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Results for "

intestinal microbiota

" in MedChemExpress (MCE) Product Catalog:

33

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1

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2

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20

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2

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • 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].
    Inulin
  • HY-N0535
    (+)-Magnoflorine chloride
    1 Publications Verification

    Magnoflorine chloride; α-Magnoflorine chloride; Thalictrine chloride

    		 Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Infection Metabolic Disease
    (+)-Magnoflorine (α-Magnoflorine) chloride is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine chloride promotes Parkin/PINK1-mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine chloride inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine chloride upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine chloride also has significant antifungal activity .
    (+)-Magnoflorine chloride
  • HY-B1172
    Lactulose
    1 Publications Verification

    4-O-β-D-Galactopyranosyl-D-fructose

    		 Bacterial Interleukin Related DNA/RNA Synthesis Infection Inflammation/Immunology Endocrinology Cancer
    Lactulose is an orally active galactose-fructose disaccharide. Lactulose suppresses upregulation of TNF-α and IL-6. Lactulose decreases the degree of DNA damage. Lactulose exhibits many of the properties of other oligosaccharides, including increasing the numbers of Bifidobacteria in feces. Lactulose restores the structure and composition of the intestinal microbiota, mitigates inflammation, and suppresses inflammatory tumorigenesis in mice with colitis-associated cancer. Lactulose can be used in the research of constipation .
    Lactulose
  • 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 .
    Allolithocholic acid
  • HY-N0334
    (+)-Magnoflorine

    Magnoflorine; α-Magnoflorine; Thalictrine

    		 Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Cardiovascular Disease Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    (+)-Magnoflorine (α-Magnoflorine) is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine also has significant antifungal activity .
    (+)-Magnoflorine
  • HY-N0468
    Rebaudioside D
    1 Publications Verification

    		 FXR Acetyl-CoA Carboxylase Metabolic Disease
    Rebaudioside D is an orally active sweetener that targets and activates FXR, modulates Acetyl-CoA Carboxylase, and inhibits 3-hydroxy-3-methylglutaryl-CoA reductase. Rebaudioside D regulates bile acid homeostasis and lipid metabolism, reduces the synthesis rates of fatty acids and cholesterol, and exerts multiple effects including anti-adipogenesis, hepatoprotection, anti-steatosis, gut microbiota modulation, enhancement of secondary bile acid metabolism, anti-endotoxin activity, regulation of bile acid transport, and inhibition of bile acid efflux. Rebaudioside D also reduces body weight gain, visceral fat accumulation, hepatic triglyceride and cholesterol accumulation, hepatic lipid peroxidation, and decreases the circulating level of lipopolysaccharide-binding protein. Rebaudioside D additionally enhances the secondary bile acid metabolic pathway of intestinal bacteria, upregulates the gene expression of ileal organic solute transporter α, and downregulates the gene expression of hepatic bile salt export pump. Rebaudioside D does not affect glucose homeostasis, alter total caloric intake or fecal energy excretion, induce weight gain, exacerbate obesity, promote hepatic steatosis, impair brown adipose tissue function, nor change skeletal muscle metabolism-related proteins. Rebaudioside D can be used in diet-induced obesity and obesity-related research .
    Rebaudioside D
  • HY-W019806
    Lacto-N-fucopentaose I

    LNFP I

    		 Endogenous Metabolite CDK Reactive Oxygen Species (ROS) Apoptosis Enterovirus Bacterial Infection Inflammation/Immunology
    Lacto-N-fucopentaose I (LNFPI) is a human milk oligosaccharide (HMO), possessing antiviral and antibacterial activity. Lacto-N-fucopentaose I can reduce capsid protein VP1 to block virus adsorption, promote CDK2 and reduce cyclin E to recover cell cycle S phase block. Lacto-N-fucopentaose I inhibits ROS production and apoptosis in virus-infected cells. Lacto-N-fucopentaose I can also regulate intestinal microbiota to affect immune system development .
    Lacto-N-fucopentaose I
  • HY-N0334A
    (+)-Magnoflorine iodide
    1 Publications Verification

