Aromasin vs arimidex

[ThE SiCkNeSs]

What's up.
I am beginning my first cycle and have decided to run aromasin. I have done a lot of research in which AI to use and I chose aromasin. In mostly everything I read aromasin seems to be the superior choice yet almost every time I read a cycle log it seems like the person is using adex. I just was wondering what I'm missing.

 

[Northern Nutrition]

Other than the obvious blocker/suicide differences, Adex is cheaper. So IMO this accounts for a large percentage of those who are on a tight budget. But they both perform well. Some respond well to Aromasin, others respond better to Adex.

 

[Gramps]

Adex is the older trusted choice. Aromasin is a bit newer. Adex plays catch and release while aromasin kills aromotose. You can recover a bit faster with the catch and release but slower with the other making your dosing take a bit more care to not crash your estradial.

 

[Docd187123]

IMO the suicidal properties of aromasin are way overhyped. Adex is cheaper, it lowers E2 more effectively, and doesn't require as frequent dosing, etc. Adex is the better choice IMO.

 

[Northern Nutrition]

I should have also included that Adex responds quicker to changes in doses compared to Aromasin. But i feel that once you have your E2 dialed in, Aromasin is the better choice IMHO.

 

[Northern Nutrition]

I knew there was something Doc and i would disagree on some day..lol

 

[ThE SiCkNeSs]

So basically aromasin stops the aromatizing effect of test while adex kills estrogen whether it's from test or what ever else?

 

[Docd187123]

So basically aromasin stops the aromatizing effect of test while adex kills estrogen whether it's from test or what ever else?

They both will inhibit aromatization of any aromatizing compound.

 

[ThE SiCkNeSs]

I think I need to do more research [emoji20]

 

[ThE SiCkNeSs]

Thanks for the insight

 

[Docd187123]

Mechanism of Action
The AIs are classified into two types: (a) type I, suicidal or noncompetitive inhibitors; and (b) type II, competitive inhibitors (13 , 14) . Type I inhibitors are steroidal compounds, and type II inhibitors are nonsteroidal drugs. Both types mimic normal substrates (androgens), competing with the substrate for access to the binding site on the enzyme. After initial binding, the next step differs for the two types: once a noncompetitive inhibitor has bound, the enzyme initiates its typical sequence of hydroxylation, but hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Enzyme activity is thus permanently blocked; even if all unattached inhibitor is removed, enzyme activity can only be restored by new enzyme synthesis. Competitive inhibitors reversibly bind to the active enzyme site, and either no enzyme activity is triggered, or it is without effect. The inhibitor can disassociate from the binding site, allowing renewed competition between the inhibitor and the substrate for binding to the site. As a result, the effectiveness of competitive inhibitors depends on the relative concentrations and affinities of the inhibitor and the substrate. Continued activity requires constant presence of inhibitor.

To compete for binding to the active site, both competitive and noncompetitive inhibitors must necessarily share important structural features with the endogenous substrate. Noncompetitive inhibitors must also share structural features with androgens, allowing them to interact with the catalytic residual on the enzyme protein. This renders them inherently selective. By contrast, most competitive inhibitors interact with the heme iron, a common feature of all cytochrome P450 enzymes. Some may also bind to the highly conserved oxygen binding site in addition to the substrate binding site. Thus, unless the specificity of a competitive inhibitor is reinforced through other structural features, it may block the activity of a variety of cytochrome P450 enzymes, as does aminoglutethimide.

Both anastrozole and letrozole are type II nonsteroidal AIs, whereas exemestane has a steroidal structure and is classified as a type I AI, also known as an aromatase inactivator because it irreversibly binds with and permanently inactivates the enzyme. The clinical relevance of these differences in mechanism of action, if any, remains to be established.


http://clincancerres.aacrjournals.org/content/9/1/468s.full

 

[tanuki]

Isn't aromasin still expensive as hell? Get whatever's cheaper if price is a concern.

Letro and adex have been tried and true for years now.

 

[Mayne]

From what I have read aromasin is far superior compared with both adex and letro, it's a TLDR info and also been posted on many forums hence why I am not copy-pasting, just continue your research. Also look for exemestane or other drugs containing exemestane, I personally use british brand pharma exemestane 25mg pills instead of aromasin, 1/4 price, I believe the real active ingredient making aromasin what it is is exemestane, correct me if needed

 

[Docd187123]

From what I have read aromasin is far superior compared with both adex and letro, it's a TLDR info and also been posted on many forums hence why I am not copy-pasting, just continue your research. Also look for exemestane or other drugs containing exemestane, I personally use british brand pharma exemestane 25mg pills instead of aromasin, 1/4 price, I believe the real active ingredient making aromasin what it is is exemestane, correct me if needed

Most posts on exemestane's efficacy are taken out of context or don't apply to us. Exemestane is the generic name while aromasin is a brand name. Same drug.

 

[Gramps]

As for price, I found ADC exemestane similar in price to adex pill for pill. I can't speak on quality, but that's where I'd start. The Pfizer was right next to that at 3x the price.

 

[Mayne]

Most posts on exemestane's efficacy are taken out of context or don't apply to us. Exemestane is the generic name while aromasin is a brand name. Same drug.

Obviously what I have read has been targeted at steroid use not in general application of exemestane. I have gone reading on more than 1 forum and aromasin has had an upper hand on any of them until this one thread here. Later I can post all the useful comments I have read backed by what I believe is scientific proof defending aromasin unless somebody else posts here counter proof defending adex, then I could have case for doubting my research.

 

[Docd187123]

Obviously what I have read has been targeted at steroid use not in general application of exemestane. I have gone reading on more than 1 forum and aromasin has had an upper hand on any of them until this one thread here. Later I can post all the useful comments I have read backed by what I believe is scientific proof defending aromasin unless somebody else posts here counter proof defending adex, then I could have case for doubting my research.

Right off the bat one of the most common claims is that aromasin kills 98% of the aromatase enzymes or estrogen. I forget which one specifically but it's one of the two and I've seen the claim on every forum I frequent. The fact of the matter is aromasin does not reduce ESTRADIOL by 98% nor does the proclaimed 98% reduction in aromatase enzymes mean it's as effective as letro or adex at lowering E2 bc the latter two are much more effective at that.

 

[Mayne]

Doesn't adex fuck your lipids up also? I have read aromasin works on E2 too, more than 50% anyway?

 

[Docd187123]

Doesn't adex fuck your lipids up also? I have read aromasin works on E2 too, more than 50% anyway?

It hasn't affected my lipids and for most I think it doesn't affect them enough to worry about.

The number is roughly 50%, I forget exactly what the studies mentioned, but I'll see if I can find them and post them up for you.

 

[Jimmyinkedup]

You have to see what works best for you. I switched from dex to stane a couple years ago and had such a hard time dialing in the stane dose that I almost gave up on it and switched back to adex. Right when I was going to switch back I got the stane dialed in and I have used it since. Both are very good choices IMO. Stane has a slightly better (very slightly) safety profile as far as lipids and igf impact but this is most likely attributed to its milder effects on e2 than dex. See what works for you is what I think is best. I do think if you can get stane to work for you and its a viable option then thats the one I would (and have) personally chose.