 9487	Amylin Receptor GCGR Insulin Receptor	Metabolic Disease
Zenagamtide (Amycretin; NN 9487) is an orally active, blood-brain barrier permeable triple agonist that targets GLP-1, amylin (Amylin Receptor) and calcitonin receptor (Calcitonin Receptor). Zenagamtide is a single peptide consisting of 68 amino acids that can target brain regions regulating food intake, significantly suppress appetite and reduce energy intake. Therefore, Zenagamtide improves body weight, waist circumference, glycated hemoglobin and lipid profile, and also alleviates the histological features of metabolic dysfunction-associated steatotic liver disease (MASLD) and enhances insulin sensitivity. Zenagamtide may cause transient increases in heart rate and fluctuations in serum calcium levels, but it is an important compound for the study of overweight, obesity, insulin resistance and related metabolic diseases .

HY-114118S1

Semaglutide-d8 tetraTFA	Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide-d₈ tetraTFA is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-114118S

Semaglutide-d8	Isotope-Labeled Compounds GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide-d₈ is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-P1723

Spexin 2 Publications Verification Neuropeptide Q	Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy	Cardiovascular Disease Neurological Disease
Spexin (Neuropeptide Q) is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin can function through both central and peripheral actions. Spexin upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .

HY-P2048A

MOTS-c(human) acetate 1 Publications Verification	AMPK GLUT	Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
MOTS-c (human) acetate is a blood-brain barrier-penetrating, mitochondrial-derived peptide that modulates the AMPK/PGC-1α pathway to enhance insulin sensitivity. MOTS-c (human) acetate inhibits the folate cycle and de novo purine synthesis, increases AICAR levels to activate AMPK, and then regulates the Nrf2/Keap1 antioxidant pathway and inhibits the NF-κB inflammatory pathway, while promoting mitochondrial biogenesis and energy metabolism. MOTS-c (human) acetate has the effects of improving glucose and lipid metabolism, anti-oxidative stress, anti-inflammatory and neuroprotection, and can be used in the study of type 2 diabetes, traumatic brain injury, inflammatory diseases and aging-related metabolic disorders .

HY-113110A

Cysteinylglycine TFA L-Cysteinylglycine TFA; Cys-Gly TFA; H-Cys-Gly-OH TFA	Endogenous Metabolite Reactive Oxygen Species (ROS) DNA/RNA Synthesis	Cardiovascular Disease Cancer
Cysteinylglycine (L-Cysteinylglycine; Cys-Gly) TFA is a dipeptide formed by the peptide bond connection of cysteine and glycine. Cysteinylglycine TFA is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine TFA can reduce trivalent iron to divalent iron, driving the redox cycle of iron, generating reactive oxygen species (ROS), stimulating oxidative reactions, inducing lipid peroxidation in human plasma LDL lipoproteins, and causing oxidative damage to DNA base. Cysteinylglycine TFA can be used as a biomarker to assess ischemic heart disease and breast cancer, etc ^[1][2][3][4].

HY-P5081

Endotrophin (Mus musculus)	TGF-β Receptor Collagen	Inflammation/Immunology
Endotrophin (Mus musculus) is an adipokine, a cleavage fragment derived from Collagen VI, whose levels are elevated in adipose tissue and breast tumors of obese mice. Endotrophin (Mus musculus) activates the TGF-β signaling pathway and reduces the expression of hormone-sensitive lipase. Endotrophin (Mus musculus) induces adipogenesis, lipid accumulation, fibrosis, inflammation, angiogenesis, adipose tissue expansion, epithelial-mesenchymal transition, and insulin resistance; it also induces Cisplatin (HY-17394) resistance in cancer cells. Endotrophin (Mus musculus) can be used in research related to metabolic diseases such as obesity and type 2 diabetes, as well as cancers such as breast cancer .