    Magnoflorine iodide; α-Magnoflorine iodide; Thalictrine iodide

    		 Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Cardiovascular Disease Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    (+)-Magnoflorine (α-Magnoflorine) iodide is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine iodide promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine iodide inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine iodide also has significant antifungal activity .
    (+)-Magnoflorine iodide
  • HY-N0237
    Atractyloside A
    3 Publications Verification

    		 Toll-like Receptor (TLR) MyD88 NF-κB Mitochondrial Metabolism Interleukin Related Aquaporin Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Atractyloside A is an orally active inhibitor of the TLR4/MyD88/NF-κB signaling pathway and also an opener of the mitochondrial permeability transition pore (MPTP). Atractyloside A interferes with the activation of the TLR4/MyD88/NF-κB pathway, thereby inhibiting intestinal inflammatory responses. Atractyloside A reverses mucin synthesis impairment, improves intestinal barrier integrity, and restores homeostasis by altering the composition of the gut microbiota. Atractyloside A can be used in studies related to spleen deficiency diarrhea and myocardial injury .
    Atractyloside A
  • HY-N1916
    Coniferyl ferulate
    1 Publications Verification

    		 Glutathione S-transferase P-glycoprotein Apoptosis iGluR CaMK p38 MAPK Reactive Oxygen Species (ROS) Bacterial Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Coniferyl ferulate is an orally active phenolic acid compound. Coniferyl ferulate is a potent inhibitor of glutathione S-transferase (GST) (IC50 = 0.3 μM), which downregulates P-gp expression, induces apoptosis in B-MD-C1 (ADR+/+) cells, and reverses multidrug resistance. Coniferyl ferulate blocks the NMDAR/NR2B-CaMKII-MAPKs signaling pathway, inhibits ROS production and mitochondrial apoptosis, while reshapes the intestinal microbiota and microbial metabolism, ameliorates colonic inflammation and alleviates depressive symptoms in mice. Coniferyl ferulate can alleviate the toxicity of xylene to hematopoietic stem and progenitor cells by targeting Mgst2. Coniferyl ferulate exhibits antibacterial activity against the Gram-positive Bacillus subtilis and Staphylococcus aureus .
    Coniferyl ferulate
  • HY-N15135
    Arabinoxylan (Medium viscosity)

    		Interleukin Related Toll-like Receptor (TLR) Fungal Metabolic Disease
    Arabinoxylan Medium viscosity is an orally active Dectin-1 splice variant modulator, glucose absorption inhibitor, and chyme viscosity enhancer. Arabinoxylan Medium viscosity inhibits particulate β-glucan-induced Dectin-1A activation and mildly suppresses Dectin-1B activation. In human dendritic cells stimulated with particulate β-glucan, Arabinoxylan Medium viscosity reduces the production of IL-10 and TNF-α, and increases the production of IL-4 and IL-23. Arabinoxylan Medium viscosity also supports antifungal immune responses without activating TLR2, TLR4 or TLR5, and does not induce cytokine production when used to stimulate human dendritic cells alone. Arabinoxylan Medium viscosity increases small intestinal chyme viscosity, gets degraded in the large intestine to produce short-chain fatty acids, reduces glucose absorption and insulin response, and improves glucose homeostasis. Arabinoxylan Medium viscosity supports microbial fermentation and the growth of beneficial microbiota in the gastrointestinal tract, prevents bile acid reabsorption, and delays starch digestion. Arabinoxylan Medium viscosity can be used in research related to type 2 diabetes, impaired glucose tolerance, and metabolic syndrome .
    Arabinoxylan (Medium viscosity)
  • HY-158766
    3-sucCA

