HCG (Humaan Choriongonadotrofine) — Onderzoekskwaliteit

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What Is HCG?

HCG (Human Chorionic Gonadotropin, CAS 9002-61-3) is a glycoprotein peptide hormone in the same gonadotropin family as luteinising hormone (LH), follicle-stimulating hormone (FSH), and thyroid-stimulating hormone (TSH). Like the other three, it is a heterodimer of an α-subunit (92 amino acids, identical across all four hormones) and a β-subunit (145 amino acids, unique to HCG). The α and β subunits are non-covalently associated and both are extensively glycosylated — the β-subunit alone carries four N-linked and four O-linked glycans, and the high sialic-acid content of these glycans is responsible for HCG’s exceptionally long plasma half-life relative to LH (33–37 h terminal, versus ~20 min for LH).

Endogenous HCG is produced by the syncytiotrophoblast of the developing placenta during pregnancy, where it maintains the corpus luteum and progesterone production for the first ~10 weeks of gestation. Outside pregnancy it is not normally present at detectable levels; its appearance in serum or urine is therefore the basis of pregnancy testing. The pharmacological utility of HCG in research, however, has nothing to do with this physiological role and everything to do with the fact that HCG binds and activates the same LH/CG receptor (LHCGR) as endogenous LH — but with far longer duration of action. HCG is therefore the standard pharmacological tool for sustained LHCGR activation in research that probes Leydig-cell function, gonadal steroidogenesis, spermatogenesis, follicular development, ovulation, and the HPG axis broadly.

Two molecular forms of HCG exist in commerce: the urinary-extracted form (uHCG, CAS 9002-61-3), purified from the urine of pregnant women, which is what we supply; and the recombinant form (rHCG or choriogonadotropin alfa, CAS 56832-30-5), produced in CHO cells and used in some clinical preparations (Ovidrel / Ovitrelle). The two forms have the same amino-acid sequence and the same LHCGR binding profile, but the glycosylation patterns differ slightly between urinary-extracted and CHO-cell expression — published bioassay comparisons report broadly equivalent in-vivo potency.

Mechanism of Action — LH/CG Receptor Activation and Steroidogenesis

HCG’s mechanism is among the most-characterised in endocrine pharmacology:

• LH/CG receptor (LHCGR) binding — HCG binds the LHCGR (a class-A Gs-coupled GPCR with a large extracellular leucine-rich-repeat domain), with high affinity and the same binding site as endogenous LH. Receptor distribution is restricted to gonadal tissue: Leydig cells of the testis (males), and ovarian theca cells, mural granulosa cells, and luteinised granulosa cells (females). The LHCGR is also expressed at lower levels on corpus-luteum cells, where HCG sustains progesterone production during early pregnancy.
• Gs-cAMP-PKA signalling cascade — Activated LHCGR couples to Gαs, raising intracellular cyclic AMP, activating PKA, and driving phosphorylation of CREB and other downstream transcription factors. cAMP also engages EPAC for some downstream effects. PKA activation in steroidogenic cells specifically upregulates the StAR protein (steroidogenic acute regulatory protein), which transports cholesterol across the mitochondrial outer membrane — the rate-limiting step in de-novo steroidogenesis.
• Steroidogenic enzyme induction — Sustained LHCGR activation by HCG drives transcriptional upregulation of the steroidogenic enzyme cascade: CYP11A1 (cholesterol side-chain cleavage), CYP17A1 (17α-hydroxylase / 17,20-lyase), 3β-HSD, and 17β-HSD. The net result in Leydig cells is sustained de-novo testosterone biosynthesis; in ovarian theca cells, the same cascade produces androstenedione (which granulosa cells convert to oestradiol via CYP19A1 / aromatase under FSH stimulation).
• Functional duration and tachyphylaxis — A single HCG bolus produces sustained LHCGR activation lasting 5–7 days in research models, because of HCG’s long plasma half-life (33–37 h) and the LHCGR’s slow internalization kinetics. Repeated high-dose HCG dosing can produce LHCGR desensitization (tachyphylaxis) — a well-documented phenomenon in published Leydig-cell research that is relevant to chronic-dosing protocols.
• Hypothalamic-pituitary feedback — Like endogenous testosterone, HCG-driven testosterone output feeds back to the hypothalamus and pituitary to suppress GnRH and LH/FSH secretion. In the context of suppressed-HPG research (testosterone replacement, AAS exposure, or pharmacological HPG suppression), HCG bypasses the hypothalamic-pituitary blockade by acting directly at the Leydig-cell LHCGR — which is why HCG is the canonical tool for probing Leydig-cell preserved function under HPG suppression.

