fatty acid synthesis pathway

Pathways Recommended:	MAPK/ERK Pathway

By Targets:	Acetyl-CoA Carboxylase (3) AMPK (2) Apoptosis (1) Biochemical Assay Reagents (1) COX (2) Endogenous Metabolite (6) FXR (4) Phospholipase (2) PROTAC Linkers (1) Reference Standards (3)
By Research Areas:	Cancer (1) Infection (2) Inflammation/Immunology (3) Metabolic Disease (10) Neurological Disease (2)
Oligonucleotides:	Phospholipids (1)

Targets Recommended: Tissue Factor Pathway Inhibitor (TFPI) DNA/RNA Synthesis Free Fatty Acid Receptor Fatty Acid Synthase (FASN) FATP FABP FAAH ELOVL

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-N9933

Tauro-β-muricholic acid 4 Publications Verification TβMCA	FXR Apoptosis	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC₅₀=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .

HY-W015924

2-Hydroxyisobutyric acid	Endogenous Metabolite	Metabolic Disease
2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

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-N8469

cis-5-Dodecenoic acid	COX	Inflammation/Immunology
cis-5-Dodecenoic acid is an inhibitor of COX-I and COX-II with anti-inflammatory activity. cis-5-Dodecenoic acid reduces prostaglandin synthesis by inhibiting COX enzyme activity and is involved in the fatty acid -β oxidative metabolic pathway. The metabolic rate of cis-5-Dodecenoic acid is significantly lower than that of saturated fatty acids. cis-5-Dodecenoic acid can be used in the research of anti-inflammation, fatty acid metabolism mechanisms and related physiological and pathological processes .

HY-P2994

3-Hydroxybutyrate dehydrogenase 3-HBDH	Endogenous Metabolite	Metabolic Disease
3-Hydroxybutyrate dehydrogenase (3-HBDH), a mitochondrial enzyme, is a key enzyme in the ketone body metabolism pathway. 3-Hydroxybutyrate dehydrogenase is the last enzyme for ketone synthesis in the liver and the first enzyme for ketone breakdown in extracellular tissues. The absence of 3-Hydroxybutyrate dehydrogenase leads to the inhibition of fatty acid oxidation in the liver during fasting in mice, resulting in lipid accumulation and the development of fatty liver .

HY-N7392A

Acetoacetyl-CoA sodium hydrate 3-Oxobutanoyl-coenzyme A sodium hydrate	Endogenous Metabolite	Metabolic Disease
Acetoacetyl CoA sodium hydrate is the precursor of HMG-CoA in the mevalonate pathway. Acetoacetyl-CoA thiolase catalyzes the reaction to form acetoacetyl-CoA sodium hydrate from two acetyl-CoA molecules. Acetoacetyl CoA sodium hydrate is essential for cholesterol biosynthesis. Acetoacetyl-CoA sodium hydrate is also a intermediate in the biological breakdown and synthesis of fatty acids .

HY-Y1139

Pimelic acid 2 Publications Verification Heptanedioic acid; 1,5-Pentanedicarboxylic acid; 1,7-Heptanedioic acid	Endogenous Metabolite PROTAC Linkers	Metabolic Disease
Pimelic acid (Heptanedioic acid; 1,5-Pentanedicarboxylic acid) is a seven-carbon α,ω-dicarboxylic acid and a downstream product of fatty acid synthesis. Pimelic acid is a key precursor in biotin biosynthesis. Pimelic acid can be converted to pimelic acid-CoA by the BioW enzyme, thereby bypassing exogenous biotin requirements to support growth in various biotinytrophic bacteria and fungi, and reversing antibiotic-induced inhibition of biotin synthesis. Furthermore, Pimelic acid has been proposed as a highly specific biomarker for oxygen-induced retinopathy in mice. Pimelic acid can be used to study retinopathy of preterm infants, oxygen-induced retinopathy, and microbial biotin metabolism .

