🇺🇸 FDA
Pipeline program

DEXMEDETOMIDINE , 18F-DPA-714

APHP200491

Phase 3 small_molecule active

Quick answer

DEXMEDETOMIDINE , 18F-DPA-714 for Patients who survive a COVID ARDS in intensive care must be weaned off invasive mechanical ventilation as quickly as possible. 60% of these patients present with intensive care delirium, a serious event that causes excess mortality and potential acute and late complications, since 30% of patients who present with delirium develop cognitive sequelae. Severe neuroinflammation is considered to be one of the main pathophysiological mechanisms causing delirium during ventilatory weaning. In addition to its sedative properties, dexmedetomidine has neuroprotective effects. In certain experimental models, it reduces cerebral inflammation by acting directly on the microglial phenotype. The role of this chronic neuroinflammatory state on cognitive capacity and reserve is beginning to emerge in the literature, regardless of the initial stress (surgery, head injury or Alzheimer's-type dementia), and is therefore capable of influencing patients' quality of life. The assessment of this neuroinflammation using non-invasive tools would appear to be of prime importance in the management of post-COVID neuro injured patients, as well as the evaluation of potential neuroprotective agents such as dexmedetomidine. is a Phase 3 program (small_molecule) at Pari Pharma GmbH with 1 ClinicalTrials.gov record(s).

Program details

Company
Pari Pharma GmbH
Indication
Patients who survive a COVID ARDS in intensive care must be weaned off invasive mechanical ventilation as quickly as possible. 60% of these patients present with intensive care delirium, a serious event that causes excess mortality and potential acute and late complications, since 30% of patients who present with delirium develop cognitive sequelae. Severe neuroinflammation is considered to be one of the main pathophysiological mechanisms causing delirium during ventilatory weaning. In addition to its sedative properties, dexmedetomidine has neuroprotective effects. In certain experimental models, it reduces cerebral inflammation by acting directly on the microglial phenotype. The role of this chronic neuroinflammatory state on cognitive capacity and reserve is beginning to emerge in the literature, regardless of the initial stress (surgery, head injury or Alzheimer's-type dementia), and is therefore capable of influencing patients' quality of life. The assessment of this neuroinflammation using non-invasive tools would appear to be of prime importance in the management of post-COVID neuro injured patients, as well as the evaluation of potential neuroprotective agents such as dexmedetomidine.
Phase
Phase 3
Modality
small_molecule
Status
active

Clinical trials