    3-Succinylated cholic acid

    		 Endogenous Metabolite Bacterial Infection Inflammation/Immunology
    3-sucCA is an orally available bacterial bile acid that exerts anti-MASH effects by promoting the growth of Akkermansia muciniphila. By remodeling the intestinal microbiota and promoting the growth of Akkermansia, 3-sucCA can improve intestinal barrier damage and reduce chronic low-level inflammation, thereby alleviating the progression of metabolic dysfunction-associated steatohepatitis (MASH). 3-sucCA accelerates the synthesis of cell wall peptidoglycan and has in vivo efficacy in the mouse MAFL-MASH model. 3-sucCA levels are low in the MAFLD model and are mainly used in the study of MASH .
    3-sucCA
  • HY-W750796
    Butyric acid-13C4 sodium

    Butanoic acid-13C4 sodium

    		 Isotope-Labeled Compounds Endogenous Metabolite
    Butyric acid-13C4 sodium (Butanoic acid-13C4 sodium) is a stable isotope labeled compound with the activity of promoting cell proliferation and regulating gene expression. Butyric acid-13C4 sodium can be used in metabolic research and compound development to help scientists gain a deeper understanding of the role of short-chain fatty acids in organisms. Butyric acid-13C4 sodium also plays an important role in nutrition and intestinal health research, especially in the regulation of probiotic function and intestinal microbiota.
    Butyric acid-13C4 sodium
  • HY-W013636C
    2-Ketoglutaric acid potassium
    5+ Cited Publications

    Alpha-Ketoglutaric acid potassium

    		 Tyrosinase Endogenous Metabolite TNF Receptor Neurological Disease Metabolic Disease
    2-Ketoglutaric acid (Alpha-Ketoglutaric acid) (potassium) is an intermediate in the production of ATP or GTP in the Krebs cycle. 2-Ketoglutaric acid potassium is a reversible and orally active inhibitor of tyrosinase with an IC50 value of 15 mM. 2-Ketoglutaric acid potassium also acts as the major carbon skeleton for nitrogen-assimilatory reactions. 2-Ketoglutaric acid potassium significantly suppresses abnormal intestinal permeability, delocalization of tight junction proteins from the intestinal cells, expression of TNFα in vitro and in vivo. 2-Ketoglutaric acid potassium directly binds to TAK1, and inhibits the TRAF6-TAK1 interaction. 2-Ketoglutaric acid potassium also alleviates inflammatory bowel disease (IBD) symptoms and gut microbiota dysbiosis, evident by the improvements in the intestine length .
    2-Ketoglutaric acid potassium
  • HY-128421
    Tridecanedioic acid

    Brassylic Acid

    		 Endogenous Metabolite Parasite Infection Metabolic Disease
    Tridecanedioic acid is an endogenous metabolite. Tridecanedioic acid is an endogenous metabolite. Tridecanedioic acid is related to the metabolic regulation of non-alcoholic fatty liver disease (NASH) and may be an important node molecule in the intestinal microbiota-host metabolism interaction network. Tridecanedioic acid is significantly accumulated in tolerant cabbage-type rapeseed varieties and has a lower content in sensitive varieties. It plays an important role in the defense response against the infection of the small cabbage moth (Plutella xylostella). Tridecanedioic acid can be used as a biomarker for plant insect resistance or a diagnostic marker for metabolic diseases .
    Tridecanedioic acid
  • HY-W718179
    Hydroxypropyl starch

    2-Hydroxypropyl starch

    		 Biochemical Assay Reagents Metabolic Disease
    Hydroxypropyl starch (2-Hydroxypropyl starch) is a type of modified starch used as a food additive. Hydroxypropyl starch is not absorbed intact by the gut, but is significantly hydrolyzed by intestinal enzymes and then fermented by intestinal microbiota .
    Hydroxypropyl starch
  • HY-P2958
    Choloylglycine hydrolase