HY-N7392

Acetoacetyl-CoA 3-Oxobutanoyl-coenzyme A	Endogenous Metabolite	Metabolic Disease
Acetoacetyl CoA is the precursor of HMG-CoA in the mevalonate pathway. Acetoacetyl-CoA thiolase catalyzes the reaction to form acetoacetyl-CoA from two acetyl-CoA molecules. Acetoacetyl CoA is essential for cholesterol biosynthesis. Acetoacetyl-CoA is also a intermediate in the biological breakdown and synthesis of fatty acids .

HY-148009

Cardiolipin (16:0/18:1/16:0/18:1) sodium 16:0-18:1 Cardiolipin sodium	Biochemical Assay Reagents	Others
Cardiolipin (16:0/18:1/16:0/18:1) (16:0-18:1 Cardiolipin) sodium is a di-saturated mitochondrial-specific anionic phospholipid sodium salt containing the long-chain fatty acid palmitic acid (HY-N0830) and the monounsaturated fatty acid oleic acid (HY-N1446). Cardiolipin (16:0/18:1/16:0/18:1) sodium undergoes in-source fragmentation via diglyceride (DG)-H₂O fragment formation and (DG-H₂O) fragment loss pathways. Cardiolipin (16:0/18:1/16:0/18:1) sodium can be used in the synthesis of lipid nanodiscs for application in in situ mass spectrometry .

HY-112747

Soy PE LPI; PE (soy)	Phospholipase	Infection
Soy PE (LPI) is the most abundant phospholipid in prokaryotes and the second most abundant found in the membrane of mammalian, plant, and yeast cells, comprising approximately 25% of total mammalian phospholipids. In the brain, phosphatidylethanolamine comprises almost half of the total phospholipids. It is synthesized mainly through the cytidine diphosphate-ethanolamine and phosphatidylserine decarboxylation pathways, which occur in the endoplasmic reticulum (ER) and mitochondrial membranes, respectively. It is a precursor in the synthesis of phosphatidylcholine and arachidonoyl ethanolamide and is a source of ethanolamine used in various cellular functions. In E.coli, phosphatidylethanolamine deficiency prevents proper assembly of lactose permease, suggesting a role as a lipid chaperone. It is a cofactor in the propagation of prions in vitro and can convert recombinant mammalian proteins into infectious molecules even in the absence of RNA. This product contains phosphatidylethanolamine molecular species with variable fatty acyl chain lengths at the sn-1 and sn-2 positions .

HY-124609

CAD031	AMPK Acetyl-CoA Carboxylase	Neurological Disease
CAD031 is an orally active AMPK/ACC1 signaling pathway activator and a derivative of the Alzheimer's disease (AD) targeted agent J147 (HY-13779) (more active than J147 in human neural stem cell assays). CAD031 can cross the blood-brain barrier, activate AMPK and inhibit ACC1, thereby increasing ac-CoA levels, improving mitochondrial function and reducing free fatty acid synthesis. CAD031 has neuroprotective, neurogenesis-promoting and memory-improving activities and can be used in the study of Alzheimer's disease and aging-related neurodegenerative diseases. CAD031 effectively enhances the memory of mice, improves dendritic structure, and stimulates cell division in the germinal zone of the brain of elderly mice .

HY-W015924R

2-Hydroxyisobutyric acid (Standard)	Reference Standards Endogenous Metabolite	Metabolic Disease
2-Hydroxyisobutyric acid (Standard) is the analytical standard of 2-Hydroxyisobutyric acid. This product is intended for research and analytical applications. 2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

HY-24547

HpFabZ-IN-1	Phospholipase	Infection
HpFabZ-IN-1 (Compound 1) is an inhibitor of the key enzyme FabZ in the Helicobacter pylori fatty acid synthesis pathway, with its IC₅₀ value being 39.8 µM. HpFabZ-IN-1 does not possess antibacterial activity .

