tryptamine

For a list of plants, fungi and animals containing tryptamines, see List of psychoactive plants and List of naturally occurring tryptamines.

Endogenous levels of tryptamine in the mammalian brain are less than 100 ng per gram of tissue. However, elevated levels of trace amines have been observed in patients with certain neuropsychiatric disorders taking medications, such as bipolar depression and schizophrenia.{{Cite journal|last=Miller|first=Gregory M.|date=2011|title=The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity|journal=Journal of Neurochemistry|volume=116|issue=2|pages=164–176|doi=10.1111/j.1471-4159.2010.07109.x|issn=0022-3042|pmc=3005101|pmid=21073468}}

Tryptamine is relatively abundant in the gut and feces of humans and rodents. Commensal bacteria, including Ruminococcus gnavus and Clostridium sporogenes in the gastrointestinal tract, possess the enzyme tryptophan decarboxylase, which aids in the conversion of dietary tryptophan to tryptamine. Tryptamine is a ligand for gut epithelial serotonin type 4 (5-HT₄) receptors and regulates gastrointestinal electrolyte balance through colonic secretions.

To yield tryptamine in vivo, tryptophan decarboxylase removes the carboxylic acid group on the α-carbon of tryptophan. Synthetic modifications to tryptamine can produce serotonin and melatonin; however, these pathways do not occur naturally as the main pathway for endogenous neurotransmitter synthesis.{{Cite web|date=2020|title=Serotonin Synthesis and Metabolism|url=https://www.sigmaaldrich.com/technical-documents/articles/biology/rbi-handbook/non-peptide-receptors-synthesis-and-metabolism/serotonin-synthesis-and-metabolism.html|website=Sigma Aldrich}}

Monoamine oxidases A and B are the primary enzymes involved in tryptamine metabolism to produce indole-3-acetaldehyde, however it is unclear which isoform is specific to tryptamine degradation.{{Cite web|title=MetaCyc L-tryptophan degradation VI (via tryptamine)|url=https://biocyc.org/META/new-image?object=PWY-3181|access-date=2020-12-11|website=biocyc.org}}

File:Biosynthesis and degradation of tryptamine.png

Tryptamine is known to act as a serotonin receptor agonist, although its potency is limited by rapid inactivation by monoamine oxidases.{{cite journal | vauthors = Mousseau DD | title = Tryptamine: a metabolite of tryptophan implicated in various neuropsychiatric disorders | journal = Metab Brain Dis | volume = 8 | issue = 1 | pages = 1–44 | date = March 1993 | pmid = 8098507 | doi = 10.1007/BF01000528 | url = }}{{cite journal | vauthors = Anwar MA, Ford WR, Broadley KJ, Herbert AA | title = Vasoconstrictor and vasodilator responses to tryptamine of rat-isolated perfused mesentery: comparison with tyramine and β-phenylethylamine | journal = Br J Pharmacol | volume = 165 | issue = 7 | pages = 2191–2202 | date = April 2012 | pmid = 21958009 | pmc = 3413856 | doi = 10.1111/j.1476-5381.2011.01706.x | url = }}{{cite journal | vauthors = Bradley PB, Humphrey PP, Williams RH | title = Tryptamine-induced vasoconstrictor responses in rat caudal arteries are mediated predominantly via 5-hydroxytryptamine receptors | journal = Br J Pharmacol | volume = 84 | issue = 4 | pages = 919–925 | date = April 1985 | pmid = 3159458 | pmc = 1987057 | doi = 10.1111/j.1476-5381.1985.tb17386.x | url = }} It has specifically been found to act as a full agonist of the serotonin 5-HT_2A receptor ({{Abbrlink|EC₅₀|half-maximal effective concentration}} = 7.36 ± 0.56{{nbsp}}nM; E_max = 104 ± 4%). Tryptamine was of much lower potency in stimulating the 5-HT_2A receptor β-arrestin pathway ({{Abbr|EC₅₀|half-maximal effective concentration}} = 3,485 ± 234{{nbsp}}nM; E_max = 108 ± 16%). In contrast to the 5-HT_2A receptor, tryptamine was found to be inactive at the serotonin 5-HT_1A receptor.