HY-P1723A

Spexin TFA Neuropeptide Q TFA	Neuropeptide Y Receptor Apoptosis Ferroptosis Autophagy	Cardiovascular Disease Metabolic Disease
Spexin (Neuropeptide Q) TFA is a selective agonist of galanin receptors GAL2 and GAL3, and is a conserved peptide that functions as a neurotransmitter/neuromodulator and endocrine factor. Spexin TFA can function through both central and peripheral actions. Spexin TFA upregulates Beclin 1 to inhibit ferroptosis induced by excessive autophagy, reduces the uptake of long-chain fatty acids by adipocytes, and regulates energy metabolism by increasing lipid oxidation (e.g., reducing the respiratory exchange ratio in rodents). Spexin TFA improves cardiac function in the Doxorubicin hydrochloride (HY-15142)-induced cardiotoxicity model, protects mitochondrial membrane potential, and reduces iron accumulation and lipid peroxidation. Spexin TFA can be used to study obesity and its related metabolic disorders, cardiovascular diseases (e.g., cardioprotection), and side effects of tumor chemotherapy .

HY-114118C

Semaglutide sodium	GLP Receptor Insulin Receptor α-synuclein Apoptosis p38 MAPK Autophagy Bcl-2 Family	Neurological Disease Metabolic Disease Cancer
Semaglutide sodium is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide sodium promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide sodium also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide sodium has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide sodium can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-P5081A

Endotrophin (Mus musculus) TFA	TGF-β Receptor Collagen	Inflammation/Immunology
Endotrophin (Mus musculus) TFA is an adipokine, a cleavage fragment derived from Collagen VI, whose levels are elevated in adipose tissue and breast tumors of obese mice. Endotrophin (Mus musculus) TFA activates the TGF-β signaling pathway and reduces the expression of hormone-sensitive lipase. Endotrophin (Mus musculus) TFA induces adipogenesis, lipid accumulation, fibrosis, inflammation, angiogenesis, adipose tissue expansion, epithelial-mesenchymal transition, and insulin resistance; it also induces Cisplatin (HY-17394) resistance in cancer cells. Endotrophin (Mus musculus) TFA can be used in research related to metabolic diseases such as obesity and type 2 diabetes, as well as cancers such as breast cancer .

Cat. No.	Nombre del producto	Category	Target	Chemical Structure

HY-113402

Gamma-glutamylcysteine 4 Publications Verification γ-Glu-Cys	Structural Classification Human Gut Microbiota Metabolites Microorganisms Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Inflammation/Immunology Disease Research Fields Source Classification	Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine 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 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 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 .

HY-W001171

3-Hydroxyanthranilic acid 1 Publications Verification	Human Gut Microbiota Metabolites Monophenols Microorganisms Classification of Application Fields Ketones, Aldehydes, Acids Other Diseases Phenols Endogenous metabolite Disease Research Fields	Endogenous Metabolite
3-Hydroxyanthranilic acid is a tryptophan metabolite in the kynurenine pathway.3-hydroxyanthranilic acid has anti-inflammatory, neuroprotective, and lipid-lowering effects. 3-hydroxyanthranilic acid can be used for researches of cardiovascular diseases, tumors, and metabolic diseases .

HY-N7075

Inulin 4 Publications Verification	Structural Classification Human Gut Microbiota Metabolites Polysaccharides Classification of Application Fields Metabolic Disease Plants Compositae Endogenous metabolite Disease Research Fields Saccharides Sophora tomentosa L. Source Classification	Endogenous Metabolite
Inulin is an orally active prebiotic targeting the intestinal microbiota, selectively promoting the proliferation and activity of beneficial bacteria such as bifidobacteria and lactic acid bacteria, and playing a role in regulating the intestinal microecology. The functions of Inulin include: Fermentation by probiotics in the colon to produce short-chain fatty acids (such as butyrate and propionate), lowering the intestinal pH and inhibiting the overgrowth of harmful bacteria; Enhancing the intestinal barrier function and reducing endotoxin translocation; Directly scavenging free radicals (such as superoxide free radicals, hydroxyl free radicals) and activating antioxidant enzymes (SOD, CAT) to reduce oxidative stress. Inulin can also be used in the study of intestinal diseases (constipation, IBD), metabolic syndrome (diabetes, obesity) and liver damage by regulating glucose and lipid metabolism (such as reducing triglycerides, improving insulin sensitivity) and immune response (enhancing NK cell activity, inhibiting inflammatory factors)[1][2][3][4].

