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liver injury diseases

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Cat. No. Product Name Target Research Areas Chemical Structure
  • 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 .
    Gamma-glutamylcysteine
  • HY-B0766
    Bicyclol

    SY801

    		 Autophagy Apoptosis HBV HCV HSP Reactive Oxygen Species (ROS) Bcl-2 Family Glutathione S-transferase p38 MAPK NF-κB Microtubule/Tubulin ERK JNK TNF Receptor Interleukin Related CDK Cyclin G-associated Kinase (GAK) mTOR P-glycoprotein Ferroptosis Infection Inflammation/Immunology Cancer
    Bicyclol (SY801) is an orally active derivative of the traditional Chinese medicine Schisandra chinensis, which has antiviral, anti-inflammatory, immunomodulatory, antioxidant, anti-steatosis, anti-fibrotic and anti-tumor activities. Bicyclol regulates the expression of heat shock proteins and plays an anti-apoptosis role in hepatocytes. Bicyclol reduces the activation of NF-κB and the levels of inflammatory factors in hepatocytes infected with hepatitis C virus (HCV) by inhibiting the activation of the ROS-MAPK-NF-κB pathway, and prevents ferroptosis in acute liver injury. Bicyclol can change the expression of Mdr-1, GSH/GST and Bcl-2, increase the intracellular concentration of anticancer drugs, and sensitize drug-resistant cells to anticancer drugs. Bicyclol inhibits the proliferation of human malignant hepatoma cells by regulating the PI3K/AKT pathway and the Ras/Raf/MEK/ERK pathway. Bicyclol can be used in the study of chronic hepatitis, acute liver injury, nonalcoholic fatty liver disease, liver fibrosis and hepatocellular carcinoma .
    Bicyclol
  • HY-N0010
    Geniposidic acid
    5+ Cited Publications

    		 FXR Sirtuin TNF Receptor Interleukin Related Metabolic Disease
    Geniposidic acid is an orally active FXR modulator and SIRT6 activator. Geniposidic acid binds to the Ser332 and His447 sites on the FXR ligand-binding domain, thereby driving nuclear translocation, coactivator recruitment, and transcription of downstream bile acid and cholesterol metabolism-related genes. Geniposidic acid improves metabolic dysfunction-related fatty liver disease by activating the SIRT6 signaling pathway. Geniposidic acid inhibits inflammation and modulates gut microbiota to alleviate colitis. Geniposidic acid can be used in research on drug-induced liver injury, inflammatory bowel disease, metabolic dysfunction-related fatty liver disease, and metabolic dysfunction-related steatohepatitis .
    Geniposidic acid
  • HY-148013
    K284-6111
    1 Publications Verification

    		 Glycosidase Amyloid-β NF-κB COX ERK NO Synthase Interleukin Related Neurological Disease Inflammation/Immunology
    K284-6111 is a high-affinity and orally active CHI3L1 inhibitor, and inhibits CHI3L1 expression. K284-6111 inhibits ERK and NF-κB pathway. K284-6111 suppresses nuclear translocation of p50 and p65, and phosphorylation of IκB. K284-6111 improves memory dysfunction by alleviating amyloidogenesis and neuroinflammation, with the reduction of inflammatory proteins (eg: iNOS, COX-2, GFAP, and Iba-1). K284-6111 reduces atopic-like skin inflammation and inhibits LPS (HY-D1056) -induced liver injury. K284-6111 can be used for the study of Alzheimer's diseases and sepsis like hepatic injury .
    K284-6111
  • HY-W008947
    SEW​2871
    5+ Cited Publications

    		 LPL Receptor ERK Akt Neurological Disease Metabolic Disease Inflammation/Immunology
    SEW2871 is an orally active, potent, highly selective S1P1 (sphingosine-1-phosphate type 1 receptor) agonist, with an EC50 of 13.8 nM. SEW2871 activates ERK, Akt, and Rac signaling pathways and induces S1P1 internalization and recycling. SEW2871 reduces lymphocyte numbers in blood. SEW2871 can be used for the research of diabetes, Alzheimer’s disease, liver fibrosis, and inflammatory responses .
    SEW​2871
  • HY-A0077
    Perphenazine
    3 Publications Verification