Tryptamine produced by mutualistic bacteria in the human gut activates serotonin GPCRs ubiquitously expressed along the colonic epithelium. Upon tryptamine binding, the activated 5-HT₄ receptor undergoes a conformational change which allows its G_s alpha subunit to exchange GDP for GTP, and its liberation from the 5-HT₄ receptor and βγ subunit. GTP-bound G_s activates adenylyl cyclase, which catalyzes the conversion of ATP into cyclic adenosine monophosphate (cAMP). cAMP opens chloride and potassium ion channels to drive colonic electrolyte secretion and promote intestinal motility.{{Cite web|date=2018-06-15|title=Microbiome-Lax May Relieve Constipation|url=https://www.genengnews.com/topics/omics/microbiome-lax-may-relieve-constipation/|access-date=2020-12-11|website=GEN - Genetic Engineering and Biotechnology News|language=en-US}}

File:Tryptamine_mechanism_of_action_in_the_human_gut.png

Tryptamine has been found to act as a monoamine releasing agent (MRA).{{cite journal | vauthors = Jones RS | title = Tryptamine: a neuromodulator or neurotransmitter in mammalian brain? | journal = Prog Neurobiol | volume = 19 | issue = 1-2 | pages = 117–139 | date = 1982 | pmid = 6131482 | doi = 10.1016/0301-0082(82)90023-5 | url = }}{{cite journal | vauthors = Blough BE, Landavazo A, Partilla JS, Decker AM, Page KM, Baumann MH, Rothman RB | title = Alpha-ethyltryptamines as dual dopamine-serotonin releasers | journal = Bioorg Med Chem Lett | volume = 24 | issue = 19 | pages = 4754–4758 | date = October 2014 | pmid = 25193229 | pmc = 4211607 | doi = 10.1016/j.bmcl.2014.07.062 | url = }} It is a releaser of serotonin, dopamine, and norepinephrine, in that order of potency ({{Abbr|EC₅₀|half-maximal effective concentration}} = 32.6{{nbsp}}nM, 164{{nbsp}}nM, and 716{{nbsp}}nM, respectively). That is, it acts as a serotonin–norepinephrine–dopamine releasing agent (SNDRA).

Tryptamine is a monoaminergic activity enhancer (MAE) of serotonin, norepinephrine, and dopamine in addition to its serotonin receptor agonism.{{cite journal | vauthors = Shimazu S, Miklya I | title = Pharmacological studies with endogenous enhancer substances: beta-phenylethylamine, tryptamine, and their synthetic derivatives | journal = Progress in Neuro-Psychopharmacology & Biological Psychiatry | volume = 28 | issue = 3 | pages = 421–427 | date = May 2004 | pmid = 15093948 | doi = 10.1016/j.pnpbp.2003.11.016 | s2cid = 37564231 }}{{cite journal | vauthors = Knoll J | title = Enhancer regulation/endogenous and synthetic enhancer compounds: a neurochemical concept of the innate and acquired drives | journal = Neurochem Res | volume = 28 | issue = 8 | pages = 1275–1297 | date = August 2003 | pmid = 12834268 | doi = 10.1023/a:1024224311289 | url = }} That is, it enhances the action potential-mediated release of these monoamine neurotransmitters. The MAE actions of tryptamine and other MAEs may be mediated by TAAR1 agonism.{{cite journal | vauthors = Harsing LG, Knoll J, Miklya I | title = Enhancer Regulation of Dopaminergic Neurochemical Transmission in the Striatum | journal = Int J Mol Sci | volume = 23 | issue = 15 | date = August 2022 | page = 8543 | pmid = 35955676 | pmc = 9369307 | doi = 10.3390/ijms23158543 | doi-access = free | url = }}{{cite journal | vauthors = Harsing LG, Timar J, Miklya I | title = Striking Neurochemical and Behavioral Differences in the Mode of Action of Selegiline and Rasagiline | journal = Int J Mol Sci | volume = 24 | issue = 17 | date = August 2023 | page = 13334 | pmid = 37686140 | pmc = 10487936 | doi = 10.3390/ijms241713334 | doi-access = free | url = }} Synthetic and more potent MAEs like benzofuranylpropylaminopentane (BPAP) and indolylpropylaminopentane (IPAP) have been derived from tryptamine.{{cite journal | vauthors = Knoll J | title = Antiaging compounds: (-)deprenyl (selegeline) and (-)1-(benzofuran-2-yl)-2-propylaminopentane, [(-)BPAP], a selective highly potent enhancer of the impulse propagation mediated release of catecholamine and serotonin in the brain | journal = CNS Drug Rev | volume = 7 | issue = 3 | pages = 317–45 | date = 2001 | pmid = 11607046 | pmc = 6494119 | doi = 10.1111/j.1527-3458.2001.tb00202.x | url = }}{{cite journal | vauthors = Yoneda F, Moto T, Sakae M, Ohde H, Knoll B, Miklya I, Knoll J | title = Structure-activity studies leading to (-)1-(benzofuran-2-yl)-2-propylaminopentane, ((-)BPAP), a highly potent, selective enhancer of the impulse propagation mediated release of catecholamines and serotonin in the brain | journal = Bioorg Med Chem | volume = 9 | issue = 5 | pages = 1197–1212 | date = May 2001 | pmid = 11377178 | doi = 10.1016/s0968-0896(01)00002-5 | url = }}{{cite journal | vauthors = Knoll J, Yoneda F, Knoll B, Ohde H, Miklya I | title = (-)1-(Benzofuran-2-yl)-2-propylaminopentane, [(-)BPAP], a selective enhancer of the impulse propagation mediated release of catecholamines and serotonin in the brain | journal = British Journal of Pharmacology | volume = 128 | issue = 8 | pages = 1723–1732 | date = December 1999 | pmid = 10588928 | pmc = 1571822 | doi = 10.1038/sj.bjp.0702995 }}