HY-W012722

4-Methyl-2-oxopentanoic acid 1 Publications Verification α-Ketoisocaproic acid	Human Gut Microbiota Metabolites Immune System Disorder Microorganisms Ketones, Aldehydes, Acids Disease markers Endogenous metabolite Source Classification	Endogenous Metabolite Autophagy mTOR SOD
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 .

HY-N9933

Tauro-β-muricholic acid 4 Publications Verification TβMCA	Structural Classification Human Gut Microbiota Metabolites Animals Endogenous metabolite Steroids Source Classification	FXR Apoptosis
Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC₅₀=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .

HY-113149A

Argininosuccinic acid disodium	Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Inflammation/Immunology Disease Research Fields Source Classification	Endogenous Metabolite Reactive Oxygen Species (ROS)
Argininosuccinic acid disodium is an intermediate metabolite in the urea cycle, and its level is associated with argininosuccinic aciduria. Argininosuccinic acid disodium can induce oxidative stress, leading to lipid and protein oxidation, reduction of glutathione, and decrease in antioxidant enzyme activity. Argininosuccinic acid disodium can be converted into guanidinosuccinic acid, a nitric oxide mimic, under the action of nitric oxide-derived free radicals. Argininosuccinic acid disodium can be used in the research of metabolic diseases, renal failure, nervous system diseases, etc .

HY-W015924

2-Hydroxyisobutyric acid	Classification of Application Fields Ketones, Aldehydes, Acids Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

HY-101036

Choline bitartrate 4 Publications Verification	Animals Ketones, Aldehydes, Acids Source Classification	mAChR Endogenous Metabolite
Choline bitartrate is a vitamin-like essential nutrient, can affect diseases such as liver disease, atherosclerosis and neurological disorders . Choline bitartrate is a precursor for the neurotransmitter acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism .

HY-143712

Allolithocholic acid 1 Publications Verification	Structural Classification Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Steroids Source Classification	Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR
Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC₅₀ = 2.7 μM) and RORγt inverse agonist (IC₅₀ = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .

HY-113110

Cysteinylglycine L-Cysteinylglycine; Cys-Gly; H-Cys-Gly-OH	Productos naturales Human Gut Microbiota Metabolites Microorganisms Disease markers Endocrine diseases Metabolic Disease Nervous System Disorder Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite Reactive Oxygen Species (ROS) DNA/RNA Synthesis
Cysteinylglycine (L-Cysteinylglycine; Cys-Gly) is a dipeptide formed by the peptide bond linkage between cysteine (Cysteine) and glycine (Glycine). Cysteinylglycine is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine reduces ferric iron to ferrous iron, drives the redox cycle of iron, generates reactive oxygen species (ROS), stimulates oxidative reactions, induces lipid peroxidation of human plasma LDL lipoproteins, and causes oxidative damage to DNA bases. Cysteinylglycine can be used as a biomarker to evaluate ischemic heart disease, breast cancer and other conditions .

HY-113402A

Gamma-glutamylcysteine TFA 4 Publications Verification γ-Glu-Cys TFA	Structural Classification Productos naturales Classification of Application Fields Endogenous metabolite Inflammation/Immunology Disease Research Fields Source Classification	Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
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 .

HY-N6677

β-Apo-8'-carotenal Apocarotenal	Other Terpenoids Structural Classification other families Classification of Application Fields Terpenoids Plants Disease Research Fields Source Classification Cancer	Cytochrome P450 DNA/RNA Synthesis
β-Apo-8'-carotenal (Apocarotenal), an orally active provitamin A carotenoid. β-Apo-8'-carotenal can induce the expression of CYP1A through the Ah receptor-dependent pathway. β-Apo-8'-carotenal can induce cancer cells DNA strand breaks and lipid peroxidation. β-Apo-8'-carotenal can be used for the researches of cancer and metabolic disease .

