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Gabapentin: Difference between revisions
>Rosie m →Subjective effects: it previously said its not very good at relieving acute pain, such as opiates which, although isnt hard to get what was meant when read literally is referring to opiates as a type of acute pain, or maybe just that opiates arent good for acute pain. i changed this to reflect what i assume was meant, that it's not effective unlike opiates, which are well known to be effective pain relief. |
>Tracer Added Category:Cycloalkylamine |
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{{headerpanel|{{DepressantOD|gabapentinoids}}}} | {{headerpanel|{{DepressantOD|gabapentinoids}}}} | ||
{{SummarySheet}} | {{SummarySheet}} | ||
{{SubstanceBox/ | {{SubstanceBox/Gabapentin}} | ||
'''Gabapentin''' (also known as '''Neurontin''') is a [[psychoactive class::depressant]] substance of the [[chemical class::gabapentinoid]] class. It is a structural analog of the [[neurotransmitter]] [[GABA]] and acts by inhibiting certain calcium channels in the brain namely α2δ subunit-containing voltage-dependent calcium channels (VGCCs).<ref name="CalandreRico-Villademoros2016">{{cite journal|last1=Calandre|first1=Elena P.|last2=Rico-Villademoros|first2=Fernando|last3=Slim|first3=Mahmoud|title=Alpha2delta ligands, gabapentin, pregabalin and mirogabalin: a review of their clinical pharmacology and therapeutic use|journal=Expert Review of Neurotherapeutics|volume=16|issue=11|year=2016|pages=1263–1277|issn=1473-7175|doi=10.1080/14737175.2016.1202764}}</ref> | '''Gabapentin''' (also known as '''Neurontin''') is a [[psychoactive class::depressant]] substance of the [[chemical class::gabapentinoid]] class. It is a structural analog of the [[neurotransmitter]] [[GABA]] and acts by inhibiting certain calcium channels in the brain, namely α2δ subunit-containing voltage-dependent calcium channels (VGCCs).<ref name="CalandreRico-Villademoros2016">{{cite journal|last1=Calandre|first1=Elena P.|last2=Rico-Villademoros|first2=Fernando|last3=Slim|first3=Mahmoud|title=Alpha2delta ligands, gabapentin, pregabalin and mirogabalin: a review of their clinical pharmacology and therapeutic use|journal=Expert Review of Neurotherapeutics|volume=16|issue=11|year=2016|pages=1263–1277|issn=1473-7175|doi=10.1080/14737175.2016.1202764}}</ref> | ||
Gabapentin was originally developed to treat epilepsy and is currently FDA approved to treat postherpetic neuralgia in adults and as an adjunctive therapy in the treatment of partial onset seizures. It is often prescribed off-label for [[restless leg syndrome]], social anxiety disorder, panic disorder, and generalized anxiety disorder.<ref>Manual of Clinical Psychopharmacology | | Gabapentin was originally developed to treat epilepsy and is currently FDA approved to treat postherpetic neuralgia in adults and as an adjunctive therapy in the treatment of partial onset seizures. It is often prescribed off-label for [[restless leg syndrome]], social anxiety disorder, panic disorder, and generalized anxiety disorder.<ref>{{cite book | vauthors=((Schatzberg, A. F.)), ((Cole, J. O.)), ((DeBattista, C.)) | date= 2010 | title=Manual of Clinical Psychopharmacology | publisher=American Psychiatric Pub. | isbn=9781585623778}}</ref><ref>{{cite book | vauthors=((Sobel, S. V.)) | date=5 November 2012 | title=Successful Psychopharmacology: Evidence-Based Treatment Solutions for Achieving Remission | publisher=W. W. Norton & Company | isbn=9780393708578}}</ref><ref>{{cite book | vauthors=((Richards, D.)), ((Aronson, J.)), ((Coleman, J.)), ((Reynolds, D. J.)) | date=10 November 2011 | title=Oxford Handbook of Practical Drug Therapy | publisher=OUP Oxford | isbn=9780199562855}}</ref> | ||
