non-enzymatic

7α-Hydroxycholesterol, a cholesterol oxide formed through both enzymatic and non-enzymatic oxidation, can serve as a biomarker for lipid peroxidation.

5-A-RU (5-Amino-6-(D-ribitylamino)uracil) is an early intermediate in riboflavin biosynthesis and is found in a variety of bacteria and yeast as well as plants. 5-A-RU is also a mucosal-associated invariant T (MAIT) cell activator that forms potent MAIT-activating antigens through non-enzymatic reactions with small molecules from other metabolic pathways.

Etravirine (R165335) is a diarylpyrimidine non-nucleoside reverse transcriptase inhibitor. Etravirine is designed to be active against HIV isolates with mutations that confer resistance to the two most commonly prescribed first-generation NNRTIs. It can bind the enzyme reverse transcriptase (RT) in multiple conformations, both for native and mutant RT, thereby blocking the enzymatic activity of RT.

LV-320 is a potent, uncompetitive ATG4B inhibitor with an IC50 of 24.5 μM and a Kd of 16 μM. LV-320 inhibits ATG4B enzymatic activity, blocks autophagic flux in cells, and is stable, non-toxic, and active in vivo. These findings suggest that LV-320 will serve as a relevant chemical tool to study the various roles of ATG4B in cancer and other contexts [1].

Reutericyclin is a selective anti-Gram-positive substance with good oral bioavailability, possessing both antibacterial and anti-obesity effects. It disrupts bacterial transmembrane potential specifically, exerting bactericidal or bacteriostatic effects on pathogenic bacteria such as Clostridium difficile and Staphylococcus aureus in a non-bacteriolytic manner, and rapidly eliminates vegetative cells and spores of Clostridium difficile. It is resistant to enzymatic degradation, has iron chelating properties, and is hardly absorbed by colonic epithelial cells. In addition to effectively eliminating Staphylococcus biofilms and inhibiting the proliferation of drug-resistant bacteria, Reutericyclin regulates intestinal flora structure and improves body energy metabolism, thereby alleviating abnormal weight gain induced by risperidone medication. Currently, Reutericyclin has been widely used in basic research on Clostridium difficile infection, drug-induced weight gain and superficial skin infection caused by Staphylococcus.

EP652 (compound 56) effectively inhibits the enzymatic activity of METTL3, with IC50 values of 2 nM in SPA, less than 10 nM in cellular assays, and 37 nM in ATPlite assays. It plays a significant role in both non-solid and solid tumor research.

Quinapril is an orally active, non-peptide, and non-thiol angiotensin-converting enzyme (ACE) inhibitor. It primarily blocks the conversion of angiotensin I to angiotensin II in both plasma and tissues. Upon enzymatic hydrolysis, Quinapril is converted into the pharmacologically active Quinaprilat and is effective in hypertension models.

CM112 is a selective degrader of protein arginine methyltransferase 1 (PRMT1), which connects a hydrophobic adamantane tag to MS023 via a 5-PEG linker. It induces the degradation of PRMT1 in various solid tumor cell lines. CM112 also targets the non-enzymatic functions of PRMT1 by reducing the stability of the orphan receptor TR3. This compound shows potential for cancer research.

Prostaglandin A3 is a non-enzymatic dehydration product of prostaglandin E3 (PGE3). It demonstrates significant affinity for canine EP2 and EP4 receptors with IC50 values of 120 nM and 20 nM, respectively. For human PPARγ, Prostaglandin A3 has a Ki value of 188 μM.

TMX-4102 is a highly selective binder of phosphatidylinositol 5-phosphate 4-kinase Type II gamma (PIP4K2C). It demonstrates binding activity to PIP4K2C with a dissociation constant (KD) of 0.45 nM, and does not significantly affect other lipid and non-lipid kinases. By specifically binding to PIP4K2C, TMX-4102 regulates its scaffold function rather than its enzymatic activity. TMX-4102 serves as a tool molecule for studying the biological functions and potential therapeutic value of PIP4K2C.

8-iso Prostaglandin F2α ethanolamide (iPF2α-III ethanolamide; 8-Isoprostane ethanolamide; 8-iso PGF2α ethanolamide) is a derivative of isoprostane ethanolamide produced through the non-enzymatic free radical oxidation of arachidonoyl ethanolamide (AEA). It is commonly used as a biomarker for oxidative stress, helping to distinguish non-enzymatic breakdown products from enzyme-mediated prostamides generated via pathways such as COX-2.

5-CNAC is an orally effective absorption enhancer with no inherent pharmacological activity. It significantly increases the gastrointestinal absorption efficiency of co-administered drugs (such as salmon calcitonin). By reversibly binding to peptide drugs in a non-covalent manner, 5-CNAC protects them from enzymatic degradation in the gastrointestinal tract and enhances lipid solubility, facilitating passive transepithelial transport without compromising intestinal epithelial integrity. It is useful in research as an adjuvant for oral peptide administration.

Bufuralol hydrochloride belongs to the class of beta-adrenoreceptor antagonists and is a potent, orally active, non-selective beta-adrenoreceptor antagonist with partial agonist activity. Bufuralol hydrochloride is a prototypical CYP2D6 probe substrate (Km = 5-50 microM) and is extensively used in biochemical studies to characterize CYP2D6 enzymatic activity and evaluate genetic variants.