    		 Dopamine Receptor Histamine Receptor 5-HT Receptor Adrenergic Receptor Apoptosis Autophagy Neurological Disease Inflammation/Immunology Endocrinology Cancer
    Perphenazine is an orally active dopamine receptor and histamine-1 receptor antagonist, with Ki values of 0.56 nM (D2), 0.43 nM (D3), 6 nM (5-HT2A), respectively. Perphenazine also binds to Alpha-1A adrenergic receptor. Perphenazine inhibits cancer cell proliferation, and induces apoptosis. Perphenazine can be used in the research of mental disease, cancer, inflammation .
    Perphenazine
  • 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 .
    Gamma-glutamylcysteine TFA
  • HY-Y1147
    Diethyl maleate
    1 Publications Verification

    Maleic acid diethyl ester

    		 Biochemical Assay Reagents Others
    Diethyl maleate (DEM) is an orally available, effective glutathione (GSH) depletor that crosses the blood-brain barrier. Diethyl maleate covalently binds irreversibly to GSH via glutathione S-transferase with an in vitro IC50 of 0.1-0.5 mM. Diethyl maleate selectively depletes GSH in liver, lung, and brain tissues, exacerbating oxidative stress and enhancing hyperbaric oxygen toxicity. Diethyl maleate promotes precursor amino acid uptake and in turn promotes GSH synthesis by upregulating the activity of the cystine-glutamate transporter XO -. Diethyl maleate can be used to study redox homeostasis and GSH protection mechanisms in oxidative stress-related diseases such as hyperbaric oxygen injury and metabolic diseases[1][2][3].
    Diethyl maleate
  • HY-N0806
    Sweroside
    3 Publications Verification

    		 Keap1-Nrf2 AMPK Sirtuin NF-κB NOD-like Receptor (NLR) Pyroptosis Apoptosis Autophagy PARP Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    Sweroside is an iridoid glycoside that targets multiple targets, including the Keap1/Nrf2 axis, NLRP3 inflammasome, SIRT1, NF-κB, AMPK/mTOR pathway, and caspase family. Sweroside promotes Nrf2 nuclear translocation by competitively binding to Keap1. Sweroside also inhibits oxidative stress and NLRP3-mediated pyroptosis by activating Nrf2, inhibits NF-κB inflammatory pathway by activating SIRT1, and promotes autophagy and induces caspase-dependent apoptosis via the AMPK/mTOR pathway. Sweroside has antioxidant, anti-inflammatory, anti-apoptotic, and lipid metabolism regulating activities, and can be used in the research of myocardial ischemia-reperfusion injury, leukemia, acute lung injury, non-alcoholic fatty liver disease, and other fields .
    Sweroside
  • HY-N1990
    Gypenoside XLIX
    2 Publications Verification

    		 PPAR Sirtuin Keap1-Nrf2 Toll-like Receptor (TLR) NF-κB Reactive Oxygen Species (ROS) NOD-like Receptor (NLR) Apoptosis Pyroptosis Autophagy Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Gypenoside XLIX is a multifunctional bioactive compound that can be isolated from Gynostemma pentaphyllum, with a Ka value of 1.58 μM for its binding to SIRT1. Gypenoside XLIX acts as a PPAR-α agonist. It inhibits the activation of TLR4-mediated NF-κB signaling pathway by activating the Sirt1/Nrf2 signaling pathway, reduces ROS accumulation, and alleviates hepatic inflammatory injury in mice with sepsis-induced liver disease. Gypenoside XLIX targets SIRT1 to block YAP-NLRP3 activation and improve sepsis-induced cardiomyopathy. Gypenoside XLIX inhibits apoptosis (Apoptosis), pyroptosis (Pyroptosis), autophagy (Autophagy), lipid peroxidation, pro-inflammatory cytokines and anti-inflammatory cytokines. Gypenoside XLIX alleviates sepsis-induced splenic injury by inhibiting inflammation and oxidative stress, and mitigates sepsis-associated encephalopathy by targeting PPAR-α. Gypenoside XLIX prevents acute kidney injury by inhibiting IGFBP7/IGF1R-mediated programmed cell death and inflammation. Gypenoside XLIX inhibits the expression and activity of vascular cell adhesion molecule-1 in cytokine-induced human endothelial cells. Gypenoside XLIX is applicable to research related to acute liver injury, lung injury, cardiomyopathy, acute splenic injury, sepsis-associated encephalopathy, acute kidney injury, atherosclerosis and chronic inflammation .
    Gypenoside XLIX
  • HY-N0660
    Jujuboside B

