Research compounds
Endothelin-1
ET-1
Endothelin-1 is the most potent endogenous vasoconstrictor known, produced by vascular endothelium. Blocking it is an approved treatment strategy for pulmonary arterial hypertension.
Also known as: endothelin 1, EDN1
- Status
- Endothelin-1 is a research compound and not approved by the FDA for human use.
- Evidence
- Early human data. Only small or early-phase studies in people so far.
- Half-life
- Approximately 4 to 7 minutes, though the vascular effect far outlasts this.
- How it's taken
- Not used therapeutically; research administration only
- Mechanism
- Other
How Endothelin-1 works
Endothelin-1 is a 21-amino-acid peptide acting at ETA receptors on vascular smooth muscle to produce intense, sustained vasoconstriction and proliferation, and at ETB receptors on endothelium where it paradoxically promotes nitric oxide release and clearance of endothelin itself. Its constrictor effect is long-lasting because it binds nearly irreversibly.
What research has looked at
- The endothelin system produced an approved drug class: bosentan, ambrisentan and macitentan are endothelin receptor antagonists used in pulmonary arterial hypertension.
- Its dual receptor system, with opposing ETA and ETB effects, explains why selective and non-selective antagonists differ clinically.
- Endothelin-1 levels are a prognostic marker in heart failure and pulmonary hypertension.
Evidence level: Early human data. Only small or early-phase studies in people so far. These are areas studied or reported, not promised effects.
Reported side effects and risks
- Endothelin-1 is a pathological mediator — the therapeutic direction is antagonism, and administering it produces profound, prolonged vasoconstriction and hypertension. No regulator has approved it, the human evidence base is limited, and material sold under this name is research chemical supply with unverified identity, purity, sterility and dose accuracy.
- Its near-irreversible receptor binding means its constrictor effect cannot be readily reversed once produced.
- It promotes vascular smooth muscle proliferation and fibrosis, contributing to remodelling in pulmonary hypertension.
- The approved antagonists carry hepatotoxicity and teratogenicity warnings, indicating how consequential this system is.
Sources
- PubMed research on endothelin-1 ETA ETB receptor antagonist pulmonary hypertension · NIH · National Library of Medicine
- DrugBank record for endothelin · DrugBank
- Active clinical trials for endothelin · U.S. National Library of Medicine
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Related compounds
Endothelin-1 FAQ
What is Endothelin-1?
Endothelin-1 is the most potent endogenous vasoconstrictor known, produced by vascular endothelium. Blocking it is an approved treatment strategy for pulmonary arterial hypertension.
How does Endothelin-1 work?
Endothelin-1 is a 21-amino-acid peptide acting at ETA receptors on vascular smooth muscle to produce intense, sustained vasoconstriction and proliferation, and at ETB receptors on endothelium where it paradoxically promotes nitric oxide release and clearance of endothelin itself. Its constrictor effect is long-lasting because it binds nearly irreversibly.
Is Endothelin-1 FDA approved?
No. Endothelin-1 is a research compound and not approved by the FDA for human use. Evidence level: early human data. Only small or early-phase studies in people so far.
What is the half-life of Endothelin-1?
Reported half-life: Approximately 4 to 7 minutes, though the vascular effect far outlasts this.
How is Endothelin-1 taken?
Not used therapeutically; research administration only.
What side effects have been reported with Endothelin-1?
Reported in the sources: Endothelin-1 is a pathological mediator — the therapeutic direction is antagonism, and administering it produces profound, prolonged vasoconstriction and hypertension. No regulator has approved it, the human evidence base is limited, and material sold under this name is research chemical supply with unverified identity, purity, sterility and dose accuracy; Its near-irreversible receptor binding means its constrictor effect cannot be readily reversed once produced; It promotes vascular smooth muscle proliferation and fibrosis, contributing to remodelling in pulmonary hypertension; The approved antagonists carry hepatotoxicity and teratogenicity warnings, indicating how consequential this system is.
Educational summary compiled from the sources listed above. Not medical advice. Peptide Vault does not sell, source or recommend any compound. Talk to a qualified clinician before starting or changing anything.