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the 1950s, longer-acting testosterone esters like testosterone enanthate and testosterone cypionate were introduced and superseded testosterone propionate.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. 
The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
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