Gabapentin | However Gabapentin's efficacy in the treatment of anxiety disorders is unclear as the evidence is "somewhat mixed".<ref>{{cite journal | vauthors=((Mula, M.)), ((Pini, S.)), ((Cassano, G. B.)) | journal=Journal of Clinical Psychopharmacology | title=The role of anticonvulsant drugs in anxiety disorders: a critical review of the evidence | volume=27 | issue=3 | pages=263–272 | date= June 2007 | issn=0271-0749 | doi=10.1097/jcp.0b013e318059361a}}</ref><ref>{{cite journal | vauthors=((Hamer, A. M.)), ((Haxby, D. G.)), ((McFarland, B. H.)), ((Ketchum, K.)) | journal=Journal of Managed Care Pharmacy | title=Gabapentin Use in a Managed Medicaid Population | volume=8 | issue=4 | pages=266–271 | date= July 2002 | url=https://www.jmcp.org/doi/abs/10.18553/jmcp.2002.8.4.266 | issn=1083-4087 | doi=10.18553/jmcp.2002.8.4.266}}</ref><ref>{{cite journal | vauthors=((Steinman, M. A.)), ((Bero, L. A.)), ((Chren, M.-M.)), ((Landefeld, C. S.)) | journal=Annals of Internal Medicine | title=Narrative Review: The Promotion of Gabapentin: An Analysis of Internal Industry Documents | volume=145 | issue=4 | pages=284–293 | date=15 August 2006 | url=https://www.acpjournals.org/doi/10.7326/0003-4819-145-4-200608150-00008 | issn=0003-4819 | doi=10.7326/0003-4819-145-4-200608150-00008}}</ref><ref>{{cite journal | vauthors=((Wijemanne, S.)), ((Jankovic, J.)) | journal=Sleep Medicine | title=Restless legs syndrome: clinical presentation diagnosis and treatment | volume=16 | issue=6 | pages=678–690 | date=1 June 2015 | url=https://www.sciencedirect.com/science/article/pii/S1389945715006474 | issn=1389-9457 | doi=10.1016/j.sleep.2015.03.002}}</ref> It is recommended as a first line agent for the treatment of neuropathic pain arising from diabetic neuropathy, post-herpetic neuralgia, and central neuropathic pain.<ref>{{cite journal | vauthors=((Attal, N.)), ((Cruccu, G.)), ((Baron, R.)), ((Haanpää, M.)), ((Hansson, P.)), ((Jensen, T. S.)), ((Nurmikko, T.)) | journal=European Journal of Neurology | title=EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision | volume=17 | issue=9 | pages=1113-e88 | date= September 2010 | issn=1468-1331 | doi=10.1111/j.1468-1331.2010.02999.x}}</ref> | ||
Gabapentin is considered to have low abuse potential compared to most recreational depressants. However, chronic use can lead to physical dependence. Additionally, there is a risk of | [[Subjective effects]] include mild to moderate [[anxiety suppression]], [[pain relief]], and [[muscle relaxation]]. Its analgesic and anxiolytic effects provide gabapentin with some recreational potential in a manner that can be compared to a mild [[benzodiazepine]]. However, these recreational effects are reported to diminish quickly with repeated usage and are typically reported by those who do not have a tolerance to this compound. | ||
Gabapentin is considered to have low abuse potential compared to most recreational depressants. However, chronic use can lead to physical dependence. Additionally, there is a increased risk of fatal overdose when it is combined with other [[depressants]] (a somewhat common practice considering its weak effects). It is highly advised to use [[harm reduction practices]] if using this substance. | |||
==Chemistry== | ==Chemistry== | ||
Gabapentin is a 3,3-disubstituted derivative of GABA. Therefore, it is a GABA analogue, as well as a γ-amino acid.<ref>Wyllie E | Gabapentin is a 3,3-disubstituted derivative of GABA. Therefore, it is a GABA analogue, as well as a γ-amino acid.<ref>{{cite book | vauthors=((Wyllie, E.)) | date= 2012 | title=Wyllie’s treatment of epilepsy: principles and practice. | isbn=9781451153484}}</ref> Specifically, it is a derivative of GABA with a pentyl disubstitution at 3 position, hence, the name - gaba''pentin'', in such a way as to form a six-membered ring. After formation of the ring, the amine and carboxylic groups are not in the same relative positions as they are in the GABA:.