Enclomiphene is not a steroid. It is a non-steroidal compound classified as a selective estrogen receptor modulator (SERM). While it can raise testosterone levels, it does so through an entirely different mechanism than anabolic steroids, and its chemical structure has nothing in common with steroid hormones.
The confusion is understandable. Enclomiphene is increasingly popular in men’s health for treating low testosterone, and anything that boosts testosterone tends to get lumped in with steroids. But the distinction matters, both chemically and in terms of what happens inside your body.
What Enclomiphene Actually Is
Enclomiphene belongs to a class of drugs called triphenylethylenes. Structurally, it looks nothing like testosterone or other steroid hormones, which all share a characteristic four-ring carbon skeleton. Triphenylethylenes are built around three connected phenyl (benzene) rings, a completely different molecular framework.
If the name sounds familiar, that’s because enclomiphene is one half of clomiphene (sold as Clomid), a fertility drug that has been on the market for decades. Clomiphene is a mixture of two mirror-image molecules, or isomers: enclomiphene (the trans-isomer) and zuclomiphene (the cis-isomer). Research in mice found that zuclomiphene was responsible for many of clomiphene’s unwanted effects, including damage to Leydig cells (the cells that produce testosterone in the testes), epididymal tissue, and seminal vesicles. Enclomiphene alone had positive effects on testosterone production with no harmful changes to testicular tissue, which is why it was developed as a standalone drug.
Enclomiphene has not been approved by the FDA for any use. It remains an unapproved drug, though it is widely available through compounding pharmacies and online clinics prescribing it off-label for low testosterone in men.
How It Raises Testosterone Without Being a Steroid
Anabolic steroids are synthetic versions of testosterone. When you inject or apply exogenous testosterone, your brain detects the high hormone levels and shuts down its own production signals. This suppresses two key hormones from the pituitary gland, LH (luteinizing hormone) and FSH (follicle-stimulating hormone), which normally tell the testes to make testosterone and sperm. The result: your testosterone comes from an outside source, your testes shrink, and sperm production drops or stops.
Enclomiphene works in the opposite direction. It blocks estrogen receptors in the hypothalamus, the part of the brain that monitors hormone levels. Normally, estrogen (converted from testosterone) signals the brain that hormone levels are adequate, keeping LH and FSH in check. When enclomiphene blocks that feedback signal, the brain responds as though estrogen is low and ramps up production of GnRH (gonadotropin-releasing hormone), which triggers more LH and FSH from the pituitary. Those hormones then stimulate the testes to produce more testosterone naturally.
The critical difference: your testes stay active. Because enclomiphene stimulates rather than replaces the body’s own hormone production, it preserves spermatogenesis. This makes it a fundamentally different tool than testosterone replacement therapy, particularly for men who want to maintain fertility.
Why It’s Banned in Sports Alongside Steroids
The World Anti-Doping Agency (WADA) prohibits enclomiphene in competition. It falls under the category of anti-estrogenic substances, which includes all SERMs. Clomiphene is listed by name, and any substance with a similar chemical structure or biological effect is also banned.
WADA bans SERMs not because they are steroids, but because they can artificially elevate testosterone production. An athlete using enclomiphene would have higher natural testosterone than their baseline, which provides a performance advantage. The substance is also sometimes used to restart natural testosterone production after a cycle of anabolic steroids, making it a tool for masking steroid use.
Side Effects Compared to Steroids
Because enclomiphene doesn’t introduce external hormones, its side effect profile is substantially different from anabolic steroids. It doesn’t cause testicular atrophy, doesn’t suppress sperm production, and doesn’t carry the cardiovascular risks associated with supraphysiological testosterone doses (liver strain, elevated red blood cell counts, cholesterol disruption).
That said, enclomiphene is not side-effect free. In clinical comparisons with clomiphene, enclomiphene performed better: only 13.8% of enclomiphene users reported adverse effects compared to 47% on clomiphene. Decreased libido occurred in 8.6% of enclomiphene users versus 33.3% on clomiphene. Reduced energy affected 5.2% on enclomiphene compared to 16.7% on clomiphene. Mood changes were absent in the enclomiphene group but affected 9.1% of clomiphene users.
One concern that applies to all clomiphene-related compounds is visual disturbances. Post-marketing reports linked to clomiphene include blurred vision, visual impairment, and photophobia, with onset ranging from days to months after starting the drug. Rare cases of serious visual disturbances potentially leading to blindness have been documented, particularly with higher doses or prolonged use. Because enclomiphene is chemically related, this risk is relevant. Any changes in vision while using enclomiphene warrant immediate discontinuation and an eye exam.
Enclomiphene vs. Testosterone Replacement
For men with secondary hypogonadism (low testosterone caused by insufficient signaling from the brain rather than testicular failure), enclomiphene offers a targeted approach. It restores the hormonal signal chain rather than bypassing it. Current American Urological Association guidelines for hypogonadism typically recommend testosterone therapy for symptomatic men, but that approach suppresses LH and FSH, reducing intratesticular testosterone and impairing sperm production.
Enclomiphene has demonstrated the ability to increase testosterone levels without suppressing LH or FSH, normalizing hormone levels while preserving fertility. For younger men, men planning to have children, or men who want to avoid the commitment of lifelong testosterone injections, this distinction is significant. However, for men with primary hypogonadism (where the testes themselves are damaged or failing), stimulating LH and FSH won’t help because the testes can’t respond to the signal.
Clinical trials have tested doses ranging from low to 25 mg daily, with the 25 mg dose producing significantly greater increases in LH than lower doses. The optimal dose for a given individual depends on their starting hormone levels and response, which is why enclomiphene use typically involves blood work monitoring over time.