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Entactogen

Topic: Chemistry

 From HandWiki - Reading time: 26 min

Entactogens, also known as empathogens or connectogens, are a class of psychoactive drugs that induce the production of experiences of emotional communion, oneness, connectedness, emotional openness—that is, empathy—as particularly observed and reported for experiences with MDMA.[1][2][3][4][5] This class of drug is distinguished from the classes of hallucinogens or psychedelics and stimulants, although entactogens, for instance MDMA, can also have these properties.[1][5][6][7] Entactogens are used both as recreational drugs[8] and are being investigated for medical use in the treatment of psychiatric disorders, for instance MDMA-assisted therapy for post-traumatic stress disorder (PTSD).[9][10][11]

Notable members of this class include the methylenedioxyphenethylamines (MDxx) MDMA, MDA, MDEA, MDOH, MBDB, and methylone, the benzofurans 5-APB, 5-MAPB, 6-APB, and 6-MAPB, the cathinone mephedrone, the 2-aminoindane MDAI, and the α-alkyltryptamines αMT and αET, among others.[1][3] Most entactogens are amphetamines, although several, such as αMT and αET, are tryptamines.[1][3] When referring to MDMA and its counterparts, the term MDxx is often used (with the exception of certain non-entactogen drugs like MDPV).

Entactogens act as serotonin releasing agents (SRAs) as their key action.[12][13][3][14][15] However, entactogens also frequently have additional actions, such as induction of dopamine and norepinephrine and serotonin 5-HT2 receptor agonism, which contributes to their effects as well.[12][13][3][14][15] It is thought that dopamine and norepinephrine release provide additional stimulant, euphoriant, and cardiovascular or sympathomimetic effects, serotonin 5-HT2A receptor agonism produces psychedelic effects of variable intensity, and both dopamine release and serotonin 5-HT2 receptor agonism may enhance the entactogenic effects and be critically involved in allowing for the qualitative "magic" of these drugs.[12][13][3][14][15] Entactogens that simultaneously induce serotonin and dopamine release, for instance MDMA, are known to produce long-lasting serotonergic neurotoxicity[16][17][3] with associated cognitive and memory deficits as well as psychiatric changes.[18][19][20][21]

MDA and MDMA were both first synthesized independently in the early 1910s.[22] The psychoactive effects of MDA were discovered in 1930 but were not described until the 1950s, MDA and MDMA emerged as recreational drugs in the 1960s, and the unique entactogenic effects of MDMA were first described in the 1970s.[22][23][24][25][26] Entactogens as a unique pharmacological class depending on induction of serotonin release was established in the mid-1980s and novel entactogens such as MBDB were developed at this time and after.[1][5][6] Gordon Alles discovered the psychoactive effects of MDA,[25][26] Alexander Shulgin played a key role in bringing awareness to MDMA and its unique effects,[24] and Ralph Metzner[27][28][29] and David E. Nichols formally defined entactogens and established them as a distinct class of drugs.[1][5][6] Many entactogens like MDMA are controlled substances throughout the world.[30][31]

Uses

Recreational

Entactogens are used as recreational drugs, including notably at raves.[8]

Medical

Psychiatrists began using entactogens as psychotherapy tools in the 1970s despite the lack of clinical trials.[32] In recent years, the scientific community has been revisiting the possible therapeutic uses of entactogens. Therapeutic models using MDMA have been studied because of its entactogenic properties.[33] This type of therapy would be applicable for treating a patient who was experiencing psychological trauma such as PTSD. Traumatic memories can be linked to fear in the patients which makes engaging with these memories difficult. Administration of an entactogen such as MDMA allows the patient to disconnect from the fear associated with the traumatic memories and engage in therapy.[33] MDMA acts by targeting the body's stress response in order to cause this therapeutic effect. In addition to reducing anxiety and a conditioned fear response, MDMA also reduces the avoidance of feelings.[33] Patients are then able to trust themselves and their therapist and engage with traumatic memories under the influence of MDMA.

Although the therapeutic effects of entactogens may be promising, drugs such as MDMA have the potential for negative effects that are counter productive in a therapy setting. For example, MDMA may make negative cognition worse. This means that a positive experience is not a guarantee and can be contingent on aspects like the setting and the patient's expectations.[34] Additionally there is no clear model of the psychopharmacological means for a positive or negative experience.[34] There is also a potential concern for the neurotoxic effects of MDMA on the fiber density of serotonin neurons in the neocortex. High doses of MDMA may cause potential depletion of serotonergic axons. The same effects may not be caused by lower doses of MDMA required for treatment, however.[35]

MDMA-assisted psychotherapy (MDMA-AT) is in late-stage clinical trials to treat PTSD as of 2025.[9][10][11]

Doses and durations

Template:Sticky

Oral doses and durations of entactogensa
Compound Class Dose Duration
MDA Amphetamine 80–160 mg (20–200 mg+) 4–8 hours
  (S)-MDA Amphetamine 160–225 mg 3 hours
  (R)-MDA Amphetamine 70–200 mg 4–8 hours
MDMA (Ecstasy; Molly; Adam) Amphetamine 80–150 mg (25–200 mg+) 3–6 hours
  (S)-MDMA Amphetamine 60–125 mg 5 hours
  (R)-MDMA Amphetamine 250–300 mg 4–5 hours
MDEA (MDE; Eve) Amphetamine 100–200 mg (30–225 mg+) 3–5 hours
MDOH (MDHA) Amphetamine 100–160 mg 3–6 hours
FLEA (MDMOH, MDHMA) Amphetamine 100–160 mg 4–8 hours
Lys-MDA Amphetamine ~164 mg ~6 hours
N-t-BOC-MDMA Amphetamine Unknown Unknown
MMDA (5-methoxy-MDA) Amphetamine 100–250 mg "Moderate"
BDB (J) Phenylisobutylamine 150–230 mg 4–8 hours
MBDB (methyl-J; Eden) Phenylisobutylamine 180–210 mg (150–250 mg+) 4–6 hours
Methylone (βk-MDMA) Cathinone 100–250 mg (60–325 mg+) 2–5 hours
Ethylone (βk-MDEA) Cathinone 150–250 mg (80–400 mg) 2–6 hours
Butylone (βk-MBDB) Cathinone 100–250 mg (20–250 mg) 2–5 hours
Mephedrone (4-MMC) Cathinone 100–200 mg (15–300 mg+) 2–5 hours
5-APB Benzofuran 60–80 mg (20–100 mg+) 3–8 hours
5-MAPB Benzofuran 30–70 mg 5–6 hours
6-APB Benzofuran 80–100 mg (15–125 mg+) 6–9 hours
6-MAPB Benzofuran 50–100 mg 6–8 hours
5-APDB Dihydrobenzofuran 50–200 mg+ Unknown
5-MAPDB Dihydrobenzofuran 50–150 mg+ Unknown
6-APDB Dihydrobenzofuran 20–130 mg+ Unknown
MDAI 2-Aminoindane 100–200 mg (20–300 mg+) 2–5 hours
MMAI 2-Aminoindane Unknown Unknown
MEAI (5-MeO-AI) 2-Aminoindane Unknown Unknown
5-IAI 2-Aminoindane 100–200 mg 2–4 hours
AMT Tryptamine 15–30 mg 12–16 hours
AET Tryptamine 100–150 mg 6–8 hours
BK-NM-AMT (βk-NM-AMT) Tryptamine Unknown Unknown
Borax combob Multipleb Variable Variable
Footnotes: a = Some of these drugs also act as robust psychedelics and/or stimulants. Examples of psychedelics include MDA, MMDA, and AMT, while examples of stimulants include mephedrone. b = The Borax combo is a combination of 5-MAPB or MDAI, 2-FMA, and 5-MeO-MiPT or 4-HO-MET and is said to closely mimic the effects and unique "magic" of MDMA. Refs: [36][37][3][31][38][39][40][41][42][43][44] Individual: [45][46][47][48][49][50][51][52][53][54][55]

