Steroid 1/2 lifes, absorption and effects in detail.


New member
Bioavailability of testosterone enanthate dependent
on genetic variation in the phosphodiesterase 7B but
not on the uridine 50
(UGT2B17) gene
Lena Ekstro¨ma
, Jenny J. Schulzea
, Chantal Guillemetteb
, Alain Belangerb
and Anders Ranea

It is a very in depth read. Over my level. They report a pretty wide range of testoserone availability and discuss genetics involved in doping test as well as testosterone replacement.

"The participants were given 500 mg of testosterone
enanthate as a single intramuscular dose (Testoviron-
Depot, kindly provided by Schering Nordiska AB, Solna
Sweden) equivalent to 360 mg testosterone."

Below are blood levels pre injection and 2 days after. Sorry for the lay out it's a copy -paste.

Testosterone (ng/ml) 5.07 (4.66***8211;5.49) 15.00 (12.29***8211;17.72) 196***

DHT (pg/ml) 400.7 (351.3***8211;450.0) 752.6 (667.3***8211;837.9) 88***

3b-Adiol (pg/ml) 64.81 (50.2***8211;79.4) 150.7 (125.4***8211;176.0) 132***

ADT (pg/ml) 418.1 (358.2***8211;478.0) 764.2 (659.0***8211;869.5) 83***

3a-Adiol-3G (ng/ml) 2.19 (1.6***8211;2.8) 4.78 (3.75***8211;5.8) 118***

ADT-G (ng/ml) 59.92 (50.18***8211;69.6) 120.7 (97.1***8211;144.3) 101***

3a-Adiol-17G (ng/ml) 4.4 (3.5***8211;5.3) 14.86 (12.2***8211;17.5) 237***

Etio-G (ng/ml) 24.5 (20.7***8211;28.3) 50.8 (40.6***8211;61.0) 107***

Pretty in depth talk on esters, genetic markets and testoserone metabolism. This will definitely have to be reread another time.

I'm trying to find specifics on hydrolosis. I found one on esters but it was specifically dealing with oral activity. The hydrolosis happened in the liver and small intestine. I should grab that just so I have it here. I lost my references on my epilepsy and endo researching except what I posted in my thread here


New member
""Carboxylesterase Catalyzed Drug Hydrolysis

Carboxylesterases catalyze the hydrolysis of a wide variety of endogenous and exogenous substrates including esters, thioesters, carbamates, and amides. However, the focus of this review is on drug substrates of carboxylesterases, and almost all known drugs that are substrates contain an ester functional group susceptible to hydrolysis. Ester hydrolysis results in the formation of the corresponding carboxylic acid and alcohol (see*Figure 1). The ******** of hydrolysis are generally more polar than the original ester resulting in an increase in water solubility, promoting renal elimination. This property of hydrolysis is widely believed to be a protective mechanism promoting the elimination of exogenously ingested esters,4*which in part helps to explain why catalytic ester hydrolysis is a highly conserved enzymatic pathway present in virtually all mammals.2

Fig 1

Ester Hydrolysis: Carboxylesterases catalyze the addition of water to an ester group producing a carboxylic acid and an alcohol, which are more polar compounds than the original ester increasing renal elimination. Substrate drugs may be prodrugs activated*..."

The role of human carboxylesterases in drug metabolism: have we overlooked their importance?

S. Casey Laizure, Pharm.D., Vanessa Herring, B.S., [...], and Robert B. Parker, Pharm.D.

Pick it apart. I don't understand huge portions of these. I'm just researching and pulling references. I don't think this is directly related but hopefully Google will do it's thing and lead me where I'm trying to go.

If I can get info sorted so I can post a post like my epilepsy AND low T thread I think it would be a sticky. I just need others to help me keep thinking on track and ensuring the references are kept in context. Liver cells in a tube are not human bodies and I don't think the hydrolosis in the intestine for oral drugs is directly relevant to injected drugs. . . .. yet more questions.