Not a Member?
Email this page
Send the page ""
to a friend, relative, colleague or yourself.
Separate multiple email address with a comma
We do not record any personal information entered above.
Thank you. Your email has been sent.
Agents for Amyotrophic Lateral Sclerosis (ALS)
Intravenous antioxidantUsed for treatment of amyotrophic lateral sclerosis (ALS)Hypersensitivity reactions, including anaphylaxis, reported
Radicava Intravenous Inj Sol: 0.3mg, 1mL
60 mg IV once daily for 14 days followed by a 14-day drug-free period for an initial treatment cycle. For subsequent treatment cycles, administer for 10 days out of 14-day periods followed by 14-day drug-free periods.
60 mg/dose IV.
Safety and efficacy have not been established.
No dosage adjustments are needed in patients with hepatic impairment.
No dosage adjustments are needed in patients with mild or moderate renal impairment (eGFR 30 to 89 mL/minute/1.73 m2). Edaravone has not been studied for use in patients with severe renal impairment.
Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.Do not use if the oxygen indicator has turned blue or purple before opening the package. The indicator will appear pink to reflect appropriate oxygen concentrations.Storage: Once the overwrap package is open, use within 24 hours.
Do not inject other medications into the infusion bag or mix with edaravone.Administer each 60 mg dose as 2 consecutive 30 mg IV infusion bags or a single 60 mg IV infusion bag over a total of 60 minutes (i.e., at a rate of approximately 1 mg/minute).
Radicava:- Discard product if it contains particulate matter, is cloudy, or discolored- Protect from light- See package insert for detailed storage information- Store at 77 degrees F; excursions permitted to 59-86 degrees F- Store in original package until time of use
Edaravone is contraindicated for use in patients with a history of a hypersensitivity to edaravone or any of the inactive ingredients, including sulfite hypersensitivity. Hypersensitivity reactions, including anaphylactic reactions, have occurred with edaravone. The edaravone product contains sodium bisulfite, which may cause hypersensitivity reactions, including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in susceptible patients. Sulfite sensitivity occurs more frequently in persons with asthma. Monitor patients closely during treatment for hypersensitivity reactions. If hypersensitivity reactions occur, discontinue edaravone, treat per standard of care, and monitor until the reaction resolves.
There are no adequate human data on the developmental risk associated with edaravone use during pregnancy. Increased mortality and other adverse developmental effects were observed during reproductive animal studies with edaravone at clinically relevant doses. Reduced fetal weight was observed in rats given edaravone (0, 3, 30, or 300 mg/kg/day) throughout organogenesis; reduced offspring weight and maternal toxicity were observed at the highest dose. The low dose is less than the recommended human dose (RHD) of 60 mg on a body surface area (BSA, mg/m2) basis. In rats given edaravone (0, 3, 20, or 200 mg/kg/day) from gestational day 17 throughout lactation, offspring mortality and increased activity were observed at the high dose and mid to high doses, respectively. There was an increase in stillbirths, offspring mortality, and physical development delay (vaginal opening) at the highest dose tested. Maternal toxicity was observed at all but the lowest dose. Offspring reproductive function was not affected. The no-effect dose for developmental toxicity (3 mg/kg/day) is less than the RHD on a BSA basis. Edaravone (0, 3, 20, or 100 mg/kg/day) administration to rabbits throughout organogenesis resulted in embryofetal death at the highest dose, which was also associated with maternal toxicity. The higher no-effect dose for embryofetal developmental toxicity is approximately 6 times the RHD on a BSA basis.
There are no data on the presence of edaravone in human milk, the effects of edaravone on the breast-fed infant, or the effects of the drug on milk production. Consider the developmental and health benefits of breast-feeding along with the mother's clinical need for edaravone and any potential adverse effects on the breast-fed infant from edaravone or the underlying maternal condition.
anaphylactoid reactions / Rapid / Incidence not knownerythema multiforme / Delayed / Incidence not known
hypoxia / Early / 6.0-6.0glycosuria / Early / 4.0-4.0dyspnea / Early / Incidence not knownhypotension / Rapid / Incidence not known
headache / Early / 10.0-10.0infection / Delayed / 4.0-4.0urticaria / Rapid / Incidence not known
There are no drug interactions associated with Edaravone products.
Edaravone is a potent free radical scavenger and antioxidant that may provide neuroprotection against oxidative stress. In motor neurons, oxidative stress may contribute to neurodegeneration and the development of amyotrophic lateral sclerosis (ALS). Antioxidant properties of edaravone include enhancement of prostacyclin production, hydroxyl radical trapping, and quenching of active oxygen.
Edaravone is administered intravenously. Edaravone is bound to human serum proteins (92%), mainly albumin. Metabolism to an inactive glucuronide conjugate occurs in the liver and kidney via glucuronide conjugation with multiple UGT isoforms (UGT1A6, UGT1A9, UGT2B7, and UGT2B17). An inactive sulfate conjugate is also formed by sulfotransferases. Excretion of edaravone mostly occurs in the urine as the glucuronide form (70% to 90% of the dose). Approximately 5% to 10% of the dose is recovered in the urine as the sulfate conjugate, and less than 1% of the dose is excreted in the urine as unchanged drug. The mean terminal half-life of edaravone is 4.5 to 6 hours. Affected cytochrome P450 isoenzymes and drug transporters: UGT1A6, UGT1A9, UGT2B7, UGT2B17Edaravone is a substrate of UGT1A6, UGT1A9, UGT2B7, UGT2B17. The pharmacokinetics of edaravone are not expected to be significantly affected by inhibitors of CYP enzymes, UGTs, or major transporters.
The maximum concentration (Cmax) of edaravone is reached by the end of the infusion (at 60 minutes). There is a more than dose-proportional increase in AUC and Cmax. Edaravone does not accumulate in plasma with multiple-dose administration.