The above table does not include atypical agents with some claimed entactogen-like effects, such as 2C-B[44][56][57] and 5-MeO-MiPT.[58]

Effects

Both terms adopted and used in naming the class of therapeutic drugs for MDMA and related compounds were chosen with the intention of providing some reflection of the reported psychological effects associated with drugs in the classification and distinguishing these compounds from classical psychedelic drugs such as LSD, mescaline, and psilocybin and major stimulants, such as methamphetamine and amphetamine.[4] Chemically, MDMA is classified as a substituted amphetamine (which includes stimulants like dextroamphetamine and psychedelics like 2,5-dimethoxy-4-methylamphetamine), which makes MDMA a substituted phenethylamine (which includes other stimulants like methylphenidate and other psychedelics like mescaline) by the definition of amphetamine. While chemically related both to psychedelics and stimulants, the psychological effects experienced with MDMA were reported to provide obvious and striking aspects of personal relatedness, feelings of connectedness, communion with others, and ability to feel what others feel—in short an empathic resonance is consistently evoked.[59] While psychedelics like LSD may sometimes yield effects of empathic resonance, these effects tend to be momentary and likely passed over on the way to some other dimension or interest. In contrast, the main characteristic that distinguishes MDMA from LSD-type experiences is the consistency of the effects of emotional communion, relatedness, emotional openness—in short, empathy and sympathy.[4]

Side effects

Side effects of entactogens like MDMA include mydriasis, nystagmus, jaw clenching, bruxism, insomnia, appetite loss, tachycardia, hypertension, and hyperthermia, among others.[3][9] Severe adverse effects of entactogens like MDMA can include dehydration, hyperthermia, seizures, rhabdomyolysis, disseminated intravascular coagulation, hyponatremia, acute renal failure, liver injury, serotonin syndrome, and valvular heart disease.[9][44] Entactogens can produce long-lasting serotonergic neurotoxicity[16][17][3] and associated cognitive and memory deficits as well as psychiatric changes.[18][19][20][21]

Overdose

Entactogens like MDMA show a much narrower margin of safety and greater toxicity in overdose than serotonergic psychedelics.[60] Whereas LSD and psilocybin have extrapolated human lethal doses relative to typical recreational doses of approximately 1,000-fold and 200-fold, respectively,[61] a reasonable estimated fatal dose of MDMA is only about 15 or 16 times a single typical recreational dose.[60]

Interactions

Entactogens like MDMA pose high risks of severe and potentially fatal serotonin syndrome and hypertensive crisis in people on monoamine oxidase inhibitors (MAOIs) due to synergistic elevations of monoamines like serotonin and norepinephrine.[62][63] MDMA also has the potential to interact with various other drugs.[64][65][66]

Pharmacology

Mechanism of action

Entactogens like MDMA are serotonin releasing agents and hence are indirect agonists of serotonin receptors.[67][68][69] They produce entactogenic effects in animals such as increased prosocial behavior like adjacent lying, enhanced empathy-like behavior, and antiaggressive effects.[67][70][12] Likewise, MDMA increases sociability, prosociality, and emotional empathy in humans.[12]

In animals, MDMA induced prosocial behavior and elevations in circulating oxytocin levels and these effects were abolished by pretreatment with the serotonin 5-HT1A receptor antagonist WAY-100635.[67][71][72][73][74] Conversely, the serotonin 5-HT1A receptor agonist 8-OH-DPAT produced prosocial behavior and increased oxytocin levels similarly to MDMA.[67][72][75] In addition, MDMA has been shown to activate oxytocinergic neurons in the hypothalamus and this too is reversed by serotonin 5-HT1A receptor antagonism.[67][72][76] Subsequent research found that direct injection of the serotonin 5-HT1A receptor WAY-100635 locally into the basolateral amygdala (BLA) suppressed MDMA-induced prosocial behavior and that direct injection of MDMA locally into the BLA significantly increased sociability.[77][73]

The serotonin 5-HT2B and 5-HT2C receptor antagonist SB-206553 has also been found to block MDMA-induced prosocial behavior, although it produced potentially confounding thigmotaxis (hyperactivity at periphery of testing chamber) as well.[71][74] Conversely, the serotonin 5-HT1B receptor antagonist GR-55562 and the serotonin 5-HT2A receptor antagonist ketanserin were both ineffective.[71][73][74] Likewise, another study found that selective antagonists of the serotonin 5-HT1B, 5-HT2A, 5-HT2C, and 5-HT4 receptors (SB-216641), volinanserin (MDL-100907), SB-242084, and SB-204070, respectively) were all ineffective in suppressing MDMA-induced prosocial activity.[77][73] Other research has found that serotonin 5-HT2B receptor inactivation abolishes the serotonin release induced by MDMA and attenuates many of its effects.[68][69][78] In addition to the preceding findings, induction of serotonin release by MDMA in the nucleus accumbens and consequent activation of serotonin 5-HT1B receptors in this area is implicated in its enhancement of prosocial behaviors, whereas consequent activation of yet-to-be-determined serotonin receptors in this area is implicated in its enhancement of empathy-like behaviors.[1][70][79][80] Injection of the serotonin 5-HT1B receptor antagonist NAS-181 directly into the nucleus accumbens blocked the prosocial behaviors of MDMA.[79]

