Estradiol's efficacy seems to vary widely with the person and the particular vehicle: I was on transdermal patches for two years ( , 2 patches changed twice weekly – considered a "high" dose of 17-beta estradiol), and my levels mostly stayed around 100 pg/mL, and I needed 100mg spironolactone daily to keep my testosterone down. When I switched to injections of Estradiol Valerate, as I was "titrating up" my testosterone was unmeasurably low at the same E2 level my patches were delivering. (I had decided to drop spiro at the same time due to it's side effects: for me it seemed to be fogging my brain and inducing suicidal ideation.) Increasing the dosage had the effect of adding a cup-size to my breasts after about two months of injections, after two years of HRT, at age 53 and with b-cup breasts already. This story is not unusual in the community, and it led me to try this form of HRT.
Flutamide acts as a selective, competitive , silent antagonist of the androgen receptor (AR).  Its active metabolite , 2-hydroxyflutamide , has between 10- to 25-fold higher affinity for the AR than does flutamide, and hence is a more powerful antiandrogen in comparison.     However, at high concentrations, unlike flutamide, 2-hydroxyflutamide is able to weakly activate the AR.   Flutamide has far lower affinity for the AR than do steroidal antiandrogens like spironolactone and cyproterone acetate, and it is a relatively weak antiandrogen in terms of potency by weight, but the large dosages at which flutamide is used appear to compensate for this.  In accordance with its selectivity for the AR, flutamide possesses no progestogenic , (direct) estrogenic , glucocorticoid , or antigonadotropic activity.   Similarly to nilutamide, bicalutamide, and enzalutamide , flutamide crosses the blood-brain-barrier and exerts central antiandrogen actions.