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Cat. No. Product Name Target Research Areas 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 .
    Semaglutide
  • HY-N8518
    Malabaricone C
    3 Publications Verification

    		 Phospholipase p38 MAPK Apoptosis NF-κB Metabolic Disease Inflammation/Immunology Cancer
    Malabaricone C is an orally active and noncompetitive sphingomyelin synthase (SMS) inhibitor with IC50 values of 3 μM and 1.5 μM for SMS 1 and SMS 2, respectively. Malabaricone C reduces body weight gain, improves glucose tolerance, and decreases lipid accumulation in the liver, showing significant prevention of high fat diet-induced fatty liver in mice. Malabaricone C has anti-inflammatory effects, which is found in the fruits of Myristica cinnamomea King. Malabaricone C is promising for research of obesity and immunological disorders caused due to hyper-activation of T-cells .
    Malabaricone C
  • 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 .
    Semaglutide acetate
  • 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 .
    Semaglutide TFA
  • HY-125848
    Ginsenoside F2

    		Apoptosis AMPK PPAR p38 MAPK PI3K Akt GSK-3 Reactive Oxygen Species (ROS) SOD Caspase Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Ginsenoside F2 is an orally active bioactive compound that participates in the regulation of metabolism and inflammation. Ginsenoside F2 promotes the phosphorylation of AMPK and ACC, binds to PPARγ, inhibits the phosphorylation of MAPK, activates the PI3K/AKT/GSK-3β pathway, reduces GLRX expression, and regulates lipid metabolism. Ginsenoside F2 reduces ROS production and MDA levels, restores SOD activity in cells, and alleviates oxidative stress. Ginsenoside F2 induces cell apoptosis (Apoptosis) and increases the number of cleaved caspase-3-positive cells. Ginsenoside F2 reduces body weight gain, adipose tissue weight and serum lipid levels in obese mice, and activates the hepatic AMPK signaling pathway and the expression of antioxidant enzymes. Ginsenoside F2 alleviates atopic dermatitis in mice by inhibiting inflammation and reshaping the gut microbiota . Ginsenoside F2 is applicable to research related to insulin resistance, obesity, atopic dermatitis, liver cancer, glioblastoma and glioma .
    Ginsenoside F2
  • HY-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 .
    Zenagamtide sodium
  • HY-145632
    Pemvidutide

    ALT-801

    		 GLP Receptor GCGR Metabolic Disease
    Pemvidutide (ALT-801) is a GLP-1R/GCGR dual agonist, shows striking reductions in body weight, liver fat and serum lipids. Pemvidutide can be used in non-alcoholic steatohepatitis (NASH) and obesity research .
    Pemvidutide
  • 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 .
    Semaglutide (crude)
  • 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 .
    Semaglutide-13C6,15N TFA
  • HY-12642
    Diethylcarbamazine citrate
    1 Publications Verification

    		 Parasite Bacterial TNF Receptor Interleukin Related Infection Metabolic Disease Inflammation/Immunology
    Diethylcarbamazine citrate is an orally active microfilaricidal agent used originally in onchocerciasis and lymphatic filiariasis. Diethylcarbamazine citrate reduces eosinophil trafficking to the lung tissue and exerts anti-allergic effects. Diethylcarbamazine citrate reduces serum levels of leptin, TNF-α, IL-6, MCP-1, glucose, insulin, and triglycerides, and ameliorates insulin resistance without altering body, liver, or adipose tissue weights. Diethylcarbamazine citrate enhances reactive oxygen intermediate expression by polymorphonuclear neutrophils, increases lymphocyte proliferation, and inhibits actinomycetoma lesion development. Diethylcarbamazine citrate can be used for the researches of bronchial asthma, insulin resistance and infection .
    Diethylcarbamazine citrate
  • HY-B0633D
    Hyaluronic acid sodium (MW 200-1560)

