lipogenesis

MT 63-78 is a specific and effective direct AMPK activator (EC50: 25 μM) that blocks prostate cancer growth by inhibiting the lipogenesis and mTORC1 pathways. It has antitumor effects and induces cell mitotic arrest and apoptosis.

Neomangiferin (Mangiferin 7-glucoside) has beneficial effects on high fat diet-induced nonalcoholic fatty liver disease in rats. Neomangiferin and mangiferin inhibit tartrate-resistant acid phosphatase, a biochemical marker of osteoclast function and bone resorption.

INT-767 is a potent farnesoid X receptor (FXR)/TGR5 dual agonist that prevents NASH and promotes visceral adipose brown lipogenesis and mitochondrial function for the study of non-alcoholic steatohepatitis.

L-(+)-Arabinose selectively inhibits intestinal sucrase in a non-competitive manner, thereby preventing glucose elevation induced by sucrose intake.

(-)-Hydroxycitric acid (Garcinia acid) is the principal acid found in the fruit rinds of Garcinia cambogia. It acts as a potent and competitive inhibitor of ATP citrate lyase, suppressing fatty acid synthesis, food intake, lipogenesis, and inducing weight loss.

SR9243, an LXR inverse agonist, can induce LXR-corepressor interaction; shows anticancer activity and selectively targets the lipogenesis and Warburg effect.

HDAC11-IN-2 (compound B6) is a highly selective inhibitor of Histone Deacetylase 11 (HDAC11). It demonstrates IC50 values of 51.1 ×10^-3 μM for HDAC11 and 5 μM for HDAC8. HDAC11-IN-2 reduces de novo lipogenesis (DNL) and enhances fatty acid oxidation, which alleviates hepatic lipid accumulation and pathological symptoms in MASLD mice. By inhibiting HDAC11, HDAC11-IN-2 enhances the phosphorylation of AMPKα1 at the Thr172 site, thereby modulating de novo lipogenesis and fatty acid oxidation in the liver.

AMPK activator17 (Compound 10g) is an orally bioavailable AMPK activator. It significantly inhibits lipogenesis (IC50: 3.4 μM) and improves dyslipidemia. By activating the AMPK pathway, AMPK activator17 suppresses early adipocyte differentiation (mitotic clonal expansion) and enhances mitochondrial function and fatty acid oxidation in mature adipocytes. It improves dyslipidemia through promoting cholesterol reverse transport. AMPK activator17 is applicable in research on obesity and associated metabolic disorders, such as type 2 diabetes and cardiovascular diseases.

TFCA is a liver X receptor α (LXRα) antagonist. It inhibits the coactivation of ligand-activated LXRα and suppresses the transcriptional expression of downstream target genes involved in fatty acid synthesis. By selectively inhibiting LXRα in the liver, TFCA reduces ligand-induced lipogenesis and fatty liver.

BGT-002 (326E) is an orally active dual ACLY inhibitor and PPARα agonist. It reduces lipogenesis by inhibiting synthesis and promoting excretion. BGT-002 has demonstrated efficacy in vivo for improving metabolic dysfunction-associated steatohepatitis (MASH) and alleviating hyperlipidemia. It is applicable for research on hypercholesterolemia and MASH.

Oltipraz metabolite M2 is the active metabolite of Oltipraz and acts as an orally effective HIF-1α inhibitor. In a high-fat diet mouse model, it enhances mitochondrial fuel oxidation and suppresses hepatic lipogenesis by dual activation of AMPK. Oltipraz metabolite M2 is applicable for research in hepatic steatosis and fatty liver disease.

Pinolenic Acid (PNLA) is an omega-6 polyunsaturated fatty acid extracted from pine nuts, with anti-inflammatory, anticancer, and lipid-lowering activities, improving oleic acid-induced lipogenesis and oxidative stress in HepG2 cells, useful in breast cancer research.

CTL-06, a Fatty Acid Synthase (FASN) inhibitor with an IC50 of 3 μM, induces apoptosis, while CTL-12 impedes cell cycle progression in the Sub-G1/S phase and modulates apoptotic and anti-apoptotic markers by upregulating caspase-9 and Bax and downregulating Bcl-xL. Additionally, CTL-12 suppresses de novo lipogenesis, curtailing the metabolic needs of tumor cells, with utilization in breast and colorectal cancer studies [1].

CTL-12, a fatty acid synthase (FASN) inhibitor (IC50: 2.5 μM), induces apoptosis and disrupts the cell cycle at the Sub-G1/S phase. It upregulates caspase-9 and the apoptosis marker Bax, while downregulating the anti-apoptotic marker Bcl-xL. By inhibiting de novo lipogenesis, CTL-12 thwarts tumor cells' metabolic requirements and is frequently employed in breast and colorectal cancer studies [1].

Haloxyfop-P-methyl, an aryloxyphenoxypropionate herbicide, is absorbed through both foliage and roots, where it inhibits lipogenesis and induces oxidative stress in susceptible plant species [1].