Tryptamine is an agonist of the trace amine-associated receptor 1 (TAAR1).{{Cite journal|last1=Gainetdinov|first1=Raul R.|last2=Hoener|first2=Marius C.|last3=Berry|first3=Mark D.|date=2018-07-01|title=Trace Amines and Their Receptors|url=https://pharmrev.aspetjournals.org/content/70/3/549|journal=Pharmacological Reviews|language=en|volume=70|issue=3|pages=549–620|doi=10.1124/pr.117.015305|issn=0031-6997|pmid=29941461|s2cid=49411553|doi-access=free}} It is a potent TAAR1 full agonist in rats, a weak TAAR1 full agonist in mice, and a very weak TAAR1 partial agonist in humans. Tryptamine may act as a trace neuromodulator in some species via activation of TAAR1 signaling.{{Cite journal|last1=Zucchi|first1=R|last2=Chiellini|first2=G|last3=Scanlan|first3=T S|last4=Grandy|first4=D K|date=2006|title=Trace amine-associated receptors and their ligands|journal=British Journal of Pharmacology|volume=149|issue=8|pages=967–978|doi=10.1038/sj.bjp.0706948|issn=0007-1188|pmc=2014643|pmid=17088868}}

The TAAR1 is a stimulatory G protein-coupled receptor (GPCR) that is weakly expressed in the intracellular compartment of both pre- and postsynaptic neurons. TAAR1 agonists have been implicated in regulating monoaminergic neurotransmission, for instance by activating G protein-coupled inwardly-rectifying potassium channels (GIRKs) and reducing neuronal firing via facilitation of membrane hyperpolarization through the efflux of potassium ions.{{Cite journal|last1=Grandy|first1=David K.|last2=Miller|first2=Gregory M.|last3=Li|first3=Jun-Xu|date=2016-02-01|title="TAARgeting Addiction" The Alamo Bears Witness to Another Revolution|journal=Drug and Alcohol Dependence|volume=159|pages=9–16|doi=10.1016/j.drugalcdep.2015.11.014|issn=0376-8716|pmc=4724540|pmid=26644139}}

TAAR1 agonists are under investigation as a novel treatment for neuropsychiatric conditions like schizophrenia, drug addiction, and depression. The TAAR1 is expressed in brain structures associated with dopamine systems, such as the ventral tegmental area (VTA) and serotonin systems in the dorsal raphe nuclei (DRN). Additionally, the human TAAR1 gene is localized at 6q23.2 on the human chromosome, which is a susceptibility locus for mood disorders and schizophrenia. Activation of TAAR1 suggests a potential novel treatment for neuropsychiatric disorders, as TAAR1 agonists produce antipsychotic-like, anti-addictive, and antidepressant-like effects in animals.

