Top Gene Interactions
- Metabolism: All pharmacological actions following gabapentin administration are due to the activity of the parent compound; gabapentin is not appreciably metabolized in humans. Route of Elimination: Gabapentin is eliminated from the systemic circulation by renal excretion as unchanged drug. Gabapentin is not appreciably metabolized in humans. Half Life: 5-7 hours
- Uses/Sources: It was originally developed for the treatment of epilepsy, and currently, gabapentin is widely used to relieve pain, especially neuropathic pain. [wikipedia]. For the management of postherpetic neuralgia in adults and as adjunctive therapy in the treatment of partial seizures with and without secondary generalization in patients over 12 years of age with epilepsy.
- Health Effects: May cause a potentially dangerous rash that may develop into Stevens Johnson syndrome, an extremely rare but potentially fatal skin disease.
- Symptoms: Symptoms of overdose include ataxia, labored breathing, ptosis, sedation, hypoactivity, and excitation.
- Treatment: Gabapentin can be removed by hemodialysis. (L1712)
- Route of Exposure: Oral. Rapid. Absorbed in part by the L-amino acid transport system, which is a carrier-mediated, saturable transport system; as the dose increases, bioavailability decreases. Bioavailability ranges from approximately 60% for a 900 mg dose per day to approximately 27% for a 4800 milligram dose per day. Food has a slight effect on the rate and extent of absorption of gabapentin (14% increase in AUC).
- Carcinogenicity: No indication of carcinogenicity to humans (not listed by IARC).
- Toxicity: LD50: >8000 mg/kg (oral,rat) [MSDS] LD50: 8053 mg/kg (oral, mouse) [MSDS]
Mechanism of Action
|Target Name||Mechanism of Action||References|
Voltage-dependent calcium channel subunit alpha-2/delta-1
Voltage-dependent calcium channel subunit alpha-2/delta-2
Voltage-dependent N-type calcium channel subunit alpha-1B
Adenosine receptor A1
Calcium channel, voltage-dependent, L type, alpha 1B subunit
Branched-chain-amino-acid aminotransferase, cytosolic
|Gabapentin interacts with cortical neurons at auxillary subunits of voltage-sensitive calcium channels. Gabapentin increases the synaptic concentration of GABA, enhances GABA responses at non-synaptic sites in neuronal tissues, and reduces the release of mono-amine neurotransmitters. One of the mechanisms implicated in this effect of gabapentin is the reduction of the axon excitability measured as an amplitude change of the presynaptic fibre volley (FV) in the CA1 area of the hippocampus. This is mediated through its binding to presynaptic NMDA receptors. Other studies have shown that the antihyperalgesic and antiallodynic effects of gabapentin are mediated by the descending noradrenergic system, resulting in the activation of spinal alpha2-adrenergic receptors. Gabapentin has also been shown to bind and activate the adenosine A1 receptor.||
Gabapentin Interacts with Diseases
|Disease||Inference Score||References/Inference Genes|
|Iron Metabolism Disorders||7.63||
|Spinocerebellar Ataxia 17||7.31||
|Diabetes Mellitus, Experimental||6.62||
|Liver Cirrhosis, Experimental||6.04||
|Chronic obstructive pulmonary disease||6.03||
|Genetic Predisposition to Disease||6.02||
|Diamond-Blackfan Anemia 10||5.99||
|Bartter syndrome, antenatal , type 2||5.97||
|DIAMOND-BLACKFAN ANEMIA 6||5.88||
|Hemiplegic migraine, familial type 1||5.76||
|Carcinoma, Non-Small-Cell Lung||5.67||