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RecruitingNCT07364162KETONES-ICUUpdated Aug 24, 2026

Exogenous Ketone Supplementation in ICU Delirium

A Phase 2 interventional study of Ketone monoester and Placebo in ICU Delirium and Critical Illness, sponsored by Vanderbilt University Medical Center. Recruiting at 1 site in United States. Open to participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2026-08-24.

Primary conditionCritical Illness(the registry's first term)UnverifiedIs this wrong?Critical Illness is a broad heading, used only when no more specific condition is named. No better condition is named, so the registry's term is kept.

Sponsored by Vanderbilt University Medical Center · Phase 2, Interventional, and Treatment

From the registry’s dates

  • Started Jun 2026; still recruiting 5 months later.
Phase
Phase 2
Study type
Interventional
Enrollment
40
Allocation
Randomized
Ages
18 Years and older
Sex
All
01

Study summary

Delirium is a common syndrome in intensive care unit (ICU) patients. Those experiencing delirium may suddenly feel confused, have trouble thinking clearly, struggle to pay attention, or see and hear things that are not real. Delirium is associated with worse long-term outcomes such as cognitive impairment, depression, and PTSD (post-traumatic stress disorder). This study examines whether an investigational medical-grade ketone supplement drink (ketone monoester [brand name: Ultrapure Ketone Monoester]) is safe and feasible to use in ICU patients, and to look for signals that it might reduce delirium or shorten its duration compared to a volume-, taste-, and calorie-matched placebo.

Read the detailed description

Delirium is a prevalent neuropsychiatric syndrome characterized by an acute disturbance in attention, cognition, and consciousness. It is associated with significant morbidity, mortality, and healthcare expenditures. Recent research has provided evidence supporting the connection between brain metabolism and delirium. During states of increased systemic inflammation, such as sepsis or trauma, the brain experiences a mismatch between energy supply and demand, which is commonly associated with delirium, especially in those with preexisting cognitive impairment.

In critically ill patients, mitochondrial dysfunction occurs in the setting of systemic inflammation, contributing to increased blood-brain barrier permeability and neuroinflammation. The downstream consequence of this is microglial activation, which amplifies the inflammatory response through the release of pro-inflammatory cytokines. The resultant mitochondrial dysfunction leads to impaired oxidative phosphorylation, decreased adenosine triphosphate (ATP) production, and increased reactive oxygen species production. In response to systemic inflammation, microglia transition to a pro-inflammatory phenotype characterized by increased aerobic glycolysis. This metabolic reprogramming depletes glucose availability for neurons and exacerbates the cerebral energy deficit. Emerging evidence suggests that activated microglia compete with neurons for metabolic substrates during inflammation. Activated microglia exhibit metabolic flexibility, shifting toward increased glycolysis to meet their heightened energy and biosynthetic demands. This competition for nutrients exacerbates the neuronal energy deficit and increases metabolic stress. The investigators hypothesize that this brain energy deficit contributes to the cognitive and neurological symptoms characteristic of delirium.

Ketones, such as β-hydroxybutyrate, are the brain's secondary source of energy when glucose is not available. After transport across the blood-brain barrier, β-hydroxybutyrate is metabolized to acetyl-CoA (acetyl coenzyme A), thereby directly entering the tricarboxylic acid cycle, bypassing the glycolytic bottleneck, to produce ATP. In addition to serving as a substrate for ATP production, ketones support mitochondrial function, limit oxidative stress, and reduce neuroinflammation. Ketones confer a two-fold therapeutic advantage in the setting of nutrient competition. Not only do they support neuronal oxidative phosphorylation by bypassing impaired glycolysis, but they also promote anti-inflammatory microglial phenotypes, inhibit inflammasome activation, and support metabolic reprogramming. This dual effect further reduces microglial glucose demand, enhancing neuronal substrate availability.

