Tamoxifen (Nolvadex)
Selective estrogen receptor modulator that competitively binds estrogen receptors, acting as an antagonist in breast tissue and hypothalamus while functioning as a partial agonist in bone and uterine tissue. Blocks negative feedback on the HPG axis, increasing GnRH pulsatility, LH, and FSH secretion. Stimulates endogenous testosterone production through central estrogen receptor antagonism.
Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.
- total-testosterone
- free-testosterone
- estradiol
- lh
- fsh
- shbg
- lipid-panel
- alt
- ast
- history-of-dvt-pe
- concurrent-warfarin
- pregnancy
- endometrial-cancer-history
- PMID:9669980Tamoxifen for prevention of breast cancer: report of the NSABP P-1 study — J Natl Cancer Inst, 1998
- PMID:11701131Tamoxifen treatment of gynecomastia and breast pain — J Clin Endocrinol Metab, 2001
- PMID:15001605Effects of tamoxifen on testosterone and gonadotropin levels in men — Fertil Steril, 2004
- PMID:26023778Tamoxifen versus clomiphene citrate for male infertility — Curr Urol Rep, 2015
Tamoxifen is the original PCT anchor. Five decades of oncology data behind it. The tissue selectivity is what makes it useful — antagonist where you need estrogen blocked (breast, hypothalamus), agonist where you want estrogenic activity (bone, lipids). The 5-7 day half-life means you are still at therapeutic concentrations a week after your last dose. That long tail is either an advantage or a liability depending on whether you understand the pharmacokinetics before you start dosing.
This is not medical advice
Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.
See Tamoxifen (Nolvadex) in a protocol matched to you