Prodolic acid is an indole derivative patented by American Home Products Corp. as antiinflammatory agent. Prodolic acid acts as non-steroidal anti-inflammatory compound and inhibits bradykinin-induced bronchoconstriction but did not affects histamine-induced bronchoconstriction in the guinea pig. In preclinical studies, Prodolic acid exhibits potent anti-inflammatory activity in adjuvant arthritic rats.

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.

Vaccenic acid (VA) (t11 octadecenoic acid) is a positional and geometric isomer of oleic acid (c9-octadecenoic acid), and is the predominant trans monoene in ruminant fats (50%–80% of total trans content). Dietary VA can be desaturated to cis-9,trans-11 conjugated linoleic acid (c9,t11-CLA) in ruminants, rodents, and humans. Hydrogenated plant oils are another source of VA in the diet, and it has been recently estimated that this source may contribute to about 13%–17% of total VA intake. In contrast to suggestions from the epidemiological studies, the majority of studies using cancer cell lines (Awad et al. 1995; Miller et al. 2003) or rodent tumors (Banni et al. 2001; Corl et al. 2003; Ip et al. 1999; Sauer et al. 2004) have demonstrated that VA reduces cell growth and (or) tumor metabolism. Animal and in vitro studies suggest that the anti-cancer properties of VA are due, in part, to the in vivo conversion of VA to c9,t11-CLA. However, several additional mechanisms for the anti-cancer effects of VA have been proposed, including changes in phosphatidylinositol hydrolysis, reduced proliferation, increased apoptosis, and inhibition of fatty acid uptake. In conclusion, although the epidemiological evidence of VA intake and cancer risk suggests a positive relationship, this is not supported by the few animal studies that have been performed. The majority of the studies suggest that any health benefit of VA may be conferred by in vivo mammalian conversion of VA to c9,t11-CLA. VA acts as a partial agonist to both peroxisome proliferator-activated receptors (PPAR)-α and PPAR-γ in vitro, with similar affinity compared to commonly known PPAR agonists. Hypolipidemic and antihypertrophic bioactivity of VA is potentially mediated via PPAR-/-dependent pathways.

Iocanlidic Acid I-123 is a radiolabeled phenylfatty acid derivative studied as a diagnostic agent for myocardial imaging

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.