Selepressin
Selective vasopressin V1a agonist
Also FE 202158, FE202158, Selepressin infusion
- Evidence
- CAnimal and cell studies
- FDA status
- In clinical trialsas of 2026-10-26
- Route
- Intravenous
- Studies cited
- 1 human0 animal or cell
A drug meant to raise blood pressure in septic shock, a life-threatening infection response. A trial of 868 adults found no benefit, and work on it stopped.
Sold for
Selepressin was meant to be a cleaner vasopressin for septic shock: raise blood pressure without the fluid leak and clotting effects of the natural hormone.
Studies say
The one large randomized trial found selepressin did not increase ventilator- and vasopressor-free days or reduce mortality compared with placebo, so the evidence does not support it.
Why grade C. One large randomized, double-blind, placebo-controlled trial (SEPSIS-ACT, 868 adults with septic shock) tested selepressin and found no benefit on its primary endpoint or on mortality. A controlled trial exists, but it was negative, so there is no evidence supporting the use for which the drug was designed. Earlier phase 2a data were small and dose-finding. 12
FDA. Selepressin is an investigational drug that is not approved by the FDA or any regulator. Its phase 2b/3 trial in septic shock was stopped for futility in 2017 and development has not resumed. 1
Written from 2 cited sources. Fact-checked 2026-10-27: 13 claims checked, 1 corrected. Last refreshed 2026-10-27. Not physician reviewed.
What this means for you
- What people take it for
- Treating septic shock.
- Can a US doctor prescribe it?
- No. It is not approved, and development has stopped after a failed trial.
- Properly tested in people?
- Partly: some human trials, with gaps: one 868-adult trial found no benefit.
Evidence checklist
- Randomised controlled trial SEPSIS-ACT, double-blind, placebo-controlledyes
- Human study over 100 people SEPSIS-ACT 868 adultsyes
- More than one research group One trial by one sponsorno
- Clinical outcomes, not surrogate markers Ventilator-free days and 90-day mortalityyes
- Human safety data beyond case reports Adverse events similar to placeboyes
Drawn from the cited studies below. A dash means the sources give no information.
What it is
Selepressin is a lab-made version of vasopressin. Vasopressin is the pituitary hormone that narrows blood vessels and conserves water. Ferring Pharmaceuticals developed selepressin to bind only the V1a receptor. This is the receptor on blood vessel muscle. It leaves two others alone. One is the V2 receptor (water retention, clotting factor release). The other is the V1b receptor (stress hormone release). 12
Vasopressin itself is already used alongside norepinephrine in septic shock. The hope was that a V1a-only drug would raise blood pressure just as well. It would avoid the fluid overload and other downsides tied to V2 activation. 2
How it works
In septic shock, blood vessels widen and leak. The body's own vasopressin stores run down within hours. V1a receptor activation tightens vessel walls. In animal models, it also cut the leak of fluid out of capillaries. It also cut the build-up of lung fluid. Selepressin was designed to prefer V1a over V2 by roughly a thousand-fold. So it should narrow vessels without triggering two V2 effects. These are kidney water retention and von Willebrand factor release. 12
What human research shows
SEPSIS-ACT was an adaptive phase 2b/3 trial. It enrolled 868 adults with septic shock who needed norepinephrine. It ran at 63 hospitals in several countries. Patients got one of several selepressin infusion rates or placebo, on top of standard care. The primary endpoint was days alive and free of both mechanical ventilation and vasopressors through day 30. Selepressin patients averaged about 15 such days. Patients on placebo also averaged about 15. There was no difference. Mortality at 90 days was around 40 percent in both groups. A planned interim analysis led to stopping the trial for futility. 1
Selepressin did cut the dose of norepinephrine needed. It also cut the amount of intravenous fluid given. This showed it was active as a vasoconstrictor. That effect on the body did not lead to any benefit patients would notice. 1
| Study | Model | Finding |
|---|---|---|
| SEPSIS-ACT | Humans, n=868, randomized, double-blind, placebo-controlled, adaptive phase 2b/3 | No difference in ventilator- and vasopressor-free days or 90-day mortality versus placebo; stopped for futility. 1 |
| SEPSIS-ACT design paper | Trial protocol and rationale | Described the adaptive design that let the trial test several infusion rates and stop early if none worked. 2 |
Safety
Adverse event rates were similar between selepressin and placebo in SEPSIS-ACT. This held for serious adverse events, arrhythmias, and limb or gut ischemia from vasoconstriction. Vasopressin-type drugs carry a known risk of reducing blood flow to the fingers, intestines and heart. The trial did not show that selepressin made this worse. One trial of 868 people cannot rule out rare harms. But the practical issue is that the drug did not help. 1
Questions for your clinician
- Is selepressin available in any trial for septic shock?
- What did SEPSIS-ACT show about survival?
- Which vasopressors are standard for septic shock?
Questions people ask
Is selepressin FDA-approved?
No. It never got past its phase 2b/3 trial, which was stopped for futility in 2017. No further trials have been registered. 1
How does it differ from vasopressin?
Vasopressin activates V1a, V1b and V2 receptors. Selepressin was built to activate V1a alone, which narrows blood vessels. It was meant to avoid V2, which drives water retention and clotting factor release. In the trial, that selectivity did not give better outcomes than standard care. 12
Did the trial show any effect at all?
Yes, a physical one. Selepressin cut the norepinephrine and intravenous fluid patients needed. That means it raised blood pressure as intended. It did not get patients off ventilators or vasopressors sooner. It did not improve survival. 1