Classes - Revision history

MDElliottMD: Em-dash sweep: replace em-dash with comma per project rule; PendellsCorner verbatim quotes preserved.

2026-05-19T03:16:06Z

Em-dash sweep: replace em-dash with comma per project rule; PendellsCorner verbatim quotes preserved.

← Older revision		Revision as of 03:16, 19 May 2026
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	=== Monoamine Oxidase Inhibitors (MAOIs) ===		=== Monoamine Oxidase Inhibitors (MAOIs) ===
	Inhibit MAO-A and/or MAO-B, increasing monoamine levels. Require strict dietary and med interaction precautions. Subclasses:		Inhibit MAO-A and/or MAO-B, increasing monoamine levels. Require strict dietary and med interaction precautions. Subclasses:
	* '''Irreversible non-selective MAOIs''' — inhibit both MAO-A and MAO-B permanently		* '''Irreversible non-selective MAOIs''', inhibit both MAO-A and MAO-B permanently
	* '''Reversible MAO-A inhibitors (RIMAs)''' — safer interaction profile; displaceable by tyramine		* '''Reversible MAO-A inhibitors (RIMAs)''', safer interaction profile; displaceable by tyramine
	* '''Selective MAO-B inhibitors''' — used primarily in Parkinson's disease; antidepressant at higher doses		* '''Selective MAO-B inhibitors''', used primarily in Parkinson's disease; antidepressant at higher doses

	=== Noradrenergic and Specific Serotonergic Antidepressants (NaSSAs) ===		=== Noradrenergic and Specific Serotonergic Antidepressants (NaSSAs) ===
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	=== First-Generation Antipsychotics (FGAs / Typicals) ===		=== First-Generation Antipsychotics (FGAs / Typicals) ===
	Primarily D2 receptor antagonists. Effective for positive symptoms; high risk of extrapyramidal side effects and tardive dyskinesia. Subclasses by chemical structure:		Primarily D2 receptor antagonists. Effective for positive symptoms; high risk of extrapyramidal side effects and tardive dyskinesia. Subclasses by chemical structure:
	* '''Phenothiazines''' — chlorpromazine, fluphenazine, perphenazine, thioridazine, trifluoperazine, prochlorperazine		* '''Phenothiazines''', chlorpromazine, fluphenazine, perphenazine, thioridazine, trifluoperazine, prochlorperazine
	* '''Butyrophenones''' — haloperidol, droperidol		* '''Butyrophenones''', haloperidol, droperidol
	* '''Thioxanthenes''' — thiothixene		* '''Thioxanthenes''', thiothixene
	* '''Dibenzoxazepines''' — loxapine		* '''Dibenzoxazepines''', loxapine
	* '''Dihydroindolones''' — molindone		* '''Dihydroindolones''', molindone
	* '''Diphenylbutylpiperidines''' — pimozide		* '''Diphenylbutylpiperidines''', pimozide

	=== Second-Generation Antipsychotics (SGAs / Atypicals) ===		=== Second-Generation Antipsychotics (SGAs / Atypicals) ===
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	=== Beta Blockers (peripheral somatic anxiolytic) ===		=== Beta Blockers (peripheral somatic anxiolytic) ===
	β-adrenergic receptor antagonists. While primarily cardiovascular meds, they are widely used off-label as peripheral anxiolytics — blunting the somatic (tachycardia, tremor, sweating) manifestations of acute anxiety without sedation or dependence liability. Particularly useful for performance anxiety, akathisia, and essential tremor. [[Propranolol]] is the prototype. See [[:Category:Beta Blockers]].		β-adrenergic receptor antagonists. While primarily cardiovascular meds, they are widely used off-label as peripheral anxiolytics, blunting the somatic (tachycardia, tremor, sweating) manifestations of acute anxiety without sedation or dependence liability. Particularly useful for performance anxiety, akathisia, and essential tremor. [[Propranolol]] is the prototype. See [[:Category:Beta Blockers]].

