Dexmedetomidine, sold under the trade name Precedex among others, is an anxiety reducing, sedative, and pain medication. Dexmedetomidine is notable for its ability to provide sedation without risk of respiratory depression (unlike other commonly used drugs such as propofol and fentanyl) and can provide cooperative or semi-rousable sedation.

Clinical data
Trade namesPrecedex, Dexdor, Dexdomitor, Sileo
License data
  • US: C (Risk not ruled out)
    Routes of
    Intravenous infusion Transmucosal
    ATC code
    Legal status
    Legal status
    • AU: S4 (Prescription only)
    • US: ℞-only
    • In general: ℞ (Prescription only)
    Pharmacokinetic data
    Protein binding94%
    MetabolismNear complete hepatic metabolism to inactive metabolites
    Elimination half-life2 hours
    CAS Number
    PubChem CID
    ECHA InfoCard100.119.391
    Chemical and physical data
    Molar mass200.28 g/mol g·mol−1
    3D model (JSmol)

    Similar to clonidine, it is an agonist of α2-adrenergic receptors in certain parts of the brain.[1] Dexmedetomidine hydrochloride is also used in veterinary medicine for dogs and cats.[2] It was developed by Orion Pharma.

    Medical uses

    Intensive care unit sedation

    Dexmedetomidine is most often used in the intensive care setting for light to moderate sedation. It is not recommended for long-term deep sedation. A feature of dexmedetomidine is that it has analgesic properties in addition to its role as a hypnotic, but is opioid sparing; thus, it is not associated with significant respiratory depression (unlike propofol).

    Many studies suggest dexmedetomidine for sedation in mechanically ventilated adults may reduce time to extubation and ICU stay.[3][4] People on dexmedetomidine can be rousable and cooperative, a benefit in some procedures.

    Compared with other sedatives, some studies suggest dexmedetomidine may be associated with less delirium.[5] However, this finding is not consistent across multiple studies.[4] At the very least, when aggregating many study results together, use of dexmedetomidine appears to be associated with less neurocognitive dysfunction compared to other sedatives.[6] Whether this observation has a beneficial psychological impact is unclear.[5] From an economic perspective, dexmedetomidine is associated with lower ICU costs, largely due to a shorter time to extubation.[7]

    Procedural sedation

    Dexmedetomidine can also be used for procedural sedation such as during colonoscopy.[8] It can be used as an adjunct with other sedatives like benzodiazepines, opioids, and propofol to enhance sedation and help maintain hemodynamic stability by decreasing the requirement of other sedatives.[9][10] Dexmedetomidine is also used for procedural sedation in children.[11]

    There is weak evidence that it can be used for sedation required for awake fibreoptic nasal intubation in patients with a difficult airway[12]


    Dexmedetomidine may be useful for the treatment of the negative cardiovascular effects of acute amphetamines and cocaine intoxication and overdose.[13][14]

    Dosage and administration

    Intravenous infusion of dexmedetomidine is commonly initiated with a loading dose followed by a maintenance infusion. There may be great individual variability in the hemodynamic effects (especially on heart rate and blood pressure), as well as the sedative effects of this drug. For this reason, the dose must be carefully adjusted to achieve the desired clinical effect.[15]

    Side effects

    There is no absolute contraindication to the use of dexmedetomidine. It has a biphasic effect on blood pressure with lower readings at lower drug concentrations and higher readings at higher concentrations.[16] Rapid IV administration or bolus has been associated with hypertension due to peripheral α2-receptor stimulation. Bradycardia can be limiting factor with infusions especially in higher doses.


    Dexmedetomidine may enhance the effects of other sedatives and anesthetics when co-administered. Similarly, drugs that lower blood pressure and heart rate, such as beta blockers, may also have enhanced effects when co-administered with dexmedetomidine.[17]



    Dexmedetomidine is a highly selective α2-adrenergic agonist. Unlike opioids and other sedatives such as propofol, dexmedetomidine is able to achieve its effects without causing respiratory depression. Dexmedetomidine induces sedation by decreasing activity of noradrenergic neurons in the locus ceruleus in the brain stem, thereby increasing the activity of inhibitory gamma-aminobutyric acid (GABA) neurons in the ventrolateral preoptic nucleus.[18] In contrast, other sedatives like propofol and benzodiazepines directly increase activity of gamma-aminobutyric acid neurons.[19] Sedation by dexmedetomidine mirrors natural sleep.[20] As such, dexmedetomidine provides less amnesia than benzodiazepines.[19] Dexmedetomidine also has analgesic effects at the spinal cord level and other supraspinal sites.[19] Thus, unlike other hypnotic agents like propofol, dexmedetomidine can be used as an adjunct medication to help decrease the opioid requirements of people in pain while still providing similar analgesia.


    Intravenous dexmedetomidine exhibits linear pharmacokinetics with a rapid distribution half-life of approximately 6 minutes and a terminal elimination half-life of approximately 2 hours. Plasma protein binding of dexemedotomindine is about 94% (mostly albumin).[21]

    Dexmedetomidine is metabolized by the liver via glucuronidation and cytochrome P450. As such, it should be used with caution in people with liver disease.[17]

    The majority of metabolized dexmedetomidine is excreted in the urine (~95%).


    Dexmedetomidine was approved in 1999 by the US Food and Drug Administration (FDA) as a short-term sedative and analgesic (<24 hours) for critically ill or injured people on mechanical ventilation in the intensive care unit (ICU). The rationale for its short-term use was due to concerns over withdrawal side effects such as rebound high blood pressure. These effects have not been consistently observed in research studies, however.[22] In 2008 the FDA expanded its indication to include non-intubated people requiring sedation for surgical or non-surgical procedures, such as colonoscopy.

    Veterinary use

    Dexmedetomidine, under the trade name Dexdomitor (Orion Corporation), was approved in the European Union in for use in cats and dogs in 2002 for sedation and induction of general anesthesia.[23] The FDA approved dexmedetomidine for use in dogs in 2006 and cats in 2007.[24]

    In 2015, the European Medicines Agency and the FDA approved an oromucosal gel form of dexmedetomidine marketed as Sileo (Zoetis) for use in dogs for relief of noise aversion.[25][26]


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