HCG and LH activate the same receptor through the same cascade, but with two key practical differences: HCG produces longer, more sustained signalling per dose (because of its longer half-life), and HCG is administered exogenously while endogenous LH is pulsatile and centrally regulated. Research protocols that need sustained, controllable LHCGR activation use HCG; protocols that need pulsatile, physiological LHCGR activation use recombinant LH or GnRH-driven endogenous LH.

Published Research Applications

HCG is used in laboratory research contexts that investigate:

• LHCGR pharmacology — the canonical reference agonist — by far the most-cited LH/CG receptor activator in the published literature; standard tool compound for receptor-internalization kinetics, signalling-bias studies, and the development of newer LHCGR-targeted small-molecule modulators
• Leydig-cell biology and gonadal steroidogenesis — HCG is the standard pharmacological stimulus for de-novo testosterone biosynthesis in primary Leydig-cell culture and ex-vivo testicular slice preparations; widely used in research on Leydig-cell function, mitochondrial cholesterol transport, StAR regulation, and steroidogenic-enzyme cascade kinetics
• HPG-axis suppression-recovery research — in research models where endogenous LH/FSH has been suppressed (by exogenous testosterone administration, anabolic-androgenic-steroid exposure, or pharmacological GnRH antagonism), HCG acts directly at the Leydig-cell LHCGR to maintain testosterone output and preserve Leydig-cell function; the canonical tool for dissecting the HPG-axis suppression-recovery dynamics
• Spermatogenesis research — used in combination with FSH or FSH-analogues in published Sertoli-cell / spermatogonial-stem-cell research; sustains the high-intratesticular-testosterone microenvironment required for spermatogenesis even in the face of suppressed circulating LH
• Ovarian follicular development and ovulation research — in female reproductive research, HCG is used to mimic the LH surge that triggers final follicular maturation, oocyte meiotic resumption, and follicular rupture; standard tool in published ovulation-trigger protocols, oocyte-maturation studies, and luteinization research
• Corpus-luteum biology — HCG sustains corpus-luteum function and progesterone production by direct LHCGR activation on luteal cells; used in published research on the luteal phase and the luteo-placental transition
• Receptor pharmacology and biased agonism — the LHCGR exhibits cAMP-vs-arrestin biased signalling, and HCG is the reference full-agonist against which biased ligands (small-molecule LHCGR allosteric modulators, ORG-43553, and others) are benchmarked
• Comparative pharmacology vs LH and recombinant choriogonadotropin alfa — published research has compared urinary-extracted HCG (uHCG, what we supply), recombinant HCG (rHCG / choriogonadotropin alfa), and recombinant LH (Luveris) head-to-head for receptor-binding, cAMP signalling, and in-vivo testosterone-output endpoints

For broader context on HPG-axis and reproductive-system research peptides in this catalogue, see Kisspeptine-10 (the upstream hypothalamic regulator of GnRH — the most direct HPG-axis peptide complement to HCG), PT-141 (Bremelanotide) (melanocortin receptor pharmacology — sexual-function research), Oxytocine Acetaat (the hypothalamic posterior-pituitary peptide hormone — reproductive / social-bonding research), and Tesamorelin (GHRH analogue — a different endocrine axis but commonly co-studied). Browse the full research peptides & compounds catalog.

Beschikbare sterktes en concentraties

MedsBase stocks HCG (urinary-extracted glycoform) in two lyophilized vial sizes calibrated to typical research-protocol dose ranges. Each strength is available in 10-vial or 20-vial pack formats:

Both strengths are the same chemical entity (lyophilized urinary-extracted HCG, ≥99% HPLC purity, WHO 5th International Standard bioassay-confirmed potency). The 10,000 IU vial provides the lowest per-IU cost for large-cohort or chronic-dosing research; the 5,000 IU vial is convenient for single-dose stimulation experiments or smaller-cohort work where vial-to-vial dosing accuracy matters more than per-IU cost. Researchers should determine specific dose ranges from peer-reviewed literature appropriate to the protocol.