    		Apoptosis PARP Caspase AMPK Autophagy VEGFR Keap1-Nrf2 STING 11β-HSD Ferroptosis PI3K Akt p38 MAPK ERK Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway . Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes .
    Jujuboside B
  • HY-108022
    Azemiglitazone
    1 Publications Verification

    MSDC-0602

    		 Mitochondrial Metabolism PPAR Neurological Disease Metabolic Disease Inflammation/Immunology
    Azemiglitazone (MSDC-0602) is an orally active thiazolidinedione (TZD) -like molecule, which binds to PPARγ with low binding and activating affinity. Azemiglitazone inhibits mitochondrial pyruvate carrier (MPC), which inhibits Alzheimer’s disease and diminishes nonalcoholic steatohepatitis (NASH) caused liver injury .
    Azemiglitazone
  • HY-19696B
    Tauroursodeoxycholate dihydrate
    Maximum Cited Publications
    104 Publications Verification

    Tauroursodeoxycholic acid dihydrate; TUDCA dihydrate; UR 906 dihydrate

    		 Caspase Apoptosis Endogenous Metabolite IRE1 NF-κB JNK Reactive Oxygen Species (ROS) Akt Neurological Disease Metabolic Disease Inflammation/Immunology
    Tauroursodeoxycholate dehydrate is an orally active taurine conjugate of Ursodeoxycholic acid (HY-13771). Tauroursodeoxycholate dehydrate inhibits caspase-3/7, Apoptosis, IRE1α/TRAF2/NF-κB, prevents JNK phosphorylation, inhibits ROS generation, and activates Akt signaling. Tauroursodeoxycholate dehydrate prevents cataract formation, reduces renal tubular damage in type 2 diabetic mice, reduces I/R injury in liver, and inhibits intestinal inflammation and barrier disruption in nonalcoholic fatty liver disease .
    Tauroursodeoxycholate dihydrate
  • HY-N0762
    Isobavachin
    5 Publications Verification

    		 Cytochrome P450 UGT p38 MAPK NF-κB NO Synthase COX Fc Receptor (FcR) RANKL/RANK Keap1-Nrf2 Reactive Oxygen Species (ROS) Apoptosis Autophagy Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Isobavachin is an orally active, blood-brain barrier-penetrating prenylated flavonoid present in Psoralea corylifolia. Isobavachin inhibits human CYP2B6, CYP2C9, CYP2C19, UGT1A1, UGT1A9, and UGT2B7. Isobavachin suppresses MAPK activation, NF-κB nuclear translocation, overexpression of iNOS/COX-2, FcεRI-mediated signaling pathways, and RANKL-induced osteoclastogenesis. Isobavachin induces autophagy, cytotoxicity, neuronal differentiation, and NRF2 activation; it alleviates oxidative damage, inflammatory responses, apoptosis, iron accumulation, mitochondrial biogenesis, and mast cell degranulation. Isobavachin is applicable to research related to liver injury, inflammatory diseases, osteoporosis, liver cancer, prostate cancer, glioma, periodontitis-induced bone loss, and Alzheimer's disease .
    Isobavachin
  • HY-N0444
    Rubiadin

    		Reactive Oxygen Species (ROS) NF-κB HBV Apoptosis Bacterial Fungal Parasite Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Rubiadin is an orally active free radical scavenger that inhibits the activation of the NF-κB pathway. Rubiadin inhibits osteoclast formation, bone resorption, lipid peroxidation, HBV DNA replication and cancer cell proliferation; reduces pro-inflammatory cytokine levels; induces cancer cell apoptosis; and possesses antifungal, antimalarial, antibacterial and anticonvulsant activities. Rubiadin can be used in the research of osteoporosis, acute inflammation, chronic inflammation, carbon tetrachloride-induced liver injury, Alzheimer's disease, breast cancer, iron overload disorders, hepatitis B virus infection, colon cancer, liver cancer, T-lymphocytic leukemia, cervical cancer, diabetic nephropathy, epileptic seizures, fungal infections, malaria and bacterial infections .
    Rubiadin
  • HY-165126
    Schizophyllan

