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lartinos
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Primordial
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Forma WTF is it?
- Thread starter Smokescreen
- Start date
cgar1228
New member
Primordial Performance.....one of the board sponsors. Tons of advertising went in to this product when it came out but like Lart said, i think the whole liquavade thing was a bust.
Who? Formestane from PP? Who's that?
Mechanism-Based (Suicide) Inhibitors
4-Hydroxyandrostenedione
Lentaron (Formestane; 4-OHA; 4-hydroxyandrost-4-ene-3,17-dione) is a structural analogue of androstenedione. It was the first steroidal suicide-type aromatase inhibitor to enter clinical trials. Using the placental aromatase assay system in vitro, 4-OHA was shown to be 60-fold more potent than aminoglutethimide (Ki=4.1δM). Extensive studies revealed no estrogenic, antiestrogenic, or antiandrogenic properties; however, transformation to 4-hydroxytestosterone occurs, and androgenic effects can be demonstrated under certain circumstances.
4-hydroxyandrostenedione (Lentaron, Formestane) has been studied extensively in postmenopausal women with breast cancer. In a phase I study, postmenopausal women received 500 to 1,000 mg of 4-OHA by weekly intramuscular injection. Although the drug has a short plasma half-life, concentrations of drug during chronic therapy and 1 week after the last injection ranged from 0.7 to 23.2 ng/mL (mean 7.8 ng/mL). This might reflect a depot effect of the injected drug. During therapy, plasma estradiol levels fell from 7.2 ± 0.8 (SEM) pg/mL to 2.6 ± 2.8 pg/mL from 1 to 41 months after initiating treatment.
Data from four phase II clinical trials of 4-OHA demonstrated a 33% objective regression rate of breast cancer in postmenopausal patients previously treated with multiple endocrine therapies. Toxicity included 6 patients with sterile abscesses due to intramuscular injections, 2 of sufficient severity to warrant discontinuation of therapy. No androgenic effects were observed.
Höffken and colleagues conducted a large trial of 4-OHA in postmenopausal women. Patients initially received 500 mg intramuscularly every 2 weeks for 6 weeks and then 250 mg every 2 weeks thereafter. Plasma estradiol levels fell from baseline values of 10 to 11 pg/mL to levels of approximately 4 pg/mL for up to 7 months of therapy. The drug appeared specific, since no reduction of cortisol or symptoms of cortisol deficiency were observed. Of 86 evaluable patients, there were 2 complete and 19 partial remissions (24%), and 26 experienced disease stabilization (30%). Side effects included minor systemic symptoms in 11% (hot flashes, constipation, alopecia, pruritus) and local symptoms in 8% (pruritus, local pain, erythema). These side effects resulted in discontinuation of therapy in only 2% of patients. Phase III trials are now ongoing to compare this inhibitor with standard endocrine therapies. In general, 4-OHA is better tolerated than aminoglutethimide.
4-hydroxyandrostenedione has also been given orally. Even though there is a marked first-pass effect with conversion in the liver to a glucuronidated derivative, oral doses of 250 mg reduce plasma estradiol by 53% and doses up to 1,000 mg produce no further suppression. The response rate after 3 months of therapy was 33%, and the only serious side effect from the oral dosage was leukopenia in a single patient.
4-Hydroxyandrostenedione
Lentaron (Formestane; 4-OHA; 4-hydroxyandrost-4-ene-3,17-dione) is a structural analogue of androstenedione. It was the first steroidal suicide-type aromatase inhibitor to enter clinical trials. Using the placental aromatase assay system in vitro, 4-OHA was shown to be 60-fold more potent than aminoglutethimide (Ki=4.1δM). Extensive studies revealed no estrogenic, antiestrogenic, or antiandrogenic properties; however, transformation to 4-hydroxytestosterone occurs, and androgenic effects can be demonstrated under certain circumstances.
4-hydroxyandrostenedione (Lentaron, Formestane) has been studied extensively in postmenopausal women with breast cancer. In a phase I study, postmenopausal women received 500 to 1,000 mg of 4-OHA by weekly intramuscular injection. Although the drug has a short plasma half-life, concentrations of drug during chronic therapy and 1 week after the last injection ranged from 0.7 to 23.2 ng/mL (mean 7.8 ng/mL). This might reflect a depot effect of the injected drug. During therapy, plasma estradiol levels fell from 7.2 ± 0.8 (SEM) pg/mL to 2.6 ± 2.8 pg/mL from 1 to 41 months after initiating treatment.
Data from four phase II clinical trials of 4-OHA demonstrated a 33% objective regression rate of breast cancer in postmenopausal patients previously treated with multiple endocrine therapies. Toxicity included 6 patients with sterile abscesses due to intramuscular injections, 2 of sufficient severity to warrant discontinuation of therapy. No androgenic effects were observed.