How It Compares — HCG vs Kisspeptin-10

HCG and Kisspeptine-10 are the two HPG-axis peptide tools in this catalogue, and they target completely different layers of the same axis. HCG acts downstream, at the Leydig-cell / theca-cell LH/CG receptor, mimicking the LH surge directly — useful when the goal is to drive Leydig-cell steroidogenesis or trigger ovulation regardless of upstream HPG state. Kisspeptin-10 acts upstream, at hypothalamic Kiss1R-expressing GnRH neurons, mimicking the kisspeptin signal that drives endogenous pulsatile GnRH and downstream LH/FSH release — useful when the goal is to interrogate the physiological HPG-axis cascade end-to-end. The two compounds are mechanistically complementary, and research protocols sometimes combine them to dissect upstream-hypothalamic vs downstream-gonadal contributions to reproductive endocrine output.

For research focused on direct gonadal-cell steroidogenesis, ovulation triggering, or downstream LHCGR pharmacology, HCG is the canonical reference compound. For research focused on hypothalamic GnRH-neuron biology, HPG-axis integration, or upstream reproductive-endocrine signalling, Kisspeptine-10 is the more targeted tool. See also PT-141 (Bremelanotide) for melanocortin-receptor pharmacology and sexual-function research, and Oxytocine Acetaat for posterior-pituitary peptide-hormone research.

Opslag en Reconstituering

Voor reconstituering: store lyophilized vials refrigerated at 2–8 °C in original packaging for short-term working stock. For long-term storage, freeze unopened vials at −20 °C (stable ≥36 months at −20 °C; ≥18 months at 2–8 °C). Lyophilized HCG is reasonably stable because the α and β subunits are held together by hydrophobic and hydrogen-bonded interactions that are not disrupted in the freeze-dried state, but the protein is sensitive to humidity exposure and to thermal cycling.

Reconstitueringsprocedure: for the 5,000 IU vial, inject 1.0 mL of bacteriostatic water down the side wall of the vial (not directly onto the lyophilized cake) — this yields a 5,000 IU/mL working stock. For the 10,000 IU vial, inject 2.0 mL of bacteriostatic water for the same 5,000 IU/mL working stock, or 1.0 mL for a 10,000 IU/mL high-concentration stock. Swirl gently to dissolve — do not shake, do not vortex. High-shear mixing dissociates the α/β heterodimer and destroys LHCGR-binding bioactivity. The mannitol-based lyophilization cake typically dissolves within 30–60 seconds with gentle swirling.

Critical storage rules for reconstituted material: once reconstituted, store at 2–8 °C and use within 30 days. Do not freeze reconstituted HCG — freeze-thaw cycles dissociate the heterodimer and irreversibly destroy bioactivity. Protect from light. Discard if cloudiness, particulates, or marked colour change appears. For research protocols that require multiple aliquots, prepare the aliquots at the time of reconstitution and store them at 2–8 °C separately rather than freezing — short-term refrigerated storage retains bioactivity better than even single freeze-thaw cycles.

Veelgestelde vragen

What is the difference between urinary-extracted HCG (uHCG) and recombinant HCG (rHCG / choriogonadotropin alfa)?

Urinary-extracted HCG (what we supply, CAS 9002-61-3) is purified from the pooled urine of pregnant women using ion-exchange and gel-filtration chromatography. Recombinant HCG (choriogonadotropin alfa, CAS 56832-30-5; clinical preparations Ovidrel / Ovitrelle) is produced in CHO cells from cloned HCG α and β subunit cDNAs. The two forms have the same amino-acid sequence and bind the LHCGR with the same affinity, but the glycosylation patterns differ slightly between urinary-derived and CHO-cell-expressed material. Published head-to-head bioassay comparisons report broadly equivalent in-vivo potency, with rHCG showing somewhat more consistent batch-to-batch glycosylation patterns and uHCG showing the slightly higher sialic-acid content typical of placental glycosylation.

How many IU is 1 mg of HCG?

The WHO 5th International Standard reference material defines HCG potency at approximately 9,300 IU per mg of pure peptide. Practically: a 5,000 IU vial contains ~0.54 mg of peptide; a 10,000 IU vial contains ~1.08 mg. The IU is a bioassay-defined unit that reflects LHCGR-binding potency rather than mass, and the IU/mg ratio varies slightly between glycoforms and between batches — which is why pharmaceutical-grade HCG is labelled in IU rather than in mg.

What published dose ranges have been used in rodent research?

