fat and glucose metabolism

By Targets:	Acetyl-CoA Carboxylase (2) Akt (4) AMPK (1) Apoptosis (5) Autophagy (1) Bacterial (1) Cytochrome P450 (1) FXR (2) Glucokinase (2) Glycosidase (1) Glycosyltransferase (1) GSK-3 (4) Insulin Receptor (1) Isotope-Labeled Compounds (2) MetAP (2) NF-κB (2) Reactive Oxygen Species (ROS) (4) Reference Standards (2)
By Research Areas:	Cancer (1) Cardiovascular Disease (3) Endocrinology (5) Infection (1) Inflammation/Immunology (1) Metabolic Disease (14) Neurological Disease (5)

Targets Recommended: Mitochondrial Metabolism GLUT Fat Mass and Obesity-associated Protein (FTO) Glucose-6-Phosphate Isomerase (GPI) SGLT

Cat. No.	상품명	Target	연구분야	Chemical Structure

HY-W014901

Bisphenol F BPF; 4,4'-Dihydroxydiphenylmethane	Reactive Oxygen Species (ROS) Akt GSK-3 Apoptosis	Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology
Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

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 .

HY-15671

GKA50	Glucokinase	Metabolic Disease
GKA50 is a potent glucokinase activator (EC₅₀=33 nM at 5 mM glucose). GKA50 stimulates insulin release from mouse islets of Langerhans. GKA50 is a glucose-like activator of beta-cell metabolism in rodent and human islets and a Ca ²⁺-dependent modulator of insulin secretion. GKA50 shows significant glucose lowering in high fat fed female rats .

HY-N2181

Acetylshikonin 3 Publications Verification	Cytochrome P450 Apoptosis Bacterial Autophagy	Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Acetylshikonin is an oral active anti-cancer, anti-inflammatory, antioxidant, anti-fertility, antibacterial, and neuroprotective agent. Acetylshikonin is a inhibitor of acetylcholinase (AChE) (IC₅₀=34.6 μM) and nonselective cytochrome P450. Acetylshikonin can induce Apoptosis and Autophagy in cancer cells. Acetylshikonin regulates blood glucose, liver fat metabolism, and renal fibrosis, and is used in the study of diabetes, diabetic nephropathy (DN), obesity, and nonalcoholic fatty liver disease (NAFLD) .

HY-14811

Beloranib ZGN-440; CKD-732 free base	MetAP NF-κB	Metabolic Disease
Beloranib (ZGN-440; CKD-732 free base) is a selective, irreversible inhibitor of methionine aminopeptidase MetAP2 that suppresses appetite and increases energy expenditure. Beloranib blocks the enzymatic cleavage of N-terminal methionine from nascent proteins by forming a covalent bond with MetAP2, thereby regulating fatty acid metabolism, adrenergic signaling, and hypothalamic NF-κB expression. Beloranib significantly reduces food intake, body weight, and fat accumulation, while improving glucose tolerance, insulin sensitivity, and lipid metabolism. Beloranib also elevates energy expenditure and fat oxidation levels, without affecting body temperature, spontaneous activity, or the inflammatory cytokine IL-1β. Beloranib can be used in research on obesity and hypothalamic obesity .

HY-14811A

Beloranib hemioxalate ZGN-440 hemioxalate; ZGN-433 hemioxalate; CDK732 hemioxalate	NF-κB MetAP	Metabolic Disease
Beloranib (ZGN-440; CKD-732 free base) hemioxalate is a selective, irreversible inhibitor of methionine aminopeptidase MetAP2 that suppresses appetite and increases energy expenditure. Beloranib hemioxalate blocks the enzymatic cleavage of N-terminal methionine from nascent proteins by forming a covalent bond with MetAP2, thereby regulating fatty acid metabolism, adrenergic signaling, and hypothalamic NF-κB expression. Beloranib hemioxalate significantly reduces food intake, body weight, and fat accumulation, while improving glucose tolerance, insulin sensitivity, and lipid metabolism. Beloranib hemioxalate also elevates energy expenditure and fat oxidation levels, without affecting body temperature, spontaneous activity, or the inflammatory cytokine IL-1β. Beloranib hemioxalate can be used in research on obesity and hypothalamic obesity .