<ref>{{cite book | vauthors=((Sneader, W.)) | date= 2005 | title=Drug Discovery A History | url=https://nbn-resolving.org/urn:nbn:de:101:1-201412158328 | isbn=9780470015520}}</ref> they are more conformationally constrained.<ref>{{cite journal | vauthors=((Levandovskiy, I. A.)), ((Sharapa, D. I.)), ((Shamota, T. V.)), ((Rodionov, V. N.)), ((Shubina, T. E.)) | journal=Future Medicinal Chemistry | title=Conformationally restricted GABA analogs: from rigid carbocycles to cage hydrocarbons | volume=3 | issue=2 | pages=223–241 | date= February 2011 | url=https://www.future-science.com/doi/10.4155/fmc.10.287 | issn=1756-8919 | doi=10.4155/fmc.10.287}}</ref> | ||
Gabapentin, or 1-(aminomethyl)cyclohexylacetic acid, is an analogue of the neurotransmitter [[GABA]]. It contains a cyclohexane ring bound to a methylamino chain CH<sub>3</sub>NH<sub>2</sub>. At the same location, R<sub>1</sub>, the cyclohexane ring is also substituted with an acetic acid group. Gabapentin is structurally analogous to GABA. GABA contains an amino group bound to the terminal carbon of a butanoic acid chain. The structure of gabapentin contains the secondary carbon R<sub>3</sub> of the butanoic acid chain in GABA incorporated into an attached cyclohexane ring, converting it into a tertiary carbon while still maintaining the chain. | Gabapentin, or 1-(aminomethyl)cyclohexylacetic acid, is an analogue of the neurotransmitter [[GABA]]. It contains a cyclohexane ring bound to a methylamino chain CH<sub>3</sub>NH<sub>2</sub>. At the same location, R<sub>1</sub>, the cyclohexane ring is also substituted with an acetic acid group. Gabapentin is structurally analogous to GABA. GABA contains an amino group bound to the terminal carbon of a butanoic acid chain. The structure of gabapentin contains the secondary carbon R<sub>3</sub> of the butanoic acid chain in GABA incorporated into an attached cyclohexane ring, converting it into a tertiary carbon while still maintaining the chain. | ||
==Pharmacology== | ==Pharmacology== | ||
Gabapentin modulates the action of [[glutamate]] decarboxylase (GAD) and branched-chain aminotransferase (BCAT), two enzymes involved in [[GABA]] biosynthesis. In human and rat studies, gabapentin was found to increase GABA biosynthesis, and to increase non-synaptic GABA neurotransmission in vitro.<ref>Mechanisms of action of gabapentin | Gabapentin modulates the action of [[glutamate]] decarboxylase (GAD) and branched-chain aminotransferase (BCAT), two enzymes involved in [[GABA]] biosynthesis. In human and rat studies, gabapentin was found to increase GABA biosynthesis, and to increase non-synaptic GABA neurotransmission in vitro.<ref>{{cite journal | vauthors=((Taylor, C. P.)) | journal=Revue Neurologique | title=Mechanisms of action of gabapentin | volume=153 Suppl 1 | pages=S39-45 | date= 1997 | issn=0035-3787}}</ref> As the GABA system is the most prolific inhibitory receptor set within the brain, its increase in biosynthesis results in the [[sedating]] and [[Anxiety_suppression|anxiolytic]] (or [[Anxiety suppression|calming effects]]) of gabapentin on the nervous system. | ||
Another study<ref>The Impact of Gabapentin Administration on Brain GABA and Glutamate Concentrations: A 7T 1H-MRS Study | Another study<ref>{{cite journal | vauthors=((Cai, K.)), ((Nanga, R. P.)), ((Lamprou, L.)), ((Schinstine, C.)), ((Elliott, M.)), ((Hariharan, H.)), ((Reddy, R.)), ((Epperson, C. N.)) | journal=Neuropsychopharmacology | title=The Impact of Gabapentin Administration on Brain GABA and Glutamate Concentrations: A 7T 1H-MRS Study | volume=37 | issue=13 | pages=2764–2771 | date= December 2012 | url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499716/ | issn=0893-133X | doi=10.1038/npp.2012.142}}</ref> based on magnetic resonance imaging done at 7 Tesla confirms that Gabapentin appears to increase cerebral GABA concentrations acutely, in vivo, by up to 79% from baseline. | ||