    		CD44 Endogenous Metabolite Bacterial Akt PI3K Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Hyaluronic acid sodium (MW 200-1560) is a biopolymer composed of repeating disaccharide units, with a molecular weight of 200-1560. Hyaluronic acid sodium is a major component of the extracellular matrix (ECM). It is synthesized on the plasma membrane. Hyaluronic acid sodium exerts its effects by binding to receptors CD44 and RHAMM. Hyaluronic acid sodium activates PI3K-Akt signaling. Hyaluronic acid sodium also enhances cell invasion and angiogenesis by promoting or stimulating the binding of proteolytic MMP-9 to the cell surface. Elevated hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion, and angiogenesis in digestive system cancers. Hyaluronic acid sodium is involved in tissue remodeling and rapid cell proliferation in several physiological processes, including embryonic morphogenesis and wound healing. Hyaluronic acid sodium can be used as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid sodium can be used as a drug delivery carrier for sodium butyrate, enhancing its anti-proliferative activity against breast cancer cell lines. Hyaluronic acid sodium can lubricate the corneal endothelium. Hyaluronic acid sodium can improve tissue hydration and enhance the resistance of cells to mechanical damage. Hyaluronic acid sodium has been conjugated with antibodies to ensure that the active compound continues to exert its effects at the site of inflammation. Hyaluronic acid sodium can be used in research in the fields of osteoarthritis, ophthalmology, cosmetic dermatology, oncology, and liver diseases .
    Hyaluronic acid sodium (MW 200-1560)
  • HY-124529
    Lunularin

    		11β-HSD Endogenous Metabolite Metabolic Disease Inflammation/Immunology Cancer
    Lunularin is an inhibitor of 11β-hydroxysteroid dehydrogenase 1, with an IC50 of 45.44 μM and a Ki of 35.8 μM against human 11β-HSD1, and an IC50 of 17.39 μM and a Ki of 10.31 μM against rat 11β-HSD1. Lunularin upregulates the transcription levels of Sirt1 and Hmox1 genes in the liver. Lunularin reduces food intake and body weight gain, and decreases blood glucose levels in mice fed a high-fat diet. Lunularin inhibits LPS-induced TLR4-mediated NF-κB pathway activation and nitric oxide production. Lunularin inhibits the proliferation and colony formation of renal cancer and colon cancer cells, and exhibits cancer cell-specific cytotoxicity. Lunularin binds to the steroid-binding site of human 11β-HSD1 and the steroid/NADPH-binding region of rat 11β-HSD1, but does not inhibit 11β-HSD2 or mouse 11β-HSD1. Lunularin can be used in research related to diet-induced obesity, renal cancer, colorectal cancer, inflammatory diseases and metabolic syndrome .
    Lunularin
  • 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 .
    Zenagamtide
  • 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 .
    Semaglutide-d8 tetraTFA
  • 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 .
    Semaglutide-d8
  • HY-P10302A
    GLP-1R/GIPR agonist-1 (soduim)

    		GLP Receptor Metabolic Disease Inflammation/Immunology
    GLP-1R/GIPR agonist-1 sodium is a dual GLP-1/GIP receptor agonist, with an EC50 of 0.57 nM for GLP-1R and an EC50 of 0.75 nM for GIPR. GLP-1R/GIPR agonist-1 sodium reduces food intake, inhibits weight gain, repairs islet damage, improves glucose tolerance, regulates serum lipid and liver enzyme levels, ameliorates hepatic vacuolization, reduces hepatic fat accumulation, delays the progression of hepatic fibrosis, and exhibits long-lasting hypoglycemic activity. GLP-1R/GIPR agonist-1 sodium can be used in research related to type 2 diabetes, obesity, and non-alcoholic steatohepatitis .
    GLP-1R/GIPR agonist-1 (soduim)
  • HY-N5112A
    β,β-Dimethylacrylalkannin
    3 Publications Verification