In a published clinical study, tryptamine, at a total dose of 23 to 277{{nbsp}}mg by intravenous infusion, produced hallucinogenic effects or perceptual disturbances similar to those of small doses of lysergic acid diethylamide (LSD).{{cite book | last=Martin | first=W. R. | last2=Sloan | first2=J. W. | title=Drug Addiction II | chapter=Pharmacology and Classification of LSD-like Hallucinogens | publisher=Springer Berlin Heidelberg | publication-place=Berlin, Heidelberg | year=1977 | isbn=978-3-642-66711-4 | doi=10.1007/978-3-642-66709-1_3 | pages=305–368 | quote=MARTIN and SLOAN (1970) found that intravenously infused tryptamine increased blood pressure, dilated pupils, enhanced the patellar reflex, and produced perceptual distortions. [...] Tryptamine, but not DMT, increases locomotor activity in the mouse, while both antagonize reserpine depression (V ANE et al., 1961). [...] In the rat, tryptamine causes backward locomotion, Straub tail, bradypnea and dyspnea, and clonic convulsions (TEDESCHI et al., 1959). [...] Tryptamine produces a variety of changes in the cat causing signs of sympathetic activation including mydriasis, retraction of nictitating membrane, piloerection, motor signs such as extension of limbs and convulsions and affective changes such as hissing and snarling (LAIDLAW, 1912). [...]}}{{cite book | last=Shulgin | first=A. | title=Tihkal: The Continuation | publisher=Transform Press | year=1997 | isbn=978-0-9630096-9-2 | url=https://books.google.com/books?id=jl_ik66IumUC | access-date=17 August 2024 | page= | at=[https://www.erowid.org/library/books_online/tihkal/tihkal53.shtml #53. T] | quote = (with 250 mg, intravenously) "Tryptamine was infused intravenously over a period of up to 7.5 minutes. Physical changes included an increases in blood pressure, in the amplitude of the patellar reflex, and in pupillary diameter. The subjective changes are not unlike those seen with small doses of LSD. A point-by-point comparison between the tryptamine and LSD syndromes reveals a close similarity which is consistent with the hypothesis that tryptamine and LSD have a common mode of action."}}{{cite journal | vauthors = Blough BE, Landavazo A, Decker AM, Partilla JS, Baumann MH, Rothman RB | title = Interaction of psychoactive tryptamines with biogenic amine transporters and serotonin receptor subtypes | journal = Psychopharmacology (Berl) | volume = 231 | issue = 21 | pages = 4135–4144 | date = October 2014 | pmid = 24800892 | pmc = 4194234 | doi = 10.1007/s00213-014-3557-7 | url = | quote = [Tryptamine (T): [...] Psychoactive effects: Psychoactive, short acting due to metabolism, increased blood pressure, similar to LSD}}{{cite journal | vauthors = Martin WR, Sloan JW | title = Effects of infused tryptamine in man | journal = Psychopharmacologia | volume = 18 | issue = 3 | pages = 231–237 | date = 1970 | pmid = 4922520 | doi = 10.1007/BF00412669 | url = }} It also produced other LSD-like effects, including pupil dilation, increased blood pressure, and increased force of the patellar reflex. Tryptamine produced side effects including nausea, vomiting, dizziness, tingling sensations, sweating, and bodily heaviness among others as well. Conversely, there were no changes in heart rate or respiratory rate. The onset of the effects was rapid and the duration was very short. This can be attributed to the very rapid metabolism of tryptamine by monoamine oxidase (MAO) and its very short elimination half-life.

