TRT Research Stack: Testosterone + HCG + Exemestane Protocol | QSC Research
QSC RESEARCH STACK PROTOCOL
TRT Research Stack: Testosterone + HCG + Exemestane Protocol
The TRT research stack models testosterone replacement therapy biology: exogenous testosterone (AR agonism, anabolic effects, HPG suppression), HCG (LH receptor agonist, intratesticular testosterone/testicular volume maintenance), and exemestane (aromatase inhibitor, oestradiol control). This is the foundational male hormone axis research model.
Testosterone cypionate 5 mg/kg SC 2x/week + HCG 50 IU SC 3x/week × 8 weeks. Vs testosterone alone. Primary: ITT (enzymatic assay of testicular homogenate), testicular volume, spermatogenesis scoring (H&E), Leydig cell morphology.
3. Aromatase inhibition — oestradiol control
Add exemestane 5 mg/kg SC 3x/week to testosterone + HCG group. Monitor plasma oestradiol, testosterone, SHBG, bone mineral density (DEXA at 8 weeks), LH/FSH. Compare vs testosterone+HCG without AI. Maps oestradiol contribution to HPG feedback.
4. SERM comparison arm
Raloxifene 1 mg/kg PO daily vs exemestane in testosterone + HCG group. Oestradiol levels (AI blocks synthesis; SERM blocks receptor without reducing oestradiol). Bone density (DEXA), cholesterol panel, gynecomastia model (tibia fat pad). Demonstrates AI vs SERM mechanistic difference.
Why this combination?
Exogenous testosterone suppresses LH/FSH via HPG axis feedback → Leydig cell atrophy → reduced intratesticular testosterone (ITT) → impaired spermatogenesis. HCG bypasses the suppressed pituitary by directly activating LH receptors on Leydig cells → maintaining ITT and testicular volume despite exogenous testosterone. Exemestane blocks aromatase (CYP19A1) irreversibly → preventing testosterone conversion to oestradiol → controlling oestrogen-related effects (gynecomastia, HPG feedback contribution, water retention). This three-compound model allows complete HPG axis pharmacological dissection.
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Frequently Asked Questions
Why is HCG used alongside testosterone in this research model?
Exogenous testosterone suppresses LH production → Leydig cells lose stimulation → intratesticular testosterone (ITT) drops → spermatogenesis is impaired. HCG activates LH receptors directly on Leydig cells — bypassing the suppressed pituitary to maintain ITT and testicular volume. This is the model for studying spermatogenesis preservation during androgen replacement.
What is the difference between exemestane and raloxifene for oestrogen control?
Exemestane is an aromatase inhibitor — it blocks CYP19A1 enzymatically, preventing testosterone-to-oestradiol conversion. This reduces total oestradiol levels. Raloxifene is a SERM — it competes at oestrogen receptors without reducing oestradiol production. In bone, raloxifene is an ER agonist (protective); in breast, an antagonist. For oestradiol reduction: exemestane. For oestrogen receptor modulation without reducing oestradiol: raloxifene.
What formats does QSC supply TRT stack compounds in?
Testosterone cypionate and HCG as injectable research solutions; exemestane and raloxifene as tablet research kits. ≥99% HPLC purity, Janoshik COA. Ships domestically in USA, EU, UK, Canada, Australia.