	== Stimulants & Wake-Promoting Agents ==		== Stimulants & Wake-Promoting Agents ==
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	=== Mu-Opioid Receptor Agonists ===		=== Mu-Opioid Receptor Agonists ===
	Analgesia, euphoria, sedation, respiratory depression, and constipation via mu (μ) opioid receptors. The primary class for moderate-to-severe pain management. Subclasses:		Analgesia, euphoria, sedation, respiratory depression, and constipation via mu (μ) opioid receptors. The primary class for moderate-to-severe pain management. Subclasses:
	* '''Natural opioids''' — derived directly from the opium poppy		* '''Natural opioids''', derived directly from the opium poppy
	* '''Semisynthetic opioids''' — modified natural opioids		* '''Semisynthetic opioids''', modified natural opioids
	* '''Synthetic opioids''' — fully synthetic; no plant-derived precursors		* '''Synthetic opioids''', fully synthetic; no plant-derived precursors

	=== Partial Mu-Opioid Agonists ===		=== Partial Mu-Opioid Agonists ===
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	== Antihistamines ==		== Antihistamines ==
	H1 receptor antagonists. First-generation agents cross the blood-brain barrier and produce sedation, anticholinergic effects, and at high doses, delirium. Divided by generation:		H1 receptor antagonists. First-generation agents cross the blood-brain barrier and produce sedation, anticholinergic effects, and at high doses, delirium. Divided by generation:
	* '''First-generation''' — lipophilic; CNS-penetrant; sedating; anticholinergic		* '''First-generation''', lipophilic; CNS-penetrant; sedating; anticholinergic
	* '''Second-generation''' — less CNS penetration; non-sedating		* '''Second-generation''', less CNS penetration; non-sedating

	== Addiction Med ==		== Addiction Med ==
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	=== Classical Psychedelics (Serotonergic) ===		=== Classical Psychedelics (Serotonergic) ===
	Primary mechanism is agonism at 5-HT2A receptors in the cortex, producing profound alterations in perception, cognition, and sense of self. Subclasses by chemical scaffold:		Primary mechanism is agonism at 5-HT2A receptors in the cortex, producing profound alterations in perception, cognition, and sense of self. Subclasses by chemical scaffold:
	* '''Tryptamines''' — indole alkaloids structurally related to serotonin		* '''Tryptamines''', indole alkaloids structurally related to serotonin
	* '''Lysergamides''' — ergoline derivatives of lysergic acid		* '''Lysergamides''', ergoline derivatives of lysergic acid
	* '''Phenethylamines''' — related to the catecholamine scaffold (mescaline and analogues)		* '''Phenethylamines''', related to the catecholamine scaffold (mescaline and analogues)
	* '''2C-x series''' — 2,5-dimethoxyphenethylamines		* '''2C-x series''', 2,5-dimethoxyphenethylamines
	* '''DOx series''' — amphetamine-based phenethylamines; very long duration		* '''DOx series''', amphetamine-based phenethylamines; very long duration
	* '''NBOMe / NBOH series''' — N-benzyl derivatives; extremely potent; no oral activity		* '''NBOMe / NBOH series''', N-benzyl derivatives; extremely potent; no oral activity

	=== Empathogens / Entactogens ===		=== Empathogens / Entactogens ===
	Primarily monoamine-releasing agents (especially serotonin) with partial 5-HT2A agonism. Produce emotional openness and prosocial effects. Core subclasses:		Primarily monoamine-releasing agents (especially serotonin) with partial 5-HT2A agonism. Produce emotional openness and prosocial effects. Core subclasses:
	* '''MDxx''' — methylenedioxy-substituted amphetamines and cathinones		* '''MDxx''', methylenedioxy-substituted amphetamines and cathinones
	* '''Benzofurans''' — related scaffold; primarily serotonergic		* '''Benzofurans''', related scaffold; primarily serotonergic

	=== Dissociatives ===		=== Dissociatives ===
	NMDA receptor antagonists producing dose-dependent detachment from self and environment. At sub-anesthetic doses: analgesia, euphoria, perceptual distortion. Subclasses:		NMDA receptor antagonists producing dose-dependent detachment from self and environment. At sub-anesthetic doses: analgesia, euphoria, perceptual distortion. Subclasses:
	* '''Arylcyclohexylamines''' — ketamine, PCP, and analogues; σ1 and dopaminergic activity		* '''Arylcyclohexylamines''', ketamine, PCP, and analogues; σ1 and dopaminergic activity
	* '''Morphinans''' — dextromethorphan, dextrorphan; also sigma-1 and serotonergic		* '''Morphinans''', dextromethorphan, dextrorphan; also sigma-1 and serotonergic
	* '''Diarylethylamines''' — diphenidine and related		* '''Diarylethylamines''', diphenidine and related
	* '''Adamantanes''' — memantine		* '''Adamantanes''', memantine
	* '''Other''' — nitrous oxide, xenon		* '''Other''', nitrous oxide, xenon

