Testosterone esters were synthesized for the first time in 1936, and were found to have greatly improved potency relative to testosterone.  Among the esters synthesized, testosterone propionate was the most potent, and for this reason, was selected for further development, subsequently being marketed.  Testosterone propionate was introduced in 1937 by Schering AG in Germany under the brand name Testoviron.  It was the first ester of testosterone to be introduced,  and was the major form of testosterone used medically before 1960.  In the 1950s, longer-acting testosterone esters like testosterone enanthate and testosterone cypionate were introduced and superseded testosterone propionate.  Although rarely used nowadays due to its short duration,  testosterone propionate remains medically available. 
In propionic acidemia , a rare inherited genetic disorder, propionate acts as a metabolic toxin in liver cells by accumulating in mitochondria as propionyl-CoA and its derivative, methylcitrate, two tricarboxylic acid cycle inhibitors. Propanoate is metabolized oxidatively by glia , which suggests astrocytic vulnerability in propionic acidemia when intramitochondrial propionyl-CoA may accumulate. Propionic acidemia may alter both neuronal and glial gene expression by affecting histone acetylation.   When propionic acid is infused directly into rodents' brains, it produces reversible behavior (., hyperactivity , dystonia , social impairment, perseveration ) and brain changes (., innate neuroinflammation, glutathione depletion) that may be used as a means to model autism in rats.