The investigators propose a prospective, randomized, placebo-controlled pilot study of exogenous ketone ester supplement administration in 40 critically ill patients to assess the safety and feasibility of this novel intervention and to generate preliminary data on its efficacy in reducing ICU delirium, as measured by delirium and coma free days (DCFDs). Exogenous ketones have been shown to support brain energetics and reduce neuroinflammation, directly targeting pathways implicated in the development of delirium. By reducing the duration of delirium or preventing its onset, this research has the potential to improve long-term cognitive outcomes for ICU survivors. The investigators propose enrolling adult patients at the time of ICU admission, with randomization to either an enteral ketone ester treatment group or a taste, volume, and calorie-matched dextrose-containing placebo. The study drug or placebo will be administered at the time of enrollment, within 24 hours of ICU admission, and every six hours thereafter for up to 7 days until ICU discharge, or death, whichever occurs first. Ketone administration will be continued after the diagnosis of delirium. In accordance with prior studies, the initial dose of β-hydroxybutyrate will be 25 g; however, subsequent doses will be titrated to maintain serum β-hydroxybutyrate levels between 1.5 and 3.5 mM, with protocolized monitoring of vital signs, serum pH, glucose levels, and adverse gastrointestinal effects. Delirium will be assessed using the Confusion Assessment Method for the ICU (CAM-ICU) delirium screening tool twice daily for a period of 7 days.

This pilot study will assess the feasibility, safety, and tolerability of oral exogenous ketone supplementation in critically ill patients. The goal is to demonstrate that ketone administration is well-tolerated, with no significant safety concerns, consistent with prior evidence that oral ketones can be administered safely, even in vulnerable patient populations. Successful completion of this aim will establish a safety profile for ketone use in the ICU, which is essential before adopting this novel therapy for critically ill patients. The investigators hypothesize that patients receiving ketones will have more DCFDs compared to those receiving a placebo. The investigators will also perform an exploratory analysis of the biological impact of ketone therapy by examining biomarkers associated with delirium and ketone metabolism through serial measurement of serum levels of peripheral inflammatory mediators, metabolic stress assays, β-hydroxybutyrate levels, and markers of central nervous system (CNS) injury.

Ketones offer a promising novel therapeutic option for delirium. By targeting the underlying neurometabolic and neuroinflammatory changes associated with delirium, they support energy production, decrease oxidative stress, and modulate inflammation. Patients with preexisting cognitive impairment, such as those with mild cognitive impairment or Alzheimer's dementia, exhibit a baseline brain energy gap due to impaired cerebral glucose metabolism. This chronic energy deficit increases the vulnerability of the aging brain to delirium. Furthermore, the neurometabolic consequences of delirium in those with preexisting cognitive impairment exacerbate the brain energy gap, accelerating cognitive decline. The safety, tolerability, and rapid induction of ketosis following oral administration of ketone esters, in addition to the aforementioned beneficial effects, suggest this may be a therapy that could be initiated upon ICU admission as a potential preventative measure in those patients at risk. Ketones have the potential to transform delirium management and improve patient care; however, this clinical trial is required to evaluate the safety and efficacy of oral ketone ester supplementation in reducing the incidence, severity, and duration of delirium in critically ill patients.

02

Conditions studied

  • ICU Delirium
  • Critical Illness

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Keywords

  • ICU
  • Intensive Care Unit
  • Critical care
  • Critical illness
  • Ketones
03

In context

Critical Illness Unverified

1,780 studies on the registry are indexed under Critical Illness; 442 are open to participants now.

This study's planned enrollment of 40 is below the median of 90 across 926 interventional studies indexed under Critical Illness.

Browse Critical Illness studies →

Lead sponsor

Vanderbilt University Medical Center is the lead sponsor of 833 studies on the registry; 155 are open to participants now.

Of its 125 completed or terminated interventional studies of FDA-regulated products, 92 (74%) have results posted.

Browse Vanderbilt University Medical Center studies →

Compared within Critical Illness, the registry's first condition term, which may not be this study's main condition. Counted across the registry records on this site, refreshed daily. How we classify →

04

Who can participate

Ages eligible
18 Years and older
Sexes eligible
All
Accepts healthy volunteers
No

Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.