	=== Deliriants ===		=== Deliriants ===
	Produce a state of true delirium — confusion, disorientation, and realistic hallucinations indistinguishable from reality. Subclasses:		Produce a state of true delirium, confusion, disorientation, and realistic hallucinations indistinguishable from reality. Subclasses:
	* '''Anticholinergics (muscarinic antagonists)''' — block muscarinic acetylcholine receptors; atropine, scopolamine, hyoscyamine, diphenhydramine		* '''Anticholinergics (muscarinic antagonists)''', block muscarinic acetylcholine receptors; atropine, scopolamine, hyoscyamine, diphenhydramine
	* '''Kainate / AMPA agonists''' — ibotenic acid		* '''Kainate / AMPA agonists''', ibotenic acid
	* '''GABAA agonists (at sedating doses)''' — muscimol		* '''GABAA agonists (at sedating doses)''', muscimol
	* '''Other''' — benzydamine, myristicin		* '''Other''', benzydamine, myristicin

	=== κ-Opioid Agonists ===		=== κ-Opioid Agonists ===

MDElliottMD: Sweep: "indications" -> "problems" sitewide terminology update (preserves MedTemplate param name)

2026-05-19T01:37:44Z

Sweep: "indications" -> "problems" sitewide terminology update (preserves MedTemplate param name)

← Older revision		Revision as of 01:37, 19 May 2026
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	=== Pharmaceutical Cannabinoids ===		=== Pharmaceutical Cannabinoids ===
	Regulated preparations of naturally-derived or synthetic cannabinoids approved for specific ~~indications~~.		Regulated preparations of naturally-derived or synthetic cannabinoids approved for specific problems.

	== Nootropics ==		== Nootropics ==

Maintenance script: Terminology: medicine → med (shorter form per user preference)

2026-05-16T02:42:47Z

Terminology: medicine → med (shorter form per user preference)

← Older revision		Revision as of 02:42, 16 May 2026
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	This page is a reference taxonomy of pharmacological '''classes''' used throughout Pharmacopedia. Click any class name to browse its members. Individual ~~medicines~~ are listed on the [[List of CNS-active medicines]] page.		This page is a reference taxonomy of pharmacological '''classes''' used throughout Pharmacopedia. Click any class name to browse its members. Individual meds are listed on the [[List of CNS-active medicines]] page.

	__TOC__		__TOC__
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	=== Monoamine Oxidase Inhibitors (MAOIs) ===		=== Monoamine Oxidase Inhibitors (MAOIs) ===
	Inhibit MAO-A and/or MAO-B, increasing monoamine levels. Require strict dietary and ~~medicine~~ interaction precautions. Subclasses:		Inhibit MAO-A and/or MAO-B, increasing monoamine levels. Require strict dietary and med interaction precautions. Subclasses:
	* '''Irreversible non-selective MAOIs''' — inhibit both MAO-A and MAO-B permanently		* '''Irreversible non-selective MAOIs''' — inhibit both MAO-A and MAO-B permanently
	* '''Reversible MAO-A inhibitors (RIMAs)''' — safer interaction profile; displaceable by tyramine		* '''Reversible MAO-A inhibitors (RIMAs)''' — safer interaction profile; displaceable by tyramine
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	=== Beta Blockers (peripheral somatic anxiolytic) ===		=== Beta Blockers (peripheral somatic anxiolytic) ===
	β-adrenergic receptor antagonists. While primarily cardiovascular ~~medicines~~, they are widely used off-label as peripheral anxiolytics — blunting the somatic (tachycardia, tremor, sweating) manifestations of acute anxiety without sedation or dependence liability. Particularly useful for performance anxiety, akathisia, and essential tremor. [[Propranolol]] is the prototype. See [[:Category:Beta Blockers]].		β-adrenergic receptor antagonists. While primarily cardiovascular meds, they are widely used off-label as peripheral anxiolytics — blunting the somatic (tachycardia, tremor, sweating) manifestations of acute anxiety without sedation or dependence liability. Particularly useful for performance anxiety, akathisia, and essential tremor. [[Propranolol]] is the prototype. See [[:Category:Beta Blockers]].

	== Stimulants & Wake-Promoting Agents ==		== Stimulants & Wake-Promoting Agents ==
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	Many anticonvulsants are also used for pain, migraine prophylaxis, mood stabilization, or anxiety.		Many anticonvulsants are also used for pain, migraine prophylaxis, mood stabilization, or anxiety.

	== Antiparkinsonian ~~Medicines~~ ==		== Antiparkinsonian Meds ==

	=== Dopamine Precursors ===		=== Dopamine Precursors ===
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	Reduce glutamate-mediated excitotoxicity and may reduce dyskinesias. Amantadine also has dopamine-releasing effects.		Reduce glutamate-mediated excitotoxicity and may reduce dyskinesias. Amantadine also has dopamine-releasing effects.

