Carbocyclic Fatty Acids

Capsaicin ((E)-Capsaicin), an active component of chili peppers, is a TRPV1 agonist. Capsaicin induces a nociceptive response by binding to its receptors. Capsaicin has analgesic effects on neurological disorders. Capsaicin has antioxidant, anti-inflammatory, anti-cancer effects.

Prostaglandin E1 (Alprostadil) is a prostanoid receptor ligand, with K_is of 1.1 nM, 2.1 nM, 10 nM, 33 nM and 36 nM for mouse EP3, EP4, EP2, IP and EP1, respectively. Prostaglandin E1 induces vasodilation and inhibits platelet aggregation. Prostaglandin E1 can be used as a vasodilator for the research of peripheral vascular diseases.

Acetyl-coenzyme A (Acetyl-CoA) trisodium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A trisodium, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A trisodium is also a key precursor of lipid synthesis.

Lactyl-CoA is an acyl-CoA formally condensed from the sulfhydryl group of CoA and the carboxyl group of lactic acid, also known as lactyl-CoA. Lactyl-CoA is essential for the biosynthesis of biodegradable and biocompatible lactic acid-based copolymers.

α-Lipoic Acid (Thioctic acid) is an antioxidant, which is an essential cofactor of mitochondrial enzyme complexes. α-Lipoic Acid inhibits NF-κB-dependent HIV-1 LTR activation. α-Lipoic Acid induces endoplasmic reticulum (ER) stress-mediated apoptosis in hepatoma cells. α-Lipoic Acid can be used with CPUL1 (HY-151802) to construct the self-assembled nanoaggregate CPUL1-LA NA, which has improved antitumor efficacy than CPUL1.

3-Ketohexanoyl-CoA is a metabolic intermediate and an enzyme activity assay substrate, which can be used for the activity determination of 3-Hydroxyacyl-CoA dehydrogenase (HY-E71706) and 3-Ketothiolase. 3-Ketohexanoyl-CoA can be converted to hexanoyl-CoA through a continuous enzymatic reaction. 3-Ketohexanoyl-CoA can be cleaved into acetyl-CoA and butyryl-CoA by BktB.

2-Methylbutyryl-CoA is a branched-chain acyl-CoA substrate. It serves as the preferred substrate for potato 2-methylbutyryl-CoA dehydrogenase (2MBCD), which catalyzes its α,β-dehydrogenation.

3-Oxotetradecanoyl-CoA is a 3-oxo fatty acyl-CoA. 3-Oxotetradecanoyl-CoA can function as a metabolite in humans, Saccharomyces cerevisiae, Escherichia coli, and mice. 3-Oxotetradecanoyl-CoA is a preferred substrate for thiolytic cleavage by P-44 (type II 3-oxoacyl-CoA thiolase).

Lipoic acid ((R)-(+)-α-Lipoic acid) is an antioxidant, which is an essential cofactor of mitochondrial enzyme complexes. (R)-(+)-α-Lipoic acid is more effective than racemic Lipoic acid.

Succinyl CoA (Succinyl-coenzyme A) sodium is a pivotal intermediate metabolite in the tricarboxylic acid cycle and a key coenzyme A metabolite. Succinyl CoA sodium is biosynthesized from α-ketoglutarate or propionyl-CoA. Succinyl CoA sodium acts as a critical precursor and substrate for heme biosynthesis and gluconeogenesis. Succinyl CoA sodium insufficiency caused by cobalamin deficiency is directly linked to growth retardation, impaired heme synthesis, tissue glycine accumulation and neurological abnormalities. Succinyl CoA sodium can be used in research on metabolic, neurological, and hematological abnormalities (such as porphyria) caused by nutritional vitamin B12 deficiency (leading to a lack of Succinyl-Coenzyme A synthesis).

Malonyl CoA (Malonyl Coenzyme A) lithium is an inhibitor of carnitine palmitoyl transferase 1 (CPT1). High Malonyl CoA lithium concentrations suppress fatty acid oxidation, while low Malonyl CoA lithium concentrations are permissive for fat oxidation.

Lipoamide ((±)-α-Lipoamide) is a monocarboxylic acid derivative of a neutral amide, formed by the condensation of the carboxyl group of lipoic acid and ammonia. Lipoamide protects against oxidative stress-mediated neuronal cell damage and also acts as a coenzyme to transfer acetyl groups and hydrogen during pyruvate deacylation. Lipoamide also stimulates mitochondrial biogenesis in adipocytes through the endothelial NO synthase-cGMP-protein kinase G signaling pathway.

(±)-Jasmonic acid is an endogenous growth regulator closely related to plant resistance to abiotic stresses, used to activate defense responses to wounding, herbivory, and pathogen attacks. (±)-Jasmonic acid does not play an independent regulatory role, but works in a complex signaling network with other plant hormone signaling pathways. In addition, (±)-Jasmonic acid can also reduce chlorophyll levels in green and etiolated barley leaf segments and inhibit the elongation of rice seedlings.

DL-β-Hydroxybutyryl coenzyme A lithium is an intermediate in the fermentation of butyric acid and the metabolism of lysine and tryptophan, and is produced from β-hydroxybutyric acid by short-chain-CoA synthase.

N-Oleoyldopamine (OLDA) is an orally active TRPV1 activator and 5-LOX inhibitor with blood-brain barrier permeability. N-Oleoyldopamine excites histaminergic neurons in the tuberomammillary nucleus via a dopamine receptor mechanism, a process independent of TRPV1 and cannabinoid receptors. On one hand, N-Oleoyldopamine promotes the release of insulin and glucose-dependent insulinotropic polypeptide through a GPR119-dependent pathway to improve glucose tolerance; on the other hand, N-Oleoyldopamine improves left ventricular function and reduces myocardial infarction size by triggering the release of substance P and calcitonin gene-related peptide. N-Oleoyldopamine is used in studies related to glycemic abnormalities and myocardial ischemia-reperfusion injury.

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.

Sterculic acid is a stearoyl-CoA desaturase-1 (SCD1) inhibitor. Sterculic acid specifically inhibits the delta-9 desaturase (Δ9D) activity with an IC₅₀ value of 0.9 μM.

Glutaryl coenzyme A lithium is an important endogenous metabolites. Glutaryl coenzyme A lithium can be used in HMG-CoA or Glutaryl-CoA related experiment.

Acetyl-coenzyme A (Acetyl-CoA) lithium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A lithium, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A lithium is also a key precursor of lipid synthesis.

Myristoyl coenzyme A lithium is lithium-labeled myristoylated coenzyme A (CoA). Myristoylation is an essential process in viruses and is generally controlled by N-myristoyltransferase (NMT). And NMT is more active in colon epithelial tumors than in normal cells. Reduced Ccoenzyme A (CoA) is known to be a key regulator of NMT activity, whereas oxidized CoA does not allow NMT to promote myristoylation. Myristoyl coenzyme A blocks the demyristoylation process and has potential anticancer and antiviral mechanisms.