    SPG

    		 C-type Lectin-like Receptors (CTLRs) Endogenous Metabolite Sirtuin JNK p38 MAPK PPAR AP-1 Infection Metabolic Disease Inflammation/Immunology Cancer
    Schizophyllan (SPG) is an orally active extracellular β-glucan produced by the fungus Schizophyllum commune. Schizophyllan improves mitochondrial function and protects against metabolic liver injury by activating the SIRT3 pathway. Schizophyllan inhibits osteoclastogenesis and promotes osteoblast differentiation by suppressing the phosphorylation of JNK/p38, as well as downregulating PGC1β/PPARγ, c-Fos and NFATc1. Recognized via Dectin-1, schizophyllan enables precise delivery of oligonucleotide drugs and antigens to antigen-presenting cells, thus holding great potential in the treatment of inflammatory diseases and vaccine development .
    Schizophyllan
  • HY-121983
    CAY10594
    1 Publications Verification

    		 Phospholipase Apoptosis GSK-3 Anaplastic lymphoma kinase (ALK) STAT Interleukin Related G Protein-coupled Receptor Kinase (GRK) CXCR Lactate Dehydrogenase Inflammation/Immunology Cancer
    CAY10594 is an orally active PLD2 inhibitor with an IC50 of 140 nM. CAY10594 has activities such as anti-tumor, anti-oxidation and liver protection. CAY10594 can be used for the research of diseases like breast cancer, acute liver injury and colitis .
    CAY10594
  • HY-N0385
    Gomisin J
    3 Publications Verification

    		 NO Synthase AMPK CaMK NF-κB Keap1-Nrf2 Cardiovascular Disease Inflammation/Immunology
    Gomisin J is a Schisandra chinensis-derived lignan that can inhibit multiple targets such as eNOS, AMPK (LKB1, CaMKIIβ), fetuin-A, NF-κB, Nrf2/HO-1, and can pass through the blood-brain barrier. Gomisin J increases NO bioavailability by activating eNOS, regulates lipid metabolism by activating the AMPK pathway, inhibits fetuin-A and NF-κB to exert anti-inflammatory effects, and activates Nrf2/HO-1 to enhance antioxidant capacity. Gomisin J has the activities of anti-hypertension, regulating liver lipid metabolism, and reducing cerebral ischemia-reperfusion injury, and can be used for research on hypertension, non-alcoholic fatty liver disease, cerebral ischemia-reperfusion injury, etc .
    Gomisin J
  • HY-N10549
    Gigantol
    1 Publications Verification

    		 Ferroptosis c-Myc Glutathione Peroxidase JNK Reactive Oxygen Species (ROS) GSK-3 Infection Metabolic Disease Cancer
    Gigantol is an orally active bibenzyl compound. Gigantol targets MYC to promote its ubiquitin-proteasomal degradation and inhibit the growth of lung cancer cells. Gigantol exerts anti-lung cancer activity by inducing ferroptosis (Ferroptosis) via the SLC7A11-GPX4 axis. Gigantol restores the sensitivity of mcr-harboring multidrug-resistant bacteria to colistin. Gigantol ameliorates carbon tetrachloride-induced liver injury by inhibiting the activation of the JNK/cPLA2/12-LOX inflammatory pathway. Gigantol promotes cholesterol metabolism and progesterone biosynthesis in Leydig cells. Gigantol can be used in studies related to diseases such as lung cancer, multidrug-resistant Gram-negative bacterial infections, and acute liver injury .
    Gigantol
  • HY-12538
    Graveoline

    Rutamine

    		 Apoptosis Autophagy Fungal Parasite Reactive Oxygen Species (ROS) Interleukin Related JAK STAT Infection Inflammation/Immunology Cancer
    Graveoline (Rutamine) is an orally active alkaloid with various activities such as antifungal, antiparasitic, anti-inflammatory, and antitumor effects. Graveoline can induce tumor cell apoptosis and autophagy through a reactive oxygen species-mediated pathway. Graveoline has an MIC of 500 μg/mL for Candida albicans. Graveoline can be used in the research of various diseases such as tumors and liver injury .
    Graveoline
  • HY-145801
    XT2
    2 Publications Verification

    		 NF-κB Inflammation/Immunology
    XT2 is a potent, orally active, and selective inhibitor of NF-κB-inducing kinase (NIK) with an IC50 of 9.1 nM. XT2 suppresses CCl4-induced upregulation of ALT, a key biomarker of acute liver injury. XT2 also decreases immune cell infiltration into the injured liver tissue. XT2 has the potential for the research of liver inflammatory diseases . XT2 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
    XT2
  • HY-N2000
    Bellidifolin
    1 Publications Verification