HY-N13248

Mulberry Leaf Extract	Glycosidase	Metabolic Disease
Mulberry Leaf Extract is a mulberry leaf extract, and its components include: 1-Deoxynojirimycin. Mulberry Leaf Extract can effectively alleviate the adverse effects of high-fat diet on blood lipids and renal function, regulate lipid metabolism abnormalities, and significantly inhibit the accumulation of glycosylated substances in glomeruli. Mulberry Leaf Extract can regulate the key signaling pathways of diabetic nephropathy, but does not directly affect blood glucose levels. .

HY-W014901S

Bisphenol F-13C6 BPF-¹³C₆; 4,4'-Dihydroxydiphenylmethane-¹³C₆	Isotope-Labeled Compounds Reactive Oxygen Species (ROS) Akt GSK-3 Apoptosis	Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology
Bisphenol F- ¹³C₆ is the ¹³C labeled Bisphenol F (HY-W014901). Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

HY-120872

AJS1669 free acid	Glycosyltransferase	Metabolic Disease
AJS1669 free acid is a potent and orally available glycogen synthase (GS) activator. AJS1669 improves glucose metabolism and reduces body fat mass in mice[1].

HY-W014901S1

Bisphenol F-13C12 BPF-¹³C₁₂; 4,4'-Dihydroxydiphenylmethane-¹³C₁₂	Isotope-Labeled Compounds Reactive Oxygen Species (ROS) Akt GSK-3 Apoptosis	Cardiovascular Disease Neurological Disease Metabolic Disease Endocrinology
Bisphenol F- ¹³C₁₂ is the ¹³C labeled Bisphenol F (HY-W014901). Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

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 .

HY-P3578

Gastric Inhibitory Polypeptide (1-30), porcine	Insulin Receptor	Endocrinology
Gastric Inhibitory Polypeptide (1-30), porcine lacks the C-terminal 12 amino acid residues of natural gastric inhibitory polypeptide (GIP), exhibits biologic activity by potentiating the release of insulin and somatostatin .

HY-15671A

GKA50 quarterhydrate	Glucokinase	Metabolic Disease
GKA50 quarterhydrate is a potent glucokinase activator (EC₅₀=33 nM at 5 mM glucose) and stimulates insulin release from mouse islets of Langerhans. GKA50 quarterhydrate is a glucose-like activator of beta-cell metabolism in rodent and human islets and a Ca ²⁺-dependent modulator of insulin secretion. GKA50 quarterhydrate shows significant glucose lowering in high fat fed female rats .

HY-162703

Lipid-lowering agent-2	AMPK	Metabolic Disease
Lipid-lowering agent-2 (Compound 14d) is an orally active lipid-lowering agent with an EC₅₀ of 0.06 μM. Lipid-lowering agent-2 inhibits the lipid synthesis, activates the AMPK signaling pathway, and exhibits anti-obesity effect. Lipid-lowering agent-2 inhibits food intake, improves the glucose metabolism, and reduces the body weight and adipose tissue in high-fat diet (HFD)-induced obese mice .

HY-W014901R

Bisphenol F (Standard) BPF (Standard); 4,4'-Dihydroxydiphenylmethane (Standard)	Reference Standards Reactive Oxygen Species (ROS) Akt GSK-3 Apoptosis	Neurological Disease Metabolic Disease Endocrinology
Bisphenol F (Standard) is the analytical standard of Bisphenol F (HY-W014901). This product is intended for research and analytical applications. Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

Cat. No.	상품명

HY-L083

Anti-Cancer Metabolism Compound Library	3,626 compounds
Mutations in oncogenes and tumor suppressor genes can modify multiple signaling pathways and in turn cell metabolism, which facilitates tumorigenesis. The paramount hallmark of tumor metabolism is “aerobic glycolysis” or the Warburg effect, coined by Otto Warburg in 1926, in which cancer cells produce most of energy from glycolysis pathway regardless of whether in aerobic or anaerobic condition. Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside. The increased uptake of glucose is facilitated by the overexpression of several isoforms of membrane glucose transporters (GLUTs). Likewise, the metabolic pathways of glutamine, amino acid and fat metabolism are also altered. Recent trends in anti-cancer drug discovery suggests that targeting the altered metabolic pathways of cancer cells result in energy crisis inside the cancer cells and can selectively inhibit cancer cell proliferation by delaying or suppressing tumor growth. MCE provides a unique collection of 3,626 compounds which cover various tumor metabolism-related signaling pathways. These compounds can be used for anti-cancer metabolism targets identification, validation as well anti-cancer drug discovery.