On the basis of the serotonin 5-HT1A receptor-mediated oxytocin release with MDMA, it has been proposed that increased oxytocinergic signaling may mediate the prosocial effects of MDMA in animals.[67][72] Accordingly, intracerebroventricular injection of the peptide oxytocin receptor antagonist tocinoic acid blocked MDMA- and 8-OH-DPAT-induced prosocial effects.[67][72][81] However, in a subsequent study, systemically administered C25, a non-peptide oxytocin receptor antagonist, failed to affect MDMA-induced prosocial behavior, whereas the vasopressin V1A receptor antagonist relcovaptan (SR-49059) was able to block MDMA-induced prosocial activity.[67][81] It might be that tocinoic acid is non-selective and also blocks the vasopressin V1A receptor or that C25 is peripherally selective and is unable to block oxytocin receptors in the brain.[67][81] More research is needed to clarify this.[81][67] In any case, in another study, the non-peptide and centrally active selective oxytocin receptor antagonist L-368899 abolished MDMA-induced prosocial behavior.[81][82] Conversely, in other studies, different oxytocin receptor antagonists were ineffective.[79]

As in animals, MDMA greatly increases circulating oxytocin levels in humans.[67] Serotonin reuptake inhibitors and norepinephrine reuptake inhibitors reduced the subjective effects of MDMA in humans, for instance increased extroversion, self-confidence, closeness, openness, and talkativeness.[12] The 5-HT2A receptor antagonist ketanserin reduced MDMA-induced increases in friendliness.[12] MDMA-induced emotional empathy was not affected by the serotonin 5-HT1A receptor antagonist pindolol or by intranasal oxytocin.[83] Similarly, MDMA-induced emotional empathy and prosocial behavior have not been associated with circulating oxytocin levels.[83][67] As such, the role of oxytocin in the entactogenic effects of MDMA in humans is controversial.[67]

Other serotonin releasing agents, like fenfluramine, show prosocial effects in animals similar to those of MDMA.[84][79] Fenfluramine has likewise been reported to improve social deficits in children with autism.[79][85] Selective agonists of the serotonin 5-HT1A and 5-HT1B receptors and of the oxytocin receptors have been or are being investigated for the potential treatment of social deficits and aggression.[86][87][88][89] Examples include batoprazine, eltoprazine (DU-28853), fluprazine (DU-27716), F-15,599 (NLX-01), zolmitriptan (ML-004), and LIT-001.[88][89][90] Serotonergic psychedelics, for instance lysergic acid diethylamide (LSD) and psilocybin, which act as non-selective serotonin receptor agonists including of the serotonin 5-HT1 and 5-HT2 receptors, have shown prosocial and empathy-enhancing effects in animals and/or humans as well, both acutely and long-term.[91][92][93]

The serotonin release of MDMA appears to be the key pharmacological action mediating the entactogenic, prosocial, and empathy-enhancing effects of the drug.[12][13][3] However, in addition to serotonin release, MDMA is also a potent releasing agent of norepinephrine and dopamine, and hence acts as a well-balanced serotonin–norepinephrine–dopamine releasing agent.[13][3] Additionally, MDMA is a direct agonist of several serotonin receptors, including of the serotonin 5-HT2 receptors, with moderate affinity.[13][3] These actions are thought to play an important role in the effects of MDMA, including in its psychostimulant, euphoriant, and mild psychedelic effects, as well as in its unique and difficult-to-replicate "magic".[13][14][3][94] It has been said by Matthew Baggott that few to no MDMA analogues, including MBDB, methylone, 6-APDB, 5-APDB, 6-APB, 5-APB, MDAT, and MDAI among others, reproduce the full quality and "magic" of MDMA.[14][15] Exceptions may anecdotally include 5-MAPB, particularly in specific enantiomer ratios, and the Borax combo.[14][15][95] The unique properties of MDMA are believed to be dependent on a very specific mixture and ratio of pharmacological activities, including combined serotonin, norepinephrine, and dopamine release and direct serotonin receptor agonism.[14][15]

Some entactogens, including the benzofurans 5-MAPB, 6-MAPB, BK-5-MAPB, and BK-6-MAPB, have unexpectedly been found to be potent serotonin 5-HT1B receptor agonists.[96] In addition to serotonin release and other actions, this property may be involved may be involved in their entactogenic effects.[96] Conversely, MDMA is inactive as a direct agonist of the serotonin 5-HT1B receptor.[96]

Ariadne, the α-ethyl analogue of the serotonergic psychedelic DOM, fully substitutes for MDMA in rodent drug discrimination tests, suggesting that it may have entactogen-like effects.[97][98] This property is unusual among psychedelics, and is in notable contrast to DOM, which at best partially substitutes for MDMA.[98][99] Besides Ariadne, the NBOMe drugs such as 25I-NBOMe and 25B-NBOMe also partially to fully substitute for MDMA in rodents.[100][101][102][103] Unlike conventional entactogens, Ariadne shows no activity at the monoamine transporters, and instead acts as a selective serotonin 5-HT2 receptor partial agonist, including as a lower-efficacy agonist of the serotonin 5-HT2A receptor.[97] Certain other psychedelics and related compounds, like low doses of 2C-B, are also selective serotonin 5-HT2 receptor partial agonists that have likewise been implicated as having entactogenic effects.[44][56][57] MDMA itself is notable in being a lower-efficacy partial agonist of the serotonin 5-HT2A receptor as well.[104][105] The stimulus effects of MDMA in the drug discrimination paradigm are partially blocked by the selective serotonin 5-HT2A receptor antagonist volinanserin in rodents.[106] Similarly, the psychoactive effects of MDMA are partially blocked by the relatively selective serotonin 5-HT2A receptor antagonist ketanserin in humans.[13][107][108][109]

History

The history of MDMA and other entactogens has been reviewed.[22][23][110][24][111][1]

Society and culture

Etymology

The term empathogen, meaning "generating a state of empathy", was coined by Ralph Metzner in 1983 as a term to denote a class of drugs that includes MDMA and other agents with similar effects.[27][28][29] Subsequently, in 1986, Nichols introduced the term entactogen, meaning "producing a touching within", to denote this class of drugs, asserting a concern with the potential for improper association of the term empathogen with negative connotations related to the Greek root πάθος páthos ("suffering; passion").[1][5][6] Additionally, Nichols wanted to avoid any association with the term pathogenesis.[112]

Nichols also thought the original term was limiting, and did not cover other therapeutic uses for the drugs that go beyond instilling feelings of empathy.[4] The hybrid word entactogen is derived from the roots en (Greek: within), tactus (Latin: touch) and -gen (Greek: produce).[5] Entactogen is not becoming dominant in usage, and, despite their difference in connotation, they are essentially interchangeable, as they refer to precisely the same chemicals.

