Rumenic acid is the major conjugated linoleic acid (CLA), probably because of successive desaturation and chain elongation and can be considered as the principal dietary form. In experiments on rodents was shown that rumenic acid possessed the protective effect against colitis, which was associated with the activation of the Nrf2 pathway.

Tridecanoic acid is a 13-carbon saturated fatty acid found in dairy products and also as a product of anaerobic biodegradation of n-hexadecane. It has been identified as a substrate of phospholipase A2. Saturated fatty acids with carbon chain lengths of C12 to C14 activated the alpha-, beta-, gamma-, and epsilon-subspecies of the protein kinase C, and this activation was synergistic with that by diacylglycerol. Tridecanoic acid(C13) was most effective among the saturated fatty acids examined.

Sodium sulfanilate is a salt of sulphanilic acid and has been used to monitor the degree of renal dysfunction in dogs.

Undecanoic acid (UDA) is a fatty acid with significant antimycotic activity. Undecanoic acid is a straight-chain, eleven-carbon saturated medium-chain fatty acid found in body fluids; the most fungitoxic of the C7:0 - C18:0 fatty acid series. It has a role as a human metabolite and an antifungal agent. It is a straight-chain saturated fatty acid and a medium-chain fatty acid. It is a conjugate acid of an undecanoate. It derives from a hydride of an undecane. Undecanoic acid inhibited the production of exocellular lipase and keratinase but stimulated the production of exocellular phospholipase A in T. rubrum undecanoic acid-resistant mutant (udar). At its minimum inhibitory concentration, undecanoic acid inhibits biosynthesis of phosphatidyl serine, phosphatidyl ethanolamine and polyphosphoinositol but does not inhibit the synthesis of phosphatidyl glycerol, phosphatidyl choline, phosphatidyl inositol and phosphatidic acid in Trichophyton rubrum. At higher concentration, however UDA inhibits biosynthesis of all phosphatides present in this dermatophyte. UDA also affects catabolism of these phosphatides. This inhibitory effect of UDA may be partially responsible for its toxic action on T. rubrum.

Tetradecylthioacetic acid (TTA) is a hypolipidemic antioxidant with immunomodulating properties involving activation of peroxisome proliferator-activated receptors (PPARs). TTA exerts both hypolipidemic and anti-inflammatory effects in psoriasis patients - TTA can be of therapeutic benefit for a subgroup of psoriatic patients. TTA may improve myocardial function in heart failure, potentially involving its ability to decrease the availability of free fatty acids in plasma and increase the myocardial proportion of n-3 polyunsaturated fatty acids. TTA attenuates dyslipidemia in patients with type 2 diabetes mellitus. These effects may occur through mechanisms involving PPAR-alpha and PPAR-delta activation, resulting in increased mitochondrial fatty acid oxidation.

1-aminocyclopropanecarboxylic acid (ACPC) is a non-proteinogenic alpha-amino acid consisting of cyclopropane having amino and carboxy substituents both at the 1-position. It has a role as a plant metabolite and a member of ethylene releasers. ACPC is produced endogenously in the tomato and other higher plants as a product of the action of 1-aminocyclopropane-1-carboxylic acid synthase in the biosynthesis of ethylene. It is a monocarboxylic acid and a non-proteinogenic alpha-amino acid. It derives from a cyclopropanecarboxylic acid. ACPC is a partial agonist at the strychnine-insensitive glycine recognition site on the N-methyl-D-aspartate (NMDA) receptor complex in the mammalian central nervous system with preclinical activity in animal models of neuroprotection and psychiatric illnesses. Half-maximal activation by ACPC as a glycine-site agonist was 0.7 to 0.9 microM. Half-maximal inhibition by ACPC was dependent on NMDA concentration. Peak responses to a >100 microM ACPC pulse in the presence of 1 microM glutamate were similar to those of glycine but decayed to a steady-state amplitude below that of glycine. The removal of ACPC initially caused an increase in inward current followed by a subsequent decrease to baseline levels. This suggests that relief of low-affinity antagonism occurs before high-affinity agonist dissociation. ACPC is shown to block convulsions and death produced by NMDA exposure, significantly reducing seizure induction and cell death of NMDA-treated hippocampal neurons.

Oxaloacetate (OAA), a salt of oxaloacetic acid, is a metabolic intermediate in many processes, e.g., urea cycle, gluconeogenesis, etc. that occur in animals. Experiments on animal have revealed that OAA was able to protect hepatocytes from hypoxia and liver ischemia/reperfusion injury. OAA also possesses a neuroprotective effect against ischemic injury, which strengthens the likelihood of its future applicability as a novel neuroprotective agent for the treatment of ischemic stroke patients. In addition, experiments on adipose stromal cells have shown that OAA directly protected cerebellar granule neurons from apoptosis induced by serum and potassium deprivation.