Inclusion criteria

  1. Adult patients (≥18 years old) admitted to the medical intensive care unit.
  2. Current ICU admission with anticipated ICU stay ≥24 hours.
  3. Enteral access in place, planned enteral access placement, or PO intake appropriate, and the ability to receive enteral dosing within 24 hours of enrollment.
  4. Ability to complete delirium assessments (CAM-ICU feasible) at time of enrollment.

Exclusion criteria

Exclusion criteria:

  1. Severe metabolic acidosis at screening: blood gas pH \<7.20 or bicarbonate \< 8 mmol/L.
  2. Diabetic ketoacidosis as an ICU admission diagnosis or hyperketonemia from any ketoacidosis state.
  3. Hypoglycemia as an ICU admission diagnosis or glucose \<60 mg/dL.
  4. Patients with a history of type 1 diabetes mellitus.
  5. \<7.0.
  6. Fulminant hepatic failure or (INR) > 3, when not attributable to therapeutic anticoagulation or another clearly non-hepatic cause.
  7. shock, defined as a sustained norepinephrine requirement ≥30 µg/min, or norepinephrine-equivalent vasopressor dose, despite appropriate resuscitation, or ongoing escalation of vasopressor support at the time of enrollment.
  8. Pregnancy (positive urine/serum hCG at screening or known pregnancy) or breastfeeding.
  9. Uncontrolled ileus or gastrointestinal condition, such as an upper gastrointestinal bleed, preventing enteral dosing.
  10. ADH/ALDH inhibitors (e.g., fomepizole, disulfiram) use in the prior 7 days or planned.
  11. Severe dementia or neurodegenerative disease, defined as either impairment that prevents the patient from living independently at baseline or IQCODE >4.5. This exclusion also pertains to mental illnesses requiring long-term institutionalization, acquired or congenital intellectual disability, severe neuromuscular disorders, Parkinson's disease, and Huntington's disease. It also excludes patients with severe deficits due to structural brain diseases such as stroke, intracranial hemorrhage, cranial trauma, , anoxic brain injury, or cerebral edema.
  12. Benzodiazepine dependency or alcohol dependency based on the medical team's decision to institute a specific treatment plan involving benzodiazepines or barbiturates (either as continuous infusions or intermittent intravenous boluses) for this dependency.
  13. Active seizures during this ICU admission being treated with intravenous benzodiazepines.
  14. Expected death within 24 hours of enrollment or lack of commitment to aggressive treatment by family/medical team (e.g., likely to withdraw life support measures within 24 hours of screening).
  15. Admission to ICU only for post-operative monitoring or frequent neurologic assessments.
  16. Incarcerated status.
  17. Inability to obtain within 24 hours from the time all inclusion criteria were met: Attending physician refusal.
  18. Inability to obtain informed consent within 24 hours from the time all inclusion criteria were met: Patient and/or surrogate refusal.
  19. Inability to obtain informed consent within 24 hours from the time all inclusion criteria were met: Patient unable to consent and no surrogate available.
  20. Current enrollment in a study that does not allow co-enrollment.
Terms in these criteria, in plain language(5)

Underlined terms in the criteria open these too. Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.

Hemoglobin (Hb)

The protein in red blood cells that carries oxygen. A low level is anaemia, which can cause tiredness and breathlessness. Measured in g/dL or g/L (9 g/dL is 90 g/L).

INR, PT and aPTT (clotting tests)

Blood tests of how long blood takes to clot. The INR is the prothrombin time (PT) put on a common scale; about 1 is usual for someone not taking a blood thinner.

Criteria often make an exception for people on a blood thinner such as warfarin, whose INR is raised on purpose.

Relapsed and refractory

Relapsed: the illness came back after treatment had worked. Refractory: it did not respond to treatment, or stopped responding while still on it.

Cancer (malignancy)

Malignancy means cancer. Criteria about another or earlier malignancy ask whether you have had a different cancer, usually within a set number of years.

Some are commonly allowed, such as treated skin cancers other than melanoma and early cancers removed completely — check the exceptions this study lists.