Gabapentin, as a gabapentinoid, has also been shown to bind to the α2δ-1 subunit of Voltage-Gated Calcium Channels to act as a VGCC blocker, which contributes to its inhibitory, analgesic, and anxiolytic effects.<ref>The mechanisms of action of gabapentin and pregabalin. | Gabapentin, as a gabapentinoid, has also been shown to bind to the α2δ-1 subunit of Voltage-Gated Calcium Channels to act as a VGCC blocker, which contributes to its inhibitory, analgesic, and anxiolytic effects.<ref>{{cite journal | vauthors=((Sills, G. J.)) | journal=Current Opinion in Pharmacology | title=The mechanisms of action of gabapentin and pregabalin | volume=6 | issue=1 | pages=108–113 | date= February 2006 | issn=1471-4892 | doi=10.1016/j.coph.2005.11.003}}</ref> It is uncertain exactly how this method of action contributes to gabapentin's psychoactive effects. | ||
The bioavailability of gabapentin is relatively low and is inversely proportional to the dose (i.e. higher doses have lower bioavailability than lower doses). The bioavailability of gabapentin is approximately 60%, 47%, | The bioavailability of gabapentin is relatively low and is inversely proportional to the dose (i.e. higher doses have lower bioavailability than lower doses). The bioavailability of gabapentin is approximately 60%, 47%, | ||
34%, 33%, and 27% following 900, 1200, 2400, 3600, and 4800 mg/day, given in divided doses of one pill per every 8 hours.<ref>Neurontin Clinical Pharmacology Biopharmaceutics Review | http://www.accessdata.fda.gov/drugsatfda_docs/nda/2002/21-397.pdf_Neurontin_BioPharmr.pdf</ref> Gabapentin is highly lipophilic, making unsaturated fats such as vegetable oil and olive oil significantly boost the total amount of absorption. This means that eating a high fat meal substantially increases gabapentin's bioavailability, due to the fact that unsaturated fats bind to gabapentin to allow for absorption, and that meals slow down and thus increase gabapentin absorption by decreasing gabapentin transporter saturation.<ref> | 34%, 33%, and 27% following 900, 1200, 2400, 3600, and 4800 mg/day, given in divided doses of one pill per every 8 hours.<ref>Neurontin Clinical Pharmacology Biopharmaceutics Review | http://www.accessdata.fda.gov/drugsatfda_docs/nda/2002/21-397.pdf_Neurontin_BioPharmr.pdf</ref> Gabapentin is highly lipophilic, making unsaturated fats such as vegetable oil and olive oil significantly boost the total amount of absorption. This means that eating a high fat meal substantially increases gabapentin's bioavailability, due to the fact that unsaturated fats bind to gabapentin to allow for absorption, and that meals slow down and thus increase gabapentin absorption by decreasing gabapentin transporter saturation.<ref name="NeurotoninMedScape">{{Citation | title=Neurontin, Gralise (gabapentin) dosing, indications, interactions, adverse effects, and more | url=https://reference.medscape.com/drug/neurontin-gralise-gabapentin-343011}}</ref> | ||
Gabapentin transporter saturation occurs when large enough doses of gabapentin are consumed in a short enough period of time to result in the body being unable to absorb any more gabapentin, causing a significant reduction in bioavailability, which largely accounts for the drop in bioavailability seen with increasing doses. | Gabapentin transporter saturation occurs when large enough doses of gabapentin are consumed in a short enough period of time to result in the body being unable to absorb any more gabapentin, causing a significant reduction in bioavailability, which largely accounts for the drop in bioavailability seen with increasing doses. | ||