In animals, tryptamine, alone and/or in combination with a monoamine oxidase inhibitor (MAOI), produces behavioral changes such as hyperlocomotion and reversal of reserpine-induced behavioral depression. In addition, it produces effects like hyperthermia, tachycardia, myoclonus, and seizures or convulsions, among others. Findings on tryptamine and the head-twitch response in rodents have been mixed, with some studies reporting no effect,{{cite journal | vauthors = Yamada J, Sugimoto Y, Horisaka K | title = The behavioural effects of intravenously administered tryptamine in mice | journal = Neuropharmacology | volume = 26 | issue = 1 | pages = 49–53 | date = January 1987 | pmid = 3561719 | doi = 10.1016/0028-3908(87)90043-8 | url = }} some studies reporting induction of head twitches by tryptamine,{{cite journal | vauthors = Haberzettl R, Bert B, Fink H, Fox MA | title = Animal models of the serotonin syndrome: a systematic review | journal = Behav Brain Res | volume = 256 | issue = | pages = 328–345 | date = November 2013 | pmid = 24004848 | doi = 10.1016/j.bbr.2013.08.045 | url = | doi-access = free }}{{cite journal | vauthors = Sugimoto Y, Yamada J, Horisaka K | title = Effect of tryptamine on the behavior of mice | journal = J Pharmacobiodyn | volume = 9 | issue = 1 | pages = 68–73 | date = January 1986 | pmid = 2940357 | doi = 10.1248/bpb1978.9.68 | url = }}{{cite journal | vauthors = Orikasa S, Sloley BD | title = Effects of 5,7-dihydroxytryptamine and 6-hydroxydopamine on head-twitch response induced by serotonin, p-chloroamphetamine, and tryptamine in mice | journal = Psychopharmacology (Berl) | volume = 95 | issue = 1 | pages = 124–131 | date = 1988 | pmid = 3133691 | doi = 10.1007/BF00212780 | url = }} and others reporting that tryptamine actually antagonized 5-hydroxytryptophan (5-HTP)-induced head twitches.{{cite journal | vauthors = Jones RS | title = In vivo pharmacological studies on the interactions between tryptamine and 5-hydroxytryptamine | journal = Br J Pharmacol | volume = 73 | issue = 2 | pages = 485–493 | date = June 1981 | pmid = 6972243 | pmc = 2071674 | doi = 10.1111/j.1476-5381.1981.tb10447.x | url = }} Another study found that combination of tryptamine with an MAOI dose-dependently produced head twitches.{{cite book | last=Irons | first=Jane | last2=Robinson | first2=C. M. | last3=Marsden | first3=C. A. | title=Neurobiology of the Trace Amines | chapter=5ht Involvement in Tryptamine Induced Behaviour in Mice | publisher=Humana Press | publication-place=Totowa, NJ | date=1984 | isbn=978-1-4612-9781-9 | doi=10.1007/978-1-4612-5312-9_35 | pages=423–427}} Head twitches in rodents are a behavioral proxy of psychedelic-like effects.{{cite journal | vauthors = Canal CE, Morgan D | title = Head-twitch response in rodents induced by the hallucinogen 2,5-dimethoxy-4-iodoamphetamine: a comprehensive history, a re-evaluation of mechanisms, and its utility as a model | journal = Drug Test Anal | volume = 4 | issue = 7-8 | pages = 556–576 | date = 2012 | pmid = 22517680 | pmc = 3722587 | doi = 10.1002/dta.1333 | url = }}{{cite book | last=Kozlenkov | first=Alexey | last2=González-Maeso | first2=Javier | title=The Neuroscience of Hallucinations | chapter=Animal Models and Hallucinogenic Drugs | publisher=Springer New York | publication-place=New York, NY | date=2013 | isbn=978-1-4614-4120-5 | doi=10.1007/978-1-4614-4121-2_14 | pages=253–277}} Many of the effects of tryptamine can be reversed by serotonin receptor antagonists like metergoline, metitepine (methiothepin), and cyproheptadine. Conversely, the effects of tryptamine in animals are profoundly augmented by MAOIs due to inhibition of its metabolism.

Tryptamine seems to also elevate prolactin and cortisol levels in animals and/or humans.

The {{Abbrlink|LD₅₀|median lethal dose}} values of tryptamine in animals include 100{{nbsp}}mg/kg i.p. in mice, 500{{nbsp}}mg/kg s.c. in mice, and 223{{nbsp}}mg/kg i.p. in rats.

Tryptamine produced endogenously or administered peripherally is readily able to cross the blood–brain barrier and enter the central nervous system.{{cite book | last=Murphy | first=D. L. | last2=Tamarkin | first2=L. | last3=Garrick | first3=N. A. | last4=Taylor | first4=P. L. | last5=Markey | first5=S. P. | title=Neuropsychopharmacology of the Trace Amines | chapter=Trace Indoleamines in the Central Nervous System | publisher=Humana Press | publication-place=Totowa, NJ | year=1985 | isbn=978-1-4612-9397-2 | doi=10.1007/978-1-4612-5010-4_36 | pages=343–360}}{{cite book | last=Kellar | first=Kenneth J. | last2=Cascio | first2=Caren S. | title=Receptor Binding | chapter=Tryptamine and Phenylethylamine Recognition Sites in Brain | publisher=Humana Press | publication-place=New Jersey | isbn=0-89603-078-4 | doi=10.1385/0-89603-078-4:119 | pages=119–138}} This is in contrast to serotonin, which is peripherally selective.