In 2024, an additional alternative term, connectogen, was proposed and introduced by Kurt Stocker and Matthias Liechti.[2]

See also

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 "Entactogens: How the Name for a Novel Class of Psychoactive Agents Originated". Front Psychiatry 13. 2022. doi:10.3389/fpsyt.2022.863088. PMID 35401275. 
  2. ↑ 2.0 2.1 "Methylenedioxymethamphetamine is a connectogen with empathogenic, entactogenic, and still further connective properties: It is time to reconcile "the great entactogen-empathogen debate"". J Psychopharmacol 38 (8): 685–689. August 2024. doi:10.1177/02698811241265352. PMID 39068642. 
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 "Beyond ecstasy: Alternative entactogens to 3,4-methylenedioxymethamphetamine with potential applications in psychotherapy". J Psychopharmacol 35 (5): 512–536. May 2021. doi:10.1177/0269881120920420. PMID 32909493. 
  4. ↑ 4.0 4.1 4.2 4.3 Cite error: Invalid <ref> tag; no text was provided for refs named NicholsYensenMetzner1993
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 Nichols, D. (1986). "Differences Between the Mechanism of Action of MDMA, MBDB, and the Classic Hallucinogens. Identification of a New Therapeutic Class: Entactogens". Journal of Psychoactive Drugs 18 (4): 305–13. doi:10.1080/02791072.1986.10472362. PMID 2880944. 
  6. ↑ 6.0 6.1 6.2 6.3 "Derivatives of 1-(1,3-benzodioxol-5-yl)-2-butanamine: representatives of a novel therapeutic class". J Med Chem 29 (10): 2009–2015. October 1986. doi:10.1021/jm00160a035. PMID 3761319. 
  7. ↑ McGregor, Iain S.; Thompson, Murray R.; Callaghan, Paul D. (2010-01-01). Stolerman, Ian P.. ed (in en). Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg. pp. 758–762. doi:10.1007/978-3-540-68706-1_154. ISBN 978-3-540-68698-9. 
  8. ↑ 8.0 8.1 "Clinical toxicology of newer recreational drugs". Clin Toxicol (Phila) 49 (8): 705–719. October 2011. doi:10.3109/15563650.2011.615318. PMID 21970769. 
  9. ↑ 9.0 9.1 9.2 9.3 "The entactogen 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) as a treatment aid in psychotherapy and its safety concerns". Arch Toxicol 98 (8): 2409–2427. August 2024. doi:10.1007/s00204-024-03765-8. PMID 38743292. Bibcode: 2024ArTox..98.2409B. 
  10. ↑ 10.0 10.1 "MDMA-Assisted Therapy for Post-Traumatic Stress Disorder: Regulatory Challenges and a Path Forward". CNS Drugs 39 (4): 339–343. April 2025. doi:10.1007/s40263-025-01162-y. PMID 39955464. 
  11. ↑ 11.0 11.1 "MDMA and MDMA-Assisted Therapy". Am J Psychiatry 182 (1): 79–103. January 2025. doi:10.1176/appi.ajp.20230681. PMID 39741438. 
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 "The prosocial effects of 3,4-methylenedioxymethamphetamine (MDMA): Controlled studies in humans and laboratory animals". Neurosci Biobehav Rev 57: 433–446. October 2015. doi:10.1016/j.neubiorev.2015.08.016. PMID 26408071. 
  13. ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 13.7 Halberstadt, Adam L.; Nichols, David E. (2020). "Serotonin and serotonin receptors in hallucinogen action". Handbook of Behavioral Neuroscience. 31. Elsevier. pp. 843–863. doi:10.1016/b978-0-444-64125-0.00043-8. ISBN 978-0-444-64125-0. 
  14. ↑ 14.0 14.1 14.2 14.3 14.4 14.5 14.6 "Beyond Ecstasy: Progress in Developing and Understanding a Novel Class of Therapeutic Medicine". PS2023 [Psychedelic Science 2023, June 19-23, 2023, Denver, Colorado]. Denver, CO: Multidisciplinary Association for Psychedelic Studies. 23 June 2023. https://2023.psychedelicscience.org/sessions/beyond-ecstasy-progress-in-developing-and-understanding-a-novel-class-of-therapeutic-medicine/. 
  15. ↑ 15.0 15.1 15.2 15.3 15.4 15.5 "Better Than Ecstasy: Progress in Developing a Novel Class of Therapeutic with Matthew Baggott, PhD.". 6 March 2024. https://www.youtube.com/watch?v=OnhJvKxwfZI&t=1048. 
  16. ↑ 16.0 16.1 Holland, J., ed (2001). "Does MDMA Cause Brain Damage?". Ecstasy: The Complete Guide: A Comprehensive Look at the Risks and Benefits of MDMA. Inner Traditions/Bear. pp. 110–145, 396–404. ISBN 978-0-89281-857-0. https://www.erowid.org/chemicals/mdma/mdma_neurotoxicity1.shtml. 
  17. ↑ 17.0 17.1 "An integrated hypothesis for the serotonergic axonal loss induced by 3,4-methylenedioxymethamphetamine". Neurotoxicology 19 (3): 427–441. June 1998. PMID 9621349. https://www.researchgate.net/publication/13663847. 
  18. ↑ 18.0 18.1 "Recreational Ecstasy/MDMA, the serotonin syndrome, and serotonergic neurotoxicity". Pharmacol Biochem Behav 71 (4): 837–844. April 2002. doi:10.1016/s0091-3057(01)00711-0. PMID 11888574. 
  19. ↑ 19.0 19.1 "MDMA, serotonergic neurotoxicity, and the diverse functional deficits of recreational 'Ecstasy' users". Neurosci Biobehav Rev 37 (8): 1466–1484. September 2013. doi:10.1016/j.neubiorev.2013.04.016. PMID 23660456. 
  20. ↑ 20.0 20.1 "Of mice and men on MDMA: A translational comparison of the neuropsychobiological effects of 3,4-methylenedioxymethamphetamine ('Ecstasy')". Brain Res 1727. January 2020. doi:10.1016/j.brainres.2019.146556. PMID 31734398. 
  21. ↑ 21.0 21.1 "Neurological and cognitive alterations induced by MDMA in humans". Exp Neurol 347. January 2022. doi:10.1016/j.expneurol.2021.113888. PMID 34624331. https://researchonline.ljmu.ac.uk/id/eprint/15629/3/Montgomery_Roberts_2021%20Review.pdf. 
  22. ↑ 22.0 22.1 22.2 Passie, Torsten (29 June 2023). The History of MDMA. Oxford University Press. doi:10.1093/oso/9780198867364.001.0001. ISBN 978-0-19-886736-4. https://books.google.com/books?id=KSvCEAAAQBAJ. 
  23. ↑ 23.0 23.1 "The origin of MDMA ("ecstasy")--separating the facts from the myth". Pharmazie 61 (11): 966–972. November 2006. PMID 17152992. 
  24. ↑ 24.0 24.1 24.2 "Rediscovering MDMA (ecstasy): the role of the American chemist Alexander T. Shulgin". Addiction 105 (8): 1355–61. August 2010. doi:10.1111/j.1360-0443.2010.02948.x. PMID 20653618. 
