Gabapentin Capsules

The mechanism of gabapentin's anticonvulsant effect is still unclear, but animal experiments suggest that gabapentin can inhibit epileptic seizures, similar to other marketed anticonvulsant drugs. Results from the maximum electric shock test in mice and rats, the benzotetrazole epilepsy seizure test, and other animal experiments (such as genetic epilepsy models) suggest that gabapentin has antiepileptic effects, but the relevance of these epilepsy models to humans is unclear. Gabapentin is structurally related to the neurotransmitter GABA, but does not interact with GABA receptors. It can neither be metabolized into GABA or GABA agonists, nor is it an inhibitor of GABA uptake or degradation. Radioligand binding assays have found that gabapentin has no affinity for many common receptor sites when the concentration reaches 100 μM, including benzodiazepine receptors, glutamate receptors, NMDA receptors, quisqualate receptors, kainate receptors, strychnine-insensitive or -sensitive aminoacetic acid receptors, α1, α2 or β receptors, adenosine A1 or A2 receptors, M or N receptors, dopamine D1 or D2 receptors, H1 receptors, 5-hydroxytryptamine S1 or S2 receptors, opioid μ, δ or k receptors, voltage-sensitive calcium channel sites labeled with nitrendipine or diltiazem, and voltage-sensitive sodium channel sites labeled with batrachotoxin A20-α-benzoate. Since the results obtained in several commonly used tests for evaluating the effects of drugs on NMDA receptors are opposite, there is currently no unified understanding of the effects of gabapentin on NMDA receptors. In vitro studies have shown that the binding sites of gabapentin in the rat brain are distributed in the neocortex and hippocampus, and its high-affinity binding protein has been confirmed to be an auxiliary subunit of the voltage-activated calcium channel, but its related functions have not yet been elucidated.

The main ingredient of this product is gabapentin, and its chemical name is: 1-(aminomethyl)-cyclohexaneacetic acid.

1. Post-herpetic neuralgia: used to treat post-herpetic neuralgia in adults. 2. Epilepsy: used as an adjuvant treatment for partial seizures with or without secondary systemic seizures in adults and children over 12 years old. It can also be used as an adjuvant treatment for partial seizures in children aged 3 to 12 years old.

1. Post-herpetic neuralgia: Take 0.3g of gabapentin once on the first day, 0.6g on the second day, divided into two doses; take 0.9g on the third day, divided into three doses. Subsequently, the dose can be gradually increased to 1.8g per day, divided into three doses, according to the need for pain relief. In foreign clinical studies, its efficacy is equivalent within the dose range of 1.8g to 3.6g per day, and doses exceeding 1.8g per day have not shown more benefits. 2. Epilepsy: Gabapentin can be used in combination with other anti-epileptic drugs for combined treatment. Gabapentin is administered orally in divided doses (3 times a day). The dosage method is to gradually increase from the initial low dose to the effective dose. Patients over 12 years old: On the first day of administration, 0.3g can be taken once a day; 0.3g twice a day on the second day, 0.3g three times a day on the third day, and then maintain this dose. According to foreign research literature, the dosage of gabapentin can be increased to 1.8g per day, and some patients can still tolerate a dosage of 2.4g per day. The safety of dosages above 2.4g per day is still uncertain.

1. Post-herpetic neuralgia: mainly dizziness, drowsiness, and peripheral edema. Other adverse events with an incidence rate higher than 1% and higher than the placebo control group in foreign clinical trials include: Systemic: weakness, infection, headache, accidental trauma, abdominal pain. Digestive system: diarrhea, constipation, dry mouth, nausea, vomiting, flatulence. Metabolic and nutritional disorders: weight gain, hyperglycemia. Nervous system: ataxia, abnormal thinking, abnormal gait, non-cooperation, and dullness of senses. Respiratory system: pharyngitis. Skin and appendages: rash. Special senses: amblyopia, diplopia, conjunctivitis, and otitis media. 2. Epilepsy: The most common adverse events are drowsiness, fatigue, dizziness, headache, nausea, vomiting, weight gain, tension, insomnia, ataxia, nystagmus, paresthesia, and anorexia. Occasionally, weakness, visual impairment (amblyopia, diplopia), tremor, joint dislocation, abnormal thinking, forgetfulness, dry mouth, depression, and emotional tendencies occur. In clinical studies, the following conditions occasionally occurred: dyspepsia, constipation, abdominal pain, urinary incontinence, increased appetite, rhinitis, pharyngitis, cough, myalgia, back pain, facial and extremity or systemic edema, decreased erectile function, dental abnormalities, gingivitis, pruritus, leukopenia, fractures, vasodilation and hypertension. In addition, aggressive behavior, emotional instability, hyperactivity (excessive exercise, partially uncontrollable), viral infection and fever were observed in clinical trials in children under 12 years old. Hemorrhagic pancreatitis has been reported in patients treated with gabapentin capsules. (See Precautions) There have been individual reports of allergic reactions (Stevens-Johnson syndrome, erythema multiforme) when taking gabapentin capsules. In clinical control studies of laboratory tests, 16% of patients had blood sugar fluctuations that may be clinically relevant (3.3mmol/L or ≥7.8mmol/L, normal range 3.5-5.5mmol/L) (see Precautions). When used simultaneously with other antiepileptic drugs, there have been reports of elevated liver function test results.