Anti-Cancer Metabolism Compound Library

3,626 compounds

Mutations in oncogenes and tumor suppressor genes can modify multiple signaling pathways and in turn cell metabolism, which facilitates tumorigenesis. The paramount hallmark of tumor metabolism is “aerobic glycolysis” or the Warburg effect, coined by Otto Warburg in 1926, in which cancer cells produce most of energy from glycolysis pathway regardless of whether in aerobic or anaerobic condition. Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside. The increased uptake of glucose is facilitated by the overexpression of several isoforms of membrane glucose transporters (GLUTs). Likewise, the metabolic pathways of glutamine, amino acid and fat metabolism are also altered. Recent trends in anti-cancer drug discovery suggests that targeting the altered metabolic pathways of cancer cells result in energy crisis inside the cancer cells and can selectively inhibit cancer cell proliferation by delaying or suppressing tumor growth.

MCE provides a unique collection of 3,626 compounds which cover various tumor metabolism-related signaling pathways. These compounds can be used for anti-cancer metabolism targets identification, validation as well anti-cancer drug discovery.

Cat. No.	상품명	Target	Research Area

HY-P3578

Gastric Inhibitory Polypeptide (1-30), porcine	Insulin Receptor	Endocrinology
Gastric Inhibitory Polypeptide (1-30), porcine lacks the C-terminal 12 amino acid residues of natural gastric inhibitory polypeptide (GIP), exhibits biologic activity by potentiating the release of insulin and somatostatin .

Cat. No.	상품명	Category	Target	Chemical Structure

HY-W014901

Bisphenol F BPF; 4,4'-Dihydroxydiphenylmethane	Classification of Application Fields Orchidaceae Galeola faberi Rolfe Phenols Polyphenols Metabolic Disease Plants Disease Research Fields Source Classification	Reactive Oxygen Species (ROS) Akt GSK-3 Apoptosis
Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

HY-N0468

Rebaudioside D 1 Publications Verification	Structural Classification other families Classification of Application Fields Terpenoids Metabolic Disease Diterpenoids Plants Disease Research Fields Sweeteners Source Classification Food Research	FXR Acetyl-CoA Carboxylase
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 .

HY-N2181

Acetylshikonin 3 Publications Verification	Quinones Classification of Application Fields Phenols Polyphenols Plants Lithospermum erythrorhizon Sieb. et Zucc. Naphthalene Quinones Boraginaceae Inflammation/Immunology Disease Research Fields Source Classification	Cytochrome P450 Apoptosis Bacterial Autophagy
Acetylshikonin is an oral active anti-cancer, anti-inflammatory, antioxidant, anti-fertility, antibacterial, and neuroprotective agent. Acetylshikonin is a inhibitor of acetylcholinase (AChE) (IC₅₀=34.6 μM) and nonselective cytochrome P450. Acetylshikonin can induce Apoptosis and Autophagy in cancer cells. Acetylshikonin regulates blood glucose, liver fat metabolism, and renal fibrosis, and is used in the study of diabetes, diabetic nephropathy (DN), obesity, and nonalcoholic fatty liver disease (NAFLD) .

HY-N0468R

Rebaudioside D (Standard)	Structural Classification other families Terpenoids Diterpenoids Plants Source Classification	Reference Standards Acetyl-CoA Carboxylase FXR
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 .

HY-W014901R

Bisphenol F (Standard) BPF (Standard); 4,4'-Dihydroxydiphenylmethane (Standard)	Orchidaceae Galeola faberi Rolfe Phenols Polyphenols Plants Source Classification	Reference Standards Reactive Oxygen Species (ROS) Akt GSK-3 Apoptosis
Bisphenol F (Standard) is the analytical standard of Bisphenol F (HY-W014901). This product is intended for research and analytical applications. Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

Cat. No.	상품명	Chemical Structure

HY-W014901S

Bisphenol F-13C6
Bisphenol F- ¹³C₆ is the ¹³C labeled Bisphenol F (HY-W014901). Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

Bisphenol F-13C6

Bisphenol F- ¹³C₆ is the ¹³C labeled Bisphenol F (HY-W014901). Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

HY-W014901S1

Bisphenol F-13C12
Bisphenol F- ¹³C₁₂ is the ¹³C labeled Bisphenol F (HY-W014901). Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

Bisphenol F-13C12

Bisphenol F- ¹³C₁₂ is the ¹³C labeled Bisphenol F (HY-W014901). Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260) .

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