HCG (Fertility)

Detailed overview

HCG (Human Chorionic Gonadotropin) is a 244-amino-acid heterodimeric glycoprotein (α + β subunit), structurally an LH analog with ~80% sequence identity on the β subunit. Endogenous source: pregnancy placental syncytiotrophoblast. In the fertility-clinic context, HCG functions as **exogenous LH replacement**: a Leydig-cell LHCGR receptor agonist that activates testosterone biosynthesis and plays a critical role in maintaining intratesticular testosterone (ITT) – the ITT concentration is 50-100× higher than serum testosterone (~600-1200 nmol/L vs. ~10-30 nmol/L serum), and this high-ITT environment is an absolute requirement for Sertoli-supported spermatogenesis. Clinical HCG sources: (1) urinary-extracted (uHCG) – purified from pregnant women's urine (Pregnyl Organon 1973, Novarel Ferring, Choragon Ferring EU); (2) recombinant (rHCG / choriogonadotropin alfa) – CHO-cell-expressed, higher purity, lower immunogenicity (Ovidrel Serono/Merck USA, Ovitrelle EMA). **Clinical indications**: (a) male hypogonadotropic hypogonadism (HH, Kallmann syndrome, pituitary insufficiency) – testosterone restoration via the Leydig-cell pathway; (b) spermatogenesis induction in HH patients (HCG monotherapy is often insufficient; HMG or rFSH co-administration is required for complete spermatogenesis initiation); (c) clinical HPTA-recovery protocol after endogenous testosterone suppression (idiopathic secondary hypogonadism, corticosteroid- or opioid-induced HPTA suppression); (d) IVF male-factor – oligospermia / azoospermia treated with a combined gonadotropin protocol. **Cross-frame note**: this is the `hcg-peptid` entry – fertility-clinic Rx framing. The `hcg-perf` counterpart entry (performance library) covers the same molecule in the AAS-PCT bridge context (atrophy prevention, doping narrative). IDENTICAL molecule, different narrative: the patient/user receives the same Pregnyl/Ovitrelle vial – only with a different intent and a different medical framing.