I found an article by Bill Roberts on the difference between the anti-estrogens. Hope this is useful reading:
Anti-estrogens are drugs which act to reduce estrogenic activity in the body. This can be done either by reducing the amount of estrogen, or by reducing the activity of whatever estrogen is present.
Competitive aromatase inhibitors, such as Cytadren, Arimidex, and probably Proviron, bind to the same binding site on the aromatase enzyme that testosterone does. By doing this, they allow less testosterone to bind to aromatase. So, less testosterone is converted to estradiol (estrogen).
Here’s an important thing: the effectiveness of competitive inhibitors decreases as the amount of the normal substrate increases. Suppose that you had equal amounts of inhibitor and normal substrate in the blood, and they bound to the enzyme equally well. Then the inhibitor would at any moment be taking up half the sites that the normal substrate otherwise would, so it would reduce conversion rate by 50%. But if the amount of substrate is increased 10 times while the amount of inhibitor remains the same, then the inhibitor would be outcompeted by the more numerous substrate molecules. It would therefore be rather ineffective.
For example, with more testosterone molecules available, and similar binding strengths, the enzyme will mostly bind testosterone. It will then mostly be working to produce estrogen. To obtain the 50% reduction we had before, then the amount of inhibitor would also have to be increased 10 times.
To be really effective, the inhibitor must either be present in higher concentration than the normal substrate, or must bind more tightly.
With Cytadren or Proviron, it takes quite a lot of inhibitor to outcompete high testosterone levels. With Arimidex, rather little, even 1 mg/day, can be sufficient because it binds so strongly.
The other general approach is estrogen receptor antagonism. If a molecule binds strongly to a hormone receptor, but does not activate that receptor and makes it unresponsive to the normal hormone, then it is a receptor antagonist. Clomid (clomiphene) and Nolvadex (tamoxifen) follow this approach. These drugs are very similar structurally. They are both what are called triphenylethylenes, and are not steroids. The differences are relatively minor, but seem to affect an important characteristic of these compounds: drug metabolism.
Both tamoxifen and clomiphene are metabolized to other related compounds which can be estrogenic or anti-estrogenic. Both act as estrogens in bone tissue, perhaps after metabolism, which is a very useful property for female patients, for whom these drugs are usually intended. (Otherwise, an anti-estrogen could lead to osteoporosis.) Tamoxifen seems particularly prone to acting as an estrogen in the liver, which may account for reduced IGF-1 levels seen when this drug is taken.
Users generally seem to agree that when tamoxifen is used, gains are a little less than what otherwise would be expected. (Let’s not take this too far though: many people have made great gains while using tamoxifen as an anti-estrogen. And it’s always hard to say what "would" have been the case if a drug had not been included.) I’ve heard nothing but good about clomiphene, though.
Proviron, an anabolic steroid, is particularly interesting. I suspect that it not only acts as an antiaromatase but in an unknown DHT-like anti-estrogenic manner. This might involve estrogen receptor downregulation for example. In any case, aromatase inhibition and/or Clomid don’t seem to give the same effect on appearance and muscle hardness as when Proviron is included.