HY-N2392

Kukoamine A 1 Publications Verification	Cardiovascular Disease Alkaloids Structural Classification other families Classification of Application Fields Other Alkaloids Phenols Polyphenols Plants Disease Research Fields Source Classification	Parasite Lipoxygenase Opioid Receptor Apoptosis Autophagy Reactive Oxygen Species (ROS) Interleukin Related TNF Receptor PGE synthase COX
Kukoamine A, a spermine alkaloid, is an orally active and brain-penetrant component found in the root barks of Lycium chinense (L. chinense) Miller. Kukoamine A inhibits purified Crithidia fasciculata trypanothione reductase and soybean lipoxygenase, activates μ-opioid receptor. Kukoamine A can inhibt cancer cell proliferation, migration and invasion, cause G0/G1 phase cell cycle arrest and induce apoptosis. Kukoamine A exerts neuroprotective effect and can induce autophagy . Kukoamine A inhibits LPS (HY-D1056)-induced NO, ROS, PGE₂, TNF-α, IL-1β, IL-6 production and COX-2 activity. Kukoamine A reverses palmitic acid-induced insulin resistance, lipid accumulation, and oxidative stress via downregulation of Srebp-1c. Kukoamine A can be used for the research of cancer, infection, inflammation, metabolic and neurological disease, such as glioblastoma and Parkinson's disease .

HY-B1189

Meglutol Dicrotalic acid; 3-Hydroxy-3-methylglutaric acid	Cardiovascular Disease Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Disease Research Fields Source Classification	HMG-CoA Reductase (HMGCR) Autophagy Endogenous Metabolite
Meglutol is a lipid-lowering agent. Meglutol can reduces cholesterol, triglycerides, serum β-lipoprotein, and phospholipids, and inhibits the activity of HMG-CoA reductase (a rate-limiting enzyme in cholesterol biosynthesis). Meglutol can induce significant lipid oxidative damage in brain tissue. It is promising for research in the field of cardiovascular diseases and metabolic diseases .

HY-113149

Argininosuccinic acid	Human Gut Microbiota Metabolites Microorganisms Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Inflammation/Immunology Disease Research Fields Source Classification	Endogenous Metabolite Reactive Oxygen Species (ROS)
Argininosuccinic acid is an intermediate metabolite in the urea cycle, and its level is associated with argininosuccinic aciduria. Argininosuccinic acid can induce oxidative stress, leading to lipid and protein oxidation, reduction of glutathione, and decrease in antioxidant enzyme activity. Argininosuccinic acid can be converted into guanidinosuccinic acid, a nitric oxide mimic, under the action of nitric oxide-derived free radicals. Argininosuccinic acid can be used in the research of metabolic diseases, renal failure, nervous system diseases, etc .

HY-126359

1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine SLPC; 18:0-18:2 PC	Structural Classification Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Lipid Source Classification	Endogenous Metabolite
1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine (SLPC; 18:0-18:2 PC) is an endogenous phospholipid marker molecule in the glycerophospholipid metabolic pathway. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine is a core component of the phospholipid bilayer of biological membranes and a key responsive lipid for radiation injury and cardiometabolic diseases. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine constitutes the phospholipid bilayers of cell membranes and high-density lipoprotein (HDL), and regulates the core activity of lipoprotein functional homeostasis. The content of 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine in mouse serum shows a significant dose-dependent decrease with increasing ionizing radiation dose, and its level in human HDL also decreases significantly in metabolic syndrome. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine can serve as a biological dosimeter marker for ionizing radiation injury, and is used for rapid and accurate assessment of radiation absorbed dose in exposed individuals. 1-Stearoyl-2-linoleoyl-sn-glycero-3-phosphocholine can also act as a lipidomics research target for cardiometabolic diseases such as lipid metabolic syndrome and early-onset coronary heart disease .

HY-N0899

Wilforine	Cardiovascular Disease Structural Classification Classification of Application Fields Terpenoids Sesquiterpenes Celastraceae Tripterygium wilfordii Hook. f. Plants Disease Research Fields Source Classification	JAK STAT Wnt β-catenin
Wilforine is an orally active JAK-STAT pathway inhibitor with immunomodulatory effects and the ability to inhibit osteoclast fusion. Wilforine disrupts lipid raft integrity, reprograms cholesterol and glycosphingolipid metabolic pathways, regulates NF-κB and the complement system, and modulates the expression of various interleukins. Wilforine also inhibits the Wnt11/β-catenin signaling pathway and suppresses the proliferation of fibroblast-like synoviocytes. Wilforine can serve as a quality and pharmacokinetic marker for Tripterygium glycoside tablets, and can be applied to research on related diseases such as rheumatoid arthritis, inflammatory osteolysis, and SAPHO syndrome .