	== Anti-Dementia ~~Medicines~~ ==		== Anti-Dementia Meds ==

	=== Acetylcholinesterase Inhibitors (AChEIs) ===		=== Acetylcholinesterase Inhibitors (AChEIs) ===
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	* '''Second-generation''' — less CNS penetration; non-sedating		* '''Second-generation''' — less CNS penetration; non-sedating

	== Addiction ~~Medicine~~ ==		== Addiction Med ==
	~~Medicines~~ used to treat substance use disorders. Mechanisms are specific to the target substance:		Meds used to treat substance use disorders. Mechanisms are specific to the target substance:
	* Opioid agonist therapy (methadone, buprenorphine)		* Opioid agonist therapy (methadone, buprenorphine)
	* Opioid antagonists (naltrexone, naloxone, nalmefene)		* Opioid antagonists (naltrexone, naloxone, nalmefene)
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	* Alpha-2 agonists for withdrawal (clonidine, lofexidine)		* Alpha-2 agonists for withdrawal (clonidine, lofexidine)

	== Migraine ~~Medicines~~ ==		== Migraine Meds ==

	=== Triptans (5-HT1B/1D Agonists) ===		=== Triptans (5-HT1B/1D Agonists) ===
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	== Research Materials ==		== Research Materials ==
	Compounds primarily of research interest, with limited or no human clinical approval. Many are analogues of approved ~~medicines~~ or classical psychoactive substances. Use of the term '''material''' is preferred over "~~medicine~~" or "substance" in this context.		Compounds primarily of research interest, with limited or no human clinical approval. Many are analogues of approved meds or classical psychoactive substances. Use of the term '''material''' is preferred over "med" or "substance" in this context.

	=== Lysergamides ===		=== Lysergamides ===

Maintenance script: Terminology sweep (site-wide): drug/medication → medicine

2026-05-16T02:30:57Z

Terminology sweep (site-wide): drug/medication → medicine

← Older revision		Revision as of 02:30, 16 May 2026
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	=== Monoamine Oxidase Inhibitors (MAOIs) ===		=== Monoamine Oxidase Inhibitors (MAOIs) ===
	Inhibit MAO-A and/or MAO-B, increasing monoamine levels. Require strict dietary and ~~drug~~ interaction precautions. Subclasses:		Inhibit MAO-A and/or MAO-B, increasing monoamine levels. Require strict dietary and medicine interaction precautions. Subclasses:
	* '''Irreversible non-selective MAOIs''' — inhibit both MAO-A and MAO-B permanently		* '''Irreversible non-selective MAOIs''' — inhibit both MAO-A and MAO-B permanently
	* '''Reversible MAO-A inhibitors (RIMAs)''' — safer interaction profile; displaceable by tyramine		* '''Reversible MAO-A inhibitors (RIMAs)''' — safer interaction profile; displaceable by tyramine
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	== Research Materials ==		== Research Materials ==
	Compounds primarily of research interest, with limited or no human clinical approval. Many are analogues of approved medicines or classical psychoactive substances. Use of the term '''material''' is preferred over "~~drug~~" or "substance" in this context.		Compounds primarily of research interest, with limited or no human clinical approval. Many are analogues of approved medicines or classical psychoactive substances. Use of the term '''material''' is preferred over "medicine" or "substance" in this context.

	=== Lysergamides ===		=== Lysergamides ===

MDElliottMD: Add Beta Blockers subsection under Anxiolytics & Sedative-Hypnotics

2026-05-15T07:23:14Z

Add Beta Blockers subsection under Anxiolytics & Sedative-Hypnotics

← Older revision		Revision as of 07:23, 15 May 2026
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	=== Barbiturates ===		=== Barbiturates ===
	Potentiate and directly activate GABAA receptors at higher concentrations. Older class; narrow therapeutic index; high overdose and dependence risk.		Potentiate and directly activate GABAA receptors at higher concentrations. Older class; narrow therapeutic index; high overdose and dependence risk.

			=== Beta Blockers (peripheral somatic anxiolytic) ===
			β-adrenergic receptor antagonists. While primarily cardiovascular medicines, they are widely used off-label as peripheral anxiolytics — blunting the somatic (tachycardia, tremor, sweating) manifestations of acute anxiety without sedation or dependence liability. Particularly useful for performance anxiety, akathisia, and essential tremor. [[Propranolol]] is the prototype. See [[:Category:Beta Blockers]].

	== Stimulants & Wake-Promoting Agents ==		== Stimulants & Wake-Promoting Agents ==

MDElliottMD: Add medicine classes taxonomy page

2026-05-13T02:08:11Z

Add medicine classes taxonomy page

New page

This page is a reference taxonomy of pharmacological '''classes''' used throughout Pharmacopedia. Click any class name to browse its members. Individual medicines are listed on the [[List of CNS-active medicines]] page.

