Anabolic androgenic steroids (AAS) are a class of steroidal compounds structurally derived from testosterone that activate the androgen receptor (AR) with varying degrees of anabolic (muscle-building, protein synthesis) and androgenic (masculinizing) activity. The term "anabolic" refers to tissue-building effects; "androgenic" refers to effects in androgen-responsive tissues (prostate, skin, hair follicles, hypothalamus).
All AAS in the QSC Peptides catalog are synthetic molecules designed to activate AR with modified selectivity, bioavailability, and half-life profiles relative to endogenous testosterone. Research applications span muscle physiology, AR pharmacology, HPTA biology, sports pharmacology, and endocrine medicine.
All AAS research compounds act via the androgen receptor (AR) — a nuclear receptor in the steroid hormone receptor superfamily. AR is a ligand-activated transcription factor expressed in skeletal muscle, prostate, skin, bone, liver, hypothalamus, and many other tissues. The AR signaling cascade:
The A:A ratio compares anabolic activity (levator ani muscle assay) to androgenic activity (prostate/seminal vesicle assay) with testosterone as 100:100 baseline. All QSC Peptides compounds:
Certain AAS are substrates for CYP19A1 (aromatase), which converts them to estrogens. Testosterone aromatizes to estradiol (E2); Dianabol to 17α-methylestradiol (potent); Nandrolone minimally to estrone (E1). Non-aromatizing AAS: Trenbolone, Anavar, Winstrol, Masteron, Anadrol (though Anadrol is a direct ER agonist). Aromatization determines the estrogenic profile of a research compound.
5α-reductase converts testosterone to DHT (3-5× higher AR affinity — amplifies androgenicity in skin/prostate/scalp). Different AAS produce different 5α-reduction products: Nandrolone → DHN (inactive — reduces androgenicity); MENT → 7α-Me-DHN (active — maintains androgenicity); Trenbolone → no reduction. DHT derivatives (Anavar, Winstrol, Masteron) cannot reduce further.
All exogenous AAS suppress the hypothalamic-pituitary-testicular axis (HPTA) via negative feedback at hypothalamic AR and ER. Strong HPTA suppressors: Trenbolone (AR + PR), MENT (AR + PR + aromatization), Testosterone (AR + E2 aromatization). Weaker: Anavar, Masteron, low-dose Nandrolone.
Injectable AAS ester half-lives determine dosing frequency in research: Suspension/no ester (<1 day), Propionate/Acetate (~2 days), Phenylpropionate (~5 days), Enanthate (~7 days), Cypionate (~8 days), Decanoate (~15 days), Undecylenate (~14 days). Oral AAS have short half-lives (3–9 hours) due to rapid hepatic metabolism.