HY-120657

9-PAHSA	Structural Classification Classification of Application Fields Ketones, Aldehydes, Acids Other Diseases Endogenous metabolite Disease Research Fields Source Classification	CGRP Receptor NF-κB
9-PAHSA is an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

HY-N4124

Poricoic acid B	Triterpenes Structural Classification Classification of Application Fields Terpenoids Polyporaceae Poria cocos Plants Disease Research Fields Source Classification Cancer	NO Synthase TNF Receptor Interleukin Related
Poricoic acid B is a triterpenoid compound that can be isolated from Poria cocos. Poricoic acid B inhibits intracellular lipid accumulation and reduces the levels of hepatocyte injury markers. Poricoic acid B inhibits the production of NO, TNF-α, IL-1β and IL-6, thereby exerting anti-inflammatory activity. Poricoic acid B can be used in the research of metabolic dysfunction-associated fatty liver disease and inflammatory diseases ^[3].

HY-142026

Vitisin A (+)-Vitisin A	Structural Classification Vitis vinifera cv. Zalema Phenols Polyphenols Plants Vitaceae Source Classification	Caspase ERK NF-κB Influenza Virus PAK LDLR PPAR PCSK9 Androgen Receptor Keap1-Nrf2 Monoamine Oxidase Cholinesterase (ChE) IKK Wnt β-catenin Reactive Oxygen Species (ROS) Apoptosis Cuproptosis
Vitisin A ((+)-Vitisin A) is an orally active natural product with multiple pharmacological activities including anti-inflammatory, anti-tumor, anti-oxidant, anti-pathogenic microorganism, hypoglycemic and lipid-regulating, anti-osteoporotic, neuroprotective and cardiovascular protective effects. Vitisin A exhibits inhibitory effects on human AChE and MAO-B with IC₅₀ values of 1.29 µM and 4.94 µM, respectively. Vitisin A inhibits the ERK, MAPK, NF-κB, STAT1, HMGCR and TRAF6 pathways, downregulates the related phosphorylation and protein expression, while activates the Nrf2/HO-1 pathway and upregulates p21 expression. Vitisin A induces tumor cell apoptosis and cell cycle arrest, inhibits adipogenesis and lipid accumulation, while alleviates oxidative stress, suppresses inflammatory responses, blocks hepatic fibrosis, Cuproptosis and cholesterol synthesis, and increases the expression levels of central BDNF and TrkB. Vitisin A can be used in the research of tumors, infectious diseases, metabolic diseases, bone and joint diseases, liver diseases, skin injuries, as well as neurodegenerative and cognitive dysfunction-related diseases .

HY-N15841

C25 Ceramide (d18:1/25:0)	Structural Classification Lipid	Ceramidase
C25 Ceramide (d18:1/25:0) is an endogenous ultra-long-chain ceramide that antagonizes the detrimental effects of long-chain ceramides on insulin sensitivity. C25 Ceramide (d18:1/25:0) is specifically enriched in oxidative skeletal muscle fibers, where it serves dual roles in providing structural support to cell membranes and regulating cellular signaling. By participating in the regulation of lipid homeostasis within muscle fibers, C25 Ceramide (d18:1/25:0) helps maintain normal insulin signaling. C25 Ceramide (d18:1/25:0) is primarily utilized in research concerning metabolic diseases—particularly in mechanistic studies investigating the muscle fiber type-specific aspects of insulin resistance .

HY-101036R

Choline bitartrate (Standard)	Structural Classification Animals Ketones, Aldehydes, Acids Source Classification	Reference Standards mAChR Endogenous Metabolite
Choline (bitartrate) (Standard) is the analytical standard of Choline (bitartrate). This product is intended for research and analytical applications. Choline bitartrate is a vitamin-like essential nutrient, can affect diseases such as liver disease, atherosclerosis and neurological disorders . Choline bitartrate is a precursor for the neurotransmitter acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism .

