Esmolol

Esmolol, sold under the brand name Brevibloc, is a cardio selective beta1 receptor blocker with rapid onset,[3] a very short duration of action, and no significant intrinsic sympathomimetic or membrane stabilising activity at therapeutic dosages.

Esmolol
Clinical data
Trade namesBrevibloc
AHFS/Drugs.comMonograph
Pregnancy
category
  • AU: C
Routes of
administration		Intravenous
ATC code
Legal status
Legal status
Pharmacokinetic data
Protein binding60%
MetabolismRed blood cell (erythrocytic)
Elimination half-life9 minutes
ExcretionKidney
Identifiers
  • methyl (RS)-3-{4-[2-hydroxy-3-(propan-2-ylamino)propoxy]phenyl}propanoate
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC16H25NO4
Molar mass295.379 g·mol−1
3D model (JSmol)
  • O=C(OC)CCc1ccc(OCC(O)CNC(C)C)cc1
  • InChI=1S/C16H25NO4/c1-12(2)17-10-14(18)11-21-15-7-4-13(5-8-15)6-9-16(19)20-3/h4-5,7-8,12,14,17-18H,6,9-11H2,1-3H3 checkY
  • Key:AQNDDEOPVVGCPG-UHFFFAOYSA-N checkY
 ☒NcheckY (what is this?)  (verify)

It is a class II antiarrhythmic.[4] Esmolol decreases the force and rate of heart contractions by blocking beta-adrenergic receptors of the sympathetic nervous system, which are found in the heart and other organs of the body. Esmolol prevents the action of two naturally occurring substances: epinephrine and norepinephrine.[5]

It was patented in 1980 and approved for medical use in 1987.[6]

Medical uses

To terminate supraventricular tachycardia,

Episodic atrial fibrillation or flutter,

Arrhythmia during anaesthesia,

To reduce HR and BP during and after cardiac surgery, and

In early treatment of myocardial infarction.

Esmolol is also used in blunting the hemodynamic response to laryngoscopy and intubation.[7]

Pharmacology

Pharmacodynamics

Esmolol is a beta blocker, or an antagonist of the β-adrenergic receptors.[8] It is selective for the β1-adrenergic receptor and has no intrinsic sympathomimetic activity.[8]

Pharmacokinetics

Esmolol is considered a soft drug,[9] one that is rapidly metabolized to an inactive form. Esmolol is rapidly metabolized by hydrolysis of the ester linkage, chiefly by the esterases in the cytosol of red blood cells and not by plasma cholinesterases or red cell membrane acetylcholinesterase. Total body clearance in man was found to be about 20 L/kg/hr, which is greater than cardiac output; thus the metabolism of esmolol is not limited by the rate of blood flow to metabolizing tissues such as the liver or affected by hepatic or renal blood flow. Esmolol's short duration of action is based on the ester-methyl side chain which allows for quick hydrolysis. Esmolol's structure is reflected in its name, es-molol as in ester-methyl. Plasma cholinesterases and red cell membrane acetylcholinesterase do not have any action. This metabolism results in the formation of a free acid and methanol. The amount of methanol produced is similar to endogenous methanol production. Esmolol has a rapid distribution half-life of about two minutes and an elimination half-life of about nine minutes.

Esmolol is classified as a beta blocker with low lipophilicity and hence lower potential for crossing the blood–brain barrier.[8] This in turn may result in fewer effects in the central nervous system as well as a lower risk of neuropsychiatric side effects.[8]

References
  1. "Brevibloc esmolol hydrochloride 2.5 g powder for injection for infusion vial (310943)". Therapeutic Goods Administration (TGA). 26 May 2022. Retrieved 29 April 2023.
  2. "Esmolol Juno (Juno Pharmaceuticals Pty Ltd)". Therapeutic Goods Administration (TGA). 13 January 2023. Archived from the original on 18 March 2023. Retrieved 29 April 2023.
  3. Deng CY, Lin SG, Zhang WC, Kuang SJ, Qian WM, Wu SL, et al. (December 2006). "Esmolol inhibits Na+ current in rat ventricular myocytes". Methods and Findings in Experimental and Clinical Pharmacology. 28 (10): 697–702. doi:10.1358/mf.2006.28.10.1037498. PMID 17235414. Archived from the original on 2019-12-10. Retrieved 2008-07-27.
  4. Jaillon P, Drici M (December 1989). "Recent antiarrhythmic drugs". The American Journal of Cardiology. 64 (20): 65J–69J. doi:10.1016/0002-9149(89)91203-4. PMID 2688391.
  5. Tripathi KD. "Antiadrenergic Drugs and Drugs for Glaucoma". Essentials of Medical Pharmacology (7th ed.). p. 149.
  6. Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 462. ISBN 978-3-527-60749-5.
  7. Sharma S, Suthar OP, Tak ML, Thanvi A, Paliwal N, Karnawat R (2018). "Comparison of Esmolol and Dexmedetomidine for Suppression of Hemodynamic Response to Laryngoscopy and Endotracheal Intubation in Adult Patients Undergoing Elective General Surgery: A Prospective, Randomized Controlled Double-blinded Study". Anesthesia: Essays and Researches. 12 (1): 262–266. doi:10.4103/aer.AER_226_17. PMC 5872877. PMID 29628593.
  8. Cojocariu SA, Maștaleru A, Sascău RA, Stătescu C, Mitu F, Leon-Constantin MM (February 2021). "Neuropsychiatric Consequences of Lipophilic Beta-Blockers". Medicina (Kaunas). 57 (2): 155. doi:10.3390/medicina57020155. PMC 7914867. PMID 33572109.
  9. Bodor N, Buchwald P (2000). "Soft drug design: General principles and recent applications". Medicinal Research Reviews. 20 (1): 58–101. doi:10.1002/(SICI)1098-1128(200001)20:1<58::AID-MED3>3.0.CO;2-X. PMID 10608921. S2CID 25119421.
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