    Arnebin 1

    		 FGFR Necroptosis Apoptosis CDK JNK Inflammation/Immunology
    β,β-Dimethylacrylalkannin (Arnebin 1) is an orally active FGFR1 inhibitor (IC50=2.5 μM) and the main active component of Lithospermum erythrorhizon. β,β-Dimethylacrylalkannin blocks downstream signaling by binding to the ATP pocket of FGFR1, and regulates the CDK1/Cdc25C pathway and ROS-JNK axis, thereby inducing G2/M phase arrest, necrosis and apoptosis in cancer cells, and inhibiting tumor proliferation. β,β-Dimethylacrylalkannin also acts as a colistin adjuvant to disrupt the cell membrane of Gram-negative bacteria. β,β-Dimethylacrylalkannin exhibits significant tumor-inhibitory effects with no obvious toxicity in PDX models, but chronic exposure to high doses may alter the relative lung/liver weights of rats, while acute exposure to high doses causes responses such as reduced motor activity. β,β-Dimethylacrylalkannin finds wide application in studies related to hepatocellular carcinoma, colorectal cancer, colistin-resistant bacterial infections, hepatitis and psoriasis .
    β,β-Dimethylacrylalkannin
  • HY-19870C
    Setmelanotide monoacetate
    5+ Cited Publications

    RM-493 monoacetate; BIM-22493 monoacetate; IRC-022493 monoacetate

    		 Melanocortin Receptor Calmodulin AMPK Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Setmelanotide monoacetate (RM-493 monoacetate) is a blood-brain barrier-permeable, selective MC4R agonist with a Ki value of 2.1 nM for hMC4R. Setmelanotide monoacetate activates the CaMKK2/AMPK signaling pathway. Setmelanotide monoacetate mediates body weight homeostasis, feeding regulation and energy expenditure modulation; it reduces food intake, induces weight loss, decreases obesity severity, increases daytime activity and energy expenditure, lowers levels of leptin, triglycerides, fasting insulin and diastolic blood pressure, improves insulin sensitivity, glucose tolerance and fatty liver condition, and reverses respiratory depression. Setmelanotide monoacetate is applicable to research related to obesity, hyperinsulinemia, fatty liver and respiratory depression .
    Setmelanotide monoacetate
  • HY-177704
    ACSL5-IN-1

    		ACSL Family Drug Derivative Metabolic Disease Cancer
    ACSL5-IN-1 (Compound A) is an ACSL5 inhibitor with body weight-reducing activity. ACSL5-IN-1 inhibits ACSL5, an enzyme linked to fatty acid metabolism. ACSL5-IN-1 reduces body weight in diet-induced obesity mice. ACSL5-IN-1 can be used for the research of obesity, metabolic dysfunction-associated steatohepatitis, metabolic syndrome, non-alcoholic fatty liver disease, type 2 diabetes, acute myeloid leukemia, colorectal cancer, and breast cancer .
    ACSL5-IN-1
  • HY-N0046
    Notoginsenoside Fe

    Notoginseng triterpenes; Ginsenoside Mb

    		 Apoptosis Src Neurological Disease Metabolic Disease Cancer
    Notoginsenoside Fe (Notoginseng triterpenes; Ginsenoside Mb) is a saponin with anti-obesity and anti-neuroblastoma activities. Notoginsenoside Fe can be isolated from leaves of Panax notoginseng. Notoginsenoside Fe specifically activates paraventricular nucleus neurons in the hypothalamus, effectively reducing body weight, improving fasting blood glucose and protecting liver function by decreasing food intake, increasing resting metabolic rate and enhancing energy expenditure. Notoginsenoside Fe also inhibits the c-Src signaling pathway, blocks the proliferation and viability of human neuroblastoma cells, while improving mitochondrial dysfunction and alleviating apoptosis. Notoginsenoside Fe can be used in studies related to diet-induced obesity and neuroblastoma .
    Notoginsenoside Fe
  • HY-156397
    HTH-02-006

    		AMPK YAP Cancer
    HTH-02-006 is a NUAK2 inhibitor, with an IC50 value of 126 nM. HTH-02-006 inhibits NUAK2-mediated signaling by reducing phosphorylation of its substrate MYPT1 at S445 and downstream MLC. HTH-02-006 shows growth inhibitory efficacy in YAP-high cancer cells (HuCCT-1, SNU475). HTH-02-006 significantly suppresses YAP-induced hepatomegaly (reduced liver/body weight ratio) in TetO-YAP S127A transgenic mice and demonstrates significant anti-tumor efficacy in mice bearing HMVP2 prostate cancer allografts. HTH-02-006 can be used for the study of liver cancer and prostate cancer .
    HTH-02-006
  • HY-116568
    Prothioconazole

