da big thinker said:
if we are talking about the same study...well,it did not give enough evidence IMO;there was no evidence that tren exerted the effects through the PR receptor...
Characterisation of the affinity of different anabolics and synthetic hormones to the human androgen receptor, human sex hormone binding globulin and to the bovine progestin receptor.
APMIS 2000 Dec;108(12):838-46 (ISSN: 0903-4641)
Bauer ER; Daxenberger A; Petri T; Sauerwein H; Meyer HH [Find other articles with these Authors]
Institut fur Physiologie, Research Center for Milk and Food Weihenstephan, Technical University Munich, Germany.
For the steroidal growth promoters trenbolone acetate (TBA) and melengestrol acetate (MGA) neither the complete spectrum of biological activities nor the potential endocrine disrupting activity of their excreted metabolites in the environment is fully understood. The potency of these substances in [3H]dihydrotestosterone ([3H]-DHT) displacement from the recombinant human androgen receptor (rhAR) and from human sex-hormone binding globulin (hSHBG) was evaluated. In addition, the potency for [3H]-ORG2058 displacement from the bovine uterine progestin receptor (bPR) was tested. For comparison, different anabolics and synthetic hormones were also tested for their binding affinities.
For 17beta-trenbolone (17beta-TbOH), the active compound after TBA administration, an affinity the rhAR similar to dihydrotestosterone (DHT) and a slightly higher affinity to the bPR than progesterone were demonstrated. The affinity of the two major metabolites, 17alpha-trenbolone and trendione, was reduced to less than 5% of the 17beta-TbOH-value. The affinity of these three compounds and of MGA to the hSHBG was much lower compared with DHT. MGA showed a 5.3-fold higher affinity than progesterone to the bPR but only a weak affinity to the rhAR. The major MGA metabolites have an affinity to the bPR between 85% and 28% of the affinity of progesterone. In consequence, MGA and TBA metabolites may be hormonally active substances, which will be present in edible tissues and in manure. We conclude that detailed investigations on biodegradation, distribution and bio-efficacy of these substances are necessary.
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What do you mean "not enough evidence"?
The study is clear about binding affinity of Tren to PR. Now, by being not sure about how it activates PR, you, probably meant if it is agonist of PR or antagoinst.
Well, it's not that complecated to prove that Tren is agonist.
As you can see from the same study, Tren's affinity to AR is the same as DHT, which means that all the users should experience "hard on" effect from Tren alone cycles, and it has to be much stronger then from Test or even Test+high dosage of Proviron combo. What do we get in real life? With few exceptions, most users experience Fina dick, or close to it, and definately nothing even close to pure DHT effect.
Why? Same as with Deca - binding to PR. That's the only possible explanation.
Now, you started that thread, saying that Tren when viewed from 3-D can't fit in PR, so how come it does?
Get your facts together.
Trenbolone and Nandrolone, both are progestogens, both derivated from 19-nortestosteron.
Tren - 4,9,11-Estratrien-17beta-ol-3-one
Nandrolone - 4-Estren-17beta-ol-3-one
Don't you see striking similarities? So, comparing these two compouds make a lot of sense.