High-quality research product.
✓ Dispatched same or next working day · 2–3 day UK delivery
Commonly combined with Enclomiphene in research protocols.
Ratings are based on published research data and are for informational purposes only.
Enclomiphene is the trans-isomer of clomiphene. Unlike clomiphene (which contains both cis and trans isomers), enclomiphene is a pure ER antagonist at the hypothalamus, stimulating LH and FSH release and restoring endogenous testosterone. Multiple Phase II/III trials by Repros Therapeutics demonstrated significant testosterone restoration in hypogonadal men without suppressing spermatogenesis, distinguishing it from exogenous testosterone therapy.
Research Post
All androgenic SARMs studied in human clinical trials produce dose-dependent suppression of endogenous testosterone via hypothalamic-pituitary-testicular (HPT) axis feedback inhibition. Post-cycle therapy (PCT) research investigates the most effective approaches to restoring HPT axis function following SARM administration.
The HPT axis operates through a negative feedback loop: the hypothalamus releases gonadotropin-releasing hormone (GnRH), stimulating the pituitary to release LH and FSH, which signal the testes to produce testosterone. When exogenous androgens (including SARMs) are present, they exert negative feedback at the hypothalamus and pituitary, reducing GnRH, LH, and FSH output. The result is reduced endogenous testosterone production.
The degree of suppression varies by compound and dose. The Basaria 2013 LGD-4033 trial documented ~50% testosterone reduction at 1 mg/day by day 21 in healthy men, with recovery documented by day 56 post-cessation. More potent SARMs (S-23, LGD-4033 at higher doses) produce more severe suppression requiring longer recovery periods.
Arimistane (Androsta-3,5-diene-7,17-dione) is a naturally occurring metabolite of DHEA that functions as an irreversible ("suicide") aromatase inhibitor. By blocking the CYP19A1 enzyme that converts androgens to oestrogens, Arimistane reduces oestrogen levels, which partially relieves the negative feedback on the HPT axis and allows LH and FSH to rise.
Unlike pharmaceutical aromatase inhibitors (Anastrozole, Letrozole), Arimistane is a prohormone-derived compound rather than a synthetic pharmaceutical. Its irreversible mechanism means that recovery of aromatase activity requires synthesis of new enzyme rather than simple drug clearance — a consideration in dose protocol design. Arimistane also has weak androgenic and cortisol-reducing properties.
Enclomiphene is the trans-isomer of clomiphene citrate and acts as a selective oestrogen receptor antagonist at the hypothalamus and pituitary. By blocking ER-mediated negative feedback at these sites, enclomiphene stimulates GnRH, LH, and FSH release — directly driving endogenous testosterone production.
The Repros Therapeutics Phase II/III clinical programme demonstrated enclomiphene's ability to restore testosterone to normal ranges in hypogonadal men while maintaining sperm production — a significant advantage over exogenous testosterone replacement, which suppresses spermatogenesis. Multiple published trials document dose-dependent testosterone restoration, providing solid human clinical data for enclomiphene's HPT axis mechanism.
Enclomiphene's advantage over the racemic mixture clomiphene is the absence of the zuclomiphene (cis-isomer), which has longer half-life and estrogenic activity at some tissues. The pure trans-isomer provides cleaner ER antagonism with less agonistic activity at peripheral oestrogen receptors.
| Parameter | Arimistane | Enclomiphene |
|---|---|---|
| Drug class | Aromatase Inhibitor (AI) | SERM (ER antagonist) |
| Mechanism | Reduces oestrogen, relieving HPT feedback | Blocks ER at hypothalamus/pituitary, stimulates LH/FSH |
| Direct LH stimulation | Indirect (via oestrogen reduction) | Direct |
| Enzyme binding | Irreversible (suicide inhibitor) | Reversible ER antagonist |
| Human clinical data | Limited published data | Multiple Phase II/III trials (Repros) |
| Typical research dose | 25–75 mg/day | 12.5–25 mg/day |
The extent of post-cycle support required depends on the degree of suppression produced by the SARM protocol. Key factors include: compound identity (more potent SARMs produce more suppression), dose, and duration. For mild protocols (e.g., low-dose Ostarine, short duration), natural recovery may be adequate without active PCT compounds. For more potent compounds (LGD-4033, RAD-140, S-23) at higher doses, active PCT with Enclomiphene and/or Arimistane is standard practice in research protocols.
Not always. For very mild SARM protocols (low-dose Ostarine, short duration), the Basaria 2013 data shows spontaneous recovery by day 56 without active intervention. However, for more potent compounds or longer/higher-dose protocols, active PCT compounds are standard in research. The Enclomiphene clinical data provides strong evidence for LH/FSH stimulation and testosterone restoration.
Clomiphene is a racemic mixture of enclomiphene (trans) and zuclomiphene (cis). The zuclomiphene isomer has a longer half-life and exhibits agonistic rather than antagonistic activity at some ER tissues, complicating the expected hormonal profile. Enclomiphene as the pure trans-isomer provides cleaner, more predictable ER antagonism at the HPT axis, making it more suitable for precise PCT research protocols.
Yes, and this combination is researched on the basis of addressing the HPT axis from two angles simultaneously: Arimistane reduces estrogenic negative feedback via aromatase inhibition; Enclomiphene directly stimulates LH/FSH release via ER antagonism at the hypothalamus/pituitary. Whether the combination is more effective than either alone in human SARM PCT contexts has not been formally studied in published trials.
