Gabapentin

2-[1-(aminomethyl)cyclohexyl]acetic acid

Overview

Gabapentin belongs to Depressants.

Key safety note: Gabapentin is often perceived as low-risk, and on its own it is relatively safe in overdose, but combined with opioids, benzodiazepines, alcohol or other CNS depressants it significantly raises the risk of sedation, respiratory depression and death.[3][4]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • At therapeutic doses: reduced neuropathic pain and seizure frequency, commonly with drowsiness, dizziness and mild unsteadiness.
  • At higher or recreational doses: alcohol-like disinhibition, relaxation, sociability and mild euphoria, sometimes with a 'floaty' or mildly dissociative quality. Effects are more pronounced in people with low tolerance.
  • Onset is slow (roughly 30 minutes to 2 hours) and effects are long (about 6–10 hours), because absorption is saturable, very large single doses give diminishing returns while still adding side effects.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral (capsules, tablets or solution). Non-medical use is also oral.. Gabapentin's oral absorption is saturable, so bioavailability falls as the dose rises and very large single doses give diminishing effect while still adding side effects. The figures below are commonly cited reference ranges, not a recommendation or a 'safe' dose. The critical harm-reduction point is combination: gabapentin taken with opioids, benzodiazepines or alcohol markedly increases the risk of respiratory depression and death, even at amounts each would tolerate alone. Dependence develops with regular use and abrupt cessation can trigger seizures: taper, do not stop suddenly.

Dose ranges

Threshold

200 mg

Light

200–900 mg

Common

900–1500 mg

Strong

1500–2400 mg

Heavy

2400 mg +

Duration

onset

30–120 minutes

total

6–10 hours

after effects

Grogginess, with regular use, tolerance, dependence and a withdrawal syndrome (seizure risk on abrupt cessation)

Chemical & Physical Properties
FormulaC9H17NO2
Molar mass171.24 g/mol
StateSolid
Melting point162–166 °C, also reported as 165–167 °C
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKa3.7
LogP1.25
Solubility>100mg/mL, In water, 4.49×10³ mg/L at 25 °C, Freely soluble in water
Refractive indexNot reported
Identifiers & Synonyms
CAS60142-96-3
CAS (enantiomer)
PubChem CID3446
InChIKeyUGJMXCAKCUNAIE-UHFFFAOYSA-N
InChIInChI=1S/C9H17NO2/c10-7-9(6-8(11)12)4-2-1-3-5-9/h1-7,10H2,(H,11,12)
SMILESC1CCC(CC1)(CC(=O)O)CN

Synonyms

  • Neurontin
  • Gralise
  • Gabapentin
Pharmacodynamics & Biochemistry

Gabapentin is a structural analogue of the neurotransmitter GABA, but, despite its name and design, it does not bind GABA receptors, is not converted to GABA, and has no meaningful effect on GABA uptake or metabolism. It is used mainly as an anticonvulsant and for neuropathic pain. Its established primary mechanism is high-affinity binding to the α2δ auxiliary subunit of voltage-gated calcium channels (α2δ-1 and α2δ-2). This reduces calcium influx at nerve terminals and dampens the release of excitatory neurotransmitters such as glutamate, noradrenaline and substance P, which underlies its analgesic and anticonvulsant effects. Gabapentin was more recently shown to be a potent activator of the KCNQ3 (Kv7.3) and KCNQ5 (Kv7.5) voltage-gated potassium channels. Opening these channels enhances the outward neuronal 'M-current' and lowers excitability: a second mechanism that may contribute to its clinical effects, and the basis of the binding data shown below. Gabapentin has a favourable but quirky pharmacokinetic profile: it is absorbed by a saturable amino-acid transporter, so oral bioavailability falls as the dose rises (dose-dependent, non-linear kinetics). It is essentially not metabolised and is eliminated unchanged by the kidneys, so doses must be reduced in renal impairment.

Biological targets

  • VGCC α2δ

Binding & functional measurements

TargetMeasurementSpecies
Kv7.5pEC50 8.7Human
Kv7.3pEC50 8.3Human
Pharmacokinetics
BioavailabilityOral, saturable and dose-dependent (≈60% falling at higher doses)
Tmax≈2–3 h
Half-life≈5–7 h
VdNot reported
Protein bindingNot reported
MetabolismNot metabolized
ExcretionRenal, unchanged (dose adjustment in renal impairment)
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

Gabapentin is often perceived as low-risk, and on its own it is relatively safe in overdose, but combined with opioids, benzodiazepines, alcohol or other CNS depressants it significantly raises the risk of sedation, respiratory depression and death. That combination is increasingly seen in overdose fatalities and drove its reclassification as a controlled drug in the UK. It has genuine misuse and dependence potential, especially in people with a history of substance use: regular high-dose use produces tolerance and a withdrawal syndrome, and abrupt discontinuation can provoke seizures, so it must be tapered rather than stopped suddenly. Common effects include dizziness, drowsiness, unsteadiness and peripheral oedema.[3][4]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Opioids Gabapentin increases opioid-related respiratory depression and overdose-death risk: the most important and dangerous interaction.[3][4]
Alcohol, Benzodiazepines Additive sedation and respiratory depression.[3]
Aluminium- or magnesium-containing antacids Aluminium- or magnesium-containing antacids reduce gabapentin absorption, so separate dosing by at least 2 hours.[2][4]

Contraindications

Known hypersensitivity to the drug hypersensitivity to gabapentin.[2]
Kidney or liver impairment dose reduction required in renal impairment (renally cleared unchanged).[4][3]
Combining with alcohol or other CNS depressants concomitant opioids or other CNS depressants (respiratory-depression risk).[3]
Abrupt discontinuation after regular use (withdrawal and seizure risk) avoid abrupt withdrawal (seizure risk), tapering on discontinuation.[3]
Usage & Context
  • Widely prescribed as an anticonvulsant (adjunct for focal seizures) and, most commonly, for neuropathic pain such as postherpetic neuralgia and diabetic neuropathy. Also used off-label for anxiety, restless-legs syndrome and other conditions.
  • Increasingly misused recreationally for a mild euphoric, alcohol-like or opioid-potentiating effect: frequently alongside opioids, which is the most dangerous pattern.
  • Commonly diverted and misused in prison and opioid-using populations, where its availability and low cost make it a frequent adjunct drug.
Sources & Evidence

Further Information