cyclofenil
- Thread starter ms84
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Popa Murph
Member
I believe cyclofenil is a weak form of estrogen itself. I do not believe it shuts off any feed back loops it mearly binds to receptor sites blocking more powerful estrogens.
Why not just use ATD. It does close to the same thing and has a much better availability. I don't know pricing on this stuff but ATD is dirt cheap, the only downside is ATD kills libido.
Why not just use ATD. It does close to the same thing and has a much better availability. I don't know pricing on this stuff but ATD is dirt cheap, the only downside is ATD kills libido.
Rostam
Well-known member
Popa Murph said:
Cyclofenil work more like SERMs than aromatase inhibitors (e.g ATD). Actually cyclofenil is a SERM.
ATD cannot and will not restore your HPTA axis as fast as cyclofenil or other SERMs. During your PCT (at least at the begining of the PCT) you need a SERM not an aromatase inhibitor.
Rostam
Well-known member
Here is a short profil of Cyclofenil.
(Cyclofenil)
This is the least popular of the three Selective Estrogen Receptor Modulators (SERM) being used in athletics today. I actually used this stuff about half a decade ago, when it was just as easy to get as Clomid, and a bit cheaper. As we already know, SERMs cause ovulation in women and (more importantly to us) increase testosterone and other beneficial hormones. This drug actually works by simulating the effects of testosterone via inhibiting the negative feedback loop caused by estrogen, with regards to testosterone production. This in turn causes the increased secretion of Gonadotropin Releasing hormone, which increases output of Luteinizing Hormone which (finally!) increases secretion of testosterone from your testes.
So what we have here is a compound which, being a SERM, will prevent gyno by binding to the estrogen receptor in breast tissue and thus preventing stronger estrogens from binding to those tissues. This should be familiar territory if you remember your facts on Clomid and Nolvadex.
The results indicate that cyclofenil, paradoxically, has two opposing actions on the hypothalamic-hypophyseal axis, one of them is estrogen-like, in that it depresses serum FSH levels and competitively binds to breast tissue (this is good, remember), and the other action is antiestrogen-like, in that it depresses serum PRL levels and raises LH levels (4). Overproduction of prolactin, as you recall will suppress Testosterone, and could induce lactation (gross!) in male breast tissue.
From the reading I’ve done on this compound, I think 400-600mgs/day would be an appropriate dose for use in Post-Cycle-Therapy, or during a cycle (4). Dan Duchaine estimated roughly the same, saying that twice as much is necessary when compared to Clomid, twice as often. Due to it’s relative expense and unavailability when compared to other SERMs, such as Nolvadex and Clomid, I can’t see this stuff making it’s way into many people’s ancillary regimen.
References:
1. Effect of cyclofenil on hormonal dynamics, follicular development and cervical mucus in normal and oligomenorrhoeic women. Hum Reprod. 1992 Jan;7(1):39-43.
2. [Cyclofenil-induced acute hepatitis. A retrospective diagnosis of a case during acute hepatitis B]
Recenti Prog Med. 1991 Apr;82(4):236-9. Italian.
3. [Induction of ovulation in 1985] J Gynecol Obstet Biol Reprod (Paris). 1985;14(7):899-913. Review
4. Plasma FSH, LH and prolactin levels in postmenopausal women undergoing cyclofenil treatment. Acta Obstet Gynecol Scand. 1982;61(6):487-90.
The reason people don't use it anymore is mainly because it is less available than other SERMs and because of the cost.
(Cyclofenil)
This is the least popular of the three Selective Estrogen Receptor Modulators (SERM) being used in athletics today. I actually used this stuff about half a decade ago, when it was just as easy to get as Clomid, and a bit cheaper. As we already know, SERMs cause ovulation in women and (more importantly to us) increase testosterone and other beneficial hormones. This drug actually works by simulating the effects of testosterone via inhibiting the negative feedback loop caused by estrogen, with regards to testosterone production. This in turn causes the increased secretion of Gonadotropin Releasing hormone, which increases output of Luteinizing Hormone which (finally!) increases secretion of testosterone from your testes.
So what we have here is a compound which, being a SERM, will prevent gyno by binding to the estrogen receptor in breast tissue and thus preventing stronger estrogens from binding to those tissues. This should be familiar territory if you remember your facts on Clomid and Nolvadex.
The results indicate that cyclofenil, paradoxically, has two opposing actions on the hypothalamic-hypophyseal axis, one of them is estrogen-like, in that it depresses serum FSH levels and competitively binds to breast tissue (this is good, remember), and the other action is antiestrogen-like, in that it depresses serum PRL levels and raises LH levels (4). Overproduction of prolactin, as you recall will suppress Testosterone, and could induce lactation (gross!) in male breast tissue.
From the reading I’ve done on this compound, I think 400-600mgs/day would be an appropriate dose for use in Post-Cycle-Therapy, or during a cycle (4). Dan Duchaine estimated roughly the same, saying that twice as much is necessary when compared to Clomid, twice as often. Due to it’s relative expense and unavailability when compared to other SERMs, such as Nolvadex and Clomid, I can’t see this stuff making it’s way into many people’s ancillary regimen.
References:
1. Effect of cyclofenil on hormonal dynamics, follicular development and cervical mucus in normal and oligomenorrhoeic women. Hum Reprod. 1992 Jan;7(1):39-43.
2. [Cyclofenil-induced acute hepatitis. A retrospective diagnosis of a case during acute hepatitis B]
Recenti Prog Med. 1991 Apr;82(4):236-9. Italian.
3. [Induction of ovulation in 1985] J Gynecol Obstet Biol Reprod (Paris). 1985;14(7):899-913. Review
4. Plasma FSH, LH and prolactin levels in postmenopausal women undergoing cyclofenil treatment. Acta Obstet Gynecol Scand. 1982;61(6):487-90.
The reason people don't use it anymore is mainly because it is less available than other SERMs and because of the cost.
Popa Murph
Member
Rostam said:
I never said use ATD for PCT, for that matter I never said use Cyclofenil for PCT or anything about PCT at all. I was under the impression he was trying to raise testosterone levels without the use of AAS. Alot like the NHA sack