the only thing I know of to fight off any tren gyno is Winstrol (winny), Winstrol (winny) will block progesterone, thats why they say to run Winstrol (winny) with your tren.
check out this link, they have any info on fina that you would ever need.
Virtually all androgens bind to the progesterone receptor to some degree; similarly progestins (and antiprogestins) bind to the androgen receptor. RU 486 binds to the androgen receptor as an antiandrogen, rendering it useless for bodybuilders.
As far as the winstrol article goes, has anyone bothered to actually read the whole study? Presumably we are supposed to believe winstrol has some kind of antiprogestin capability because it blocked FGF stimulated DNA synthesis.
The effect on DNA synthesis was measured by thymidine uptake. Less thymidine uptake means less DNA synthesis. Quoting from page 38 of the article,
" A significant inhibition of thymidine uptake was seen in response to stanozolol in both cell types. The steroids nortestosterone, oxymetholone, and progesterone itself were also tested for their effect on thymidine uptake to determine whether the effects of stanozolol on DNA synthesis were unique. These other compounds also inhibited DNA synthesis in both cell types"
In other words, winstrol has THE SAME effect as progesterone on progesterone receptor mediated DNA synthesis: they both block it. So rather than acting as an antiprogesterone in this study, winstrol, as well as nandrolone and oxymetholone, act in the same manner as progesterone.
Ellis AJ, Cawston TE, Mackie EJ.
Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK.
The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.