    		Biochemical Assay Reagents Metabolic Disease
    Choloylglycine hydrolase is a conjugated bile salt hydrolase that catalyses the hydrolysis of amide bond in conjugated bile acids. Choloylglycine hydrolase is expressed by intestinal microbiota. Choloylglycine hydrolase can be studied in research on type 2 diabetes .
    Choloylglycine hydrolase
  • HY-N7635
    Oleanolic acid 28-O-β-D-glucopyranoside

    β-D-Glucopyranosyl oleanolate

    		 NO Synthase COX Interleukin Related Claudin p38 MAPK Akt PI3K Inflammation/Immunology
    Oleanolic acid 28-O-β-D-glucopyranoside (β-D-Glucopyranosyl oleanolate) is an orally active pentacyclic triterpenoid compound. Oleanolic acid 28-O-β-D-glucopyranoside has anti-inflammatory effects. In ulcerative colitis models, Oleanolic acid 28-O-β-D-glucopyranoside can inhibit the inflammatory response, enhance the intestinal epithelial barrier function, and modulate the gut microbiota. Its mechanism of action is related to the PI3K-AKT and MAPK signaling pathways. Oleanolic acid 28-O-β-D-glucopyranoside can be used in the research of diseases such as colitis .
    Oleanolic acid 28-O-β-D-glucopyranoside
  • HY-135319
    Strictinin

    		Bacterial Antibiotic ERK JNK NF-κB ROR Apoptosis Caspase GSK-3 Akt PI3K Infection Metabolic Disease Inflammation/Immunology Cancer
    Strictinin is an orally active phenolic compound. Strictinin reduces xanthine oxidase activity, uric acid production, and the activation of ERK1/2, JNK, NF-κB, and NLRP3 inflammasome components in hepatocytes treated with Xanthine (HY-W017389). Strictinin decreases elevated serum uric acid levels and enhanced xanthine oxidase activity in mice treated with potassium oxonate. Strictinin acts as a ROR1 inhibitor and exhibits anticancer activity against highly aggressive non-androgen-dependent prostate cancer. Strictinin induces cancer cell apoptosis (apoptosis), arrests cell cycle, and inhibits cancer cell migration, invasion, and epithelial-mesenchymal transition. Strictinin modulates gut microbiota, inhibits bacterial growth and biofilm formation, accelerates small intestinal transit, and blocks viral entry and replication. Strictinin can be used in research related to hyperuricemia, androgen receptor-negative non-androgen-dependent prostate cancer, triple-negative breast cancer, bacterial infections, constipation, coronavirus infections, dental caries, and infections caused by influenza A, influenza B, and human parainfluenza virus type 1 .
    Strictinin
  • HY-N6612B
    Glucuronic acid sodium
    1 Publications Verification

    		 Bacterial Inflammation/Immunology
    Glucuronic acid sodium is a polysaccharide that exhibits anti-inflammatory activity, supporting the healing of ulcerative colitis. Glucuronic acid sodium also enhances the intestinal barrier by upregulating tight junction proteins like ZO-1 and Occludin. Furthermore, Glucuronic acid sodium plays a role in modulating gut microbiota by increasing beneficial bacterial populations while suppressing harmful ones.
    Glucuronic acid sodium
  • HY-128421R
    Tridecanedioic acid (Standard)

    Brassylic Acid (Standard)

    		 Reference Standards Endogenous Metabolite Parasite Infection Metabolic Disease
    Tridecanedioic acid (Standard) is the analytical standard of Tridecanedioic acid (HY-128421). This product is intended for research and analytical applications. Tridecanedioic acid is an endogenous metabolite. Tridecanedioic acid is an endogenous metabolite. Tridecanedioic acid is related to the metabolic regulation of non-alcoholic fatty liver disease (NASH) and may be an important node molecule in the intestinal microbiota-host metabolism interaction network. Tridecanedioic acid is significantly accumulated in tolerant cabbage-type rapeseed varieties and has a lower content in sensitive varieties. It plays an important role in the defense response against the infection of the small cabbage moth (Plutella xylostella). Tridecanedioic acid can be used as a biomarker for plant insect resistance or a diagnostic marker for metabolic diseases.
    Tridecanedioic acid (Standard)
  • HY-136896
    FFA3 agonist 1