  25. ↑ 25.0 25.1 Gordon A. Alles (1959). "Some Relations Between Chemical Structure and Physiological Action of Mescaline and Related Compounds / Structure and Action of Phenethylamines". Neuropharmacology: Transactions of the Fourth Conference, September 25, 26, and 27, 1957, Princeton, N. J.. New York: Josiah Macy Foundation. pp. 181–268. OCLC 9802642. https://bitnest.netfirms.com/external/Books/NeuropharmacologyTrans.4.181#page=5. 
  26. ↑ 26.0 26.1 Gordon A. Alles (1959). "Subjective Reactions to Phenethylamine Hallucinogens". A Pharmacologic Approach to the Study of the Mind. Springfield: CC Thomas. pp. 238–250 (241–246). ISBN 978-0-398-04254-7. https://archive.org/details/pharmacologicapp0000univ/page/238/mode/1up. 
  27. ↑ 27.0 27.1 Eisner, Bruce (1989). "Chapter II. What is an Empathogen?". Ecstasy: The MDMA Story. Berkeley, California: Ronin Pub.. pp. 33–50. ISBN 978-0-914171-25-6. OCLC 27935523. https://books.google.com/books?id=oIM4AQAAIAAJ. Retrieved 25 April 2025. 
  28. ↑ 28.0 28.1 Holland, J., ed (2001). "Using MDMA in Healing, Psychotherapy, and Spiritual Practice". Ecstasy: The Complete Guide: A Comprehensive Look at the Risks and Benefits of MDMA. Inner Traditions/Bear. pp. 182–207. ISBN 978-0-89281-857-0. https://books.google.com/books?id=CUCcyklcO00C. "The term "empathogenic," meaning "generating a state of empathy," was independently proposed for these substances in 1983—84 by Ralph Metzner, a psychologist and psychopharmacologist, and David Nichols, a professor of medicinal chemistry at Purdue University. Nichols subsequently rejected the term and now prefers "entactogenic," meaning "touching within," for MDMA. We continue to use the term "empathogenic."" 
  29. ↑ 29.0 29.1 Ralph Metzner (May 1983). "[Lecture presented at the Psychedelics and Spirituality Conference"]. Psychedelics and Spirituality, University of California, Santa Barbara, May 13–14, 1983. https://scholar.google.com/scholar?cluster=16938435501563008121. "Another group of drugs are the phenethylamines, of which MDA [and MDMA] is an example. Instead of calling these "psychedelic drugs," I'd like to suggest the name "empathogenic." Empathogenic means "empathy generating." Everyone I've mentioned this name to thinks it is a good one. These drugs don't produce visions as LSD does. They don't produce multileveled thinking or objectivity toward your mind as LSD and the psychedelics do. They generate a profound state of empathy for self and other in the most general and profound terms. A state of empathy where the feeling is that the self, the other, and the world is basically good, is all right. This state can be referred to as the ground of being, the core of our being, a still point of our being. Then individuals using these substances in therapy can look at their own problems from the standpoint of stillness and empathy. They are able to do changework on themselves very rapidly, compared to ordinary therapy." 
  30. ↑ Shulgin, Alexander (1992). Controlled Substances: A Chemical and Legal Guide to the Federal Drug Laws. Ronin Pub.. ISBN 978-0-914171-50-8. https://books.google.com/books?id=rO4MAAAACAAJ. Retrieved 25 April 2025. 
  31. ↑ 31.0 31.1 Shulgin, A.; Manning, T.; Daley, P.F. (2011). The Shulgin Index, Volume One: Psychedelic Phenethylamines and Related Compounds. 1. Berkeley: Transform Press. ISBN 978-0-9630096-3-0. https://books.google.com/books?id=68-huAAACAAJ. 
  32. ↑ Malamud, Ozer, Yvette; Yuri, Ito (2010-01-01). Encyclopedia of emotion. Greenwood Press. ISBN 978-0-313-34574-6. OCLC 934324453. 
  33. ↑ 33.0 33.1 33.2 Caiuby, Labate, Beatriz; Clancy, Cavnar (2014-01-01). The therapeutic use of Ayahuasca. Springer. ISBN 978-3-642-40425-2. OCLC 876696992. 
  34. ↑ 34.0 34.1 Parrott, A. C. (2007-04-01). "The psychotherapeutic potential of MDMA (3,4-methylenedioxymethamphetamine): an evidence-based review" (in en). Psychopharmacology 191 (2): 181–193. doi:10.1007/s00213-007-0703-5. ISSN 0033-3158. PMID 17297639. 
  35. ↑ F., Quenzer, Linda (2013-05-06). Psychopharmacology: drugs, the brain, and behavior. Sinauer. ISBN 978-0-87893-510-9. OCLC 869923492. 
  36. ↑ Shulgin, Alexander; Shulgin, Ann (September 1991). PiHKAL: A Chemical Love Story. Berkeley, California: Transform Press. ISBN 0-9630096-0-5. OCLC 25627628. http://www.erowid.org/library/books_online/pihkal/pihkal.shtml. 
  37. ↑ (in de) Phenethylamine: von der Struktur zur Funktion. Nachtschatten-Science (1 ed.). Solothurn: Nachtschatten-Verlag. 2013. pp. 465–468, 555–557, 578–630, 659–660, 721, 745–746, 828–831, 905–906. ISBN 978-3-03788-700-4. OCLC 858805226. https://books.google.com/books?id=-Us1kgEACAAJ. 
  38. ↑ "Structure-Activity Relationships of the Classic Hallucinogens and Their Analogs". Hallucinogens: An Update. National Institute on Drug Abuse Research Monograph Series. 146. National Institute on Drug Abuse. 1994. pp. 74–91. https://bibliography.maps.org/resources/download/11534. 
  39. ↑ "Basic Pharmacology and Effects". Hallucinogens: A Forensic Drug Handbook. Forensic Drug Handbook Series. Elsevier Science. 2003. pp. 67–137. ISBN 978-0-12-433951-4. https://bibliography.maps.org/resources/download/12634. 
  40. ↑ "Psychotomimetic Agents". Psychopharmacological Agents: Use, Misuse and Abuse. Medicinal Chemistry: A Series of Monographs. 4. Academic Press. 1976. pp. 59–146. doi:10.1016/b978-0-12-290559-9.50011-9. ISBN 978-0-12-290559-9. https://bitnest.netfirms.com/external/10.1016/B978-0-12-290559-9.50011-9. 
  41. ↑ Shulgin, Alexander T. (1978). "Psychotomimetic Drugs: Structure-Activity Relationships". Stimulants. Boston, MA: Springer US. pp. 243–333. doi:10.1007/978-1-4757-0510-2_6. ISBN 978-1-4757-0512-6. https://bitnest.netfirms.com/external/10.1007/978-1-4757-0510-2_6. 