Single-bolus rodent protocols typically use 50–250 IU SC or IM for cAMP / receptor-internalization studies, and 500–5,000 IU SC for sustained testosterone-output protocols (3–7 day duration of action per bolus). Chronic protocols use 100–500 IU/day for 2–4 weeks. The published ovulation-trigger dose in rodents is typically 5–10 IU per mouse or 10–50 IU per rat IP. In-vitro Leydig-cell stimulation protocols typically use 0.1–10 IU/mL in culture medium. Researchers should consult primary literature appropriate to the species, model, and endpoint of interest.

Why does HCG have a much longer half-life than LH?

The β-subunit of HCG carries four N-linked glycans and four O-linked glycans, with exceptionally high sialic-acid (NeuAc) content at the terminal positions of these glycans. The asialoglycoprotein receptor (ASGR) on hepatocytes is the major route by which gonadotropin-family hormones are cleared from circulation — ASGR recognises terminal galactose / N-acetylgalactosamine residues exposed after sialidase removal of terminal sialic acid. Because HCG’s β-subunit is so heavily and terminally sialylated, hepatic ASGR-mediated clearance is much slower than for the more lightly-sialylated LH β-subunit, producing the dramatic half-life difference (HCG 33–37 h vs LH ~20 min).

Why can’t reconstituted HCG be frozen?

HCG is a heterodimer of two non-covalently associated subunits. The α/β interaction is stable in the lyophilized cake (because there’s no water for the subunits to drift apart in) and stable in refrigerated aqueous solution at 2–8 °C (because the kinetics of dissociation are slow at low temperature). But the ice-crystal formation during freezing physically pulls the subunits apart, and once dissociated they re-associate only inefficiently on thawing. The result is that frozen-and-thawed HCG retains a large fraction of immunoreactivity (the β-subunit is still detectable by antibody) but loses a large fraction of bioactivity (the dissociated subunits do not productively engage the LHCGR). Lyophilized HCG can be frozen and is stable at −20 °C; reconstituted HCG cannot.

What is the WADA regulatory status of HCG?

HCG is on the World Anti-Doping Agency (WADA) Prohibited List under class S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). It is prohibited at all times — both in-competition and out-of-competition — for male athletes only. Female athletes are exempt because HCG is a natural pregnancy hormone and therefore detectable in any pregnant woman regardless of administration. Researchers conducting human-subject research with HCG need to be aware of this regulatory status. For laboratory in-vitro and rodent in-vivo research the WADA status is informational only.

Can HCG be combined with Kisspeptin-10, FSH, or testosterone in research protocols?

Yes — these compounds target different layers of the HPG axis (upstream, mid, downstream) and are commonly combined in research that aims to dissect axis integration. The most-published combinations are HCG with FSH (or FSH analogues) for spermatogenesis or follicular-development research; HCG with Kisspeptine-10 for upstream-vs-downstream dissection; HCG with exogenous testosterone (for HPG-suppression-recovery research, where the testosterone suppresses LH and HCG bypasses the suppression). Reconstitute each separately and follow each compound’s specific storage rules — HCG in particular must not be frozen reconstituted (see above).

How does this research-grade HCG compare with the branded clinical preparations (Eutrig, HUCOG, ZyHCG, Pregnyl, Ovidrel)?

The branded clinical preparations are urinary-extracted HCG (Eutrig HP, HUCOG, ZyHCG, Pregnyl) or recombinant HCG (Ovidrel / Ovitrelle) packaged under various manufacturer SKUs for clinical use in fertility and reproductive medicine. The research-grade HCG supplied here is the same urinary-extracted glycoform (uHCG, CAS 9002-61-3) at ≥99% HPLC purity, supplied without a clinical-use label and intended for laboratory research only. Researchers seeking clinical-use HCG should obtain it through a clinical supply chain; researchers seeking research-grade material for in-vitro receptor pharmacology, rodent in-vivo work, or other laboratory applications can use the material supplied here.

Other Research Peptides for HPG-Axis and Reproductive Research

• Kisspeptine-10 — Hypothalamic Kiss1R agonist — upstream HPG-axis regulator, drives GnRH pulsatility
• PT-141 (Bremelanotide) — Melanocortin-4 receptor agonist — sexual-function research
• Oxytocine Acetaat — Posterior pituitary nonapeptide — reproductive and social-bonding research
• Tesamorelin — GHRH analogue — different endocrine axis, commonly co-studied
• Sermorelin — GHRH 1-29 analogue — pituitary GH-axis research
• BAC Water (Bacteriostatisch Water) — Required for reconstituting any lyophilized vial — sterile, 0.9% benzyl-alcohol-preserved diluent

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