KHK-IN-3 (Example 1), a ketohexokinase (KHK) inhibitor, plays a crucial role in the study of various diseases including kidney disease, nonalcoholic steatohepatitis (NASH), diabetes, and heart failure. KHK, a pivotal rate-limiting enzyme and fructokinase, facilitates the metabolism of fructose by catalyzing the transformation of fructose into fructose-1-phosphate (FIP) utilizing ATP. This process lacks feedback inhibition, leading to the buildup of metabolites involved in lipogenesis, gluconeogenesis, and oxidative phosphorylation [1].

NNMTi (5-Amino-1-methylquinolinium) is a substrate site-targeting, selective nicotinamide N-methyltransferase (NNMT) inhibitor (IC50 = 1.2 μM; 50 μM SAM, 100 μM NCA) that reduces 3T3-L1 lipogenesis (EC50 = 30μM) and adipocytes 1-methylnicotinamide level (EC50 = 2.3 μM) without affecting related methyltransferases & enzymes in the NAD+ salvage pathway

Semaglutide-13C6,15N trifluoroacetic acid isotopes, is a form of Semaglutide trifluoroacetic acid. This compound is a long-acting, selective, competitive, orally active GLP-1R agonist capable of crossing the blood-brain barrier. Upon GLP-1R activation, it stimulates insulin secretion, inhibits gastric emptying and appetite, and enhances autophagy while reducing oxidative stress and apoptosis (apoptosis). Additionally, it modulates mitochondrial function and lipid metabolism, such as reducing hepatic de novo lipogenesis. Semaglutide trifluoroacetic acid exhibits activities including blood glucose reduction, weight loss, neuroprotection (such as improving motor function in Parkinson’s disease models and reducing α-synuclein aggregation), and amelioration of hepatic steatosis. It is useful for research into type 2 diabetes, obesity, Parkinson’s disease, metabolic-associated steatotic liver disease (MASLD), other neurodegenerative conditions, liver diseases, and cancer.

Semaglutide-d8 is the deuterium-labeled form of Semaglutide. Semaglutide, a long-acting, selective, competitive GLP-1R agonist, can cross the blood-brain barrier. Upon GLP-1R activation, it promotes insulin secretion, inhibits gastric emptying and appetite, and enhances autophagy while suppressing oxidative stress and apoptosis. It also regulates mitochondrial function and lipid metabolism, such as reducing hepatic de novo lipogenesis. Semaglutide exhibits activities like lowering blood glucose, weight reduction, neuroprotection (e.g., improving motor function in Parkinson’s models and reducing α-synuclein aggregation), and amelioration of hepatic steatosis. It is used in the research of type 2 diabetes, obesity, Parkinson’s disease, metabolic-associated steatotic liver disease (MASLD), other neurodegenerative diseases, liver disorders, and cancer.

Semaglutide-d8tetraTFA is a deuterium-labeled form of Semaglutide. Semaglutide is a long-acting, selective, competitive GLP-1 receptor agonist that crosses the blood-brain barrier. Upon activating the GLP-1 receptor, it enhances insulin secretion, suppresses gastric emptying and appetite, and improves mitochondrial function and lipid metabolism (such as reducing hepatic de novo lipogenesis). It offers antihyperglycemic, weight-reduction, neuroprotective (such as improving motor function in Parkinson's disease models and reducing α-synuclein aggregation), and hepatosteatosis amelioration effects. It is applicable in research on type 2 diabetes, obesity, Parkinson’s disease, metabolic-associated steatotic liver disease (MASLD), and certain neurodegenerative and liver diseases, as well as cancer.

D-Fructose (Standard) is the analytical standard of D-Fructose, primarily used for quantitative analysis and metabolomics research. D-Fructose is a predominant monosaccharide. Fructose metabolism (fructolysis) is distinct as it bypasses the key rate-limiting step of glycolysis (PFK1), leading to its significant role in lipogenesis and research concerning metabolic disorders.

Haloxyfop-P-methyl (Standard) is the standard substance of Haloxyfop-P-methyl, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Haloxyfop-P-methyl, an aryloxyphenoxypropionate herbicide, is absorbed through both foliage and roots, where it inhibits lipogenesis and induces oxidative stress in susceptible plant species .

L-(+)-Arabinose (Standard) is the standard substance of L-(+)-Arabinose, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. L-(+)-Arabinose inhibits intestinal sucrase activity, thereby reducing sucrose utilization, and consequently decreasing lipogenesis.

Palmitelaidic Acid (Standard) is a standard substance that can be used for analysis, and usually used as a reference standard sample in the research and analysis of palmitelaidic acid. Palmitelaidic acid is the trans isomer of palmitoleic acid, which belongs to trans monounsaturated fatty acid. Palmitelaidic Acid can enhance the phosphorylation of AMPK, up-regulate the expression of glucokinase and PPARα [2], and down-regulate the mRNA level of lipogenesis related genes (such as FAS] [3].