Long COVID Patterns in the RECOVER-Adult Study
November 21, 2025
Brand Name :
Enlon-plus, Enlon
Synonyms :
edrophonium
Class :
Antidote; Acetylcholinesterase Inhibitor; Diagnostic Agent
Dosage Forms & StrengthsÂ
Intravenous solutionÂ
2mgÂ
Intramuscular solutionÂ
10mgÂ
Initial dose-2mg
If there is a significant improvement after 90 seconds, the test is declared positive and can be discontinued. If the symptoms return, another 2 mg dosage may be given.
If there isn't a noticeable difference after the first dosage, you may give the patient another dose of 3 mg and watch them for another 90 seconds. If the test is negative, give them the last dose of 5 mg and watch them for another three to five minutes.
Assessment of myasthenia gravis therapy needs:
Administer 1 to 2 mg Intravenously given 1 hour after oral anticholinesterase dosage.
Intravenously administer 1 mg; repeat after 1 minute to differentiate cholinergic from myasthenic crises. If the patient is experiencing a cholinergic crisis, intubation, and controlled breathing may be necessary.
Nondepolarizing neuromuscular blockers are reversed.
Administer 0.5 to 1 mg/kg intravenously as the usual dosage.
Dosage Forms & StrengthsÂ
Intravenous solutionÂ
0.5mgÂ
1mgÂ
2mgÂ
Intramuscular solutionÂ
2mgÂ
5mgÂ
10mgÂ
Infants-Administer 0.5mg intravenously
Children and Adults:
>34kg- Administer 2 mg. If there is no reaction after 45 seconds, the dose can be increased by 1 mg every 30 to 45 seconds, up to a maximum of 10 mg.
Administer 5mg intramuscularly.
<34 kgs- Administer 1 mg. If there is no reaction after 45 seconds, the dose can be increased by 1 mg every 30 to 45 seconds, up to a maximum of 10 mg.
Administer 2 mg intramuscularly.
Neutralization of nondepolarizing neuromuscular blockers
Usual dose: Administer 0.5 to 1 mg/kg/dose intravenously;
minimum dose: Administer 0.3 mg/kg/dose intravenously
Refer adult dosingÂ
may increase the bradycardic effect of Bradycardia-Causing Agents
may increase the bradycardic effect of Bradycardia-Causing Agents
corticosteroids may increase the risk of adverse effects of acetylcholinesterase Inhibitors
corticosteroids may increase the risk of adverse effects of acetylcholinesterase Inhibitors
corticosteroids may increase the risk of adverse effects of acetylcholinesterase Inhibitors
corticosteroids may increase the risk of adverse effects of acetylcholinesterase Inhibitors
corticosteroids may increase the risk of adverse effects of acetylcholinesterase Inhibitors
acetylcholinesterase Inhibitors may diminish the therapeutic effect of anticholinergic Agents
acetylcholinesterase Inhibitors may diminish the therapeutic effect of anticholinergic Agents
acetylcholinesterase Inhibitors may diminish the therapeutic effect of anticholinergic Agents
acetylcholinesterase Inhibitors may diminish the therapeutic effect of anticholinergic Agents
acetylcholinesterase Inhibitors may diminish the therapeutic effect of anticholinergic Agents
acetylcholinesterase Inhibitors may enhance the neurotoxic (central) effect of antipsychotic Agents
acetylcholinesterase Inhibitors may enhance the neurotoxic (central) effect of antipsychotic Agents
acetylcholinesterase Inhibitors may enhance the neurotoxic (central) effect of antipsychotic Agents
acetylcholinesterase Inhibitors may enhance the neurotoxic (central) effect of antipsychotic Agents
acetylcholinesterase Inhibitors may enhance the neurotoxic (central) effect of antipsychotic Agents
it enhance the neurotoxic (central) effect of antipsychotic Agents
it enhance the neurotoxic (central) effect of antipsychotic Agents
it enhance the neurotoxic (central) effect of antipsychotic Agents
it enhance the neurotoxic (central) effect of antipsychotic Agents
it enhance the neurotoxic (central) effect of antipsychotic Agents
may increase the therapeutic effect of Acetylcholinesterase Inhibitors
may diminish the therapeutic effect of Acetylcholinesterase Inhibitors
may diminish the therapeutic effect of Acetylcholinesterase Inhibitors
may diminish the therapeutic effect of Acetylcholinesterase Inhibitors
may diminish the therapeutic effect of Acetylcholinesterase Inhibitors
may diminish the therapeutic effect of Acetylcholinesterase Inhibitors
may increase the bradycardic effect of Acetylcholinesterase Inhibitors
may increase the bradycardic effect of each other
may increase the bradycardic effect of each other
may increase the bradycardic effect of each other
may increase the bradycardic effect of each other
may increase the bradycardic effect of each other
may increase the AV-blocking effect when combined
