Clomiphene Citrate (Clomid) 50mg | 100-Count
SERM · HPTA restoration · ↑LH/FSH
QSC Peptides · ~5 day t½
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≥99% Pure · COA
The complete QSC Peptides PCT research reference — covering SERMs (Clomid, Nolvadex), aromatase inhibitors (Aromasin, Arimidex), and HCG for HPTA axis restoration research following exogenous AAS administration models.
Understanding the HPTA feedback loop is fundamental to PCT research. AAS suppress endogenous production via negative feedback; SERMs and AIs act at different points to restore it.
| Compound | Class | Mechanism | ER Activity | AI Activity | Half-Life | QSC Dose |
|---|---|---|---|---|---|---|
| Clomiphene (Clomid) | SERM | Blocks hypothalamic/pituitary ER → ↑LH/FSH | Antagonist (hypo) / Agonist (bone, endometrium) | None | ~5 days | 50mg tablets |
| Tamoxifen (Nolvadex) | SERM | Blocks hypothalamic ER → ↑GnRH → ↑LH/FSH | Tissue-selective antagonist/agonist | None | ~7 days | 20mg tablets |
| Exemestane (Aromasin) | Steroidal AI | Irreversible CYP19A1 inhibitor → ↓E2 | None | Irreversible (suicidal) | ~24 hrs | 25mg tablets |
| Anastrozole (Arimidex) | Non-steroidal AI | Reversible CYP19A1 inhibitor → ↓E2 | None | Reversible (competitive) | ~48 hrs | 1mg tablets |
| HCG | Gonadotropin analog | LH analog → Stimulates testicular T production directly | None | None | ~30 hrs | 5,000 IU |
Clomiphene (Clomid) and Tamoxifen (Nolvadex) are the two principal SERMs in PCT research. Both block estrogen receptors in the hypothalamus and pituitary, disrupting the E2-mediated negative feedback loop that suppresses GnRH, LH, and FSH secretion during AAS administration.
By blocking hypothalamic ER, SERMs cause the hypothalamus to perceive low estrogen — triggering increased GnRH pulse frequency and amplitude → increased pituitary LH/FSH secretion → increased testicular testosterone production. This is the core HPTA restoration mechanism studied in AAS recovery research.
Clomiphene has two active isomers: zuclomiphene (ER antagonist, ~20%) and enclomiphene (ER agonist, ~80%). Tamoxifen is tissue-selective — ER antagonist in hypothalamus/pituitary and breast, but partial agonist in bone, endometrium, and liver. In HPTA restoration research, both drive LH/FSH recovery but with different estrogenic side effect profiles in peripheral tissues.
Exemestane (Aromasin) is a steroidal "suicidal" AI — it irreversibly inactivates CYP19A1 (aromatase) by forming a covalent bond after the enzyme's initial oxidation step. Because inactivation is permanent, E2 suppression persists after drug clearance until new aromatase enzyme is synthesized (~3 days).
Anastrozole (Arimidex) is a non-steroidal competitive (reversible) AI — it binds the CYP19A1 active site in competition with androgen substrates. E2 suppression reverses rapidly after discontinuation as anastrozole clears. This kinetic difference makes Aromasin vs Arimidex a valuable comparison in CYP19A1 inhibition research.
Human Chorionic Gonadotropin (HCG) is a glycoprotein hormone with LH-like activity at LH/hCG receptors in Leydig cells. It directly stimulates testicular testosterone production independent of the HPTA axis — making it useful in research where primary testicular stimulation (bypassing pituitary LH) is required, and in studies comparing direct vs axis-mediated testosterone restoration.
QSC Peptides PCT Research Note: The combination of a SERM (for HPTA axis stimulation) with an AI (for estrogen control during recovery) and HCG (for direct testicular support) represents the standard tri-compound PCT research protocol. QSC Peptides stocks all three compound classes.
QSC Peptides · ~5 day t½
QSC Peptides · ~7 day t½
QSC Peptides · ↓E2 permanently per dose
QSC Peptides · ~48 hr t½
* All products research use only. Purchase links direct to qscpeptide.com.