__TOC__

== Antidepressants ==

=== Selective Serotonin Reuptake Inhibitors (SSRIs) ===
Block presynaptic reuptake of serotonin via SERT. First-line for most depressive and anxiety disorders.

=== Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs) ===
Block reuptake of both serotonin and norepinephrine. Used in depression, anxiety, and neuropathic pain.

=== Norepinephrine–Dopamine Reuptake Inhibitors (NDRIs) ===
Block reuptake of norepinephrine and dopamine. Minimal serotonergic activity; lower sexual side-effect burden.

=== Norepinephrine Reuptake Inhibitors (NRIs) ===
Selective for norepinephrine reuptake. Used in depression and ADHD.

=== Tricyclic Antidepressants (TCAs) ===
Older class; block SERT and NET with broad receptor antagonism (H1, muscarinic, alpha-1). High side-effect burden; significant overdose risk.

=== Monoamine Oxidase Inhibitors (MAOIs) ===
Inhibit MAO-A and/or MAO-B, increasing monoamine levels. Require strict dietary and drug interaction precautions. Subclasses:
* '''Irreversible non-selective MAOIs''' — inhibit both MAO-A and MAO-B permanently
* '''Reversible MAO-A inhibitors (RIMAs)''' — safer interaction profile; displaceable by tyramine
* '''Selective MAO-B inhibitors''' — used primarily in Parkinson's disease; antidepressant at higher doses

=== Noradrenergic and Specific Serotonergic Antidepressants (NaSSAs) ===
Alpha-2 antagonists that increase norepinephrine and serotonin release; also potent H1 antagonists (sedating).

=== Serotonin Antagonist and Reuptake Inhibitors (SARIs) ===
Block SERT and antagonize 5-HT2A/2C receptors. Sedating; low sexual side-effect burden.

=== Melatonin Agonist / Serotonin Antagonist ===
Agonism at MT1/MT2 melatonin receptors and 5-HT2C antagonism; circadian-focused antidepressant mechanism.

=== Multimodal Serotonergic Agents ===
Act on multiple serotonin receptor subtypes simultaneously (SERT inhibition + receptor agonism/antagonism).

== Antipsychotics / Neuroleptics ==

=== First-Generation Antipsychotics (FGAs / Typicals) ===
Primarily D2 receptor antagonists. Effective for positive symptoms; high risk of extrapyramidal side effects and tardive dyskinesia. Subclasses by chemical structure:
* '''Phenothiazines''' — chlorpromazine, fluphenazine, perphenazine, thioridazine, trifluoperazine, prochlorperazine
* '''Butyrophenones''' — haloperidol, droperidol
* '''Thioxanthenes''' — thiothixene
* '''Dibenzoxazepines''' — loxapine
* '''Dihydroindolones''' — molindone
* '''Diphenylbutylpiperidines''' — pimozide

=== Second-Generation Antipsychotics (SGAs / Atypicals) ===
D2 and 5-HT2A antagonists (or partial agonists). Lower EPS risk; higher metabolic side-effect burden.

=== Third-Generation Antipsychotics ===
D2/D3 partial agonists with 5-HT1A partial agonism. Intended to stabilize rather than fully block dopamine signaling.

== Mood Stabilizers ==
Reduce episode frequency and severity in bipolar disorder. Mechanisms vary widely:
* Sodium channel blockers
* GABA enhancers
* Histone deacetylase inhibitors
* Unknown/multiple mechanisms (lithium)

== Anxiolytics & Sedative-Hypnotics ==

=== Benzodiazepines ===
Positive allosteric modulators at GABAA receptors (benzodiazepine site). Increase chloride channel opening frequency. Used for anxiety, seizures, muscle spasm, alcohol withdrawal, and procedural sedation. Dependence liability with chronic use.

=== Thienodiazepines ===
Structurally related to benzodiazepines with a thiophene ring substitution. Similar mechanism and effects.

=== Z-Drugs (Non-Benzodiazepine Hypnotics) ===
GABAA positive allosteric modulators with greater selectivity for alpha-1-containing receptors. Primarily hypnotic; lower anxiolytic/anticonvulsant activity than benzodiazepines.

=== Orexin Receptor Antagonists ===
Block orexin (hypocretin) signaling to promote sleep onset and maintenance. Lower dependence potential than GABAergic hypnotics.

=== Azapirones ===
5-HT1A partial agonists with D2 antagonism. Anxiolytic without sedation or dependence; slow onset of effect.

