Absorption
The absolute bioavailability of acamprosate calcium after oral administration is about 11%. Steady-state plasma concentrations of acamprosate are reached within 5 days of dosing. Steady-state peak plasma concentrations after acamprosate calcium doses of 2 x 333 mg tablets three times daily average 350 ng/mL and occur at 3-8 hours post-dose. Coadministration of acamprosate calcium with food decreases bioavailability as measured by C
maxand AUC, by approximately 42% and 23%, respectively. The food effect on absorption is not clinically significant and no adjustment of dose is necessary.
Distribution
The volume of distribution for acamprosate following intravenous administration is estimated to be 72-109 liters (approximately 1 L/kg
).Plasma protein binding of acamprosate is negligible.
Metabolism
Acamprosate does not undergo metabolism.
Elimination
After oral dosing of 2 x 333 mg of acamprosate calcium, the terminal half-life ranges from approximately 20-33 hours. Following oral administration of acamprosate calcium, the major route of excretion is via the kidneys as acamprosate.
Special Populations
Gender:Acamprosate calcium does not exhibit any significant pharmacokinetic differences between male and female subjects.
Age:The pharmacokinetics of acamprosate calcium have not been evaluated in a geriatric population. However, since renal function diminishes in elderly patients and acamprosate is excreted unchanged in urine, acamprosate plasma concentrations are likely to be higher in the elderly population compared to younger adults.
Pediatrics:The pharmacokinetics of acamprosate calcium have not been evaluated in a pediatric population.
Renal Impairment:Peak plasma concentrations after administration of a single dose of 2 x 333 mg acamprosate calcium delayed-release tablets to patients with moderate or severe renal impairment were about 2-fold and 4-fold higher, respectively, compared to healthy subjects. Similarly, elimination half-life was about 1.8-fold and 2.6-fold longer, respectively, compared to healthy subjects. There is a linear relationship between creatinine clearance values and total apparent plasma clearance, renal clearance and plasma half-life of acamprosate. A dose of 1 x 333 mg acamprosate calcium delayed-release tablets, three times daily, is recommended in patients with moderate renal impairment (creatinine clearance of 30-50 mL/min,
[
see Use in Specific Populations (8.6)].
Acamprosate calcium is contraindicated in patients with severe renal impairment (creatinine clearance of ≤30 mL/min)
[
see Dosage and Administration (2.1),
Contraindications (4.2),
Warnings and Precautions (5.1),
and
Use in Specific Populations (8.6)].
Hepatic Impairment:Acamprosate is not metabolized by the liver and the pharmacokinetics of acamprosate calcium are not altered in patients with mild to moderate hepatic impairment (groups A and B of the Child-Pugh classification). No adjustment of dosage is recommended in such patients.
Alcohol-dependent subjects:A cross-study comparison of acamprosate calcium at doses of 2 x 333 mg three times daily indicated similar pharmacokinetics between alcohol-dependent subjects and healthy subjects.
Drug-Drug Interactions
Acamprosate had no inducing potential on the cytochrome CYP1A2 and 3A4 systems, and
in vitroinhibition studies suggest that acamprosate does not inhibit
in vivometabolism mediated by cytochrome CYP1A2, 2C9, 2C19, 2D6, 2E1, or 3A4. The pharmacokinetics of acamprosate calcium were unaffected when co-administered with alcohol, disulfiram or diazepam. Similarly, the pharmacokinetics of ethanol, diazepam and nordiazepam, imipramine and desipramine, naltrexone and 6-beta naltrexol were unaffected following co-administration with acamprosate calcium. However, co-administration of acamprosate calcium with naltrexone led to a 33% increase in the C
maxand a 25% increase in the AUC of acamprosate. No adjustment of dosage is recommended in such patients.