    JAU-6476

    		 Fungal Cytochrome P450 Microtubule/Tubulin Mitochondrial Metabolism DNA/RNA Synthesis Apoptosis Fatty Acid Synthase (FASN) Infection Metabolic Disease Endocrinology
    Prothioconazole is an orally active broad-spectrum fungicide. Prothioconazole weakly inhibits CaCYP51 activity in Candida albicans, with an apparent IC50 of approximately 120 μM. Prothioconazole disrupts Microtubule stability by reducing the acetylation level of α-tubulin. Prothioconazole induces Mitochondrial dysfunction, oxidative stress, DNA damage, and Apoptosis. Prothioconazole accumulates 14-methylated sterols and depletes ergosterol in cells, culture media, plants, and animals. Prothioconazole interferes with pyruvate metabolism and glycolysis/gluconeogenesis processes in mouse liver, downregulates Fasn mRNA expression, and induces hepatotoxicity and renal metabolic disorders. Prothioconazole reduces the fertility of female mice. Prothioconazole inhibits body weight gain and increases liver/kidney indices in mice. Prothioconazole can be used in studies related to candidiasis .
    Prothioconazole
  • HY-N14035
    Garcinia cambogia extract

    		FABP PPAR Metabolic Disease
    Garcinia cambogia extract is an orally active anti-obesity agent . Garcinia cambogia extract upregulates the gene expression of aP2, SREBP1c, PPARγ2 and C/EBPα. Garcinia cambogia extract reduces the rate of body weight gain, visceral fat accumulation, lipid levels in blood and liver, as well as plasma insulin and leptin levels . Garcinia cambogia extract ameliorates high-fat diet-induced obesity .
    Garcinia cambogia extract
  • HY-12642A
    Diethylcarbamazine
    1 Publications Verification

    		 Parasite Bacterial TNF Receptor Interleukin Related Infection Metabolic Disease Inflammation/Immunology
    Diethylcarbamazine is an orally active microfilaricidal agent used originally in onchocerciasis and lymphatic filiariasis. Diethylcarbamazine reduces eosinophil trafficking to the lung tissue and exerts anti-allergic effects. Diethylcarbamazine reduces serum levels of leptin, TNF-α, IL-6, MCP-1, glucose, insulin, and triglycerides, and ameliorates insulin resistance without altering body, liver, or adipose tissue weights. Diethylcarbamazine enhances reactive oxygen intermediate expression by polymorphonuclear neutrophils, increases lymphocyte proliferation, and inhibits actinomycetoma lesion development. Diethylcarbamazine can be used for the researches of bronchial asthma, insulin resistance and infection .
    Diethylcarbamazine
  • 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 .
    Tartronic acid
  • HY-N4177
    Rubrofusarin gentiobioside

    Rubrofusarin-6-β-gentiobioside

    		 Phosphatase Monoamine Oxidase PPAR mTOR AMPK Metabolic Disease
    Rubrofusarin gentiobioside (Rrubrofusarin-6-β-gentiobioside) is an orally active weak inhibitor of PTP1B and MAO-A (IC50 >100 μM), and its glycosylation modification results in lower biological activity than its aglycone Rubrofusarin (HY-130307). Rubrofusarin gentiobioside promotes AMPK phosphorylation in an LKB1-independent manner and inhibits the mTOR signaling pathway, thereby downregulating the expressions of PPARγ, C/EBPα, as well as FAS, LPL and aP2. Rubrofusarin gentiobioside inhibits lipid accumulation, reduces body weight and epididymal white adipose tissue volume, improves fatty liver, and shows no cytotoxicity to hepatocytes. Rubrofusarin gentiobioside is widely used in obesity-related studies .
    Rubrofusarin gentiobioside
  • HY-145632A
    Pemvidutide TFA

    ALT-801 TFA

    		 GLP Receptor GCGR Metabolic Disease
    Pemvidutide (ALT-801) TFA is a GLP-1R/GCGR dual agonist, shows striking reductions in body weight, liver fat and serum lipids. Pemvidutide TFA can be used in non-alcoholic steatohepatitis (NASH) and obesity research .
    Pemvidutide TFA
  • HY-168049
    ZLY06