=== Barbiturates ===
Potentiate and directly activate GABAA receptors at higher concentrations. Older class; narrow therapeutic index; high overdose and dependence risk.

== Stimulants & Wake-Promoting Agents ==

=== Amphetamines ===
Monoamine releasing agents; reverse transporter function to flood the synapse with dopamine, norepinephrine, and (to varying degrees) serotonin. Used for ADHD, narcolepsy, and obesity.

=== Methylphenidates (Phenidates) ===
Dopamine and norepinephrine reuptake inhibitors; structurally distinct from amphetamines. First-line for ADHD.

=== Eugeroics (Wakefulness-Promoting Agents) ===
Promote wakefulness through incompletely understood mechanisms involving dopamine reuptake inhibition and orexin pathway activation. Lower abuse potential than amphetamines.

=== Xanthines ===
Adenosine receptor antagonists. Mild CNS stimulation; widely consumed (caffeine). Theophylline also inhibits phosphodiesterase.

=== Alpha-2 Agonists (for ADHD) ===
Activate presynaptic and postsynaptic alpha-2A adrenergic receptors in prefrontal cortex. Non-stimulant; used for ADHD, tics, and opioid/nicotine withdrawal.

=== Norepinephrine Reuptake Inhibitors (ADHD) ===
Selective NET inhibitors approved for ADHD. Non-stimulant; full antidepressant-level NRI activity.

=== Histamine H3 Antagonists / Inverse Agonists ===
Block presynaptic H3 autoreceptors, increasing histamine (and other monoamine) release. Used for narcolepsy with cataplexy.

== Opioids ==

=== Mu-Opioid Receptor Agonists ===
Analgesia, euphoria, sedation, respiratory depression, and constipation via mu (μ) opioid receptors. The primary class for moderate-to-severe pain management. Subclasses:
* '''Natural opioids''' — derived directly from the opium poppy
* '''Semisynthetic opioids''' — modified natural opioids
* '''Synthetic opioids''' — fully synthetic; no plant-derived precursors

=== Partial Mu-Opioid Agonists ===
Ceiling effect on respiratory depression; used for addiction treatment and pain.

=== Mixed Agonist-Antagonists ===
Kappa agonists with mu partial agonism or antagonism. Analgesic but may precipitate withdrawal in opioid-dependent patients.

=== Kappa-Opioid Receptor Agonists ===
Dysphoria, hallucinations, sedation, analgesia. Endogenous stress response mediators; relevant to dissociative and psychedelic pharmacology.

=== Opioid Antagonists ===
Competitive blockade of opioid receptors. Used for overdose reversal and addiction treatment.

=== Opioid Receptor Modulator + NMDA Antagonists ===
Dual-mechanism opioids that add NMDA antagonism (methadone, levorphanol). Useful for complex pain; longer half-life.

== GABAergics ==

=== GABAB Receptor Agonists ===
Activate metabotropic GABAB receptors. Muscle relaxation, analgesia, euphoria/reinforcement at high doses. Includes baclofen and sodium oxybate (GHB).

=== GABAA Positive Allosteric Modulators (General) ===
Enhance chloride influx via GABAA receptors. Umbrella category covering benzodiazepines, barbiturates, Z-drugs, neurosteroids, and several other classes.

=== GABA Reuptake Inhibitors ===
Block GAT-1 transporter to raise synaptic GABA. Anticonvulsant application.

=== GABA-Transaminase Inhibitors ===
Irreversibly inhibit the enzyme that degrades GABA, raising brain GABA levels overall. Anticonvulsant.

=== GHB Receptor Agonists ===
Activate the endogenous GHB receptor in addition to GABAB. Sedative-hypnotic; used for narcolepsy and alcohol withdrawal.

== Anticonvulsants / Antiepileptics ==
Heterogeneous class united by seizure suppression. Mechanisms include:
* Sodium channel blockers
* Calcium channel blockers (T-type or N/P/Q-type)
* GABA enhancement (multiple mechanisms)
* Glutamate/AMPA antagonists
* SV2A ligands (synaptic vesicle protein)
* Carbonic anhydrase inhibitors

Many anticonvulsants are also used for pain, migraine prophylaxis, mood stabilization, or anxiety.

== Antiparkinsonian Medicines ==

=== Dopamine Precursors ===
Levodopa, converted to dopamine in the brain, replenishes the depleted dopaminergic pathway in Parkinson's disease.

=== Dopamine Agonists ===
Directly stimulate D2/D3 receptors, bypassing presynaptic neurons. Also used for restless legs syndrome and hyperprolactinemia.

