Heart & blood Selective vasopressin V1a agonist
Selepressin
Regulatory status
Status at a glance
503A compounding status
Not nominated
We found no pending nomination for the 503A bulks list. Unless the substance has another legal pathway (for example, a USP monograph or use in an FDA-approved drug), 503A pharmacies generally may not compound with it.
- FDA approval
- Not FDA-approved for any use
- 503B outsourcing
- Not determined
- Anti-doping (WADA)
- Not on the WADA Prohibited List
- DEA schedule
- Not a controlled substance
About peptide status
Most peptides discussed here are not FDA-approved for any use, and products labeled “research use only” are not for human use. Removal from Category 2 does not authorize compounding. PCAC votes are non-binding recommendations; FDA and HHS make the final decisions.
This is not medical or legal advice, and we do not publish dosing, sourcing or reconstitution information. Talk with a licensed clinician before using any peptide.
If you think you are having a medical emergency, call 911.
Key takeaway
Selepressin is an investigational selective vasopressin V1a receptor agonist, developed by Ferring Pharmaceuticals as an intravenous blood-pressure support for septic shock. Its pivotal trial was stopped for futility and showed no benefit over placebo, and development has been discontinued. As of 2026 it is not approved.
At a glance
- FDA status
- Investigational peptide, not approved by the FDA
- What it is
- Selective vasopressin V1a receptor agonist given by intravenous infusion for septic shock
- Research
- Pivotal trial (SEPSIS-ACT) stopped for futility with no benefit
- Development status
- Discontinued
- Evidence strength
- Low research
Summary
Selepressin is an investigational V1a receptor agonist once studied for septic shock. Learn how it works and why its pivotal trial showed no benefit.
What is selepressin?
Selepressin is an experimental vasopressor, a drug that raises blood pressure. It was being developed for septic shock by Ferring Pharmaceuticals under the code FE-202158. Unlike natural vasopressin, which acts on several receptors, selepressin was designed to act selectively on the V1a receptor. It is given by continuous intravenous infusion in intensive care. It is investigational, and its development has been discontinued.
How does it work?
Selepressin selectively activates the vasopressin V1a receptor, which causes blood vessels to constrict and raises blood pressure. Targeting V1a alone had three aims:
- Achieve this pressor effect
- Avoid the fluid retention and other effects linked to the V2 receptor that non-selective vasopressin also activates
- Reduce reliance on catecholamine drugs like norepinephrine
This describes the mechanism; as the trial below shows, it did not translate into improved outcomes.
Is it FDA-approved?
Safety note
Status: Investigational peptide, not approved by the FDA
Category: In clinical trials · Primary body area: Heart & blood
No. Selepressin is investigational and not approved, and its development program has been stopped.
What does the research show?
Editor’s note
Evidence strength: Low research
Its one pivotal trial was stopped for futility with no benefit on the primary or key secondary outcomes.
The decisive evidence is negative. According to PubMed, the adaptive Phase 2b/3 SEPSIS-ACT trial in adults with septic shock was stopped for futility. There was no significant difference from placebo in the primary endpoint of ventilator- and vasopressor-free days, nor in key secondary outcomes including 90-day mortality. A companion design paper describes the trial's adaptive methods. The human evidence does not support a benefit.
Sources: the SEPSIS-ACT trial (Laterre et al., JAMA, 2019, DOI: 10.1001/jama.2019.14607) and its design paper (Lewis et al., Annals of the American Thoracic Society, 2018, DOI: 10.1513/AnnalsATS.201708-669SD), both indexed on PubMed. This document is educational, is not medical advice or a health claim, and is not an offer to sell any product.
Registered human trials
0 registered human trials on ClinicalTrials.gov that we reviewed
Sources
- [1]
- [2]
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