Gabapentin is a potent activator of voltage-gated potassium channels KCNQ3 and KCNQ5, even at low nanomolar concentrations. However, this activation is unlikely to be the dominant mechanism of gabapentin's therapeutic effects.<ref>Manville | Gabapentin is a potent activator of voltage-gated potassium channels KCNQ3 and KCNQ5, even at low nanomolar concentrations. However, this activation is unlikely to be the dominant mechanism of gabapentin's therapeutic effects.<ref>{{cite journal | vauthors=((Manville, R. W.)), ((Abbott, G. W.)) | journal=Molecular Pharmacology | title=Gabapentin Is a Potent Activator of KCNQ3 and KCNQ5 Potassium Channels | volume=94 | issue=4 | pages=1155–1163 | date=1 October 2018 | url=https://molpharm.aspetjournals.org/content/94/4/1155 | issn=0026-895X | doi=10.1124/mol.118.112953}}</ref> | ||
==Subjective effects== | ==Subjective effects== | ||
The decreasing bioavailability of gabapentin can be lessened by taking lower doses more often instead of higher doses less frequently. As a general rule, using any more than 250-300 mg of gabapentin every 30-45 minutes will result in wasting a significant portion of the total dose of gabapentin, although this number varies depending on the individual. Alkaline environments inhibit the absorption of gabapentin, so lowering the pH of one's stomach using acidic substances (such as soft drinks) will boost bioavailability as well. It is generally not recommended to take antacids 2 hours before or after taking gabapentin, because although not dangerous, it will severely lower the total absorption of gabapentin.<ref> | The decreasing bioavailability of gabapentin can be lessened by taking lower doses more often instead of higher doses less frequently. As a general rule, using any more than 250-300 mg of gabapentin every 30-45 minutes will result in wasting a significant portion of the total dose of gabapentin, although this number varies depending on the individual. Alkaline environments inhibit the absorption of gabapentin, so lowering the pH of one's stomach using acidic substances (such as soft drinks) will boost bioavailability as well. It is generally not recommended to take antacids 2 hours before or after taking gabapentin, because although not dangerous, it will severely lower the total absorption of gabapentin.<ref>{{Citation | title=gabapentin, Michigan Medicine | url=https://www.uofmhealth.org/health-library/d03182a1}}</ref> | ||
{{Preamble/SubjectiveEffects}} | {{Preamble/SubjectiveEffects}} | ||
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*'''[[Effect::Amnesia]]''' - Gabapentin induces a substantially lower amount of amnesia compared to other [[GABA |GABAergic]] drugs such as [[Benzodiazepine |benzodiazepines]]. | *'''[[Effect::Amnesia]]''' - Gabapentin induces a substantially lower amount of amnesia compared to other [[GABA |GABAergic]] drugs such as [[Benzodiazepine |benzodiazepines]]. | ||
*'''[[Effect::Sleepiness]]''' | *'''[[Effect::Sleepiness]]''' | ||
*'''[[Effect::Suicidal ideation]]'''<ref> Anticonvulsant medications and the risk of suicide, attempted suicide, or violent death. | *'''[[Effect::Suicidal ideation]]'''<ref name="Patorno2010">{{cite journal | vauthors=((Patorno, E.)), ((Bohn, R. L.)), ((Wahl, P. M.)), ((Avorn, J.)), ((Patrick, A. R.)), ((Liu, J.)), ((Schneeweiss, S.)) | journal=JAMA | title=Anticonvulsant medications and the risk of suicide, attempted suicide, or violent death | volume=303 | issue=14 | pages=1401–1409 | date=14 April 2010 | issn=1538-3598 | doi=10.1001/jama.2010.410}}</ref> | ||
}} | }} | ||
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{{toxicity}} | {{toxicity}} | ||
[[File:Gabapentin FDA prescription document.jpg|300px|thumbnail|This document, provided with prescription gabapentin, contains detailed information regarding its toxicity and harm potential.]] | [[File:Gabapentin FDA prescription document.jpg|300px|thumbnail|This document, provided with prescription gabapentin, contains detailed information regarding its toxicity and harm potential.]] | ||
