Enclomiphene
Enclomifene, Androxal, trans-clomiphene
Selective oestrogen receptor modulator that raises testosterone by restarting your own axis instead of replacing it - which is why it preserves fertility where TRT does not.
Human trials
Not FDA-approved as a standalone product; an approval attempt under the name Androxal was unsuccessful. Widely prescribed off-label via telehealth, and also sold as research material. Clomiphene citrate, the mixed isomer, is approved for female infertility.
What it is
Clomiphene citrate is a mixture of two isomers with different behaviour. Enclomiphene is the trans isomer - the one responsible for the oestrogen-antagonist effect at the hypothalamus - isolated from zuclomiphene, the longer-lived isomer associated with much of the mood and visual side effect burden.
Mechanism, and why fertility is preserved
Testosterone production is governed by a feedback loop: the hypothalamus releases GnRH, the pituitary releases LH and FSH, the testes make testosterone and sperm. Testosterone aromatises to oestradiol, which signals the hypothalamus to slow down.
Enclomiphene blocks that oestrogen receptor at the hypothalamus. The brain reads low oestrogen, increases GnRH, and LH and FSH rise - driving both testosterone production and spermatogenesis.
Exogenous testosterone does the opposite. The loop reads high testosterone, shuts down LH and FSH, and spermatogenesis stops along with them. This is the single practical difference that decides which option someone should be on:
| Enclomiphene | Testosterone replacement | |
|---|---|---|
| Testosterone | Rises | Rises |
| LH / FSH | Rise | Suppressed |
| Sperm production | Preserved or improved | Significantly reduced |
| Requires functioning testes | Yes | No |
| Works for primary hypogonadism | No | Yes |
What the evidence shows
Randomised trials found enclomiphene at 12.5-25 mg daily normalised testosterone comparably to topical testosterone, while increasing LH and FSH and conserving sperm counts - where the testosterone arm reduced them. Meta-analysis of SERM trials in male hypogonadism reports mean total testosterone increases in the region of 270 ng/dL over placebo, with parallel rises in LH and FSH.
The critical constraint: enclomiphene works by asking the testes to produce more. If the testes cannot respond - primary hypogonadism - it does nothing. It treats secondary (central) hypogonadism only. Establishing which one you have requires bloodwork including LH and FSH, not a symptom checklist.
Practical notes
- Get baseline labs first: total and free testosterone, LH, FSH, oestradiol, SHBG, prolactin. Without LH and FSH you cannot tell secondary from primary hypogonadism, and the drug only works for one of them.
- Visual symptoms mean stop. This is not a side effect to push through.
- Oestradiol rises alongside testosterone - that is expected, and reflexively reaching for an aromatase inhibitor tends to cause more problems than it solves.
- It is not a bodybuilding drug. It restores your own production to a normal range; it does not exceed it.
Side effects and warning signs
Commonly reported
- Visual disturbances - floaters, light trails, difficulty adjusting to darkness. Uncommon but characteristic of the SERM class and a reason to stop
- Mood changes, irritability or low mood
- Headache
- Nausea
- Elevated oestradiol as more testosterone becomes available for aromatisation
Stop and get medical help
- Any visual change - floaters, blurring, light sensitivity. This is the class-defining adverse effect and warrants stopping and seeing an ophthalmologist
- Marked mood deterioration
- Signs of a clot: unilateral leg swelling, chest pain, sudden breathlessness. SERMs carry thromboembolic risk
Sources
From the community
Discussion for this compound concentrates in r/Biohackers and r/PeptideForum.
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