Gabapentin capsules are contraindicated in patients with known allergies to any of the ingredients in this drug and patients with acute pancreatitis. Gabapentin capsules are ineffective for patients with primary systemic seizures, such as absence seizures.

Gabapentin is poorly metabolized and does not interfere with the metabolism of other commonly used antiepileptic drugs. The drug interaction data described in this section were obtained from studies in healthy adults and patients with epilepsy. Phenytoin: Single and multiple doses of gabapentin (0.4 g three times daily) were studied in patients with epilepsy who had been taking phenytoin for at least 2 months (N=8). The results showed that gabapentin had no effect on the steady-state plasma concentration of phenytoin, and phenytoin had no effect on the pharmacokinetics of gabapentin. Carbamazepine Administration of gabapentin (0.4 g three times daily; N=12) did not affect the steady-state plasma concentrations of carbamazepine and carbamazepine 10,11 epoxide. Similarly, administration of carbamazepine did not alter the pharmacokinetics of gabapentin. Valproic acid There were no differences in the mean steady-state plasma concentrations of valproic acid before and during concurrent administration of gabapentin (0.4 g three times daily; N=17), and the pharmacokinetic data of gabapentin were not affected by valproic acid. Sedatives Hypnotics Steady-state pharmacokinetic data for sedatives hypnotics or gabapentin (0.3 g three times daily; N=12) were similar whether administered alone or in combination. Gabapentin absorption increased by 12% to 15% when naproxen sodium capsules (250 mg) and Neurontin (125 mg) were administered concomitantly. Gabapentin had no effect on the pharmacokinetic parameters of naproxen. The doses given for both agents were below their respective therapeutic doses. The interaction is unclear at the recommended dose range. The Cmax and AUC of hydrocodone (10 mg, N=50) were decreased after the coadministration of gabapentin (0.125 to 0.5 g; N=48) with hydrocodone, in a dose-dependent manner. Co-administration of gabapentin (0.125 g) reduces the Cmax and AUC of dihydrocodone (10 mg, N=50) by about 3% to 4%, and co-administration of gabapentin (0.5 g) reduces the Cmax and AUC of dihydrocodone (10 mg, N=50) by about 21% to 22%. The mechanism of this interaction is not clear. Dihydrocodone can increase the AUC of gabapentin by about 14%. The interaction of other doses is not clear. Morphine According to literature reports, when 0.6 g of gabapentin capsules (N=12) were given 2 hours after 60 mg of controlled-release morphine capsules, the average AUC of gabapentin increased by 44% compared with the absence of morphine (see Warnings). The pharmacokinetic parameters of morphine did not change after taking gabapentin. The interaction with other doses is not clear. Cimetidine Administration of cimetidine 0.3 g 4 times daily (N=12) decreased the mean apparent oral clearance of gabapentin by 14% and creatinine clearance by 10%. Thus, cimetidine may alter the renal excretion of gabapentin to creatinine. The small decrease in gabapentin excretion caused by cimetidine is not clinically important. The effect of gabapentin on cimetidine was not evaluated. Oral contraceptives After administration of tablets containing 2.5 mg of norethindrone acetate and 50 μg of ethinyl estradiol, the AUC and half-life of norethindrone acetate and ethinyl estradiol were similar, regardless of the concomitant administration of gabapentin (0.4 g tid; N=13). When coadministered with gabapentin, the Cmax of norethindrone increased by 13%; this interaction is not clinically important. Antacids (aluminum hydroxide) Aluminum hydroxide decreases the bioavailability of gabapentin by approximately 20%. When gabapentin is taken 2 hours after aluminum hydroxide, the bioavailability decreases by approximately 5%. Therefore, it is recommended that gabapentin should be taken at least 2 hours after aluminum hydroxide. Effects of probenecid (carbenesulfonamide): Probenecid is a renal tubular secretion blocker. Comparison of pharmacokinetic parameters of gabapentin with or without probenecid demonstrated that gabapentin cannot flow through the renal tubular pathway blocked by probenecid.

Keep tightly closed and avoid high temperature storage.

0.1 g