GABApentin has a [[Toxicity::low toxicity]] relative to dose. The most common side effects of gabapentin in adult patients include dizziness, fatigue, drowsiness, weight gain, and peripheral edema (swelling of extremities).<ref>http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020235s041,020882s028,021129s027lbl.pdf</ref> Gabapentin may also produce sexual dysfunction in some patients whose symptoms of which may include loss of libido, inability to reach orgasm, and erectile dysfunction.<ref> | GABApentin has a [[Toxicity::low toxicity]] relative to dose. The most common side effects of gabapentin in adult patients include dizziness, fatigue, drowsiness, weight gain, and peripheral edema (swelling of extremities).<ref>http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020235s041,020882s028,021129s027lbl.pdf</ref> Gabapentin may also produce sexual dysfunction in some patients whose symptoms of which may include loss of libido, inability to reach orgasm, and erectile dysfunction.<ref>{{cite book | vauthors=((Aronson, J. K.)) | date=4 March 2014 | title=Side Effects of Drugs Annual: A worldwide yearly survey of new data in adverse drug reactions | publisher=Newnes | isbn=9780444626363}}</ref> Gabapentin should be used carefully in patients with renal impairment due to possible accumulation and toxicity.<ref>http://www.accessdata.fda.gov/drugsatfda_docs/label/2014/020235s057,020882s041,021129s039lbl.pdf</ref> | ||
It is strongly recommended that one use [[responsible drug use|harm reduction practices]] when using this drug. | It is strongly recommended that one use [[responsible drug use|harm reduction practices]] when using this drug. | ||
===Suicide=== | ===Suicide=== | ||
In 2009, the U.S. Food and Drug Administration issued a warning of an increased risk of depression and suicidal thoughts and behaviors in patients taking gabapentin (along with other [[anticonvulsant]] drugs),<ref>http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm100190.htm</ref> modifying the packaging insert to reflect this. A 2010 meta-analysis confirmed the increased risk of suicide associated with gabapentin use.<ref>https:// | In 2009, the U.S. Food and Drug Administration issued a warning of an increased risk of depression and suicidal thoughts and behaviors in patients taking gabapentin (along with other [[anticonvulsant]] drugs),<ref>http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm100190.htm</ref> modifying the packaging insert to reflect this. A 2010 meta-analysis confirmed the increased risk of suicide associated with gabapentin use.<ref name="Patorno2010" /> | ||
In 2010, a study conducted by Patorno E, Bohn RL, Wahl PM, et al, found that the use of gabapentin compared to the use of [[topiramate]] may be associated with an increase in suicidal acts and or violent deaths.<ref>{{cite journal | vauthors=((Patorno, E.)), ((Bohn, R. L.)), ((Wahl, P. M.)), ((Avorn, J.)), ((Patrick, A. R.)), ((Liu, J.)), ((Schneeweiss, S.)) | journal=JAMA | title=Anticonvulsant Medications and the Risk of Suicide, Attempted Suicide, or Violent Death | volume=303 | issue=14 | pages=1401–1409 | date=14 April 2010 | url=https://doi.org/10.1001/jama.2010.410 | issn=0098-7484 | doi=10.1001/jama.2010.410}}</ref> | |||
It should be noted that in both studies along with others that the patients evaluated had a higher suicide risk and the studies were both limited and imprecise.<ref name="Patorno2010" /> | |||
===Lethal dosage=== | ===Lethal dosage=== | ||
