In Vitro Binding of Amantadine to Plasma Proteins

Liu, P; Cheng, Peng; Ing, Todd S.; Daugirdas, John T.; Jeevanandhan, R; Soung, Lian-Sen; Galinis, S

doi:10.1097/00002826-198406000-00005

Cited by 13 publications

(10 citation statements)

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“…Namely, plasma protein binding of 1-ADA of 68-52% was observed. Liu et al have shown that approximately two-thirds of the 1-ADA was found to be protein bound in the concentration range of 0.1-2 g/ml [27]. Our results were nearly consistent with previous data, suggesting that our HPLC assay is appropriate for determining the unbound fraction of 1-ADA in the filtrate.…”

Section: Bindings Of 1-ada and 2-ada To Human Plasma Proteinsupporting

confidence: 92%

Liquid chromatographic determination of 1-adamantanamine and 2-adamantanamine in human plasma after pre-column derivatization with o-phthalaldehyde and 1-thio-β-d-glucose

Higashi

Fujii

2004

Journal of Chromatography B

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Section: Bindings Of 1-ada and 2-ada To Human Plasma Proteinsupporting

confidence: 92%

Liquid chromatographic determination of 1-adamantanamine and 2-adamantanamine in human plasma after pre-column derivatization with o-phthalaldehyde and 1-thio-β-d-glucose

Higashi

Fujii

2004

Journal of Chromatography B

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“…Using blood bank samples from apparently healthy subjects, Liu et al (1984) determined that amantadine in plasma was approximately 67% protein bound and that the percentage of drug bound was independent of amantadine concentration between 100 and 2000 p.glL. Mean total plasma protein concentration in these samples was 61 ± 5 giL, with 35 ± 4 giL as albumin.…”

Section: Anatomicmentioning

confidence: 99%

Clinical Pharmacokinetics of Amantadine Hydrochloride

Aoki

Sitar

1988

Clinical Pharmacokinetics

188

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Amantadine is a drug with diverse uses ranging from prevention of influenza A illness to the treatment of patients with Parkinson's disease. It is available only in oral formulations from which it is well absorbed and widely distributed, little drug being present in the circulation. Apparent volume of distribution is inversely related to dose over the therapeutic range and accounts in part for a noteworthy logarithmic increase in plasma concentration as a function of dose. Elimination is primarily by renal clearance by both glomerular filtration and tubular secretion. Amantadine accumulates in patients with renal dysfunction. Hence, doses must be reduced in such patients to avoid toxicity. Interactions with other drugs appear uncommon. Relationships have been demonstrated between amantadine therapeutic effects and plasma concentrations in different study cohorts, but not in individual patients. Dose schedules have been suggested for individuals in whom amantadine kinetics are different from healthy subjects. However, these schedules are controversial in their choice of target concentrations and in being untested as to predictive value.

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“…In both healthy volunteers and patients with Parkinson's disease, steady-state plasma concentrations are reached in 4 to 7 days (Pacifici et al 1976) and are proportional to dose in young, healthy individuals (Aoki et al 1979). Amantadine binds to plasma proteins in vitro (Liu et al 1984), but the extent of in vivo protein binding has not been determined.…”

Section: Absorptionmentioning

confidence: 99%

Clinical Pharmacokinetics of Anti-Parkinsonian Drugs

Cedarbaum

1987

Clinical Pharmacokinetics

171

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Of the neurological disorders, none can claim a battery of therapeutic agents based upon as rational a pharmacology as can Parkinson's disease. In this review, the clinical pharmacokinetics of the major classes of anti-Parkinsonian drugs is discussed. Although they are the oldest drugs in the anti-Parkinsonian armamentarium, little pharmacokinetic data are available regarding the anticholinergic and antihistaminic agents. Based on elimination half-lives of 10 to 18 hours, most could probably be effectively given on a twice-daily schedule. Amantadine is unique among anti-Parkinsonian agents both in lacking a clearly defined mechanism of action and in being eliminated from the body exclusively by renal excretion of unchanged drug. Thus the normal decline of renal function in the elderly Parkinsonian population becomes an important factor in avoiding potential drug toxicity. The pharmacokinetics and pharmacodynamics of levodopa are complex. Since it is an amino acid, it follows metabolic pathways and must compete for absorption and brain uptake with a number of large neutral amino acids. It has a short elimination half-life and, as Parkinson's disease progresses, the brain loses its capacity to store the drug and becomes dependent in a moment-to-moment fashion on plasma levodopa concentrations, creating therapeutic response fluctuations in over 50% of patients. Pharmacokinetic considerations in the management of these response fluctuations are discussed. The newest class of anti-Parkinsonian agents are the direct acting dopamine receptor agonists. These drugs, all derivatives of ergot, have more prolonged durations of anti-Parkinsonian action than levodopa. However, other than bromocriptine, clinical experience with members of this class of drugs is still limited.

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In Vitro Binding of Amantadine to Plasma Proteins

Cited by 13 publications

References 0 publications

Liquid chromatographic determination of 1-adamantanamine and 2-adamantanamine in human plasma after pre-column derivatization with o-phthalaldehyde and 1-thio-β-d-glucose

Liquid chromatographic determination of 1-adamantanamine and 2-adamantanamine in human plasma after pre-column derivatization with o-phthalaldehyde and 1-thio-β-d-glucose

Clinical Pharmacokinetics of Amantadine Hydrochloride

Clinical Pharmacokinetics of Anti-Parkinsonian Drugs

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