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Pregabalin and gabapentin are members of a unique class of compounds characterized by high affinity binding to the alpha-2-delta (α2δ) protein in the CNS. Both have been shown to be effective as adjunctive therapy for partial seizures and neuropathic pain disorders. Clinical pharmacology studies conducted to characterize the pharmacokinetics, bioavailability, and drug-drug interaction Gabapentin is a novel anticonvulsant drug. The anticonvulsant mechanism of gabapentin is not known. Based on the amino acid structure of gabapentin we explored its possible effects on glutamate and γ-aminobutyric acid (GABA) metabolism in brain as they may relate to its anticonvulsant mechanisms of action. Gabapentin is absorbed slowly after oral administration, with maximum plasma concentrations attained within 3-4 hours. Orally administered gabapentin exhibits saturable absorption--a nonlinear (zero-order) process--making its pharmacokinetics less predictable. Plasma concentrations of gabapentin do not increase proportionally with increasing dose. In man, no biotransformation of gabapentin is observed. In rats, biotransformation is only minor. In dogs, however, a remarkable formation of N-methyl-gabapentin is found. Elimination half-lives range between 2-3 h in rats, 3-4 h in dogs, and 5-6 h in man. Gabapentin is nearly exclusively eliminated via the kidneys. Gabapentin, sold under the brand name Neurontin among others, is an anticonvulsant medication primarily used to treat neuropathic pain and also for partial seizures [10] [7] of epilepsy. It is a commonly used medication for the treatment of neuropathic pain caused by diabetic neuropathy , postherpetic neuralgia , and central pain . [ 11 ] The pharmacokinetic (PK) properties of gabapentin, including absorption, distribution, metabolism, and excretion (ADME), were investigated during the development of Neurontin®, an immediate-release (IR) formulation of gabapentin that is orally administered three-times daily. Lin HC, Huang YH, Chao TH, et al. Gabapentin reverses central hypersensitivity and suppresses medial prefrontal cortical glucose metabolism in rats with neuropathic pain. Mol Pain 2014; 10: 63. Crossref Gabapentin pharmacokinetics are not affected by repeated administration, and steady state plasma concentrations are predictable from single dose data. Gabapentin is not appreciably metabolized in humans, is eliminated solely by renal excretion, and can be removed from plasma by hemodialysis. Metabolism. Gabapentin is not appreciably metabolized. Gabapentin enacarbil, the prodrug of gabapentin, is rapidly and efficiently converted to gabapentin by first-pass hydrolysis following oral administration. Elimination Route. Excreted renally as unchanged drug. Half-life. Approximately 5–7 hours. Special Populations The metabolism of Mestranol can be increased when combined with Gabapentin. Metaxalone The risk or severity of CNS depression can be increased when Metaxalone is combined with Gabapentin. As a result, metabolism-related factors do not necessitate dosage alterations of gabapentin and concomitant AEDs after prolonged therapy. The drug is excreted unchanged in urine; plasma clearance is linearly related to creatinine clearance; and dosage is readily adjusted based on renal function. Gabapentin is a new antiepileptic drug (AED) with an attractive pharmacokinetic profile. It is absorbed by an active and saturable transport system, and has a high volume of distribution. Gabapentin is not bound to plasma proteins, does not induce hepatic enzymes and is not metabolized. At steady st gabapentin 1800 mg/day to pregabalin 300 mg/day and gabapentin 900 mg/day to enhanced recovery pathways, hypersensitivity and suppresses medial prefrontal cortical glucose metabolism . in Absorption of gabapentin is solely dependent on LAT that are easily saturable, resulting in dose-dependent pharmacokinetics. As the dose of gabapentin increases, the area under the plasma concentration–time curve (AUC) does not increase proportionally. As a drug, gabapentin was formerly considered as a structural analogue of the inhibitory neurotransmitter γ-aminobutyric acid (GABA). However, preliminary studies proposed that gabapentin did not bind to either GABA-A or GABA-B receptors 11, nor was it transform metabolically into GABA. 12 Gabapentin is effective as monotherapy for partial seizures (Beydoun 1999).However, although few studies have compared the effectiveness of gabapentin with other AEDs in the management of partial epilepsy, available evidence suggests that monotherapy with gabapentin is less effective than traditional agents such as carbamazepine and the newer antiepileptic drug lamotrigine (Marson et al. 2007). Results with human and rat brain NMR spectroscopy indicate that gabapentin increases GABA synthesis. Gabapentin increases non-synaptic GABA responses from neuronal tissues in vitro. In vitro, gabapentin reduces the release of several mono-amine neurotransmitters. Gabapentin is eliminated from the systemic circulation by renal excretion as unchanged drug. Gabapentin is not appreciably metabolized in humans. Gabapentin elimination half-life is 5 to 7 hours and is unaltered by dose or following multiple dosing. Metabolism: In humans, gabapentin undergoes minimal metabolic alteration, largely retaining the original structure. Gabapentin does not induce or inhibit CYP enzymes. Also, none of the CYP enzyme inhibitors alter their pharmacokinetics. Gabapentin is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but it does not modify GABAA or GABAB radioligand binding, it is not converted metabolically into GABA or
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