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.

Aceburic acid is the acetyl ester of gamma-hydroxybutyrate (GHB), it has analgesic effects as a prodrug to GHB. GHB is used medically as an anesthetic as well as a treatment for several neurologically affecting diseases.

Iodofiltic Acid I-123 is a single-photon branching free fatty acid radiopharmaceutical with potential application in single-photon emission computed tomography (SPECT). Assessment of fatty acid metabolism by radionuclide techniques has a potential role for the early detection of myocardial ischaemia and the assessment of the severity of ischaemic heart disease. The Iodofiltic Acid I-123 scan is preferable because it can provide suitable information for risk stratification just after an acute myocardial infarction (AMI) without requiring the patient to exercise; it can also detect previous ischaemic insult even after recovery of myocardial perfusion, the so- called "ischaemic memory".

Betulinic acid (BA) is a plant-derived pentacyclic triterpenoid that exerts potent anti-cancer effects in vitro and in vivo. It`s anticancer property is linked to its ability to induce apoptotic cell death in cancer cells by triggering the mitochondrial pathway of apoptosis. In contrast to the cytotoxicity of betulinic acid against a variety of cancer types, normal cells and tissue are relatively resistant to betulinic acid, pointing to a therapeutic window. Compounds that exert a direct action on mitochondria present promising experimental cancer therapeutics, since they may trigger cell death under circumstances in which standard chemotherapeutics fail. Thus, mitochondrion-targeted agents such as betulinic acid hold great promise as a novel therapeutic strategy in the treatment of human cancers. Betulinic acid has antiretroviral, antimalarial, and anti-inflammatory properties. Betulinic acid exerts its inhibitory effect by preventing topoisomerase I-DNA interaction as a result of which the 'cleavable complex' is not formed. In consequence, it also acts as an antagonist to camptothecin-mediated cleavage. The antitumor pharmacological effects of BA consist of triggering apoptosis via the mitochondrial pathway, regulating the cell cycle and the angiogenic pathway via factors, including specificity protein transcription factors, cyclin D1 and epidermal growth factor receptor, inhibiting the signal transducer and activator of transcription 3 and nuclear factor‑κB signaling pathways, preventing the invasion and metastasis of tumor cells, and affecting the expression of topoisomerase I, p53 and lamin B1. Betulinic Acid has also been used in trials studying the treatment of Dysplastic Nevus Syndrome. Betulinic acid acts as anti-melanoma agent through inhibiting aminopeptidase N activity with IC50 of 7.3 uM. Betulinic acid is an inhibitor of HIV-1 with EC50 of 1.4 uM.

Diprogulic acid (Dikegulac) is used as a precursor in vitamin C synthesis. It is plant growth regulator for hedges. Dikegulac is used to differentially kill terminal apices, and it analogously inhibits basic metabolic functions in dividing cells, but not stationary cells, in suspension culture. At the lowest concentrations, dikegulac partially suppresses division of the isolated tobacco protoplasts. Higher concentrations are required to produce visual cytoplasmic damage to the protoplasts, which probably first occurs at the level of the plasmalemma, as the vacuoles can be released intact. Later, tonoplast disruption occurs. It does not inhibit mature leaves.

Hydroxytoluic acid is a long-acting derivative of salicylate with antilipidemic properties. It shows fibrinolytic activity in human plasma by activating the fibrinolytic system and has been shown to lower plasma free fatty acid, cholesterol levels, and to raise metabolic oxygen consumption.