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Infectious Disease · Clinical trials

Sepsis Clinical Trials

Approved therapies, the pivotal-trial endpoints they were judged on, the magnitude of benefit — and the drugs that failed their endpoints, and why.

Indication overview

About sepsis — and why its trials are hard

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection; septic shock is its most severe form, marked by profound circulatory and metabolic derangement. It is a leading cause of hospital death worldwide and a syndrome rather than a single disease, which has profoundly shaped its therapeutics. There is no approved sepsis-specific drug that treats the underlying dysregulated response. Management rests entirely on supportive care: prompt source control, early broad-spectrum antibiotics, intravenous fluids, vasopressors, and organ support, guided by frameworks such as the Surviving Sepsis Campaign. The field is notorious for a graveyard of failed targeted therapies. Drotrecogin alfa (Xigris), an activated protein C approved in 2001, was withdrawn in 2011 after the PROWESS-SHOCK trial showed no survival benefit. Numerous anti-inflammatory, anticoagulant, and immunomodulatory agents targeting endotoxin, cytokines, and Toll-like receptors have failed in large trials, reflecting sepsis heterogeneity. Current research emphasizes patient subphenotyping and precision-medicine enrichment to succeed where broad approaches failed.

Indication
Sepsis
ICD-10-CM
A41.9 — Sepsis, unspecified organism

Where trials have failed

Drugs that missed their endpoint — and what contributed

The most instructive lessons in sepsis development come from programmes that failed the endpoint that mattered.

Drug / trialEndpoint outcomeWhat contributed
Drotrecogin alfa (activated protein C) — PROWESS-SHOCK (confirmatory)No mortality benefit in septic shock; drug voluntarily withdrawn worldwide in 2011Initial PROWESS approval (2001) not confirmed; bleeding risk without survival gain led to withdrawal
Eritoran (TLR4 antagonist) — ACCESSFailed to reduce 28-day mortality in severe sepsisTargeting endotoxin/TLR4 signaling did not improve survival across a heterogeneous population
Selepressin (selective vasopressin V1a agonist) — SEPSIS-ACTFailed to improve ventilator- and vasopressor-free days in septic shockDid not meet primary or key secondary endpoints; trial stopped for futility
High-dose vitamin C (with thiamine/hydrocortisone) — VITAMINS / CITRIS-ALINo improvement in resolution of organ dysfunction or key clinical outcomesMetabolic resuscitation hypothesis not confirmed in rigorous randomized trials
Anti-TNF agents (e.g., afelimomab) — Multiple anti-cytokine sepsis trialsLittle to no consistent mortality benefitBlocking single mediators failed given the redundant, heterogeneous host response

Choosing the right endpoint

Primary endpoints that matter in sepsis trials

  • 28-day (or 90-day) all-cause mortality — The definitive and most common primary endpoint in sepsis interventional trials
  • Vasopressor-free days — Reflects reversal of shock; used as a shorter-term efficacy signal
  • Ventilator-free days — Captures respiratory organ support burden and recovery
  • Resolution of organ dysfunction (SOFA) — Change in Sequential Organ Failure Assessment score tracks organ recovery

How iNGENū runs sepsis trials

Physician-led design, built for FDA submission

Endpoint & biomarker strategy

Board-certified specialists design endpoints and patient selection aligned to current FDA guidance for this indication.

FDA-ready data

Built to ICH-GCP and 21 CFR 312.120, with direct FDA submission — data accepted by the FDA, EMA and MHRA.

Faster, lower-cost delivery

~4-week ethics via the TGA CTN scheme, up to 43.5% R&D rebate, and 80–90% below US CRO cost.

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Frequently asked questions

Sepsis clinical trials — FAQs

Is there a drug that treats sepsis itself?
No. There is no approved sepsis-specific therapy targeting the dysregulated host response; care relies on early antibiotics, source control, fluids, vasopressors, and organ support.
What happened to Xigris (drotrecogin alfa)?
Approved in 2001 for severe sepsis, it was voluntarily withdrawn in 2011 after the confirmatory PROWESS-SHOCK trial found no survival benefit while bleeding risk remained.
Why have so many sepsis drugs failed?
Sepsis is a heterogeneous syndrome, so single-target anti-inflammatory or anticoagulant agents tested in broad populations have repeatedly failed; research now focuses on identifying subphenotypes for precision enrichment.

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