may increase the AV-blocking effect when combined
may increase the AV-blocking effect when combined
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may increase the toxic effect of Acetylcholinesterase Inhibitors
may decrease the neuromuscular-blocking effect when combined
may decrease the neuromuscular-blocking effect when combined
may decrease the neuromuscular-blocking effect when combined
may decrease the neuromuscular-blocking effect when combined
may decrease the neuromuscular-blocking effect when combined
edrophonium: they may increase the bradycardic effect of Bradycardia-Causing Agents
When edrophonium is used together in combination with profenamine, this leads to reduction in therapeutic effectiveness of profenamine
Actions and Spectrum:Â
The mechanism of action of edrophonium involves the following steps:Â
Frequency not definedÂ
Cardiac arrhythmiaÂ
ECG changesÂ
HypotensionÂ
TachycardiaÂ
Atrioventricular blockÂ
Cardiac arrestÂ
FlushingÂ
SyncopeÂ
ThrombophlebitisÂ
DizzinessÂ
DysarthriaÂ
DiarrheaÂ
DysphagiaÂ
Urinary urgencyÂ
WeaknessÂ
DiplopiaÂ
ConvulsionsÂ
DrowsinessÂ
HeadacheÂ
FlatulenceÂ
Urinary frequencyÂ
FasciculationsÂ
Conjunctival hyperemiaÂ
Black box warning:Â
NoneÂ
Contraindications/caution:Â
Contraindications:Â
Caution:Â
Pregnancy consideration: Insufficient data availableÂ
Lactation: Excretion of the drug in human breast milk is unknownÂ
Pregnancy category:Â
Category A: well-controlled and Satisfactory studies show no risk to the fetus in the first or later trimester.Â
Category B: there was no evidence of risk to the fetus in animal studies, and there were not enough studies on pregnant women.Â
Category C: there was evidence of risk of adverse effects in animal reproduction studies, and no adequate evidence in human studies must take care of potential risks in pregnant women.   Â
Category D: adequate data with sufficient evidence of human fetal risk from various platforms, but despite the potential risk, and used only in emergency cases for potential benefits.   Â
Category X: Drugs listed in this category outweigh the risks over benefits. Hence these categories of drugs need to be avoided by pregnant women.   Â
Category N: There is no data available for the drug under this categoryÂ
Pharmacology:Â
edrophonium is a short-acting reversible acetylcholinesterase inhibitor with pharmacological properties that involve its interaction with the cholinergic system.Â
Pharmacokinetics:Â
AbsorptionÂ
edrophonium is typically administered intravenously, which ensures rapid and complete absorption into the bloodstream. Â
The Onset of action:Â
Intramuscular (IM): 2 to 10 minutesÂ
Intravenous (IV): 30 to 60 secondsÂ
Duration:Â
Intramuscular: 5 to 30 minutesÂ
Intravenous: 10 minutesÂ
DistributionÂ
edrophonium is distributed throughout the body after intravenous administration. It readily crosses the blood-brain barrier, allowing it to act centrally and peripherally. The extent of protein binding for edrophonium is minimal.Â
The volume of distribution (Vd):Â
Infants: 1.18 ± 0.2 L/kgÂ
Children: 1.22 ± 0.74 L/kgÂ
Adults: 0.9 ± 0.13 L/kgÂ
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MetabolismÂ
edrophonium undergoes minimal metabolism in the body. It is primarily hydrolyzed by cholinesterases, including plasma cholinesterase and acetylcholinesterase, to its inactive metabolites. The metabolism of edrophonium is relatively rapid, leading to its short duration of action. Â
Elimination and ExcretionÂ
The elimination of edrophonium and its metabolites occurs primarily through renal excretion. The exact percentage of excretion in urine has not been widely reported.Â
Half-life elimination:Â
Infants: 73 ± 30 minutesÂ
Children: 99 ± 31 minutesÂ
Adults: 126 ± 59 minutesÂ
Anephric patients: 2.4 to 4.4 hoursÂ
Excretion:Â
Adults: Primarily excreted in urine (67%)Â
Clearance:Â
Infants: 17.8 mL/kg/minuteÂ
Children: 14.2 mL/kg/minuteÂ
Adults: 8.3 ± 2.9 mL/kg/minuteÂ
Administration:Â
Intravenous administrationÂ
edrophonium is administered as a slow IV injection over several minutes. The medication should not be administered as a rapid bolus to avoid adverse effects.Â
Patient information leafletÂ
Generic Name: edrophoniumÂ
Why do we use edrophonium?Â
edrophonium is primarily used for diagnostic purposes in evaluating myasthenia gravis, a neuromuscular disorder characterized by muscle weakness and fatigue. The main use of edrophonium is to differentiate between myasthenic and cholinergic crises in patients with myasthenia gravis. Here are the key uses of edrophonium:Â