    		 STAT PI3K mTOR Akt Neurological Disease Inflammation/Immunology Cancer
    Bellidifolin is an orally active compound with antiproliferative, anti-inflammatory and antioxidant properties. Bellidifolin modulates key signaling pathways including STAT3, PI3K-Akt, mTOR and BRD4, and inhibits the viral protein R (Vpr). Bellidifolin induces cell cycle arrest and apoptosis, exerts significant antifibrotic effects, and protects the heart, liver and nervous system. Bellidifolin is applicable to the research of various diseases such as lung cancer, non-alcoholic fatty liver disease, myocardial hypertrophy and ischemic cranial nerve injury .
    Bellidifolin
  • HY-N6850
    Calenduloside E
    1 Publications Verification

    		 Apoptosis Pyroptosis AMPK Bcl-2 Family JAK STAT Calcium Channel Interleukin Related TNF Receptor SOD Reactive Oxygen Species (ROS) PPAR Cardiovascular Disease Inflammation/Immunology
    Calenduloside E is a pentacyclic triterpenoid saponin that can be extracted from the bark and roots of Aralia ovata, and has anti-inflammatory and anti-apoptotic activities. Calenduloside E alleviates atherosclerosis by regulating macrophage polarization, improves mitochondrial function by regulating the AMPK-SIRT3 pathway, and alleviates acute liver injury. In addition, Calenduloside E promotes the interaction between L-type calcium channels and Bcl-2 related apoptosis genes, inhibits calcium overload, and alleviates myocardial ischemia/reperfusion injury. Calenduloside E also improves non-alcoholic fatty liver disease by regulating heat shock-dependent pathways, and inhibits ROS mediated JAK1-STAT3 pathways to reduce cellular inflammatory responses .
    Calenduloside E
  • HY-N13250
    Hawthorn Extract

    		Apoptosis AMPK Elastase Bcl-2 Family Interleukin Related Caspase PI3K Akt SOD Cardiovascular Disease
    Hawthorn Extract is an orally active hawthorn extract. Hawthorn Extract decreases Bax expression and increases Bcl-2 expression in the aorta. Hawthorn Extract regulates the AMPK signaling pathway, induces apoptosis, enhances the hepatic antioxidant system, and ameliorates symptoms of liver injury, inflammation and cancer. Hawthorn Extract reduces plasma levels of pro-inflammatory factors, increases plasma levels of anti-inflammatory adiponectin, and alleviates atherosclerotic plaque lesions in the aorta. Hawthorn Extract improves symptoms associated with chronic heart failure . Hawthorn Extract inhibits FMLP-induced superoxide anion production, Elastase release, ILB4 generation and calcium signaling in neutrophils, and also reduces LPS-induced cytokine production in neutrophils. Hawthorn Extract induces autophagy and inhibits the proliferation of intestinal stem cells. Hawthorn Extract can be used in research related to atherosclerosis, hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, hepatocellular carcinoma, chronic heart failure and hypotension .
    Hawthorn Extract
  • HY-15800A
    CZC-25146

    		TNK1 LRRK2 Neurological Disease Inflammation/Immunology
    CZC-25146 is a potent and orally active LRRK2 inhibitor with IC50 values of 4.76 nM and 6.87 nM for wild-type LRRK2 and G2019S LRRK2, respectively. CZC-25146 inhibits PLK4, GAK, TNK1, CAMKK2 and PIP4K2C as well. CZC-25146 prevents mutant LRRK2-induced injury of neurons in vitro. CZC-25146 exhibits relatively favorable pharmacokinetic properties in mice. CZC-25146 can increase normal α-1-antitrypsin (AAT) secretion and reduce inflammatory cytokines. CZC-25146 can be used to research Parkinson's disease and liver diseases .
    CZC-25146
  • 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].
    Poricoic acid B
  • HY-N5073
    Vitexin-4''-O-glucoside