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-N8469R

cis-5-Dodecenoic acid (Standard)	Reference Standards COX	Inflammation/Immunology
cis-5-Dodecenoic acid (Standard) is the analytical standard of cis-5-Dodecenoic acid (HY-N8469). This product is intended for research and analytical applications. cis-5-Dodecenoic acid is an inhibitor of COX-I and COX-II with anti-inflammatory activity. cis-5-Dodecenoic acid reduces prostaglandin synthesis by inhibiting COX enzyme activity and is involved in the fatty acid -β oxidative metabolic pathway. The metabolic rate of cis-5-Dodecenoic acid is significantly lower than that of saturated fatty acids. cis-5-Dodecenoic acid can be used in the research of anti-inflammation, fatty acid metabolism mechanisms and related physiological and pathological processes .

HY-183279

FXR antagonist 4	FXR AMPK	Metabolic Disease
FXR antagonist 4 (Compound 4l) is an orally active, selective FXR antagonist with an IC₅₀ of 0.70 μM. FXR antagonist 4 binds to FXR, differentially regulates bile acid and lipid transporter genes, and exerts no effect on gluconeogenesis-related genes. FXR modulator 1 activates the AMPK signaling pathway to inhibit fatty acid synthesis. FXR modulator 1 alleviates hepatic steatosis, ballooning degeneration and fibrosis, and improves dyslipidemia. FXR modulator 1 can be used for research on metabolic dysfunction-associated steatohepatitis .

Cat. No.	Product Name

HY-L064

Glutamine Metabolism Compound Library	1,690 compounds
Glutamine is an important metabolic fuel that helps rapidly proliferating cells meet the increased demand for ATP, biosynthetic precursors, and reducing agents. Glutamine Metabolism pathway involves the initial deamination of glutamine by glutaminase(GLS), yielding glutamate and ammonia. Glutamate is converted to the TCA cycle intermediate α-ketoglutarate (α-KG) by either glutamate dehydrogenase (GDH) or by the alanine or aspartate transaminases (TAs), to produce both ATP and anabolic carbons for the synthesis of amino acids, nucleotides and lipids. During periods of hypoxia or mitochondrial dysfunction, α-KG can be converted to citrate in a reductive carboxylation reaction catalyzed by IDH2. The newly formed citrate exits the mitochondria where it is used to synthesize fatty acids and amino acids and produce the reducing agent, NADPH. Cancer cells display an altered metabolic circuitry that is directly regulated by oncogenic mutations and loss of tumor suppressors. Mounting evidence indicates that altered glutamine metabolism in cancer cells has critical roles in supporting macromolecule biosynthesis, regulating signaling pathways, and maintaining redox homeostasis, all of which contribute to cancer cell proliferation and survival. Thus, intervention in glutamine metabolic processes could provide novel approaches to improve cancer treatment. MCE owns a unique collection of 1,690 compounds targeting the mainly proteins and enzymes involved in glutamine metabolism pathway. Glutamine Metabolism compound library is a useful tool for intervention in glutamine metabolic processes.

Glutamine Metabolism Compound Library

1,690 compounds

Glutamine is an important metabolic fuel that helps rapidly proliferating cells meet the increased demand for ATP, biosynthetic precursors, and reducing agents. Glutamine Metabolism pathway involves the initial deamination of glutamine by glutaminase(GLS), yielding glutamate and ammonia. Glutamate is converted to the TCA cycle intermediate α-ketoglutarate (α-KG) by either glutamate dehydrogenase (GDH) or by the alanine or aspartate transaminases (TAs), to produce both ATP and anabolic carbons for the synthesis of amino acids, nucleotides and lipids. During periods of hypoxia or mitochondrial dysfunction, α-KG can be converted to citrate in a reductive carboxylation reaction catalyzed by IDH2. The newly formed citrate exits the mitochondria where it is used to synthesize fatty acids and amino acids and produce the reducing agent, NADPH.

Cancer cells display an altered metabolic circuitry that is directly regulated by oncogenic mutations and loss of tumor suppressors. Mounting evidence indicates that altered glutamine metabolism in cancer cells has critical roles in supporting macromolecule biosynthesis, regulating signaling pathways, and maintaining redox homeostasis, all of which contribute to cancer cell proliferation and survival. Thus, intervention in glutamine metabolic processes could provide novel approaches to improve cancer treatment.

