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Gonadorelin 2mg
SKU: GONADRLN-2M
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Contact Us →Gonadorelin (synthetic GnRH/LHRH) is a synthetic decapeptide identical in sequence to the endogenous hypothalamic gonadotropin-releasing hormone. Pulsatile GnRH receptor (GnRHR) activation drives pulsatile LH and FSH release from pituitary gonadotrophs; continuous receptor activation produces GnRHR downregulation and gonadotropin suppression. Research applications include GnRHR pharmacology, HPG-axis pulsatility investigation, gonadotropin secretion dynamics, and pulse-versus-continuous agonism comparison studies.
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3D Molecular Structure of C55H75N17O13
CarbonHydrogenFluorineNitrogenOxygenSulfur
| Chemical Formula | C55H75N17O13 |
|---|---|
| Synonyms | Luliberin, Dirigestran, Fertagyl, Gonadorelina, Gonadorelinum, Gonadotropin-releasing hormone, LH-releasing factor |
| Molar Mass | 1,182.31 g/mol |
| CAS Number | 33515-09-02 |
| PubChem CID | 638793 |
| Total Compound Content | 2 mg per vial |
| Shelf Life | 36 months |
Gonadorelin (pyroGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2) is a synthetic decapeptide identical in sequence to endogenous gonadotropin-releasing hormone (GnRH). It functions as a full agonist of the gonadotropin-releasing hormone receptor (GnRHR), a Gq/11-coupled GPCR expressed on gonadotroph cells. Receptor activation stimulates phospholipase C signalling, resulting in IP3/DAG generation, intracellular calcium mobilization, and downstream gonadotropin-associated signalling pathways. A defining feature of GnRHR biology is its dependence on pulsatile stimulation; transient receptor activation and continuous receptor activation produce markedly different signalling outcomes due to receptor desensitization and internalization mechanisms. Because gonadorelin is structurally identical to endogenous GnRH and possesses a very short plasma half-life, it remains the reference compound for studies investigating GnRHR pharmacology, pulsatile peptide signalling, receptor regulation, gonadotroph signalling dynamics, and comparative GnRH analogue research. Supplied as lyophilized preparation (2 mg/vial). Independently third-party HPLC-tested; COA available per batch.
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Why does pulsatile GnRH stimulate receptor signalling while continuous GnRH produces receptor desensitisation?
GnRHR is a Gq/11-coupled receptor whose signalling output is highly dependent on the pattern of ligand exposure. Intermittent receptor activation allows signalling pathways to reset between stimulation events, maintaining receptor availability and responsiveness. In contrast, continuous receptor occupancy promotes receptor phosphorylation, β-arrestin recruitment, internalisation, and desensitisation mechanisms that reduce subsequent signalling capacity. This pulse-frequency dependence is a defining characteristic of GnRHR biology and makes gonadorelin an important research tool for investigating receptor regulation, signal-transduction dynamics, and temporal control of GPCR signalling.
How does gonadorelin differ from long-acting GnRH analogues in research applications?
Gonadorelin is the native GnRH decapeptide and serves as the reference compound for studies of physiological GnRHR activation. Long-acting GnRH analogues incorporate structural modifications that increase receptor affinity, enzymatic stability, and duration of action. As a result, gonadorelin is typically used when investigating acute receptor activation, pulsatile signalling dynamics, and endogenous GnRH pathway biology, whereas longer-acting analogues are valuable tools for studying receptor desensitisation, sustained receptor occupancy, and long-duration GnRHR signalling mechanisms.
Why is gonadorelin considered the reference compound for GnRHR pharmacology?
Because gonadorelin is structurally identical to endogenous GnRH, it provides the benchmark against which synthetic GnRH analogues are compared. Its receptor-binding properties, signalling characteristics, and pharmacological profile have been extensively characterised, making it a standard tool for studies of GnRHR activation, receptor regulation, signalling kinetics, ligand-receptor interactions, and comparative GnRH analogue pharmacology.
