Search Result
Results for "
prevents lipid accumulation
" in MedChemExpress (MCE) Product Catalog:
6
Isotope-Labeled Compounds
| Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
-
- HY-B0415
-
|
|
Glucocorticoid Receptor
Wnt
|
Inflammation/Immunology
Endocrinology
|
|
Fluocinolone is a glucocorticoid glucocorticoid receptor agonist. Fluocinolone is effective in preventing both lipid accumulation and inflammation. Fluocinolone can promote the proliferation of DPCs and has the potential role in repairing injured pulp tissues. Fluocinolone can be used to study the prevention of chemotherapy-induced peripheral neuropathy caused by Paclitaxel (HY-B0015) .
|
-
-
- HY-N2515
-
|
|
NF-κB
PI3K
JAK
Apoptosis
|
Inflammation/Immunology
Cancer
|
|
Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures .
Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB .
Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis .
Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway .
|
-
-
- HY-133707
-
|
|
Endogenous Metabolite
|
Metabolic Disease
|
|
β-Muricholic acid is a potent and orally active biliary cholesterol-desaturating agent. β-Muricholic acid prevents cholesterol gallstones. β-Muricholic acid inhibits lipid accumulation. β-Muricholic acid has the potential for the research of nonalcoholic fatty liver disease (NAFLD) .
|
-
-
- HY-143712
-
|
|
Drug Metabolite
G protein-coupled Bile Acid Receptor 1
ROR
|
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC50 = 2.7 μM) and RORγt inverse agonist (IC50 = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .
|
-
-
- HY-N1990
-
|
|
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 .
|
-
-
- HY-161929
-
|
|
Glutathione Peroxidase
Ferroptosis
|
Cardiovascular Disease
|
|
GPX4 activator 2 is a GPX4 activator with a Ka value of 0.426 μM for human GPX4. GPX4 activator 2 reduces lipid hydroperoxide levels, prevents lipid peroxide accumulation, and inhibits ferroptosis. GPX4 activator 2 rescues cell death induced by Erastin (HY-15763). GPX4 activator 2 exerts cardioprotective effects in a mouse model of doxorubicin (HY-15142A)-induced myocardial injury .
|
-
-
- HY-161928
-
|
|
Glutathione Peroxidase
Ferroptosis
|
Cancer
|
|
GPX4 activator 1 (Compound A9) is a allosteric activator of GPX4 (Kd = 5.86 μM, EC50 = 19.19 μM). GPX4 activator 1 can selectively act on ferroptosis and prevent the accumulation of intracellular lipid peroxides caused by ferroptosis inducers .
|
-
-
- HY-120657
-
|
|
CGRP Receptor
NF-κB
|
Neurological Disease
Metabolic Disease
Inflammation/Immunology
|
|
9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-108571
-
|
|
PPAR
|
Cardiovascular Disease
Metabolic Disease
|
|
CP-775146 is a selective PPARα agonist (Ki of 24.5 nM) that binds strongly to the PPARα ligand. CP-775146 has no observable affinity for PPARβ and PPARγ.CP-775146 shows hypolipidemic activity. CP-775146 efficiently alleviates obesity-induced liver damage, prevents lipid accumulation by activating the liver fatty acid β-oxidation pathway .
|
-
-
- HY-W770410
-
|
|
Isotope-Labeled Compounds
CGRP Receptor
NF-κB
|
Others
|
|
9-PAHSA- 13C4 is 13C-labeled 9-PAHSA. 9-PAHSAis an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSAsignificantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSAinduces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSAregulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSAdoes not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSAcan be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-143712S1
-
|
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 .
|
-
-
- HY-120657S
-
|
|
Isotope-Labeled Compounds
CGRP Receptor
NF-κB
|
Others
|
|
9-PAHSA-d4 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-161985
-
|
|
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 .
|
-
-
- HY-B0415R
-
|
|
Reference Standards
Glucocorticoid Receptor
Wnt
|
Inflammation/Immunology
Endocrinology
|
|
Fluocinolone (Acetonide) (Standard) is the analytical standard of Fluocinolone (Acetonide). This product is intended for research and analytical applications. Fluocinolone is a glucocorticoid glucocorticoid receptor agonist. Fluocinolone is effective in preventing both lipid accumulation and inflammation. Fluocinolone can promote the proliferation of DPCs and has the potential role in repairing injured pulp tissues. Fluocinolone can be used to study the prevention of chemotherapy-induced peripheral neuropathy caused by Paclitaxel (HY-B0015) .