MCE owns a unique collection of 1,690 compounds targeting the mainly proteins and enzymes involved in glutamine metabolism pathway. Glutamine Metabolism compound library is a useful tool for intervention in glutamine metabolic processes.

Cat. No.	Product Name	Type

HY-N7392

Acetoacetyl-CoA 3-Oxobutanoyl-coenzyme A	Biochemical Assay Reagents
Acetoacetyl CoA is the precursor of HMG-CoA in the mevalonate pathway. Acetoacetyl-CoA thiolase catalyzes the reaction to form acetoacetyl-CoA from two acetyl-CoA molecules. Acetoacetyl CoA is essential for cholesterol biosynthesis. Acetoacetyl-CoA is also a intermediate in the biological breakdown and synthesis of fatty acids .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N9933

Tauro-β-muricholic acid 4 Publications Verification TβMCA	Structural Classification Human Gut Microbiota Metabolites Animals Endogenous metabolite Steroids Source Classification	FXR Apoptosis
Tauro-β-muricholic acid (TβMCA) is an orally active trihydroxylated bile acid and a competitive, reversible FXR antagonist (IC₅₀=40 μM). Tauro-β-muricholic acid inhibits bile acid-induced hepatocyte apoptosis by maintaining mitochondrial membrane potential, while simultaneously inhibiting intestinal FXR signaling, affecting bile acid synthesis, hepatic lipid metabolism, and insulin sensitivity. Accumulation of tauro-β-muricholic acid disrupts metabolic homeostasis, promoting cancer stem cell proliferation and tumor progression. The mechanisms of tauro-β-muricholic acid involve two aspects: first, inhibiting the translocation of the pro-apoptotic protein Bax to mitochondria and maintaining mitochondrial membrane potential (MMP); and second, blocking the FXR signaling pathway to regulate bile acid metabolism, reduce serum ceramide production, and downregulate the hepatic SREBP1C/CIDEA pathway. Tauro-β-muricholic acid possesses anti-hepatocyte apoptosis, bile acid homeostasis regulation, and liver fat accumulation reduction properties, and also functions as a biomarker, making it useful in the study of diseases such as bile acid metabolism disorders, non-alcoholic fatty liver disease, colorectal cancer, and liver fibrosis .

HY-W015924

2-Hydroxyisobutyric acid	Classification of Application Fields Ketones, Aldehydes, Acids Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

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-N8469

cis-5-Dodecenoic acid	Microorganisms Classification of Application Fields Ketones, Aldehydes, Acids Inflammation/Immunology Disease Research Fields Source Classification	COX
cis-5-Dodecenoic acid is an inhibitor of COX-I and COX-II with anti-inflammatory activity. cis-5-Dodecenoic acid reduces prostaglandin synthesis by inhibiting COX enzyme activity and is involved in the fatty acid -β oxidative metabolic pathway. The metabolic rate of cis-5-Dodecenoic acid is significantly lower than that of saturated fatty acids. cis-5-Dodecenoic acid can be used in the research of anti-inflammation, fatty acid metabolism mechanisms and related physiological and pathological processes .

HY-N7392A

Acetoacetyl-CoA sodium hydrate 3-Oxobutanoyl-coenzyme A sodium hydrate	Alkaloids Microorganisms Classification of Application Fields Metabolic Disease Disease Research Fields Indole Alkaloids Source Classification	Endogenous Metabolite
Acetoacetyl CoA sodium hydrate is the precursor of HMG-CoA in the mevalonate pathway. Acetoacetyl-CoA thiolase catalyzes the reaction to form acetoacetyl-CoA sodium hydrate from two acetyl-CoA molecules. Acetoacetyl CoA sodium hydrate is essential for cholesterol biosynthesis. Acetoacetyl-CoA sodium hydrate is also a intermediate in the biological breakdown and synthesis of fatty acids .