    		Free Fatty Acid Receptor Metabolic Disease Inflammation/Immunology
    FFA3 agonist 1 is an agonist of free fatty acid receptor 3 (FFA3). FFA3 agonist 1 regulates the health effect of intestinal microbiota by activating FFA3 .
    FFA3 agonist 1
  • HY-143712S1
    Allolithocholic Acid-d4

    3α-hydoxy-5α-Cholaoic Acid-d4, allo-LCA-d4

    		 Isotope-Labeled Compounds Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR Metabolic Disease Inflammation/Immunology Cancer
    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 .
    Allolithocholic Acid-d4
  • HY-N0468R
    Rebaudioside D (Standard)

    		Reference Standards Acetyl-CoA Carboxylase FXR Metabolic Disease
    Rebaudioside D (Standard) is the analytical standard of Rebaudioside D. This product is intended for research and analytical applications. Rebaudioside D is an orally active sweetener that targets and activates FXR, modulates Acetyl-CoA Carboxylase, and inhibits 3-hydroxy-3-methylglutaryl-CoA reductase. Rebaudioside D regulates bile acid homeostasis and lipid metabolism, reduces the synthesis rates of fatty acids and cholesterol, and exerts multiple effects including anti-adipogenesis, hepatoprotection, anti-steatosis, gut microbiota modulation, enhancement of secondary bile acid metabolism, anti-endotoxin activity, regulation of bile acid transport, and inhibition of bile acid efflux. Rebaudioside D also reduces body weight gain, visceral fat accumulation, hepatic triglyceride and cholesterol accumulation, hepatic lipid peroxidation, and decreases the circulating level of lipopolysaccharide-binding protein. Rebaudioside D additionally enhances the secondary bile acid metabolic pathway of intestinal bacteria, upregulates the gene expression of ileal organic solute transporter α, and downregulates the gene expression of hepatic bile salt export pump. Rebaudioside D does not affect glucose homeostasis, alter total caloric intake or fecal energy excretion, induce weight gain, exacerbate obesity, promote hepatic steatosis, impair brown adipose tissue function, nor change skeletal muscle metabolism-related proteins. Rebaudioside D can be used in diet-induced obesity and obesity-related research .
    Rebaudioside D (Standard)
  • HY-N13218
    Pueraria Extract

    		Others Cardiovascular Disease
    Pueraria Extract is a kudzu extract, and its components include: Isoflavones. Pueraria Extract (ethanol extract) can significantly improve cardiac damage in rats with acute myocardial infarction. Pueraria Extract improves bile acid levels by increasing the expression of CYP7A1 and restoring the diversity of intestinal microbiota. Pueraria Extract can also inhibit the FXR-FGF15 signaling pathway and increase the expression of OST-α to increase bile acid reabsorption and fecal excretion. .
    Pueraria Extract
  • HY-143712R
    Allolithocholic acid (Standard)

    		Reference Standards Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR Metabolic Disease Inflammation/Immunology Cancer
    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 .
    Allolithocholic acid (Standard)
  • HY-173397
    β-Glucuronidase-IN-3

    		β-glucuronidase Bacterial Metabolic Disease
    β-Glucuronidase-IN-3 (Compound 49) is a covalent allosteric β-glucuronidase inhibitor. β-Glucuronidase-IN-3 has potent inhibitory activity against Escherichia coli β-glucuronidase (EcGUS) (IC50: 12.9 nM). β-Glucuronidase-IN-3 exerts its inhibitory effect by reversibly covalently modifying the cysteine residues (Cys28, Cys443, and Cys197) of EcGUS. β-Glucuronidase-IN-3 can be used in the study of intestinal microbiota-related diseases, especially to alleviate the toxic side effects of Irinotecan (HY-16562) and nonsteroidal anti-inflammatory drugs (NSAIDs) .
    β-Glucuronidase-IN-3
  • HY-N17698
    Cyclogaleginoside B