Höffken and colleagues conducted a large trial of 4-OHA in postmenopausal women. Patients initially received 500 mg intramuscularly every 2 weeks for 6 weeks and then 250 mg every 2 weeks thereafter. Plasma estradiol levels fell from baseline values of 10 to 11 pg/mL to levels of approximately 4 pg/mL for up to 7 months of therapy. The drug appeared specific, since no reduction of cortisol or symptoms of cortisol deficiency were observed. Of 86 evaluable patients, there were 2 complete and 19 partial remissions (24%), and 26 experienced disease stabilization (30%). Side effects included minor systemic symptoms in 11% (hot flashes, constipation, alopecia, pruritus) and local symptoms in 8% (pruritus, local pain, erythema). These side effects resulted in discontinuation of therapy in only 2% of patients. Phase III trials are now ongoing to compare this inhibitor with standard endocrine therapies. In general, 4-OHA is better tolerated than aminoglutethimide.
4-hydroxyandrostenedione has also been given orally. Even though there is a marked first-pass effect with conversion in the liver to a glucuronidated derivative, oral doses of 250 mg reduce plasma estradiol by 53% and doses up to 1,000 mg produce no further suppression. The response rate after 3 months of therapy was 33%, and the only serious side effect from the oral dosage was leukopenia in a single patient.
Did I read this correctly? It's NOT an anti-estrogen? But instead converts to a potent androgen? Huh?
"Extensive studies revealed no estrogenic, antiestrogenic, or antiandrogenic properties; however, transformation to 4-hydroxytestosterone occurs, and androgenic effects can be demonstrated under certain circumstances."
"Extensive studies revealed no estrogenic, antiestrogenic, or antiandrogenic properties; however, transformation to 4-hydroxytestosterone occurs, and androgenic effects can be demonstrated under certain circumstances."
O
OrbitNutrition.com
Guest
Formestane = steroidal AI nuff said.
skyling35
New member
Given that your post on winstrol indicated you are having a problem with both estradiol and progesterone. I would give a formestane product a try. There is plenty of research that indicates it works.
Fertil Steril. 1991 May;55(5):922-6.
Effect of the aromatase inhibitor 4-hydroxyandrostene-3,17-dione progesterone synthesis by human luteal cells.
Devoto L, Vega M, Castro O, Kohen P.
University of Chile, School of Medicine, Santiago.
Abstract
The authors studied the effects of 4-hydroxyandrostene-3,17-dione (4-OHA) on progesterone (P), 17 beta-estradiol (E2), and 20 alpha-hydroxy-4-pregnen-3-one synthesis and pregnenolone accumulation in cultured human midluteal cells. A dose-dependent inhibition with and without human chorionic gonadotropin (hCG) of E2 and P production was observed. The accumulation of pregnenolone was significantly enhanced three to fourfold by 4-OHA in this culture system, as compared with control value. In addition, a sevenfold increase on pregnenolone accumulation was observed in the presence of 4-OHA plus 10 IU of hCG as compared with control values and 2.2-fold as compared with the 4-OHA treatments. These in vitro findings indicate a direct effect of 4-OHA on luteal steroidogenesis. Nevertheless, the suppressive effect of 4-OHA on P and E2 production is located at different sites of the steroidogenic pathway. In addition, the results demonstrate that hCG in the presence of 4-OHA stimulated pregnenolone accumulation, suggesting that the inhibition of P synthesis is in some steps after the formation of pregnenolone. These data indicate that the actions of 4-OHA on P or E2 formation have different inhibitory mechanisms.
PMID: 2022270 [PubMed - indexed for MEDLINE]
Fertil Steril. 1991 May;55(5):922-6.
Effect of the aromatase inhibitor 4-hydroxyandrostene-3,17-dione progesterone synthesis by human luteal cells.
Devoto L, Vega M, Castro O, Kohen P.
University of Chile, School of Medicine, Santiago.
Abstract
The authors studied the effects of 4-hydroxyandrostene-3,17-dione (4-OHA) on progesterone (P), 17 beta-estradiol (E2), and 20 alpha-hydroxy-4-pregnen-3-one synthesis and pregnenolone accumulation in cultured human midluteal cells. A dose-dependent inhibition with and without human chorionic gonadotropin (hCG) of E2 and P production was observed. The accumulation of pregnenolone was significantly enhanced three to fourfold by 4-OHA in this culture system, as compared with control value. In addition, a sevenfold increase on pregnenolone accumulation was observed in the presence of 4-OHA plus 10 IU of hCG as compared with control values and 2.2-fold as compared with the 4-OHA treatments. These in vitro findings indicate a direct effect of 4-OHA on luteal steroidogenesis. Nevertheless, the suppressive effect of 4-OHA on P and E2 production is located at different sites of the steroidogenic pathway. In addition, the results demonstrate that hCG in the presence of 4-OHA stimulated pregnenolone accumulation, suggesting that the inhibition of P synthesis is in some steps after the formation of pregnenolone. These data indicate that the actions of 4-OHA on P or E2 formation have different inhibitory mechanisms.
PMID: 2022270 [PubMed - indexed for MEDLINE]
Forma Stanzol is awesome..
You got transdermal forma with DMSO to penetrate skin beter.
You have phyto serms.
This all equals lowered estrogen, drying out, heightened libido, strength gains and slight lean mass gains
..I love TD formastane
Haven't a clue what all of this meant. :-( I guess I'm that stupid. :-(
To me it was more like...."blah blah blah pregno something blah blah blah"
I didn't read anything stating it lowered progesterone. And if it "increases" pregnolone...that's not good for me! That means it will lead to the increase of EVERY other hormone there is! DHEA, Estogen, Progesterone etc etc etc.
