Phenoxyacetic acid is found in cocoa and cocoa products. Phenoxyacetic acid is a flavouring ingredient. Phenoxyacetic acid is on the FDA list of approved food additives (PART 172 - FOOD ADDITIVES PERMITTED FOR DIRECT ADDITION TO FOOD FOR HUMAN CONSUMPTION; Subpart F--Flavoring Agents and Related Substances Sec. 172.515 Synthetic flavoring substances and adjuvants.). Research has shown that Phenoxyacetic acid induced hematopoietic cell proliferation, providing potential for oral therapeutics which stimulate proliferation of hematopoietic cells of multiple lineages, as well as inducing fetal globin, important for therapy of hemoglobinopathies.

D-(-)-tartaric acid is isomer of tartaric acid, that industrially produced in the largest amounts. D-(-)-Tartaric acid may be used in the preparation of enantiospecific homochiral cis-4-formyl β-lactams. It may also be used as a starting material in the synthesis of D-erythro-sphingosine and L-lyxo-phytosphingosine. D-(-)-tartaric acid is widely used as an acidizing agent for beverages and other foods, and this use is similar to citric acid. Tartaric acid can be used as an acid dye mordant when it is combined with tannin. It is also used for some development and fixing operations in the photographic industry. D-(-)-Tartaric Acid is used in the preparation of synthetic analgesics. Tartaric acid is metabolically inert in the human body. When taken by mouth, only about 20% of ingested tartrate is eliminated in the urine; the remainder is not absorbed as such since it is destroyed in the intestinal tract by bacterial action. Sodium tartrate in daily doses of up to 10 or even 20 g has been used in medical practice as a laxative.

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.