  42. ↑ "Monoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and Psychedelics". Int J Neuropsychopharmacol 21 (10): 926–931. October 2018. doi:10.1093/ijnp/pyy047. PMID 29850881. 
  43. ↑ Ballentine, Galen; Friedman, Samuel Freesun; Bzdok, Danilo (March 2022). "Trips and neurotransmitters: Discovering principled patterns across 6850 hallucinogenic experiences". Sci Adv 8 (11). doi:10.1126/sciadv.abl6989. PMID 35294242. Bibcode: 2022SciA....8L6989B. 
  44. ↑ 44.0 44.1 44.2 44.3 "Designer drugs: mechanism of action and adverse effects". Arch Toxicol 94 (4): 1085–1133. April 2020. doi:10.1007/s00204-020-02693-7. PMID 32249347. Bibcode: 2020ArTox..94.1085L. "In one of the few clinical studies of a designer drug, 4-bromo-2,5-dimethoxyphenylethylamine (2C-B) was shown to induce euphoria, well-being, and changes in perception, and to have mild stimulant properties (Gonzalez et al. 2015). 2C-B may thus be classified as a psychedelic with entactogenic properties, an effect profile that is similar to various other phenethylamine psychedelics (Shulgin and Shulgin 1995).". 
  45. ↑ "Dosing Psychedelics and MDMA". Curr Top Behav Neurosci 56: 3–21. 2022. doi:10.1007/7854_2021_270. PMID 34734392. 
  46. ↑ "Absolute Configuration and Psychotomimetic Activity". QuaSAR: Quantitative Structure Activity Relationships Of Analgesics, Narcotic Antagonists, And Hallucinogens. National Institute on Drug Abuse Research Monograph Series. 22. National Institute on Drug Abuse. 1978. pp. 8–15. https://archives.nida.nih.gov/sites/default/files/monograph22.pdf#page=19. 
  47. ↑ "Acute effects of R-MDMA, S-MDMA, and racemic MDMA in a randomized double-blind cross-over trial in healthy participants". Neuropsychopharmacology 50 (2): 362–371. August 2024. doi:10.1038/s41386-024-01972-6. PMID 39179638. 
  48. ↑ "Effects of the Psychedelic Amphetamine MDA (3,4-Methylenedioxyamphetamine) in Healthy Volunteers". Journal of Psychoactive Drugs 51 (2): 108–117. 2019-03-15. doi:10.1080/02791072.2019.1593560. PMID 30967099. 
  49. ↑ "Acute effects of MDMA, MDA, lysine-MDMA, and lysine-MDA in a randomized, double-blind, placebo-controlled, crossover trial in healthy participants". Neuropsychopharmacology. September 2025. doi:10.1038/s41386-025-02248-3. PMID 40999236. 
  50. ↑ "The preclinical pharmacology of mephedrone; not just MDMA by another name". Br J Pharmacol 171 (9): 2251–2268. May 2014. doi:10.1111/bph.12628. PMID 24654568. "The normal routes of mephedrone administration in recreational users are reported to be oral and insufflation. Extrapolation from dosing to plasma levels is difficult as there are no detailed dose–concentration curves available and pharmacokinetic studies on the drug in humans have yet to be performed. However, it is suggested that a ‘normal’ recreational oral dose is 100–200 mg, while somewhat lower doses are used when the drug is insufflated (EROWID, 2013). This oral dose is similar to the usual oral MDMA dose typically resulting from ingestion of two tablets (140–180 mg), but an important difference with mephedrone is that the reported short duration of the psychoactive response often leads to rapid repeat dosing (Schifano et al., 2012).". 
  51. ↑ "Clinical Pharmacology of the Synthetic Cathinone Mephedrone". Curr Top Behav Neurosci 32: 313–331. 2017. doi:10.1007/7854_2016_61. PMID 28012094. "Mephedrone oral dosage ranges from 15 to 300 mg, whereas nasal insufflation dosage is somewhat lower and ranges from 5 to 200 mg. Intravenous/intramuscular injection has been reported at approximately half or one-third of oral dosage, whilst 100 mg is described as a usual rectal dose [26, 38]. The initial impact is felt by recreational users approximately 30 min after oral ingestion, with effects lasting for 2–5 h [39]; in contrast, intravenous and rectal administration produce earlier onset of action and shorter duration [40].". 
  52. ↑ "Acute psychotropic, autonomic, and endocrine effects of 5,6-methylenedioxy-2-aminoindane (MDAI) compared with 3,4-methylenedioxymethamphetamine (MDMA) in human volunteers: A self-administration study". Drug Test Anal 16 (9): 1002–1011. September 2024. doi:10.1002/dta.3622. PMID 38056906. 
  53. ↑ "MDAI (5,6-methylenedioxy-2-aminoindane; 6,7-dihydro-5H-cyclopenta[f][1,3]benzodioxol-6-amine; 'sparkle'; 'mindy') toxicity: a brief overview and update". Hum Psychopharmacol 28 (4): 345–355. July 2013. doi:10.1002/hup.2298. PMID 23881883. "Doses range from 70–300 mg; typical doses appear to be 150–200 mg of active ingredient (equivalent to half of a 300 mg capsule or a whole 200 mg capsule). A ‘low’ dose of 70–80 mg produces subtle but noticeable effects; a strong dose is considered to be 250–300 mg. Redosing often occurs; typically a ‘booster’ of 100–150 mg is administered after the initial positive effects have worn off (Drugs-Forum, 2009a; Bluelight, 2010a; Herbalhighs, 2012a; Partyvibe, 2012).". 
  54. ↑ Shulgin, Alexander; Shulgin, Ann (September 1997). TiHKAL: The Continuation. Berkeley, California: Transform Press. ISBN 0-9630096-9-9. OCLC 38503252. http://www.erowid.org/library/books_online/tihkal/tihkal.shtml. 
  55. ↑ "α-Ethyltryptamine: A Ratiocinatory Review of a Forgotten Antidepressant". ACS Pharmacol Transl Sci 6 (12): 1780–1789. December 2023. doi:10.1021/acsptsci.3c00139. PMID 38093842. 
  56. ↑ 56.0 56.1 Barceloux, Donald G., ed (9 March 2012). "Psychoactive Phenethylamine, Piperazine, and Pyrrolidinophenone Derivatives". Medical Toxicology of Drug Abuse: Synthesized Chemicals and Psychoactive Plants. Wiley. pp. 156–192. doi:10.1002/9781118105955.ch10. ISBN 978-0-471-72760-6. "DOSE EFFECT: Anecdotal data suggests that recreational doses of 2C-B range from 4—30 mg with lower doses (4—10 mg) producing entactogenic effects, whereas high doses (10— 20 mg) cause psychedelic and sympathomimetic effects." 
