Etomidate Powder for sale

Etomidate (USAN, INN, BAN; marketed as Amidate) is a short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation for short procedures such as reduction of dislocated joints, tracheal intubation, cardioversion and electroconvulsive therapy. Etomidate Powder

Etomidate is an ultrashort-acting, non-barbiturate hypnotic intravenous anesthetic agent.[1] Etomidate does not have any analgesic properties. It is administered only by intravenous route. Etomidate has a favorable hemodynamic profile on induction, with minimal blood pressure depression, making it ideal for shock trauma, hypovolemic patients, or patients with significant cardiovascular disease.[2] Etomidate has been approved for use during induction of general anesthesia and rapid sequence intubation.[3] Etomidate is indicated for procedural sedation.

Etomidate is also used to maintain anesthesia and for short operative procedures such as reducing dislocated joints, tracheal intubation, cardioversion, dilation, curettage, or cervical conization.[5https://www.pureresearchchemical.com/product/etomidate-powder/][6] Etomidate is used to increase the seizure duration potential and has shown to be superior to propofol and thiopental.[7] Etomidate has been used off-label to inhibit steroidogenesis in patients with Cushing syndrome. Etomidate Powder

Mechanism of Action

Etomidate contains a carboxylated imidazole ring-containing anesthetic compound (R-1-ethyl-1-[a-methylbenzyl] imidazole-5-carboxylate) and is structurally unrelated to other anesthetic agents. The imidazole ring provides water solubility in acidic solutions and lipid solubility at physiological pH. Therefore, etomidate is dissolved in propylene glycol, which often causes pain on injection but can be reduced by prior intravenous injection of lidocaine.

Etomidate has a chiral carbon atom and exists in the form of 2 enantiomers. Only the R (+) isomer is hypnotically active. The S (-) enantiomer has a 20-fold lower hypnotic effect.[2] Etomidate interacts with gamma-Aminobutyric acid type A (GABA) receptors by binding directly to specific sites and increasing the affinity of the inhibitory neurotransmitter GABA (positive modulation of GABA-mediated activity).[6] GABA is the principal inhibitory neurotransmitter within the central nervous system (CNS) and works with the adrenergic neurotransmitter system to counterbalance the action of excitatory neurotransmitters. Etomidate may have disinhibitory effects on the parts of the nervous system that control extrapyramidal motor activity. This disinhibition offers a potential explanation for the 30% to 60% incidence of myoclonus during induction with etomidate.

Pharmacokinetics

The onset of action: 30 to 60 seconds, Peak effect: 1 minute

Distribution: 2 to 4.5 L/kg. Limited pharmacokinetic data in patients with cirrhosis and esophageal varices suggest that the volume of distribution and elimination half-life of etomidate are approximately double that seen in healthy subjects.

Metabolism: Metabolism is primarily hepatic by ester hydrolysis to inactive metabolites. Minimal anesthetic plasma levels of unchanged drug are equal to or higher than 0.23 mcg/mL; they decrease rapidly up to 30 minutes following injection and more slowly with a half-life value of about 75 minutes.

Excretion: 75% of the administered dose is excreted in the urine on the first day after injection. The chief metabolite is R-(+)-1-(1-phenylethyl)-1H-imidazole-5-carboxylic acid, resulting from hydrolysis of etomidate, and accounts for about 80% of the urinary excretion. Another route of excretion is bile. Like most intravenous anesthetics, etomidate is highly protein-bound (77%). Thus, it can achieve a higher concentration in the brain in low albumin states since it will be less bound to albumin, and more free-drug would be available in the brain.