|
-
-
- HY-W777281
-
|
|
Isotope-Labeled Compounds
Glucocorticoid Receptor
Wnt
|
Endocrinology
|
|
Fluocinolone acetonide- 13C3 is the 13C-labeled Fluocinolone (Acetonide) (HY-B0415). Fluocinolone is a glucocorticoid glucocorticoid receptor agonist. Fluocinolone is effective in preventing both lipid accumulation and inflammation. Fluocinolone can promote the proliferation of DPCs and has the potential role in repairing injured pulp tissues. Fluocinolone can be used to study the prevention of chemotherapy-induced peripheral neuropathy caused by Paclitaxel (HY-B0015) .
|
-
-
- HY-143712R
-
|
|
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 .
|
-
-
- HY-N2515R
-
|
|
Reference Standards
NF-κB
PI3K
JAK
Apoptosis
|
Inflammation/Immunology
Cancer
|
|
Ginsenoside Rk1 (Standard) is the analytical standard of Ginsenoside Rk1. This product is intended for research and analytical applications. Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures .
Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB .
Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis .
Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway .
|
-
-
- HY-120657R
-
|
|
Reference Standards
CGRP Receptor
NF-κB
|
Cardiovascular Disease
Inflammation/Immunology
|
|
Flumethrin (Standard) is the analytical standard of Flumethrin. This product is intended for research and analytical applications. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-144026S
-
|
|
CGRP Receptor
NF-κB
|
Inflammation/Immunology
|
|
9-PAHSA-d9 is the deuterium labeled 9-PAHSA (HY-120657). 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-120657S1
-
|
|
Isotope-Labeled Compounds
CGRP Receptor
NF-κB
|
Others
|
|
9-PAHSA-d31 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-180398
-
|
|
PPAR
PGC-1α
|
Metabolic Disease
|
|
PA-082 is a selective PPAR-γ modulator that functions as a partial agonist. PA-082 causes partial recruitment of SRC1, TIF2, SRC3 and full recruitment of PGC1-α to PPAR-γ ligand-binding domain. PA-082 prevents triglyceride accumulation during de novo adipogenesis and antagonizes Rosiglitazone (HY-17386)-induced lipid accumulation. PA-082 potentiates insulin-stimulated glucose uptake in adipocytes and protects against TNFα-induced insulin resistance. PA-082 can be used for the research of type 2 diabetes .
|
-
-
- HY-153149
-
|
|
Adenosine Receptor
Apoptosis
PGC-1α
|
Metabolic Disease
Inflammation/Immunology
|
|
LJ-2698 is an orally active adenosine A3 receptor antagonist. LJ-2698 induces increased levels of anti-inflammatory cytokines in macrophages and significantly elevates the number of anti-inflammatory M2 macrophages in the lung. LJ-2698 prevents alveolar cavity enlargement, restores pulmonary function, inhibits matrix metalloproteinase activity and pulmonary cell apoptosis in the lung tissues of mice. LJ-2698 prevents renal injury, inhibits renal lipid accumulation, and increases PGC1α levels in renal tissues of mice with diabetic nephropathy. LJ-2698 is applicable to the research of emphysema and diabetic nephropathy .
|
-
-
- HY-181062
-
|
|
HSP
Apoptosis
Autophagy
ULK
RIP kinase
CDK
|
Cancer
|
|
VWK147 is a second-generation HSP90 C-terminal domain (CTD) inhibitor. VWK147 targets the CTD dimerization interface, prevents HSP90 CTD dimerization, disrupts co-chaperone PPID binding to HSP90 CTD, and inhibits HSP90 chaperone function dependent on dimerization. VWK147 reduces protein levels of HSP90 client proteins ULK1, RIPK1, and CDK4 without inducing a heat shock response. VWK147 induces cell death, including apoptosis, in Cisplatin (HY-17394)-sensitive and -resistant urothelial carcinoma cells. VWK147 induces LC3-II accumulation, inhibits autophagosome-lysosome fusion to block canonical autophagy, and induces non-canonical LC3 lipidation independent of ULK1 and PIK3C3 complexes. VWK147 can be used for the research of urothelial carcinoma .