=== MAO-B Inhibitors ===
Reduce dopamine catabolism in the striatum by inhibiting the MAO-B isoform. Mild antiparkinsonian and neuroprotective effects.

=== COMT Inhibitors ===
Reduce peripheral and central metabolism of levodopa, extending its duration of action.

=== Anticholinergics (Antiparkinsonian) ===
Reduce the relative excess of cholinergic activity resulting from dopamine depletion in the striatum. Effective for tremor; significant cognitive side effects.

=== NMDA Antagonists (Antiparkinsonian) ===
Reduce glutamate-mediated excitotoxicity and may reduce dyskinesias. Amantadine also has dopamine-releasing effects.

== Anti-Dementia Medicines ==

=== Acetylcholinesterase Inhibitors (AChEIs) ===
Prevent the breakdown of acetylcholine, increasing cholinergic transmission in the cortex and hippocampus. First-line for Alzheimer's and other dementias.

=== NMDA Receptor Antagonists ===
Block pathological NMDA receptor overactivation (excitotoxicity). Used adjunctively in moderate-to-severe Alzheimer's.

=== Anti-Amyloid Monoclonal Antibodies ===
Clear amyloid-beta plaques from the brain. Disease-modifying approach; newer class with contested clinical benefit.

== Anesthetics ==

=== General (IV) Anesthetics ===
Intravenous agents for induction and/or maintenance of anesthesia. Mechanisms vary:
* GABAA potentiators (propofol, etomidate, barbiturates)
* NMDA antagonists (ketamine)

=== Inhalational Anesthetics ===
Volatile agents for maintenance of anesthesia. Primarily GABAA potentiation and NMDA antagonism. Dose-dependent CNS depression.

=== Dissociative Anesthetics ===
NMDA antagonists producing analgesia, amnesia, and cataleptic state without loss of airway reflexes. See [[#Dissociatives]].

=== Local Anesthetics ===
Sodium channel blockers that block nerve conduction locally. CNS toxicity (including seizures) may occur with systemic absorption.

=== Alpha-2 Agonist Sedatives ===
Dexmedetomidine: highly selective alpha-2A agonist producing sedation that closely resembles natural sleep. Used for ICU sedation and procedural sedation.

== Muscle Relaxants (CNS-acting) ==
Centrally-acting agents that reduce skeletal muscle tone via spinal cord or supraspinal mechanisms. Distinct from peripherally-acting neuromuscular blocking agents.

== Antihistamines ==
H1 receptor antagonists. First-generation agents cross the blood-brain barrier and produce sedation, anticholinergic effects, and at high doses, delirium. Divided by generation:
* '''First-generation''' — lipophilic; CNS-penetrant; sedating; anticholinergic
* '''Second-generation''' — less CNS penetration; non-sedating

== Addiction Medicine ==
Medicines used to treat substance use disorders. Mechanisms are specific to the target substance:
* Opioid agonist therapy (methadone, buprenorphine)
* Opioid antagonists (naltrexone, naloxone, nalmefene)
* Aversion agents (disulfiram)
* NMDA/GABA modulators for alcohol (acamprosate)
* Nicotinic partial agonists (varenicline)
* Alpha-2 agonists for withdrawal (clonidine, lofexidine)

== Migraine Medicines ==

=== Triptans (5-HT1B/1D Agonists) ===
Selective serotonin agonists at 5-HT1B and 5-HT1D receptors. Cause vasoconstriction and inhibit trigeminal pain transmission. Acute treatment.

=== Gepants (CGRP Receptor Antagonists) ===
Block calcitonin gene-related peptide (CGRP) receptors. Effective for acute and preventive migraine treatment without vasoconstriction.

=== Ditans (5-HT1F Agonists) ===
Serotonin agonists selective for the 5-HT1F receptor. Inhibit trigeminal pain without vasoconstriction; CNS side effects (dizziness, sedation) are common.

=== Ergotamines ===
Ergot alkaloids; 5-HT1B/1D agonists with additional vasoconstrictor activity. Older class; significant side-effect burden.