    4''-O-Glucosylvitexin

    		 JNK p38 MAPK Interleukin Related TNF Receptor Caspase Lactate Dehydrogenase Apoptosis Cardiovascular Disease Metabolic Disease
    Vitexin-4''-O-glucoside (4''-O-Glucosylvitexin) is an orally active natural flavonoid component with multiple pharmacological effects including antioxidation, anti-inflammation, cytoprotection and anti-apoptosis. Vitexin-4''-O-glucoside regulates the MAPK signaling pathway by downregulating the phosphorylation levels of JNK and p38, thereby blocking endoplasmic reticulum stress responses. Vitexin-4''-O-glucoside alleviates oxidative stress by reducing MDA content and upregulating the activities of SOD and CAT, attenuates inflammation by downregulating the expressions of inflammatory factors TNF-α, IL-1β and IL-6, and also reduces LDH release and inhibits caspase-3 activation. Vitexin-4''-O-glucoside effectively improves drug-induced acute liver injury and exerts significant protective effects against myocardial hypoxia/reoxygenation injury. Vitexin-4''-O-glucoside can be used in studies on acute liver injury, cardiovascular diseases and myocardial hypoxia-reoxygenation injury .
    Vitexin-4''-O-glucoside
  • HY-N2082
    Isorhamnetin 3-O-galactoside
    1 Publications Verification

    Cacticin

    		 Thrombin COX ERK JNK Factor Xa Cardiovascular Disease Inflammation/Immunology
    Isorhamnetin 3-O-galactoside (Cacticin) is a flavonoid glycoside that can be isolated from Oenanthe javanica, with antithrombotic and profibrinolytic activities. Isorhamnetin 3-O-galactoside inhibits the activities of thrombin and factor Xa (FXa) and reduces thrombin-catalyzed fibrin polymerization maximum rate. Isorhamnetin 3-O-galactoside suppresses TNF-α-induced PAI-1 secretion, decreases the PAI-1/tissue-type plasminogen activator (t-PA) ratio, and inhibits FXa production and FVa/FXa-mediated thrombin generation. Isorhamnetin 3-O-galactoside exerts protective effects against Carbon tetrachloride (CCl4) (HY-Y0298)-induced hepatic injury in mice. Isorhamnetin 3-O-galactoside can be used for the study of liver injury-related diseases and thrombotic vascular diseases .
    Isorhamnetin 3-O-galactoside
  • HY-N6924
    Zingibroside R1
    1 Publications Verification

    		 HIV PIN1 Fungal GLUT Reactive Oxygen Species (ROS) Infection Neurological Disease Metabolic Disease Cancer
    Zingibroside R1 is an orally active triterpene saponin with multiple biological activities including antioxidant, anti-inflammatory, antiviral, and metabolic regulatory properties. Zingibroside R1 reduces the expression of PIN family members, inhibits the expression of PLT1/PLT2, WOX5, SHR, and SCR, disrupts auxin transport and distribution, triggers plant ROS responses, and inhibits root growth. Zingibroside R1 extends the lifespan of Caenorhabditis elegans, enhances its heat stress resistance, and improves its motor ability. Hydrogel derivatives of Zingibroside R1 inhibit the proliferation of Candida albicans by binding to its β-1,3-glucan and exhibit antifungal activity. Zingibroside R1 inhibits GLUT1-mediated uptake and alleviates liver injury. Zingibroside R1 can be used in research related to neurodegenerative diseases, vulvovaginal candidiasis, acute liver injury, Ehrlich ascites tumor and HIV-1 infection .
    Zingibroside R1
  • 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 .
    Vitisin A
  • HY-130437
    p-nitro-Pifithrin-α

    		MDM-2/p53 TGF-β Receptor Caspase Infection Metabolic Disease
    p-nitro-Pifithrin-α, a cell-permeable analog of pifithrin-α, is a potent p53 inhibitor. p-nitro-Pifithrin-α suppresses p53-mediated TGF-β1 expression in HK-2 cells. p-nitro-Pifithrin-α inhibits the activation of caspase-3 by Zika virus (ZIKV) strains. p-nitro-Pifithrin-α attenuates steatosis and liver injury in mice fed a high-fat diet [4]. non-alcoholic fatty liver disease .
    p-nitro-Pifithrin-α
  • HY-P3016B
    Aspartate aminotransferase, Human liver

    EC 2.6.1.1, Human liver; GOT, Human liver; AST, Human liver

    		 Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), Human liver is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Human liver comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Human liver also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Human liver is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, Human liver
  • HY-D3000
    NIR-RED ROS-H2O2 Probe

