I found this to be very informative on helping me understand what each PCT tools (SEMS/AI) do what... Kinda a long read but well worth it!
SERM:
Clomid, stimulates the hypophysis to release more gonadotropin so that
a faster and higher release of follicle stimulating hormone aud
luteinizing hormone occurs. This results in an increase of the body's
own testosterone production. Clomid is a synthetic estrogen, however
it does also work as an anti-estrogen. How does it work? Because it is
a weak synthetic estrogen, it will bind to the estrogen receptor (ER)
and not cause any problems. At the same time the increase in estrogen
from steroids are blocked from attaching to the ER.
Nolvadex, is very comparable to Clomid, behaves in the same manner in
all tissues, and is a mixed estrogen agonist/antagonist of the same
type as Clomid. The two molecules are also very similar in structure.
It is not correct that Nolvadex reduces levels of estrogen: rather, it
blocks estrogen from estrogen receptors and, in those tissues where it
is an antagonist, causes the receptor to do nothing.
Cyclofenil, similar to HCG and Clomid in action. This drug is most
commonly used to increase endogenous testosterone levels after a cycle
in an attempt to avoid a hard crash while waiting for your hormone
levels to naturally balance. Similar to HCG and Clomid, cyclofenil
seems to quickly and effectively raise natural levels. Cyclofenil is
an estrogen that works as an anti-estrogen as well as a testosterone
booster.
AI:
Femara, (letrozole tablets) for oral administration contain 2.5 mg of
letrozole, a nonsteroidal aromatase inhibitor (inhibitor of estrogen
synthesis). Letrozole is a nonsteroidal competitive inhibitor of the
aromatase enzyme system; it inhibits the conversion of androgens to
estrogens.
Cytadren, (aminoglutethimide) at moderate doses, is a fairly effective
inhibitor of aromatase and a weak inhibitor of desmolase (an enzyme needed for the
production of all steroids), and at higher doses becomes an effective
inhibitor of desmolase. It is therefore useful when using aromatizable
steroids, though it is not the drug of choice for this purpose.
Aromasin, tablets for oral administration contain 25 mg of exemestane,
an irreversible, steroidal aromatase inactivator. Exemestane is
chemically described as 6-methylenandrosta-1,4-diene-3,17 -dione.
Anastrozole,(Arimidex) is the aromatase inhibitor of choice. The drug
is appropriately used when using substantial amounts of aromatizing
steroids, or when one is prone to gynecomastia and using moderate
amounts of such steroids. It is manufactured by Zenica Pharmaceuticals
and was approved for use in the United States at the end of Dec 1995.
Proviron, is also an estrogen antagonist which prevents the
aromatization of steroids. Unlike the antiestrogen Nolvadex which only
blocks the estrogen receptors (see Nolvadex) Proviron already prevents
the aromatizing of steroids. Therefore gynecomastia and increased water
retention are successfully blocked. Since Proviron strongly suppresses
the forming of estrogens no re-bound effect occurs.
Teslac,is unique in its effectiveness as an antiestrogen. Like
Proviron, it prevents the aromatizing process of the steroids from the
basis. Thus, Teslac prevents almost completely the introduction of more
estrogens into the blood and subsequent bonding with the estrogen
receptors.
The Androgen Receptor
All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and
activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.
Testosterone, Nandrolone and Methenolone
Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced[i]. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone[ii]. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.
Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?
When we look at Primobolan® (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone[iii]. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan® is a non-aromatizable steroid is more relevant.
If you have taken the time to read all of this I think that like me you have a much better understanding of PCT and what meds do what.
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TEAM BIG PAY CHECK 
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all in like 5 minutes... okay days... FINE YEARS, gimme a break, sheesh...