Informed consent

Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.

You can keep asking questions during the study, you are told of new information that matters, and you can choose to leave at any time.

05

Study design

Phase
Phase 2
Primary purpose
Treatment
Allocation
Randomized
Intervention model
Parallel assignment
Masking
Quadruple (Participant, Care provider, Investigator, Outcomes assessor)
Enrollment
40 participants (estimated)

Study arms

  • Experimental
    Ketone monoester

    Drug: Ketone monoester

  • Placebo comparator
    Placebo

    Drug: Placebo

Interventions

  • DrugKetone monoester

    Ketone monoester diluted to a total volume of 74 mL with water and administered enterally (oral/feeding tube). Dosing is protocolized with an initial dose of 25 g and subsequent dose titration based on serum β-hydroxybutyrate levels to target a prespecified serum β-hydroxybutyrate range, administered every 6 hours for up to 7 days (or ICU discharge or death, whichever occurs first).

    Also known as: (R)-3-hydroxybutyl (R)-3-hydroxybutyrate, D-β-hydroxybutyrate monoester, D-BHB monoester, (R)-hydroxybutyl (R)-3-hydroxybutyrate;, [(3R)-3-hydroxybutyl] (3R)-3-hydroxybutanoate)

  • DrugPlacebo

    Placebo consists of 74 mL of dextrose 50% in water (D50W) plus 50 mg sucrose octaacetate for taste matching; administered enterally (oral/feeding tube) on the same schedule as the experimental arm.

06

What researchers measure

Primary outcomes

  1. Mean composite Confusion Assessment Method for the Intensive Care Unit-7 (CAM-ICU-7) delirium severity score

    Delirium severity will be assessed using the Confusion Assessment Method for the Intensive Care Unit-7 (CAM-ICU-7) delirium severity scale. The CAM-ICU-7 score ranges from 0 to 7, with higher scores indicating more severe delirium. A composite CAM-ICU-7 delirium severity score will be calculated for each participant by summing all available CAM-ICU-7 scores from enrollment through study day 7. The primary outcome will compare the mean composite CAM-ICU-7 delirium severity score between treatment arms. A clinically meaningful treatment effect is defined as a 25% lower mean composite CAM-ICU-7 score in the intervention arm compared with the control arm.

    Time frame: From enrollment through study day 7.

Secondary outcomes

  1. Feasibility: Proportion of participants achieving target peak serum β-hydroxybutyrate (1.5-3.5 mmol/L) on at least 50% of dosing days

    Peak serum β-hydroxybutyrate will be measured once daily using a post-dose blood draw collected 60-90 minutes after the morning ketone dose. A dosing day will be considered evaluable if a valid post-dose serum β-hydroxybutyrate measurement is obtained. A dosing day will be considered within target range if the post-dose serum β-hydroxybutyrate concentration is 1.5-3.5 mmol/L. This feasibility outcome is the proportion of ketone-group participants with post-dose serum β-hydroxybutyrate within the target range on at least 50% of evaluable dosing days. Feasibility will be considered met if at least 70% of ketone-group participants meet this criterion.

    Time frame: From enrollment through study day 7 or ICU discharge.

  2. Feasibility: Proportion of scheduled post-dose serum β-hydroxybutyrate draws completed

    The proportion of scheduled daily post-dose serum β-hydroxybutyrate draws that are successfully collected during the dosing period will be calculated and summarized. Feasibility performance will be summarized relative to a target of ≥80% completion.

    Time frame: From enrollment through study day 7 or ICU discharge.

  3. Feasibility: Proportion of post-dose serum β-hydroxybutyrate measurements >4.0 mmol/L

    In participants assigned to the ketone group, the proportion of valid daily post-dose serum β-hydroxybutyrate measurements greater than 4.0 mmol/L will be calculated during the dosing period. Performance will be summarized relative to a target of fewer than 10% of post-dose measurements greater than 4.0 mmol/L.

    Time frame: From enrollment through study day 7 or ICU discharge.

