Classes

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.

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 med 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.

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.

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 Meds

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 Meds

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 Med

Meds 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 Meds

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 problems.

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 meds or classical psychoactive substances. Use of the term material is preferred over "med" 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