    Cyc B

    		 Drug Metabolite Others
    Cyclogaleginoside B (Cyc B) is a metabolize of Astragaloside IV (HY-N0431) by intestinal microbiota .
    Cyclogaleginoside B
  • HY-169411
    α-Glucosidase-IN-77

    		Glycosidase Metabolic Disease
    α-Glucosidase-IN-77 (Compound H7) is a non-competitive inhibitor for α-glucosidase with an IC50 of 1.25 μM. α-Glucosidase-IN-77 lowers blood glucose levels, improves glucose tolerance, regulates intestinal microbiota, and exhibits hepatoprotective effect in mouse type 2 diabetes model .
    α-Glucosidase-IN-77
  • HY-N19420
    Theasinensin C

    		Renin Bacterial Interleukin Related TNF Receptor Cardiovascular Disease Inflammation/Immunology
    Theasinensin C is an orally effective renin inhibitor and gut microbiota modulator, with an IC50 of 40.21 μM against renin activity. Theasinensin C selectively enriches Akkermansia muciniphila in the gut microbiota, enhances the Akkermansia muciniphila-mediated hydrolysis of the PTS domain of mucin, drives the accumulation of luminal glutamine and serine, and regulates the gut-kidney-liver glutamine/serine metabolic signaling pathway to promote creatine biosynthesis. Theasinensin C improves cognitive function, reduces pro-inflammatory cytokines, alleviates neuropathological changes and restores intestinal barrier integrity. Theasinensin C can be used in research related to hypertension and neuroinflammation induced by high-fructose diet .
    Theasinensin C
  • HY-W854443
    L-Fucose

    6-Deoxy-L-galactopyranose

    		 Endogenous Metabolite Inflammation/Immunology Cancer
    L-Fucose (6-Deoxy-L-galactopyranose) is an orally active dietary sugar. L-Fucose is one of the key metabolites involved in the interaction between humans and the intestinal microbiota. L-Fucose binds to proteins as a post-translational modification through the fucosylation process, thereby regulating the behavior and function of proteins. L-Fucose has shown the ability to inhibit tumor growth and increase the infiltration of immune cells within tumors. L-Fucose can be used in cancer and anti-tumor immune research .
    L-Fucose
  • HY-N17383
    Ligusticum cycloprolactam

    		Toll-like Receptor (TLR) NF-κB Collagen Interleukin Related Cadherin NOD-like Receptor (NLR) TGF-β Receptor FXR Apoptosis Metabolic Disease Inflammation/Immunology
    Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease .
    Ligusticum cycloprolactam
  • HY-179476
    3-Oxochol-5-en-24-oic acid

    		Androgen Receptor Endogenous Metabolite Inflammation/Immunology Cancer
    3-Oxochol-5-en-24-oic acid is a rare bile acid produced by the intestinal microbiota. 3-Oxochol-5-en-24-oic acid is a potent antagonist of the human androgen receptor (hAR), with an IC50 of 119.4 nM. 3-Oxochol-5-en-24-oic acid has no significant agonistic or antagonistic effects on estrogen receptors (ER) or glucocorticoid receptors (GR). 3-Oxochol-5-en-24-oic acid effectively inhibits the growth of prostate cancer cells. In animal models, it enhances the efficacy of anti-PD-1 therapy by regulating the differentiation of CD8 + T cells. 3-Oxochol-5-en-24-oic acid can be used for research on regulating host immunity and anti-tumor studies .
    3-Oxochol-5-en-24-oic acid

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