HY-Y1139

Pimelic acid 2 Publications Verification Heptanedioic acid; 1,5-Pentanedicarboxylic acid; 1,7-Heptanedioic acid	Structural Classification Immune System Disorder Classification of Application Fields Ketones, Aldehydes, Acids Disease markers Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite PROTAC Linkers
Pimelic acid (Heptanedioic acid; 1,5-Pentanedicarboxylic acid) is a seven-carbon α,ω-dicarboxylic acid and a downstream product of fatty acid synthesis. Pimelic acid is a key precursor in biotin biosynthesis. Pimelic acid can be converted to pimelic acid-CoA by the BioW enzyme, thereby bypassing exogenous biotin requirements to support growth in various biotinytrophic bacteria and fungi, and reversing antibiotic-induced inhibition of biotin synthesis. Furthermore, Pimelic acid has been proposed as a highly specific biomarker for oxygen-induced retinopathy in mice. Pimelic acid can be used to study retinopathy of preterm infants, oxygen-induced retinopathy, and microbial biotin metabolism .

HY-N7392

Acetoacetyl-CoA 3-Oxobutanoyl-coenzyme A	Human Gut Microbiota Metabolites Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Endogenous Metabolite
Acetoacetyl CoA is the precursor of HMG-CoA in the mevalonate pathway. Acetoacetyl-CoA thiolase catalyzes the reaction to form acetoacetyl-CoA from two acetyl-CoA molecules. Acetoacetyl CoA is essential for cholesterol biosynthesis. Acetoacetyl-CoA is also a intermediate in the biological breakdown and synthesis of fatty acids .

HY-W015924R

2-Hydroxyisobutyric acid (Standard)	Structural Classification Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	Reference Standards Endogenous Metabolite
2-Hydroxyisobutyric acid (Standard) is the analytical standard of 2-Hydroxyisobutyric acid. This product is intended for research and analytical applications. 2-Hydroxyisobutyric acid (2-HIBA) is a selective modulator of the Insulin/IGF-1 pathway and the p38 MAPK pathway, which reduces reactive oxygen species (ROS) and fat accumulation in Caenorhabditis elegans. 2-Hydroxyisobutyric acid promotes β-oxidation and inhibits fatty acid synthesis by upregulating SKN-1/NRF2 and downregulating SREBP-1c transcription factors. 2-Hydroxyisobutyric acid has anti-aging and lipid-lowering effects, and can be used to study metabolic diseases such as obesity and diabetes. 2-Hydroxyisobutyric acid is also a renewable precursor of methacrylate through 2-HIB-CoA mutase-mediated biosynthesis[1][2].

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-N8469R

cis-5-Dodecenoic acid (Standard)	Microorganisms Ketones, Aldehydes, Acids Source Classification	Reference Standards COX
cis-5-Dodecenoic acid (Standard) is the analytical standard of cis-5-Dodecenoic acid (HY-N8469). This product is intended for research and analytical applications. cis-5-Dodecenoic acid is an inhibitor of COX-I and COX-II with anti-inflammatory activity. cis-5-Dodecenoic acid reduces prostaglandin synthesis by inhibiting COX enzyme activity and is involved in the fatty acid -β oxidative metabolic pathway. The metabolic rate of cis-5-Dodecenoic acid is significantly lower than that of saturated fatty acids. cis-5-Dodecenoic acid can be used in the research of anti-inflammation, fatty acid metabolism mechanisms and related physiological and pathological processes .

Cat. No.	Product Name		Classification

HY-148009

Cardiolipin (16:0/18:1/16:0/18:1) sodium 16:0-18:1 Cardiolipin sodium		Phospholipids
Cardiolipin (16:0/18:1/16:0/18:1) (16:0-18:1 Cardiolipin) sodium is a di-saturated mitochondrial-specific anionic phospholipid sodium salt containing the long-chain fatty acid palmitic acid (HY-N0830) and the monounsaturated fatty acid oleic acid (HY-N1446). Cardiolipin (16:0/18:1/16:0/18:1) sodium undergoes in-source fragmentation via diglyceride (DG)-H₂O fragment formation and (DG-H₂O) fragment loss pathways. Cardiolipin (16:0/18:1/16:0/18:1) sodium can be used in the synthesis of lipid nanodiscs for application in in situ mass spectrometry .

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fatty acid synthesis pathway

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