HY-113402R

Gamma-glutamylcysteine (Standard) γ-Glu-Cys (Standard)	Structural Classification Human Gut Microbiota Metabolites Microorganisms Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine 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 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 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.

HY-W015924R

2-Hydroxyisobutyric acid (Standard)	Structural Classification Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	Reference Standards Endogenous Metabolite
2-Hydroxyisobutyric acid (Standard) is the analytical standard of 2-Hydroxyisobutyric acid. This product is intended for research and analytical applications. 2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

HY-113110A

Cysteinylglycine TFA L-Cysteinylglycine TFA; Cys-Gly TFA; H-Cys-Gly-OH TFA	Structural Classification Productos naturales Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite Reactive Oxygen Species (ROS) DNA/RNA Synthesis
Cysteinylglycine (L-Cysteinylglycine; Cys-Gly) TFA is a dipeptide formed by the peptide bond connection of cysteine and glycine. Cysteinylglycine TFA is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine TFA can reduce trivalent iron to divalent iron, driving the redox cycle of iron, generating reactive oxygen species (ROS), stimulating oxidative reactions, inducing lipid peroxidation in human plasma LDL lipoproteins, and causing oxidative damage to DNA base. Cysteinylglycine TFA can be used as a biomarker to assess ischemic heart disease and breast cancer, etc ^[1][2][3][4].

HY-N11924

Foenumoside B	Triterpenes Terpenoids Lysimachia foenum-graecum Hance Plants Primulaceae Source Classification	AMPK PPAR
Foenumoside B is a triterpene saponin isolated from Lysimachia foenum-graecum. Foenumoside B activates AMPK signaling, inhibits PPARγ-induced adipogenesis, and shifts lipid metabolism toward lipolysis. Foenumoside B can be used in the study of obesity and obesity-related metabolic diseases .

HY-113402AR

Gamma-glutamylcysteine TFA (Standard) γ-Glu-Cys TFA (Standard)	Structural Classification Productos naturales Endogenous metabolite Source Classification	Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis
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.

HY-113110R

Cysteinylglycine (Standard) L-Cysteinylglycine (Standard); Cys-Gly (Standard); H-Cys-Gly-OH (Standard)	Productos naturales Human Gut Microbiota Metabolites Microorganisms Disease markers Endocrine diseases Nervous System Disorder Endogenous metabolite Source Classification	Reference Standards Endogenous Metabolite Reactive Oxygen Species (ROS) DNA/RNA Synthesis
Cysteinylglycine (Standard) is the analytical standard of Cysteinylglycine. This product is intended for research and analytical applications. Cysteinylglycine is a dipeptide formed by the peptide bond linkage between cysteine (Cysteine) and glycine (Glycine). Cysteinylglycine is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine reduces ferric iron to ferrous iron, drives the redox cycle of iron, generates reactive oxygen species (ROS), stimulates oxidative reactions, induces lipid peroxidation of human plasma LDL lipoproteins, and causes oxidative damage to DNA bases. Cysteinylglycine can be used as a biomarker to evaluate ischemic heart disease, breast cancer and other conditions .

HY-B1189R

Meglutol (Standard) Dicrotalic acid (Standard); 3-Hydroxy-3-methylglutaric acid (Standard)	Structural Classification Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	HMG-CoA Reductase (HMGCR) Autophagy Endogenous Metabolite Reference Standards
Meglutol (Standard) is the analytical standard of Meglutol. This product is intended for research and analytical applications. Meglutol is a lipid-lowering agent. Meglutol can reduces cholesterol, triglycerides, serum β-lipoprotein, and phospholipids, and inhibits the activity of HMG-CoA reductase (a rate-limiting enzyme in cholesterol biosynthesis). Meglutol can induce significant lipid oxidative damage in brain tissue. It is promising for research in the field of cardiovascular diseases and metabolic diseases .