    		PPAR Akt Metabolic Disease
    ZLY06 is an orally active dual agonist of peroxisome proliferator-activated receptor (PPAR) δ and γ (PPAR δ: EC50=341 nM; PPAR γ: EC50=237 nM). ZLY06 induces hepatic lipid accumulation by inhibiting the phosphorylation of AKT1, mediating the upregulation of CD36. In addition, ZLY06 significantly improves glucose and lipid metabolism without increasing body weight, and alleviates fatty liver by promoting β-oxidation of fatty acids and inhibiting hepatic lipogenesis .
    ZLY06
  • HY-W020788
    Benoxacor

    CGA 154281

    		 Environmental Pollutants Glutathione S-transferase Estrogen Receptor/ERR Pregnane X Receptor (PXR) FXR Metabolic Disease Cancer
    Benoxacor (CGA 154281) is a herbicide safener and xenobiotic metabolism regulator. Benoxacor protects maize from the toxicity of metolachlor mainly by inducing detoxifying enzymes such as Glutathione S-transferase. Benoxacor also activates FXR, PXR and ERRα, and inhibits aromatase (aromatase). However, Benoxacor exhibits potential subacute oral toxicity and a high risk of hepatotoxicity in animal models. Benoxacor induces reactive oxygen species accumulation, interferes with embryonic heart development, and causes increased liver and kidney weights as well as alterations in gut microbiota in mice. Benoxacor can be used in studies related to hepatic steatosis, infertility, breast cancer and developmental toxicity .
    Benoxacor
  • HY-B1341
    Norethynodrel

    Enidrel; SC-4642; NSC 15432

    		 Endogenous Metabolite Progesterone Receptor Cancer
    Norethynodrel (Enidrel; SC-4642) is an orally active progestogen analog that reduces estrogen-like effects and enhances progestogen-like responses in endometrial stromal cells. Norethynodrel also promotes cell maturation and predecidual cell formation by inducing organelle hyperplasia and glycogen accumulation. Norethynodrel competitively inhibits drug-metabolizing enzymes in rat liver microsomes, thereby prolonging Pentobarbital sleep time, while exhibiting multiple effects including reduced body weight gain, attenuated heart rate elevation and ovulation inhibition. In mouse models, Norethynodrel significantly increases the incidence of mammary adenocarcinoma, cervical cancer and pituitary tumors. Norethynodrel can be used for mechanism research on related diseases such as mammary adenocarcinoma, cervical cancer, ovarian tubular adenoma and pituitary adenoma .
    Norethynodrel
  • HY-159595
    PCSK9-IN-29

    		LDLR PCSK9 Metabolic Disease Inflammation/Immunology
    PCSK9-IN-29 is a lipid-lowering agent. PCSK9-IN-29 can increase low-density lipoprotein receptor (LDLR) protein expression and decrease PCSK9 protein expression in hepG2 cells. PCSK9-IN-29 can reduce the levels of serum LDL-C, TC, and liver enzyme ALT in crab eating macaques fed a high-fat diet, lower body weight and fat, and increase bone mineral content. PCSK9-IN-29 can be used for research on non-alcoholic fatty liver disease and obesity .
    PCSK9-IN-29
  • HY-W451406B
    NH2-PEG1000-NH2

    		Drug Intermediate Biochemical Assay Reagents Metabolic Disease
    NH2-PEG1000-NH2 is a double-ended amino polyethylene glycol with a number-average molecular weight of 1000, which serves as a synthetic raw material for adamantyl polyethylene glycol amine. NH2-PEG1000-NH2 can be used for the preparation of reduction-responsive liver-targeted polymeric micelles .
    NH2-PEG1000-NH2
  • HY-P3491
    Pegloxenatide

    Polyethylene glycol loxenatide; PEX 168

    		 GCGR PI3K Akt Reactive Oxygen Species (ROS) Autophagy Interleukin Related Sirtuin AMPK Apoptosis Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Pegloxenatide (Polyethylene glycol loxenatide) is a long-acting glucagon-like peptide-1 receptor (GLP-1RA) agonist. Pegloxenatide has various activities such as lowering blood glucose, lowering blood lipids, improving body weight, anti-inflammation, promoting wound healing, protecting the liver, and protecting the heart. Pegloxenatide can be used in the research of type 2 diabetes and its multiple complications .
    Pegloxenatide
  • HY-W001925
    7-Methoxy-1-tetralone

