Glucocorticoid antagonists...

Not an answer to your question, but are you saying you can run test and tren seperately, but not together?

Have you tried dostinex?

A1: Yes

A2: No, for the life of me I can not figure out how dostinex would help this problem. I've seen prolactin elevation in ONE study using Testosterone alone, and it wasn't even that great. From my reading, estrogen can elevate prolactin. Yet, I've tried to run Tren A s the base with 100mgs of Test Prop split twice a week and still had gyno issues. I wouldn't think prolactin would be a big issue when keeping the aromatizing steroids to a minimum.

Didn't know that test and tren would lead to gyno. Can anyone give more info on that.

That is the 1st time I have heard of the combo leading to gyno.

By what interaction could the 2 cause gyno, that either would no on its own?

I know of a few people who got gyno from tren, but not test, and dostinex worked for them.

Interesting subject.

Test gives me gyno, but I can control it with adex. Tren doesn't give me gyno when run solo because there is no estrogen present in the system.

Test + tren = estrogen + progesterone = "super estrogen"

Re: Glucocorticoid antagonists...

Posted by: ready2explode

I've been busy lately, so for this question I was hoping I could get away with cheating rather than doing my own research.

Glucocorticoid antagonists also tend to have progesterone receptor antagonistic abilities which vary back and forth.

Does any one know halo's PR antagonistic abilities?

Also, what types of side effects does one run into with an antiglucocorticoid?

Last, would it be possible to use an antiglucocorticoid for two purposes: (1) block a progestin (tren, deca) and (2) reap the benefits during a time of potential catabolism (cutting cycle)?

Just playing around with ideas. I can't run test/tren due to gyno issues. No amount of nolva or combination of nolva and anti-aromatase helps. It's not a huge deal, I love my solo test cycles, and solo tren is my second favorite. Just been wondering...

androgens are glucocorticoid antagonists.

Although both the 17a-methyl and the 11b-substituent cause a slight shift toward PR, there is nothing to point in the direction of halo being remotely antagonistic toward the PR. For the 11b by the way, its usually rule of thumb that the bulkier the substituent, the more PR binding you get, and an OH group isn't really that bulky. (Ojasoo and Raynaud, 1978 and 1995)

THe typical effects of too much gluco blocking are increased agression, painful joints, bouts of feeling faint due to blood sugar problems etc. That's usually a sign that you need to stop or lower dosages.

As to your question, if you had such a product, of course it would. But there is no reason to believe we get any real ill effect from the minor progestagenic effects of tren and deca to warrant the use of an anti-PR, and generally androgens (we all know this I assume, for those who didn't OS just chimed in with another useless fact) reduce GR effects sufficiently not to need more GR blocking.

What exactly are you trying to achieve/work out here ?

Posted by: Big Cat

...But there is no reason to believe we get any real ill effect from the minor progestagenic effects of tren and deca to warrant the use of an anti-PR...

What exactly are you trying to achieve/work out here ?

I can't run a test & tren cycle due to gyno issues. This lead me to playing with some ideas in my head, that's all. As aforementioned, it's really not a big deal. I finally got five minutes of my own time to sit and relax, and sadly that's what popped into my head.

Thank you for answering my questions.

I've stumbled across many of these types of abstracts in the past. They are what gave me this idea:

The novel progesterone receptor antagonists RTI 3021-012 and RTI 3021-022 exhibit complex glucocorticoid receptor antagonist activities: implications for the development of dissociated antiprogestins.

Wagner BL, Pollio G, Giangrande P, Webster JC, Breslin M, Mais DE, Cook CE, Vedeckis WV, Cidlowski JA, McDonnell DP.

Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.

We have identified two novel compounds (RTI 3021-012 and RTI 3021-022) that demonstrate similar affinities for human progesterone receptor (PR) and display equivalent antiprogestenic activity. As with most antiprogestins, such as RU486, RTI 3021-012, and RTI 3021-022 also bind to the glucocorticoid receptor (GR) with high affinity. Unexpectedly, when compared with RU486, the RTI antagonists manifest significantly less GR antagonist activity. This finding indicates that, with respect to antiglucocorticoid function, receptor binding affinity is not a good predictor of biological activity. We have determined that the lack of a clear correlation between the GR binding affinity of the RTI compounds and their antagonist activity reflects the unique manner in which they modulate GR signaling. Previously, we proposed a two step "active inhibition" model to explain steroid receptor antagonism: 1) competitive inhibition of agonist binding; and 2) competition of the antagonist bound receptor with that activated by agonists for DNA response elements within target gene promoters. Accordingly, we observed that RU486, RTI 3021-012, and RTI 3021-022, when assayed for PR antagonist activity, accomplished both of these steps. Thus, all three compounds are "active antagonists" of PR function. When assayed on GR, however, RU486 alone functioned as an active antagonist. RTI 3021-012 and RTI 3021-022, on the other hand, functioned solely as "competitive antagonists" since they were capable of high affinity GR binding, but the resulting ligand receptor complex was unable to bind DNA. These results have important pharmaceutical implications supporting the use of mechanism based approaches to identify nuclear receptor modulators. Of equal importance, RTI 3021-012 and RTI 3021-022 are two new antiprogestins that may have clinical utility and are likely to be useful as research reagents with which to separate the effects of antiprogestins and antiglucocorticoids in physiological systems.

Yes, its certainly holds true for some PR antagonists, I know it also holds true for the likes of Spironolactone and such. Chances are these products also (certainly spiro and RU486) exhibit mild to moderate anti-androgenic effects as well. The RU486 family (bulky 11b-substituents and often a more acidic A-ring) tend to be all-round blockers, likely due to hindering of the binding of co-activators to the Activating Function-2 binding pocket of the receptor they attach too.

Thanks BC. Wouldn't have gotten a solid answer without you.