  4. Safety and tolerability: Number of participants with ≥1 prespecified safety or tolerability event

    A prespecified safety or tolerability event is defined as any of the following occurring from enrollment through study day 7: acid-base abnormality (blood gas pH \<7.20 or serum bicarbonate \<8 mmol/L), off-target hyperketonemia (peak serum β-hydroxybutyrate \>3.5 mmol/L despite dose reduction), hypoglycemia (\<60 mg/dL), renal or hepatic safety signal (new dialysis initiation; aspartate aminotransferase (AST) or alanine aminotransferase (ALT) \>5× upper limit of normal, or total bilirubin \>3 mg/dL without alternative explanation), or hemodynamic instability temporally related to dosing. Gastrointestinal symptoms (nausea, vomiting, diarrhea, cramping) will be reported separately as tolerability adverse events. The outcome will be summarized as the proportion of participants with ≥1 prespecified event by treatment arm.

    Time frame: From enrollment through study day 7.

  5. Feasibility: Adherence to ketone dose-titration algorithm

    In those participants assigned to the treatment group, adherence will be defined as the proportion of dosing decisions during the dosing period that follow the prespecified dose-titration algorithm based on post-dose serum β-hydroxybutyrate results and protocol-defined dose adjustment rules. Adherence will be summarized relative to a target of ≥80%.

    Time frame: From enrollment through study day 7 or ICU discharge.

  6. Delirium- and coma-free days (DCFDs) through study day 7

    Delirium- and coma-free days (DCFDs) is defined as the number of days from enrollment through study day 7 during which participants are alive and free of both delirium and coma. Delirium is defined as any positive assessment on the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) administered twice daily while participants remain in the intensive care unit. Coma is defined as a Richmond Agitation-Sedation Scale score of -4 or -5, or an equivalent protocol-defined coma assessment. Days after ICU discharge will be counted as delirium- and coma-free if the participant is alive. Days after death will be counted as not delirium- and coma-free. Delirium- and coma-free days will be summarized by treatment arm.

    Time frame: From enrollment through study day 7.

  7. Peak serum beta-hydroxybutyrate concentration following dosing

    Post-dose serum β-hydroxybutyrate concentration will be measured once daily using a blood draw collected 60-90 minutes after the morning dose. For each participant, the mean post-dose serum β-hydroxybutyrate concentration during the dosing period will be calculated and reported in mmol/L by treatment arm.

    Time frame: From enrollment through study day 7 or ICU discharge.

Other outcomes

  1. Change from baseline in serum interleukin-1 beta (IL-1β) concentration

    Serum interleukin-1 beta (IL-1β) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  2. Change from baseline in serum interleukin-6 (IL-6) concentration

    Serum interleukin-6 (IL-6) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  3. Change from baseline in serum interleukin-8 (IL-8) concentration

    Serum interleukin-8 (IL-8) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  4. Change from baseline in serum interleukin-10 (IL-10) concentration

    Serum interleukin-10 (IL-10) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  5. Change from baseline in serum interleukin-18 (IL-18) concentration

    Serum interleukin-18 (IL-18) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  6. Change from baseline in serum C-reactive protein (CRP) concentration

    Serum C-reactive protein (CRP) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  7. Change from baseline in serum monocyte chemoattractant protein-1 (MCP-1) concentration

    Serum monocyte chemoattractant protein-1 (MCP-1) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  8. Change from baseline in serum tumor necrosis factor alpha (TNF-α) concentration

    Serum tumor necrosis factor alpha (TNF-α) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  9. Change from baseline in serum brain-derived neurotrophic factor (BDNF) concentration

    Serum brain-derived neurotrophic factor (BDNF) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  10. Change from baseline in serum glial fibrillary acidic protein (GFAP) concentration

    Serum glial fibrillary acidic protein (GFAP) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

  11. Change from baseline in serum neurofilament light chain (NfL) concentration

    Serum neurofilament light chain (NfL) concentration will be measured at baseline and on study days 1, 3, 5, and 7 and reported as change from baseline by treatment arm.