Secoisolariciresinol diglucoside (LGM2605) was cytoprotective in an in vitro model of iron overload-induced redox-inflammatory damage. Secoisolariciresinol diglucoside (25 mg/kg b.w.) exerts the antihyperglycemic effect by preventing the liver from peroxidation damage through inhibition of ROS level mediated increased level of enzymatic and non-enzymatic antioxidants.

(±)11-HETE is one of the six monohydroxy fatty acids produced by the non-enzymatic oxidation of arachidonic acid . The individual R and S isomers of racemic HETEs have been separated and identified using chiral phase HPLC. The racemic HETEs have been quantified as an index of lipid peroxidation using GC/MS.

(±)18-HEPE is produced by non-enzymatic oxidation of EPA. It contains equal amounts of 18(S)-HEPE and 18(R)-HEPE. Specific biological activity attributed to (±)18-HEPE has not been documented.

(±)12-HEPE is produced by non-enzymatic oxidation of EPA, resulting in equal amounts of 12(S)-HEPE and 12(R)-HEPE. The biological activity of (±)12-HEPE is likely mediated by one of the individual isomers, primarily the 12(S) isomer in mammalian systems. 12-HEPE inhibits platelet aggregation with an IC50 of 24 μM, similar to 12-HETE (IC50 = 25 μM), and both compounds also inhibit U46619-induced contraction of rat aorta with IC50 values between 8.6-8.8 μM. [1][2]

(±)14-HDHA is a hydroxydocosahexaenoic acid, an oxidized metabolite of DHA generated intracellularly by enzymatic or non-enzymatic reactions, is one of the specific substrates of 15-PGDH and can be further oxidized to the anti-inflammatory 14-oxoDHA, and in primary alveolar macrophages, 14-HDoHE itself significantly inhibits LPS-induced IL-6 mRNA expression in primary alveolar macrophages, which may be relevant to inflammatory diseases such as asthma.

(±)15-HEDE is produced by non-enzymatic oxidation of 11,14-eicosadienoic acid. There are no reports in the literature of biological activity associated with (±)15-HEDE.

Advanced glycation end products (AGEs) are compounds formed by non-enzymatic chemical reactions following the bonding of sugars to proteins or lipids during diabetes, uremia, aging, rheumatic arthritis, and other conditions. A receptor for the AGEs (RAGE) binds certain members of this class to initiate cell signaling.[1][2] Pentosidine is a well-characterized natural AGE that is often used as a biomarker for the production of all AGEs. While pentosidine can be measured in urine, the majority of this AGE is catabolized before excretion.[3] Reference:[1]. Neeper, M., Schmidt, A.M., Brett, J., et al. Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. The Journal of Biological Chemisty 267(21), 14998-15004 (1992).[2]. Brett, J., Schmidt, A.M., Yan, S.D., et al. Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. American Journal of Pathology 143(6), 1699-1712 (1993).[3]. Miyata, T., Ueda, Y., Horie, K., et al. Renal catabolism of advanced glycation end products: The fate of pentosidine. Kidney International 53, 416-422 (1998).

Isoprostanes are produced by the non-enzymatic, free radical peroxidation of phospholipid-esterified arachidonic acid. They have been used as biomarkers of oxidative stress, but they also have been found to have potent biological activity. ent-8-iso-15(S)-Prostaglandin F2α (ent-8-iso-15(S)-PGF2α) is a potent vasoconstrictor of porcine retinal and brain microvessels with EC50 values of 15 and 24 nM, respectively. This isoprostane is about ten-fold more potent than 8-iso-PGF2α in a whole blood platelet aggregation inhibition assay.

8-iso Prostaglandin F2β (8-iso PGF2β) is an isomer of PGF2α of non-enzymatic origin. It is one of 64 possible isomers of PGF2α which can be produced by free radical peroxidation of arachidonic acid. 8-iso PGF2β exhibits very weak contraction of human umbilical vein artery and does not promote aggregation of human whole blood. However, 8-iso PGF2β moderately contracts both the canine and porcine pulmonary vein, although the effect is much weaker than that exhibited by other isoprostanes such as 8-iso PGE1, 8-iso PGE2, or 8-iso PGF2α. 8-iso-15-keto PGF2β is a potential metabolite of 8-iso PGF2β via the 15-hydroxy PG dehydrogenase pathway. There are no published reports on the formation or biological activity of 8-iso-15-keto PGF2β.

Prostaglandin B2 (PGB2) is a non-enzymatic dehydration product resulting from the treatment of PGE2 or PGA2 with strong base. It has weak agonist activity on TP receptors and can increase pulmonary blood pressure in the rabbit at relatively high doses (5 ug/kg). [1]

(±)9-HETE is one of the six monohydroxy fatty acids produced by the non-enzymatic oxidation of arachidonic acid. The individual R and S isomers of racemic HETEs have been separated and identified using chiral phase HPLC. The racemic HETEs have been quantified as an index of lipid peroxidation using GC/MS.