|
-
| Cat. No. |
Product Name |
Category |
Target |
Chemical Structure |
-
- HY-N2515
-
-
-
- HY-133707
-
-
-
- HY-143712
-
|
|
Structural Classification
Classification of Application Fields
Metabolic Disease
Endogenous metabolite
Disease Research Fields
Steroids
Source Classification
|
Drug Metabolite
G protein-coupled Bile Acid Receptor 1
ROR
|
|
Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC50 = 2.7 μM) and RORγt inverse agonist (IC50 = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .
|
-
-
- HY-N1990
-
|
|
Cardiovascular Disease
Triterpenes
Structural Classification
Classification of Application Fields
Terpenoids
Cucurbitaceae
Plants
Gynostemma pentaphyllum (Thunb.) Makino
Disease Research Fields
Source Classification
|
PPAR
Sirtuin
Keap1-Nrf2
Toll-like Receptor (TLR)
NF-κB
Reactive Oxygen Species (ROS)
NOD-like Receptor (NLR)
Apoptosis
Pyroptosis
Autophagy
|
|
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 .
|
-
-
- HY-120657
-
|
|
Structural Classification
Classification of Application Fields
Ketones, Aldehydes, Acids
Other Diseases
Endogenous metabolite
Disease Research Fields
Source Classification
|
CGRP Receptor
NF-κB
|
|
9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-143712R
-
|
|
Structural Classification
Endogenous metabolite
Steroids
Source Classification
|
Reference Standards
Drug Metabolite
G protein-coupled Bile Acid Receptor 1
ROR
|
|
Allolithocholic acid (Standard) is the analytical standard of Allolithocholic acid (HY-143712). This product is intended for research and analytical applications. Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC50 = 2.7 μM) and RORγt inverse agonist (IC50 = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .
|
-
-
- HY-N2515R
-
|
|
Panax ginseng C. A. Meyer
Triterpenes
Structural Classification
Terpenoids
Plants
Araliaceae
Source Classification
|
Reference Standards
NF-κB
PI3K
JAK
Apoptosis
|
|
Ginsenoside Rk1 (Standard) is the analytical standard of Ginsenoside Rk1. This product is intended for research and analytical applications. Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures .
Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB .
Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis .
Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway .
|
-
-
- HY-120657R
-
|
|
Structural Classification
Ketones, Aldehydes, Acids
Endogenous metabolite
Source Classification
|
Reference Standards
CGRP Receptor
NF-κB
|
|
Flumethrin (Standard) is the analytical standard of Flumethrin. This product is intended for research and analytical applications. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
| Cat. No. |
Product Name |
Chemical Structure |
-
- HY-W770410
-
|
|
|
9-PAHSA- 13C4 is 13C-labeled 9-PAHSA. 9-PAHSAis an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSAsignificantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSAinduces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSAregulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSAdoes not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSAcan be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-143712S1
-
|
|
|
Allolithocholic Acid-d4 (3α-hydoxy-5α-Cholaoic Acid-d4, allo-LCA-d4) is deuterium labeled Allolithocholic acid (HY-143712). Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC50 = 2.7 μM) and RORγt inverse agonist (IC50 = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease .
|
-
-
- HY-120657S
-
|
|
|
9-PAHSA-d4 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-W777281
-
|
|
|
Fluocinolone acetonide- 13C3 is the 13C-labeled Fluocinolone (Acetonide) (HY-B0415). Fluocinolone is a glucocorticoid glucocorticoid receptor agonist. Fluocinolone is effective in preventing both lipid accumulation and inflammation. Fluocinolone can promote the proliferation of DPCs and has the potential role in repairing injured pulp tissues. Fluocinolone can be used to study the prevention of chemotherapy-induced peripheral neuropathy caused by Paclitaxel (HY-B0015) .
|
-
-
- HY-144026S
-
|
|
|
9-PAHSA-d9 is the deuterium labeled 9-PAHSA (HY-120657). 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
|
-
-
- HY-120657S1
-
|
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9-PAHSA-d31 is the deuterium labeled 9-PAHSA. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease .
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