    		Apoptosis NF-κB c-Met/HGFR Akt MMP Cancer
    7-Methoxy-1-tetralone is a potent antitumor agent. 7-Methoxy-1-tetralone inhibits cancer cell proliferation and migration, and induces hepatocellular carcinoma cell (HCC) apoptosis. 7-Methoxy-1-tetralone decreased the protein levels of NF-κB, matrix metallopeptidase 2 (MMP2)/MMP9, and p-AKT. 7-Methoxy-1-tetralone showed antitumor activity in nude mice and had no effect on body weight and liver, spleen and organ index .
    7-Methoxy-1-tetralone
  • HY-W020788R
    Benoxacor (Standard)

    CGA 154281 (Standard)

    		 Reference Standards Glutathione S-transferase Estrogen Receptor/ERR Pregnane X Receptor (PXR) FXR Others
    Benoxacor (Standard) is the analytical standard of Benoxacor. This product is intended for research and analytical applications. Benoxacor (CGA 154281) is a herbicide safener and xenobiotic metabolism regulator. Benoxacor protects maize from the toxicity of metolachlor mainly by inducing detoxifying enzymes such as Glutathione S-transferase. Benoxacor also activates FXR, PXR and ERRα, and inhibits aromatase (aromatase). However, Benoxacor exhibits potential subacute oral toxicity and a high risk of hepatotoxicity in animal models. Benoxacor induces reactive oxygen species accumulation, interferes with embryonic heart development, and causes increased liver and kidney weights as well as alterations in gut microbiota in mice. Benoxacor can be used in studies related to hepatic steatosis, infertility, breast cancer and developmental toxicity .
    Benoxacor (Standard)
  • HY-119449
    Florantyrone

    Zanchol

    		 Others Inflammation/Immunology
    Florantyrone (Zanchol) is a bile-promoting agent. Florantyrone increases the volume of bile rather than the content of bile acids. Zanchol can stimulate the synthesis of cholesterol in the liver, significantly raising the plasma cholesterol level, increasing the weight of the liver, but has no significant effect on the synthesis of cholesterol in the intestine. Florantyrone can be used in research on biliary motility disorders .
    Florantyrone
  • HY-161985
    PPARγ-IN-3

    		PPAR Metabolic Disease
    PPARγ-IN-3 (compound 9ga) is a potent and orally active PPARγ inhibitor. PPARγ-IN-3 reduces triglyceride (TG) accumulation with low cytotoxicity. PPARγ-IN-3 preventes the excessive growth of body weight and lessened fat mass as well as liver mass, decreases lipid accumulation in the liver and blood. PPARγ-IN-3 has the potential for the research of diet-induced obesity .
    PPARγ-IN-3
  • HY-N8518R
    Malabaricone C (Standard)

    		Reference Standards Phospholipase p38 MAPK Apoptosis NF-κB Metabolic Disease Inflammation/Immunology Cancer
    Malabaricone C is an orally active and noncompetitive sphingomyelin synthase (SMS) inhibitor with IC50 values of 3 μM and 1.5 μM for SMS 1 and SMS 2, respectively. Malabaricone C reduces body weight gain, improves glucose tolerance, and decreases lipid accumulation in the liver, showing significant prevention of high fat diet-induced fatty liver in mice. Malabaricone C has anti-inflammatory effects, which is found in the fruits of Myristica cinnamomea King. Malabaricone C is promising for research of obesity and immunological disorders caused due to hyper-activation of T-cells .
    Malabaricone C (Standard)
  • HY-12642AR
    Diethylcarbamazine (Standard)