HY-143712R

Allolithocholic acid (Standard)	Structural Classification Endogenous metabolite Steroids Source Classification	Reference Standards Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR
Allolithocholic acid (Standard) is the analytical standard of Allolithocholic acid (HY-143712). This product is intended for research and analytical applications. Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC₅₀ = 2.7 μM) and RORγt inverse agonist (IC₅₀ = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .

HY-120657R

9-PAHSA (Standard)	Structural Classification Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	Reference Standards CGRP Receptor NF-κB
Flumethrin (Standard) is the analytical standard of Flumethrin. This product is intended for research and analytical applications. 9-PAHSA is an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

Cat. No.	Nombre del producto	Chemical Structure

HY-114118S3

Semaglutide-13C6,15N TFA

Semaglutide- ¹³C₆, ¹⁵N TFA is the ¹³C- and ¹⁵N-labeled Semaglutide TFA (HY-114118A). Semaglutide TFA is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-114118S1

Semaglutide-d8 tetraTFA

Semaglutide-d₈ tetraTFA is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-114118S

Semaglutide-d8

Semaglutide-d₈ is the deuterium labeled Semaglutide (HY-114118). Semaglutide is a long-acting, selective, competitive GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer .

HY-W770410

9-PAHSA-13C4

9-PAHSA- ¹³C₄ is ¹³C-labeled 9-PAHSA. 9-PAHSAis an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSAsignificantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSAinduces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSAregulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSAdoes not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSAcan be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

HY-143712S1

Allolithocholic Acid-d4

Allolithocholic Acid-d₄ (3α-hydoxy-5α-Cholaoic Acid-d₄, allo-LCA-d₄) is deuterium labeled Allolithocholic acid (HY-143712). Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC₅₀ = 2.7 μM) and RORγt inverse agonist (IC₅₀ = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .

HY-120657S

9-PAHSA-d4

9-PAHSA-d₄ is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

HY-144026S

9-PAHSA-d9

9-PAHSA-d9 is the deuterium labeled 9-PAHSA (HY-120657). 9-PAHSA is an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

HY-120657S1

9-PAHSA-d31

9-PAHSA-d₃₁ is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC₅₀=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .

HY-W355700S

1-Oleoyl-2-hydroxy-sn-glycero-3-phosphoethanolamine-d31

1-Oleoyl-2-hydroxy-sn-glycero-3-phosphoethanolamine-d₃₁ is the deuterium labeled 1-Oleoyl-2-hydroxy-sn-glycero-3-phosphoethanolamine (HY-W355700). 1-oleoyl-sn-glycero-3-phosphoethanolamine (LysoPE 18:1) is a lysophosphatidylethanolamine molecule involved in phospholipid metabolism, targeting cell membrane receptors (such as G protein-coupled receptors) to regulate cell signaling pathways. 1-oleoyl-sn-glycero-3-phosphoethanolamine may activate mitogen-activated protein kinase (MAPK) signaling, promote cell migration, regulate inflammatory responses and lipid metabolism, and has both pro-inflammatory and anti-inflammatory activities. 1-oleoyl-sn-glycero-3-phosphoethanolamine is mainly used in the screening of biomarkers for metabolic diseases (such as non-alcoholic fatty liver disease and obesity), as well as the study of the mechanism of lysophospholipids in cell membrane homeostasis and signal transduction .

Cat. No.	Nombre del producto		Classification

HY-W355700

1-Oleoyl-2-hydroxy-sn-glycero-3-phosphoethanolamine		Phospholipids
1-oleoyl-sn-glycero-3-phosphoethanolamine (LysoPE 18:1) is a lysophosphatidylethanolamine molecule involved in phospholipid metabolism, targeting cell membrane receptors (such as G protein-coupled receptors) to regulate cell signaling pathways. 1-oleoyl-sn-glycero-3-phosphoethanolamine may activate mitogen-activated protein kinase (MAPK) signaling, promote cell migration, regulate inflammatory responses and lipid metabolism, and has both pro-inflammatory and anti-inflammatory activities. 1-oleoyl-sn-glycero-3-phosphoethanolamine is mainly used in the screening of biomarkers for metabolic diseases (such as non-alcoholic fatty liver disease and obesity), as well as the study of the mechanism of lysophospholipids in cell membrane homeostasis and signal transduction .

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