    		Fluorescent Dye Metabolic Disease
    NIR-RED ROS-H2O2 Probe is a near-infrared fluorescent probe used for detecting hydrogen peroxide (H₂O₂) and featuring dual-modal fluorescence/photoacoustic imaging capabilities. NIR-RED ROS-H2O2 Probe successfully detects the upregulated fluorescence signal of H₂O₂ in HepG2 cells and a mouse liver injury model. NIR-RED ROS-H2O2 Probe can be used as a biomarker detection tool for drug-induced liver injury (DILI) .
    NIR-RED ROS-H2O2 Probe
  • HY-179473
    MK-0626

    		Dipeptidyl Peptidase NO Synthase Cardiovascular Disease Metabolic Disease
    MK-0626 is a selective, orally active DPP-4 inhibitor with an IC50 of 6.3 nM. MK-0626 increases endothelial nitric oxide synthetase expression. MK-0626 improves neovascularization, attenuates hepatic steatosis, attenuates pancreatic islet injury. MK-0626 can be used in the research of diabetes and non-alcoholic fatty liver disease .
    MK-0626
  • HY-D2999
    NIR-RED ATP Probe

    		Fluorescent Dye Metabolic Disease
    NIR-RED ATP Probe is a NIR-II fluorescent probe. NIR-RED ATP Probe exhibits high affinity and selectivity for ATP and can non-invasively and with high contrast detect changes in ATP concentration at the cellular level, with minimal interference to the abundant biomolecules within the cells. NIR-RED ATP Probe can be used as a biomarker detection tool for drug-induced liver injury (DILI) .
    NIR-RED ATP Probe
  • HY-N0444R
    Rubiadin (Standard)

    		Reference Standards Reactive Oxygen Species (ROS) Apoptosis Fungal Parasite NF-κB HBV Bacterial Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Rubiadin (Standard) is the analytical standard of Rubiadin (HY-N0444). This product is intended for research and analytical applications. Rubiadin is an orally active free radical scavenger that inhibits the activation of the NF-κB pathway. Rubiadin inhibits osteoclast formation, bone resorption, lipid peroxidation, HBV DNA replication and cancer cell proliferation; reduces pro-inflammatory cytokine levels; induces cancer cell apoptosis; and possesses antifungal, antimalarial, antibacterial and anticonvulsant activities. Rubiadin can be used in the research of osteoporosis, acute inflammation, chronic inflammation, carbon tetrachloride-induced liver injury, Alzheimer's disease, breast cancer, iron overload disorders, hepatitis B virus infection, colon cancer, liver cancer, T-lymphocytic leukemia, cervical cancer, diabetic nephropathy, epileptic seizures, fungal infections, malaria and bacterial infections.
    Rubiadin (Standard)
  • HY-W008947R
    SEW​2871 (Standard)

    		Reference Standards LPL Receptor ERK Akt Neurological Disease Metabolic Disease Inflammation/Immunology
    SEW2871 is an orally active, potent, highly selective S1P1 (sphingosine-1-phosphate type 1 receptor) agonist, with an EC50 of 13.8 nM. SEW2871 activates ERK, Akt, and Rac signaling pathways and induces S1P1 internalization and recycling. SEW2871 reduces lymphocyte numbers in blood. SEW2871 can be used for the research of diabetes, Alzheimer’s disease, liver fibrosis, and inflammatory responses .
    SEW​2871 (Standard)
  • HY-15800
    CZC-25146 hydrochloride

    		TNK1 LRRK2 Neurological Disease Inflammation/Immunology
    CZC-25146 hydrochloride is a potent LRRK2 inhibitor with IC50 values of 4.76 nM and 6.87 nM for wild-type LRRK2 and G2019S LRRK2, respectively. CZC-25146 hydrochloride inhibits PLK4, GAK, TNK1, CAMKK2 and PIP4K2C as well. CZC-25146 hydrochloride prevents mutant LRRK2-induced injury of neurons in vitro. CZC-25146 hydrochloride exhibits relatively favorable pharmacokinetic properties in mice. CZC-25146 hydrochloride can increase normal α-1-antitrypsin (AAT) secretion and reduce inflammatory cytokines. CZC-25146 hydrochloride can be used to research Parkinson's disease and liver diseases .
    CZC-25146 hydrochloride
  • HY-A0077A
    Perphenazine dihydrochloride