== Psychedelics ==

=== Classical Psychedelics (Serotonergic) ===
Primary mechanism is agonism at 5-HT2A receptors in the cortex, producing profound alterations in perception, cognition, and sense of self. Subclasses by chemical scaffold:
* '''Tryptamines''' — indole alkaloids structurally related to serotonin
* '''Lysergamides''' — ergoline derivatives of lysergic acid
* '''Phenethylamines''' — related to the catecholamine scaffold (mescaline and analogues)
* '''2C-x series''' — 2,5-dimethoxyphenethylamines
* '''DOx series''' — amphetamine-based phenethylamines; very long duration
* '''NBOMe / NBOH series''' — N-benzyl derivatives; extremely potent; no oral activity

=== Empathogens / Entactogens ===
Primarily monoamine-releasing agents (especially serotonin) with partial 5-HT2A agonism. Produce emotional openness and prosocial effects. Core subclasses:
* '''MDxx''' — methylenedioxy-substituted amphetamines and cathinones
* '''Benzofurans''' — related scaffold; primarily serotonergic

=== Dissociatives ===
NMDA receptor antagonists producing dose-dependent detachment from self and environment. At sub-anesthetic doses: analgesia, euphoria, perceptual distortion. Subclasses:
* '''Arylcyclohexylamines''' — ketamine, PCP, and analogues; σ1 and dopaminergic activity
* '''Morphinans''' — dextromethorphan, dextrorphan; also sigma-1 and serotonergic
* '''Diarylethylamines''' — diphenidine and related
* '''Adamantanes''' — memantine
* '''Other''' — nitrous oxide, xenon

=== Deliriants ===
Produce a state of true delirium — confusion, disorientation, and realistic hallucinations indistinguishable from reality. Subclasses:
* '''Anticholinergics (muscarinic antagonists)''' — block muscarinic acetylcholine receptors; atropine, scopolamine, hyoscyamine, diphenhydramine
* '''Kainate / AMPA agonists''' — ibotenic acid
* '''GABAA agonists (at sedating doses)''' — muscimol
* '''Other''' — benzydamine, myristicin

=== κ-Opioid Agonists ===
Kappa receptor activation produces dysphoric, dissociative, and oneirogenic effects distinct from classical psychedelics and mu-opioid analgesia.

== Cannabinoids ==

=== Phytocannabinoids ===
Naturally occurring compounds in ''Cannabis sativa''. Act primarily at CB1 (CNS) and CB2 (immune) receptors.

=== Synthetic Cannabinoids ===
Fully synthetic full agonists at CB1/CB2. Often far more potent than THC; unpredictable toxicity profile.

=== Pharmaceutical Cannabinoids ===
Regulated preparations of naturally-derived or synthetic cannabinoids approved for specific indications.

== Nootropics ==

=== Racetams ===
Positive allosteric modulators at AMPA receptors; some also affect choline uptake or acetylcholine synthesis.

=== Eugeroics ===
See [[#Eugeroics (Wakefulness-Promoting Agents)]] above.

=== Peptide Nootropics ===
Short peptide sequences (e.g., Semax) with neurotrophic and neuroprotective activity.

=== Dietary Precursors and Cofactors ===
Amino acids, vitamins, and metabolites that support neurotransmitter synthesis or neuronal function.

== Research Materials ==
Compounds primarily of research interest, with limited or no human clinical approval. Many are analogues of approved medicines or classical psychoactive substances. Use of the term '''material''' is preferred over "drug" or "substance" in this context.

=== Lysergamides ===
LSD analogues and prodrugs, typically N-substituted at the amide position. Share the ergoline scaffold.

=== Novel Tryptamines ===
4-substituted and 5-substituted tryptamine analogues. Many are prodrugs of known psychedelics (e.g., 4-AcO-DMT → psilocin).

=== Novel Phenethylamines ===
Analogues of mescaline, 2C-x, and DOx compounds. Potency varies enormously; some (NBOMe series) are active at microgram doses.

=== Cathinones ===
Beta-keto amphetamine analogues. Stimulant and/or empathogenic; high abuse potential.

=== Pyrrolidinophenones ===
Cathinone-related stimulants with pyrrolidine ring substitution. Potent dopamine/norepinephrine reuptake inhibitors.

=== Novel Amphetamines ===
Fluorinated and other amphetamine analogues with modified pharmacokinetic or receptor profiles.

=== Novel Phenidates ===
Methylphenidate analogues with modified ester or ring substitutions.

=== Novel Dissociatives (Arylcyclohexylamines) ===
Ketamine and PCP analogues with various halogen, methoxy, or hydroxyl substitutions altering potency, duration, and receptor selectivity.

=== Novel / Designer Benzodiazepines ===
Benzodiazepine analogues including triazolo- and thienodiazepines. Structural modifications alter potency, duration, and subunit selectivity.

=== Beta-Carbolines ===
MAOI-active alkaloids found in plants used in ayahuasca preparations (harmine, harmaline, tetrahydroharmine). Also exhibit NMDA antagonism and 5-HT2A activity at higher doses.

== See also ==
* [[List of CNS-active medicines]]
* [[Main Page]]

[[Category:Reference]]
[[Category:Medicines]]