    Time frame: From enrollment through study day 7.

07

Study locations

1 of 1 sites recruiting
08

References and documents

Publications

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  • Ota M, Matsuo J, Ishida I, Takano H, Yokoi Y, Hori H, Yoshida S, Ashida K, Nakamura K, Takahashi T, Kunugi H. Effects of a medium-chain triglyceride-based ketogenic formula on cognitive function in patients with mild-to-moderate Alzheimer's disease. Neurosci Lett. 2019 Jan 18;690:232-236. doi: 10.1016/j.neulet.2018.10.048. Epub 2018 Oct 24. PubMed 30367958 ↗
  • Jensen NJ, Nilsson M, Ingerslev JS, Olsen DA, Fenger M, Svart M, Moller N, Zander M, Miskowiak KW, Rungby J. Effects of beta-hydroxybutyrate on cognition in patients with type 2 diabetes. Eur J Endocrinol. 2020 Feb;182(2):233-242. doi: 10.1530/EJE-19-0710. PubMed 31821157 ↗
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  • Myette-Cote E, Soto-Mota A, Cunnane SC. Ketones: potential to achieve brain energy rescue and sustain cognitive health during ageing. Br J Nutr. 2022 Aug 14;128(3):407-423. doi: 10.1017/S0007114521003883. Epub 2021 Sep 28. PubMed 34581265 ↗
  • Stagg DB, Gillingham JR, Nelson AB, Lengfeld JE, d'Avignon DA, Puchalska P, Crawford PA. Diminished ketone interconversion, hepatic TCA cycle flux, and glucose production in D-beta-hydroxybutyrate dehydrogenase hepatocyte-deficient mice. Mol Metab. 2021 Nov;53:101269. doi: 10.1016/j.molmet.2021.101269. Epub 2021 Jun 8. PubMed 34116232 ↗
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Individual participant data

Plan to share: Yes — De-identified individual participant data (IPD) for all randomized participants that underlie reported results, including: baseline demographics and clinical characteristics; eligibility variables; treatment assignment and dosing history; serum β-hydroxybutyrate and other protocol safety labs (e.g., glucose, acid-base measures); delirium/coma assessments (CAM-ICU, CAM-ICU-7) and derived delirium- and coma-free days through study day 7; key clinical outcomes (e.g., ICU/hospital length of stay, mortality); adverse events, dose holds/reductions/discontinuations; and research biomarker assay results. A data dictionary will be provided. Direct identifiers and free-text clinical notes will not be shared.

Supporting information: Study protocol, Statistical analysis plan, Analytic code

Time frame: IPD and supporting documents will be available beginning 9 months after publication of the primary results and will remain available for 36 months following publication.

Access criteria: De-identified IPD and supporting documents will be shared with qualified researchers who submit a methodologically sound proposal. Access requires approval by the study team, execution of a data use agreement, and IRB/ethics approval as applicable. Data will be provided via secure electronic transfer. Requestors must agree not to attempt re-identification and to use the data only for the approved purpose.

09

Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Aug 24, 2026, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
10

Registry details

Key details

Study ID
NCT07364162
Lead sponsor
Vanderbilt University Medical Center
Responsible party
Ryan Smith (Pulmonary & Critical Care Medicine Fellow, Vanderbilt University Medical Center, Vanderbilt University Medical Center) — Principal investigator
First posted
Jan 23, 2026
Start date
Jun 9, 2026
Primary completion
Dec 31, 2026 (estimated)
Completion
Dec 31, 2027 (estimated)
Last update
Aug 24, 2026

Study contacts

Ryan J Smith, MD, JD
Contact
ryan.j.smith@vumc.org
(602) 538-5003
Rebecca Abel, MA
Contact
wes.ely@vumc.org
6158753763
E. Wes Ely, MD, MPH
study director · Vanderbilt University Medical Center
Ryan J Smith, MD, JD
principal investigator · Vanderbilt University Medical Center

Oversight

Data monitoring committee
No
FDA-regulated drug
Yes
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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