Tryptamine is metabolized by monoamine oxidase (MAO) to form indole-3-acetic acid (IAA). Its metabolism is described as extremely rapid and its elimination half-life and duration as very short. In addition, its duration is described as shorter than that of dimethyltryptamine (DMT). Brain tryptamine levels are increased up to 300-fold by MAOIs in animals. In addition, the effects of exogenous tryptamine are strongly augmented by monoamine oxidase inhibitors (MAOIs).

Tryptamine is excreted in urine and its rate of urinary excretion has been reported to be pH-dependent.{{cite journal | vauthors = Franzen F, Gross H | title = Tryptamine, N,N-dimethyltryptamine, N,N-dimethyl-5-hydroxytryptamine and 5-methoxytryptamine in human blood and urine | journal = Nature | volume = 206 | issue = 988 | pages = 1052 | date = June 1965 | pmid = 5839067 | doi = 10.1038/2061052a0 | url = }}{{cite journal | vauthors = Price J | title = The dependence of tryptamine excretion on urinary pH | journal = Clin Chim Acta | volume = 65 | issue = 3 | pages = 339–342 | date = December 1975 | pmid = 1161 | doi = 10.1016/0009-8981(75)90259-4 | url = }}

Tryptamine is a substituted tryptamine derivative and trace amine and is structurally related to the amino acid tryptophan.

The experimental log P of tryptamine is 1.55.{{cite web | title=Tryptamine | website=PubChem | url=https://pubchem.ncbi.nlm.nih.gov/compound/1150 | access-date=7 November 2024}}

{{Main|Substituted tryptamine}}

The endogenous monoamine neurotransmitters serotonin (5-hydroxytryptamine or 5-HT) and melatonin (5-methoxy-N-acetyltryptamine), as well as trace amines like N-methyltryptamine (NMT), N,N-dimethyltryptamine (DMT), and bufotenin (N,N-dimethylserotonin), are derivatives of tryptamine.

File:Tryptamine Alkaloids 2.png

A variety of drugs, including both naturally occurring and pharmaceutical substances, are derivatives of tryptamine. These include the tryptamine psychedelics like psilocybin, psilocin, DMT, and 5-MeO-DMT; tryptamine stimulants, entactogens, psychedelics, and/or antidepressants like α-methyltryptamine (αMT) and α-ethyltryptamine (αET); triptan antimigraine agents like sumatriptan; certain antipsychotics like oxypertine; and the sleep aid melatonin.

Various other drugs, including ergolines and lysergamides like the psychedelic lysergic acid diethylamide (LSD), the antimigraine agents ergotamine, dihydroergotamine, and methysergide, and the antiparkinsonian agents bromocriptine, cabergoline, lisuride, and pergolide; β-carbolines like harmine (some of which are monoamine oxidase inhibitors (MAOIs)); Iboga alkaloids like the hallucinogen ibogaine; yohimbans like the α₂ blocker yohimbine; antipsychotics like ciclindole and flucindole; and the MAOI antidepressant metralindole, can all be thought of as cyclized tryptamine derivatives.

Drugs very closely related to tryptamines, but technically not tryptamines themselves, include certain triptans like avitriptan and naratriptan; the antipsychotics sertindole and tepirindole; and the MAOI antidepressants pirlindole and tetrindole.

{{Reflist|2}}

• [https://www.erowid.org/psychoactives/faqs/faqs_tryptamine.shtml Tryptamine FAQ]
• [http://www.tryptamind.com/tryptamine.html Tryptamine Hallucinogens and Consciousness]
• [http://www.tryptamind.com/ Tryptamind Psychoactives], reference site on tryptamine and other psychoactives.
• [http://isomerdesign.com/PiHKAL/read.php?domain=tk&id=53 Tryptamine (T) entry in TiHKAL • info]

{{Neurotransmitters}}

{{Psychedelics}}

{{Navboxes

| title = Biological activities

| titlestyle = background:#ccccff

| list1 =

{{Serotonin receptor modulators}}

{{TAAR ligands}}

{{Monoamine releasing agents}}

{{Monoaminergic activity enhancers}}

}}

{{Tryptamines}}

{{Chemical classes of psychoactive drugs}}

{{Chocolate}}

Category:5-HT1A agonists

Category:5-HT2A agonists

Category:5-HT2B agonists

Category:5-HT2C agonists

Category:Biogenic amines

Category:Monoaminergic activity enhancers

Category:Psychedelic tryptamines

Category:Serotonin receptor agonists

Category:Serotonin-norepinephrine-dopamine releasing agents

Category:TAAR1 agonists

Category:Trace amines

Category:Aminoethyl compounds