    		Dopamine Receptor Histamine Receptor 5-HT Receptor Adrenergic Receptor Apoptosis Autophagy Neurological Disease Inflammation/Immunology Endocrinology Cancer
    Perphenazine dihydrochloride is an orally active dopamine receptor and histamine-1 receptor antagonist, with Ki values of 0.56 nM (D2), 0.43 nM (D3), 6 nM (5-HT2A), respectively. Perphenazine dihydrochloride also binds to Alpha-1A adrenergic receptor. Perphenazine dihydrochloride inhibits cancer cell proliferation, and induces apoptosis. Perphenazine dihydrochloride can be used in the research of mental disease, cancer, inflammation .
    Perphenazine dihydrochloride
  • HY-168332
    FXR agonist 11

    		FXR Metabolic Disease
    FXR agonist 11 (Compound 14) is an FXR agonist with an EC50 of 1.2 μM and a maximum effect of 73.7%. FXR agonist 11 can significantly increase GSH levels in the liver and is used to study drug-induced liver injury diseases .
    FXR agonist 11
  • HY-162220
    HSD17B13-IN-94

    		Estrogen Receptor/ERR 17β-HSD Metabolic Disease
    HSD17B13-IN-94 (Compound 12) is an effective inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for Estradiol (HY-B0141). HSD17B13-IN-94 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD, NASH, or drug-induced liver injury (DILI) .
    HSD17B13-IN-94
  • HY-171857
    Cytaphat

    		Reactive Oxygen Species (ROS) Metabolic Disease Inflammation/Immunology
    Cytaphat is a compound with hepatoprotective activity. Cytaphat has antioxidant, membrane-stabilizing and choleretic effects. Cytaphat can be used in the research of diseases such as acute toxic hepatopathy and liver injury .
    Cytaphat
  • HY-113402B
    Gamma-glutamylcysteine ammonium

    γ-Glu-Cys ammonium

    		 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 ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium 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 ammonium 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 ammonium 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 .
    Gamma-glutamylcysteine ammonium
  • HY-163243
    HSD17B13-IN-29

    		17β-HSD Metabolic Disease
    HSD17B13-IN-29 (Compound 53) is an inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for estradiol. HSD17B13-IN-29 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD or NASH, as well as drug-induced liver injury (DILI) .
    HSD17B13-IN-29
  • HY-163249
    HSD17B13-IN-49

    		17β-HSD Metabolic Disease
    HSD17B13-IN-49 (Compound 81) is an inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for estradiol. HSD17B13-IN-49 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD or NASH, as well as drug-induced liver injury (DILI) .
    HSD17B13-IN-49
  • HY-161229
    HSD17B13-IN-69

    		17β-HSD Metabolic Disease
    HSD17B13-IN-69 (Compound 11) is an inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for estradiol. HSD17B13-IN-69 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD or NASH, as well as drug-induced liver injury (DILI) .
    HSD17B13-IN-69
  • HY-162209
    HSD17B13-IN-63

    		17β-HSD Metabolic Disease
    HSD17B13-IN-63 (Compound 160) is an inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for estradiol. HSD17B13-IN-63 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD or NASH, as well as drug-induced liver injury (DILI) .
    HSD17B13-IN-63
  • HY-163254
    HSD17B13-IN-57

    		17β-HSD Metabolic Disease
    HSD17B13-IN-57 (Compound 93) is an inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for estradiol. HSD17B13-IN-57 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD or NASH, as well as drug-induced liver injury (DILI) .
    HSD17B13-IN-57
  • HY-163263
    HSD17B13-IN-80

    		17β-HSD Metabolic Disease
    HSD17B13-IN-80 (Compound 151) is an inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for estradiol. HSD17B13-IN-80 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD or NASH, as well as drug-induced liver injury (DILI) .
    HSD17B13-IN-80
  • HY-163264
    HSD17B13-IN-81

    		17β-HSD Metabolic Disease
    HSD17B13-IN-81 (Compound 154) is an inhibitor of hydroxysteroid 17β-dehydrogenase 13 (HSD17B13) with an IC50 value of ≤ 0.1 μM for estradiol. HSD17B13-IN-81 can be used for research on liver diseases, metabolic diseases, or cardiovascular diseases, such as NAFLD or NASH, as well as drug-induced liver injury (DILI) .
    HSD17B13-IN-81

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