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Gabapentin is a prescription-only medicine and can only be prescribed following a consultation with a doctor.{{citation needed}} | Gabapentin is a prescription-only medicine and can only be prescribed following a consultation with a doctor.{{citation needed}} | ||
*'''Germany:''' Gabapentin is a prescription medicine, according to Anlage 1 AMVV.<ref>https://www.gesetze-im-internet.de/amvv/BJNR363210005.html</ref> | *'''Germany:''' Gabapentin is a prescription medicine, according to Anlage 1 AMVV.<ref>{{Citation | title=AMVV - Verordnung über die Verschreibungspflicht von Arzneimitteln | url=https://www.gesetze-im-internet.de/amvv/BJNR363210005.html}}</ref> | ||
*'''Switzerland:''' Gabapentin is listed as a "Abgabekategorie B" pharmaceutical, which requires a prescription.{{citation needed}} | *'''Switzerland:''' Gabapentin is listed as a "Abgabekategorie B" pharmaceutical, which requires a prescription.{{citation needed}} | ||
*'''United States:''' Gabapentin is not a scheduled substance but may only be sold with prescription.<ref>Peckham, A. M., Ananickal, M. J., | *'''United Kingdom''': Gabapentin is available as a prescription.<ref>[https://www.nhs.uk/medicines/baclofen/about-baclofen/ Baclofen: muscle relaxant that relieves muscle spasms - NHS]</ref> | ||
**''' | *'''United States:''' Gabapentin is not a scheduled substance but may only be sold with prescription.<ref>{{cite journal | vauthors=((Peckham, A. M.)), ((Ananickal, M. J.)), ((Sclar, D. A.)) | journal=Risk Management and Healthcare Policy | title=Gabapentin use, abuse, and the US opioid epidemic: the case for reclassification as a controlled substance and the need for pharmacovigilance | volume=11 | pages=109–116 | date=17 August 2018 | url=https://www.dovepress.com/gabapentin-use-abuse-and-the-us-opioid-epidemic-the-case-for-reclassif-peer-reviewed-fulltext-article-RMHP | doi=10.2147/RMHP.S168504}}</ref> | ||
**'''Exceptions:''' Gabapentin is a Schedule 5 controlled substance in: Alabama, Kentucky, Michigan, North Dakota, Tennessee, Virginia, and West Virginia. With prescription drug monitoring in: Connecticut, District of Columbia, Indiana, Kansas, Massachusetts, Minnesota, Nebraska, New Jersey, Ohio, Oregon, Utah, and Wyoming.<ref>{{cite journal | vauthors=((Collins, S.)) | journal=Pharmacy Today | title=More states make gabapentin a Schedule V Controlled Substance | volume=27 | issue=10 | pages=33 | date= October 2021 | url=https://linkinghub.elsevier.com/retrieve/pii/S1042099121007301 | issn=10420991 | doi=10.1016/j.ptdy.2021.09.016}}</ref> | |||
==See also== | ==See also== | ||
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*[[GABA]] | *[[GABA]] | ||
*[[Pregabalin]] | *[[Pregabalin]] | ||
*[[Phenibut]] | |||
==External links== | ==External links== | ||
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*[https://en.wikipedia.org/wiki/Gabapentin Gabapentin (Wikipedia)] | *[https://en.wikipedia.org/wiki/Gabapentin Gabapentin (Wikipedia)] | ||
*[https://www.erowid.org/pharms/gabapentin/ Gabapentin (Erowid Vault)] | *[https://www.erowid.org/pharms/gabapentin/ Gabapentin (Erowid Vault)] | ||
*[https://isomerdesign.com/PiHKAL/explore.php?id=8697 Gabapentin ( | *[https://isomerdesign.com/PiHKAL/explore.php?id=8697 Gabapentin (Isomer Design)] | ||
*[https://go.drugbank.com/drugs/DB00996 Gabapentin (DrugBank)] | |||
*[https://www.drugs.com/gabapentin.html Gabapentin (Drugs.com)] | |||
*[https://drugs-forum.com/wiki/Gabapentin Gabapentin (Drugs-Forum)] | |||
==References== | ==References== | ||
<references /> | <references /> | ||
[[Category:Psychoactive substance]] | [[Category:Psychoactive substance]] | ||
[[Category:Cycloalkylamine]] | |||
[[Category:Gamma-Amino acid]] | |||
[[Category:Depressant]] | [[Category:Depressant]] | ||
[[Category:Anxiolytics]] | [[Category:Anxiolytics]] | ||
[[Category:Gabapentinoid]] | [[Category:Gabapentinoid]] | ||
{{#set:Featured=true}} | |||