L-threonine is an optically active form of threonine having L-configuration. It has a role as a micronutrient, a nutraceutical, a mouse metabolite, a Saccharomyces cerevisiae metabolite, a plant metabolite, an Escherichia coli metabolite, a human metabolite and an algal metabolite. It is a L-alpha-amino acid, an aspartate family amino acid, a threonine and a proteinogenic amino acid. It is a conjugate base of a L-threoninium. It is a conjugate acid of a L-threoninate. L-Threonine is a natural amino acid, can be produced by microbial fermentation, and is used in food, medicine, or feed.

Lanosterol is a tetracyclic triterpenoid that is lanosta-8,24-diene substituted by a beta-hydroxy group at the 3beta position. It is the compound from which all steroids are derived. It has a role as a mouse metabolite, a Saccharomyces cerevisiae metabolite, a plant metabolite, a bacterial metabolite and a human metabolite. It is a 14alpha-methyl steroid, a tetracyclic triterpenoid and a 3beta-sterol. It derives from a hydride of a lanostane. Lanosterol is a key triterpenoid intermediate in the biosynthesis of Cholesterol. Lanosterol induces mild depolarization of mitochondria and promotes autophagy, it is indicative of altered Lanosterol metabolism during PD pathogenesis. 10 μM Lanosterol during IVM in medium without serum and bases on recombinant human chorionic gonadotrophin has a positive effect on maturation of prepubertal ewe oocytes.

Corynoxine B, a natural autophagy inducer, restores the deficient cytosolic translocation of HMGB1 and autophagy in cells overexpressing SNCA, which may be attributed to its ability to block SNCA-HMGB1 interaction. Corynoxine B exhibits prolongation of the thiopental-induced hypnosis on oral administration in mice. Corynoxine B is a member of indolizines. It has a role as a metabolite.

Mogroside V is a widely used sweetener, has in vitro AMPK activating effect, it also has anti-inflammatory potential in murine macrophages and a murine ear edema model, and has the potential to protect against LPS-induced airway inflammation in a model of ALI.