    		Reference Standards Parasite Bacterial TNF Receptor Interleukin Related Infection Metabolic Disease Inflammation/Immunology
    Diethylcarbamazine (Standard) is the analytical standard of Diethylcarbamazine (HY-12642A). This product is intended for research and analytical applications. Diethylcarbamazine is an orally active microfilaricidal agent used originally in onchocerciasis and lymphatic filiariasis. Diethylcarbamazine reduces eosinophil trafficking to the lung tissue and exerts anti-allergic effects. Diethylcarbamazine reduces serum levels of leptin, TNF-α, IL-6, MCP-1, glucose, insulin, and triglycerides, and ameliorates insulin resistance without altering body, liver, or adipose tissue weights. Diethylcarbamazine enhances reactive oxygen intermediate expression by polymorphonuclear neutrophils, increases lymphocyte proliferation, and inhibits actinomycetoma lesion development. Diethylcarbamazine can be used for the researches of bronchial asthma, insulin resistance and infection .
    Diethylcarbamazine (Standard)
  • HY-12642R
    Diethylcarbamazine citrate (Standard)

    		Reference Standards Parasite Bacterial TNF Receptor Interleukin Related Infection Metabolic Disease Inflammation/Immunology
    Diethylcarbamazine citrate (Standard) is the analytical standard of Diethylcarbamazine citrate (HY-12642). This product is intended for research and analytical applications. Diethylcarbamazine citrate is an orally active microfilaricidal agent used originally in onchocerciasis and lymphatic filiariasis. Diethylcarbamazine citrate reduces eosinophil trafficking to the lung tissue and exerts anti-allergic effects. Diethylcarbamazine citrate reduces serum levels of leptin, TNF-α, IL-6, MCP-1, glucose, insulin, and triglycerides, and ameliorates insulin resistance without altering body, liver, or adipose tissue weights. Diethylcarbamazine citrate enhances reactive oxygen intermediate expression by polymorphonuclear neutrophils, increases lymphocyte proliferation, and inhibits actinomycetoma lesion development. Diethylcarbamazine citrate can be used for the researches of bronchial asthma, insulin resistance and infection .
    Diethylcarbamazine citrate (Standard)
  • HY-W093416
    3,3-Azo-1-butanol

    		TRP Channel Metabolic Disease
    3,3-Azo-1-butanol is an orally active hypoglycemic agent. 3,3-Azo-1-butanol increases liver weight and induces fat infiltration .
    3,3-Azo-1-butanol
  • HY-W040305
    2,6-Dichloro-4-nitroaniline

    		Environmental Pollutants Fungal Mitochondrial Metabolism Herbicide Infection
    2,6-Dichloro-4-nitroaniline is an orally active Herbicide, Fungicide and uncoupler. 2,6-Dichloro-4-nitroaniline uncouples oxidative phosphorylation and inhibits electron transport. 2,6-Dichloro-4-nitroaniline induces biphenyl hydroxylase activity in rat liver. 2,6-Dichloro-4-nitroaniline increases the relative liver weight of rats via hepatomegaly without altering their body weight .
    2,6-Dichloro-4-nitroaniline
  • HY-P11610
    KBP-089

    		Amylin Receptor CGRP Receptor Metabolic Disease
    KBP-089 is a dual Amylin and Calcitonin Receptor agonist. KBP-089 reduces body weight, decreases adipose tissue mass and improves glucose tolerance in obese rats. KBP-089 also eliminates lipid accumulation in the liver and muscle, and ameliorates glycemic homeostasis and insulin sensitivity. KBP-089 is applicable to the research of diseases such as obesity and type 2 diabetes .
    KBP-089
  • HY-181091
    α-Glucosidase-IN-109

    		Glycosidase Metabolic Disease
    α-Glucosidase-IN-109 is an orally active α-glucosidase inhibitor with an IC50 of 0.0136 μM. α-Glucosidase-IN-109 modulates carbohydrate and lipid metabolism, reduces fasting blood glucose levels, alleviates weight loss, and exhibits protective effects on liver and kidney function. α-Glucosidase-IN-109 can be used in research related to type 2 diabetes .
    α-Glucosidase-IN-109
  • 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 .
    Semaglutide sodium
  • HY-182287
    PRDX1-IN-4