  57. ↑ 57.0 57.1 "Acute Effects of the Novel Psychoactive Drug 2C-B on Emotions". BioMed Research International 2015. 2015-10-12. doi:10.1155/2015/643878. PMID 26543863. 
  58. ↑ "DEA Proposes Adding Five Psychedelic Compounds to Schedule 1" (in en-US). 2022-01-25. https://www.lucid.news/dea-proposes-five-psychedelic-compounds-schedule-1/. 
  59. ↑ Metzner, Ralph (1993). "Letter from Ralph Metzner". Newsletter of the Multidisciplinary Association for Psychedelic Studies MAPS 4 (1). http://www.maps.org/news-letters/v04n1/04143met.html. Retrieved 8 January 2015. 
  60. ↑ 60.0 60.1 "Hofmann vs. Paracelsus: Do Psychedelics Defy the Basics of Toxicology?-A Systematic Review of the Main Ergolamines, Simple Tryptamines, and Phenylethylamines". Toxics 11 (2): 148. February 2023. doi:10.3390/toxics11020148. PMID 36851023. Bibcode: 2023Toxic..11..148H. 
  61. ↑ Thomas, Kelan (2024). Toxicology and Pharmacological Interactions of Classic Psychedelics. Current Topics in Behavioral Neurosciences. Berlin, Heidelberg: Springer Berlin Heidelberg. doi:10.1007/7854_2024_508. https://link.springer.com/10.1007/7854_2024_508. Retrieved 14 May 2025. 
  62. ↑ "Serotonin toxicity of serotonergic psychedelics". Psychopharmacology (Berl) 239 (6): 1881–1891. June 2022. doi:10.1007/s00213-021-05876-x. PMID 34251464. 
  63. ↑ "Clinically Relevant Drug Interactions with Monoamine Oxidase Inhibitors". Health Psychol Res 10 (4). 2022. doi:10.52965/001c.39576. PMID 36425231. 
  64. ↑ "MDMA interactions with pharmaceuticals and drugs of abuse". Expert Opin Drug Metab Toxicol 16 (5): 357–369. May 2020. doi:10.1080/17425255.2020.1749262. PMID 32228243. 
  65. ↑ "Drug-drug interactions between psychiatric medications and MDMA or psilocybin: a systematic review". Psychopharmacology (Berl) 239 (6): 1945–1976. June 2022. doi:10.1007/s00213-022-06083-y. PMID 35253070. 
  66. ↑ "MDMA: interactions with other psychoactive drugs". Pharmacol Biochem Behav 99 (4): 759–774. October 2011. doi:10.1016/j.pbb.2011.06.032. PMID 21756931. 
  67. ↑ 67.00 67.01 67.02 67.03 67.04 67.05 67.06 67.07 67.08 67.09 67.10 67.11 67.12 "Dark Classics in Chemical Neuroscience: 3,4-Methylenedioxymethamphetamine". ACS Chem Neurosci 9 (10): 2408–2427. October 2018. doi:10.1021/acschemneuro.8b00155. PMID 30001118. 
  68. ↑ 68.0 68.1 Martinez-Price, Diana; Krebs-Thomson, Kirsten; Geyer, Mark (1 January 2002). "Behavioral Psychopharmacology of MDMA and MDMA-Like Drugs: A Review of Human and Animal Studies". Addiction Research & Theory (Informa UK Limited) 10 (1): 43–67. doi:10.1080/16066350290001704. ISSN 1606-6359. 
  69. ↑ 69.0 69.1 "Mice in ecstasy: advanced animal models in the study of MDMA". Curr Pharm Biotechnol 11 (5): 421–433. August 2010. doi:10.2174/138920110791591508. PMID 20420576. 
  70. ↑ 70.0 70.1 "MDMA enhances empathy-like behaviors in mice via 5-HT release in the nucleus accumbens". Sci Adv 10 (17). April 2024. doi:10.1126/sciadv.adl6554. PMID 38657057. Bibcode: 2024SciA...10L6554R. 
  71. ↑ 71.0 71.1 71.2 "Effect of drugs of abuse on social behaviour: a review of animal models". Behav Pharmacol 26 (6): 541–570. September 2015. doi:10.1097/FBP.0000000000000162. PMID 26221831. 
  72. ↑ 72.0 72.1 72.2 72.3 72.4 "A role for oxytocin and 5-HT(1A) receptors in the prosocial effects of 3,4 methylenedioxymethamphetamine ("ecstasy")". Neuroscience 146 (2): 509–514. May 2007. doi:10.1016/j.neuroscience.2007.02.032. PMID 17383105. 
  73. ↑ 73.0 73.1 73.2 73.3 "Role of 5-HT1A receptors in the basolateral amygdala on 3,4-methylenedioxymethamphetamine-induced prosocial effects in mice". Eur J Pharmacol 946. May 2023. doi:10.1016/j.ejphar.2023.175653. PMID 36907260. 
  74. ↑ 74.0 74.1 74.2 "Serotonin (1A) receptor involvement in acute 3,4-methylenedioxymethamphetamine (MDMA) facilitation of social interaction in the rat". Prog Neuropsychopharmacol Biol Psychiatry 29 (5): 648–657. June 2005. doi:10.1016/j.pnpbp.2005.04.009. PMID 15908091. 
  75. ↑ "Divergent pathways mediate 5-HT1A receptor agonist effects on close social interaction, grooming and aggressive behaviour in mice: Exploring the involvement of the oxytocin and vasopressin systems". J Psychopharmacol 34 (7): 795–805. July 2020. doi:10.1177/0269881120913150. PMID 32312154. 
  76. ↑ "MDMA-induced c-Fos expression in oxytocin-containing neurons is blocked by pretreatment with the 5-HT-1A receptor antagonist WAY 100635". Brain Res Bull 86 (1–2): 65–73. August 2011. doi:10.1016/j.brainresbull.2011.06.011. PMID 21745546. 
  77. ↑ 77.0 77.1 "Therapeutic mechanisms of psychedelics and entactogens". Neuropsychopharmacology 49 (1): 104–118. January 2024. doi:10.1038/s41386-023-01666-5. PMID 37488282. 
  78. ↑ "Serotonin 5-HT2B receptors are required for 3,4-methylenedioxymethamphetamine-induced hyperlocomotion and 5-HT release in vivo and in vitro". J Neurosci 28 (11): 2933–2940. March 2008. doi:10.1523/JNEUROSCI.5723-07.2008. PMID 18337424. 
  79. ↑ 79.0 79.1 79.2 79.3 79.4 "Distinct neural mechanisms for the prosocial and rewarding properties of MDMA". Sci Transl Med 11 (522). December 2019. doi:10.1126/scitranslmed.aaw6435. PMID 31826983. 
  80. ↑ "Systemic enhancement of serotonin signaling reverses social deficits in multiple mouse models for ASD". Neuropsychopharmacology 46 (11): 2000–2010. October 2021. doi:10.1038/s41386-021-01091-6. PMID 34239048. 
  81. ↑ 81.0 81.1 81.2 81.3 81.4 "The Role of Oxytocin and Vasopressin in Drug-Induced Reward-Implications for Social and Non-Social Factors". Biomolecules 13 (3): 405. February 2023. doi:10.3390/biom13030405. PMID 36979340. 
  82. ↑ "Looking for prosocial genes: ITRAQ analysis of proteins involved in MDMA-induced sociability in mice". Eur Neuropsychopharmacol 24 (11): 1773–1783. November 2014. doi:10.1016/j.euroneuro.2014.08.007. PMID 25241352. 
