Product InformationRegistration Status: Active
ROCURONIUM-HAMELN INJECTION 10MG/ML is approved to be sold in Singapore with effective from 2017-05-16. It is marketed by ZYFAS MEDICAL CO, with the registration number of SIN15237P.
This product contains Rocuronium 10mg/1ml in the form of INJECTION, SOLUTION. It is approved for INTRAVENOUS use.
This product is manufactured by Hameln Pharmaceuticals GMBH in GERMANY.
It is a Prescription Only Medicine that can only be obtained from a doctor or a dentist, or a pharmacist with a prescription from a Singapore-registered doctor or dentist.
Rocuronium (rapid onset-curonium) is a desacetoxy analogue of vecuronium with a more rapid onset of action. It is an aminosteroid non-depolarizing neuromuscular blocker or muscle relaxant used in modern anaesthesia, to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Introduced in 1994, rocuronium has rapid onset, and intermediate duration of action. It is marketed under the trade name of Zemuron in the United States and Esmeron in most other countries. There is considered to be a risk of allergic reaction to the drug in some patients (particularly those with asthma), but a similar incidence of allergic reactions has been observed by using other members of the same drug class (non-depolarizing neuromuscular blocking drugs). The γ-cyclodextrin derivative sugammadex (trade name Bridion) has been recently introduced as a novel agent to reverse the action of rocuronium.
For inpatients and outpatients as an adjunct to general anesthesia to facilitate both rapid sequence and routine tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation.
Mechanism of Action
Rocuronium acts by competing for cholinergic receptors at the motor end-plate. This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine and edrophonium. Rocuronium acts by competitively binding to nicotinic cholinergic receptors. The binding of vecuronium decreases the opportunity for acetylcholine to bind to the nicotinic receptor at the postjunctional membrane of the myoneural junction. As a result, depolarization is prevented, calcium ions are not released and muscle contraction does not occur. Evidence also suggests that nondepolarizing agents can affect ACh release. It has been hypothesized that nondepolarzing agents bind to postjunctional ("curare") receptors and may therefore interfere with the sodium and potassium flux, which is responsible for depolarization and repolarization of the membranes involved in muscle contraction.
- Poorly absorbed from the GI tract.
- * 0.3 L/kg [3 to <12 mos] * 0.26 L/kg [1 to <3 yrs] * 0.21 L/kg [3 to <8 yrs]
- Rocuronium is metabolized to a less active metabolite, 17-desacetyl-rocuronium, and is eliminated primarily by the liver.
* 0.25 L/kg/hr [Adults (Ages 27 to 58 years)] * 0.21 L/kg/hr [Geriatrics (>=65 yrs)] * 0.16 L/kg/hr [Normal ewnal and hepatice function] * 0.13 L/kg/hr [Renal transplant patients] * 0.13 L/kg/hr [Hepatic dysfunction patients] * 0.35 +/- 0.08 L/kg/hr [Pediatric Patients 3 to <12 mos] * 0.32 +/- 0.07 L/kg/hr [Pediatric Patients 1 to 3 yrs] * 0.44 +/- 0.16 L/kg/hr [Pediatric Patients 3 to 8 yrs]
No cases of significant accidental or intentional overdose have been reported. Overdosage with neuromuscular blocking agents may result in neuromuscular block beyond the time needed for surgery and anesthesia.
Rocuronium | Rocuronium |
Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.