    		Reactive Oxygen Species (ROS) NOD-like Receptor (NLR) Metabolic Disease
    PRDX1-IN-4 is a PRDX1 inhibitor with an IC50 of 122 nM against human targets and high subtype selectivity. PRDX1-IN-4 covalently binds to PRDX1 to promote ROS accumulation. PRDX1-IN-4 inhibits NLRP3 inflammasome activation, blocks hepatic stellate cell activation and reduces collagen deposition. PRDX1-IN-4 induces apoptosis in activated hepatic stellate cells. PRDX1-IN-4 has good safety profile, with no significant body weight loss or hepatotoxicity observed in mice at a dose of 20 mg/kg. PRDX1-IN-4 ameliorates CCl4-induced liver injury and liver fibrosis in mice at a dose of 1 mg/kg. PRDX1-IN-4 can be used for the research of liver fibrosis .
    PRDX1-IN-4
  • HY-N19083
    Tecomella undulata extract

    		Bacterial Inflammation/Immunology
    Tecomella undulata Extract, also known as Rohida extract, is a valuable botanical extract derived from the bark and leaves of the Tecomella undulata plant native to the Indian Thar Desert and is rich in bioactive compounds such as flavonoids, quinones, triterpenoids, and other phytochemicals that contribute to its diverse therapeutic properties. This extract is widely recognized for its hepatoprotective effects demonstrated through its ability to protect against liver damage induced by toxins such as paracetamol and carbon tetrachloride by normalizing elevated liver enzyme levels reducing oxidative stress and improving liver function. Additionally, it exhibits significant anti-inflammatory activity comparable to standard drugs like indomethacin and has been used to treat conditions like ascites and hepatosplenomegaly while also showing immunomodulatory effects by enhancing both humoral and cell-mediated immune responses and possessing antimicrobial properties that make it effective against various pathogens. Recent research suggests that Tecomella undulata may have potential in managing nonalcoholic steatohepatitis (NASH) by reducing body weight insulin resistance and improving liver function markers making it a versatile natural remedy with significant applications in hepatoprotection anti-inflammation and immune support.
    Tecomella undulata extract
  • HY-181709
    TPM003

    TG062

    		 GLP Receptor GCGR Metabolic Disease Inflammation/Immunology
    TPM003 (TG062) is a triple agonist of GLP-1R, GIPR and GCGR, with EC50 values of 33.9, 12.5 and 92.9 pM, respectively. TPM003 suppresses appetite, regulates blood glucose, enhances insulin sensitivity, reduces gastrointestinal intolerance, promotes hepatic lipid mobilization and increases energy expenditure. TPM003 induces weight loss, improves metabolic parameters, reverses hepatic steatosis and optimizes liver function markers. TPM003 is applicable for research on obesity and non-alcoholic steatohepatitis .
    TPM003
  • HY-183878
    Zincov

    		Bacterial Infection Metabolic Disease
    Zincov is an orally active hydroxamic acid derivative and bacterial metalloproteinase inhibitor. Zincov blocks chloride ion binding by binding to the active site of thermolysin, thereby inhibiting the hydrolysis and blood coagulation reactions catalyzed by this enzyme. Meanwhile, Zincov attenuates cytotoxicity, prevents protein degradation and ZO-1 rearrangement without affecting the functions of other common proteases. Zincov exhibits blood glucose-regulating and antioxidant activities; it reduces blood glucose levels and increases liver dry weight in diabetic rats, but elevates blood glucose levels in normal rats. Zincov is widely used in studies related to cholera and diabetes .
    Zincov
  • HY-119578
    Imiprothrin

    		Cytochrome P450 Cancer
    Imiprothrin is an inducer that induces CYP1A2 and metallothionein 1a, with significant genotoxicity and cytotoxicity. In rat hepatocytes, Imiprothrin initiates detoxification responses by triggering the overexpression of these two genes. Imiprothrin induces chromosomal aberrations and micronucleus formation in rat bone marrow cells, and causes DNA damage in hepatocytes. Imiprothrin triggers oxidative stress in rats, leading to lipid peroxidation, excessive reactive oxygen species production and redox imbalance, which in turn impairs liver and kidney functions and causes tissue damage. Imiprothrin inhibits weight gain in mice, and even causes high mortality in female mice at high doses. However, it shows no carcinogenicity in rat experiments; among relevant indicators, aspartate aminotransferase and total protein are identified as sensitive toxicity biomarkers .
    Imiprothrin

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