  83. ↑ 83.0 83.1 "No evidence that MDMA-induced enhancement of emotional empathy is related to peripheral oxytocin levels or 5-HT1a receptor activation". PLOS ONE 9 (6). 2014. doi:10.1371/journal.pone.0100719. PMID 24972084. Bibcode: 2014PLoSO...9j0719K. 
  84. ↑ "Exploring the regulatory framework of psychedelics in the US & Europe". Asian J Psychiatr 102. September 2024. doi:10.1016/j.ajp.2024.104242. PMID 39305768. 
  85. ↑ "Review of fenfluramine in the treatment of the developmental disabilities". J Am Acad Child Adolesc Psychiatry 28 (4): 549–565. July 1989. doi:10.1097/00004583-198907000-00014. PMID 2670881. 
  86. ↑ "5-HT1A and 5-HT1B receptor agonists and aggression: a pharmacological challenge of the serotonin deficiency hypothesis". Eur J Pharmacol 526 (1–3): 125–139. December 2005. doi:10.1016/j.ejphar.2005.09.065. PMID 16310183. 
  87. ↑ "Serotonin and aggression". Ann N Y Acad Sci 1036 (1): 382–392. December 2004. doi:10.1196/annals.1330.022. PMID 15817750. Bibcode: 2004NYASA1036..382O. 
  88. ↑ 88.0 88.1 "Pharmacotherapy of Primary Impulsive Aggression in Violent Criminal Offenders". Front Psychol 12. 2021. doi:10.3389/fpsyg.2021.744061. PMID 34975633. 
  89. ↑ 89.0 89.1 "Biased agonism in drug discovery: Is there a future for biased 5-HT1A receptor agonists in the treatment of neuropsychiatric diseases?". Pharmacol Ther 227. November 2021. doi:10.1016/j.pharmthera.2021.107872. PMID 33905796. 
  90. ↑ "The Current Status of Drug Discovery for the Oxytocin Receptor". Oxytocin. Methods Mol Biol. 2384. 2022. pp. 153–174. doi:10.1007/978-1-0716-1759-5_10. ISBN 978-1-0716-1758-8. 
  91. ↑ "Evaluating the Potential Use of Serotonergic Psychedelics in Autism Spectrum Disorder". Front Pharmacol 12. 2021. doi:10.3389/fphar.2021.749068. PMID 35177979. 
  92. ↑ "The effect of psilocybin on empathy and prosocial behavior: a proposed mechanism for enduring antidepressant effects". npj Ment Health Res 3 (1). February 2024. doi:10.1038/s44184-023-00053-8. PMID 38609500. 
  93. ↑ "From antidepressants and psychotherapy to oxytocin, vagus nerve stimulation, ketamine and psychedelics: how established and novel treatments can improve social functioning in major depression". Front Psychiatry 15. 2024. doi:10.3389/fpsyt.2024.1372650. PMID 39469469. 
  94. ↑ "Experimental strategies to discover and develop the next generation of psychedelics and entactogens as medicines". Neuropharmacology 225. March 2023. doi:10.1016/j.neuropharm.2022.109375. PMID 36529260. 
  95. ↑ "Advantageous benzofuran compositions for mental disorders or enhancement". 8 December 2022. https://patents.google.com/patent/US11767305B2/. 
  96. ↑ 96.0 96.1 96.2 Matthew Baggott, "Advantageous benzofuran compositions for mental disorders or enhancement", US patent 20230150963, published 2023 May 18, assigned to Tactogen
  97. ↑ 97.0 97.1 "Pharmacological Mechanism of the Non-hallucinogenic 5-HT2A Agonist Ariadne and Analogs". ACS Chemical Neuroscience 14 (1): 119–135. January 2023. doi:10.1021/acschemneuro.2c00597. PMID 36521179. "In rat drug discrimination assays, Ariadne substituted responding in LSD trained animals in one study, in another showed full substitution for MDMA stimulus.14,15 [...] 15). Glennon RA MDMA-like Stimulus Effects of α-Ethyltryptamine and the α-Ethyl Homolog of Dom. Pharmacology Biochemistry and Behavior 1993, 46 (2), 459–462. [PubMed: 7903460]". 
  98. ↑ 98.0 98.1 "MDMA-like stimulus effects of alpha-ethyltryptamine and the alpha-ethyl homolog of DOM". Pharmacol Biochem Behav 46 (2): 459–462. October 1993. doi:10.1016/0091-3057(93)90379-8. PMID 7903460. 
  99. ↑ "Stereoselective aspects of hallucinogenic drug action and drug discrimination studies of entactogens". Purdue University. May 1989. https://bitnest.netfirms.com/external/Theses/Oberlender1989. "The results of initial studies (Nichols et al., 1986) generally demonstrated the lack of LSD-Iike discriminative stimulus properties for the members of the entactogen drug class. This was confirmed and extended to other hallucinogens in tests with rats trained on entactogens. These results are summarized in Table 12. Table 12. Results of DD tests comparing entactogens and hallucinogens. [...] It seems clear that entactogen activity is distinct from that of hallucinogens. [...]" 
  100. ↑ "25X-NBOMe compounds - chemistry, pharmacology and toxicology. A comprehensive review". Crit Rev Toxicol 53 (1): 15–33. January 2023. doi:10.1080/10408444.2023.2194907. PMID 37115704. "For a better understanding of the actions of different NBOMes resulting from their molecular structure and receptor binding affinity, drug discrimination studies were performed. Animals trained with 4-methyl-2,5-dimethoxyamphetamine (DOM) and 3,4-methylenedioxymethamphetamine (MDMA) were used in the drug discrimination paradigm. 25B- and 25CNBOMe completely (80%) substituted DOM, while 25INBOMe produced 74% drug-appropriate responding (Gatch et al. 2017). On the other hand, only 25B-NBOMe fully substituted for MDMA, suggesting that this compound could be used as both a hallucinogen and an entactogen.". 
  101. ↑ "NBOMes-Highly Potent and Toxic Alternatives of LSD". Front Neurosci 14: 78. 2020. doi:10.3389/fnins.2020.00078. PMID 32174803. "Gatch et al. (2017) tested 25B-NBOMe, 25C-NBOMe, and 25I-NBOMe for discriminative stimulus effects similar to a prototypical psychedelic/hallucinogen DOM and to an empathogen, 3,4-methylenedioxymethamphetamine (MDMA). In DOM-trained rats 25B-NBOMe and 25C-NBOMe, but not 25I-NBOMe, fully substituted for this drug. 25B-NBOMe also fully substituted for MDMA. In both tests, the dose-effect curves for 25B-NBOMe had an inverted U-shape. It is suggested that 25B-NBOMe and 25C-NBOMe are most likely used as recreational psychedelics, although 25B-NBOMe may also be used as an empathogenic compound (Gatch et al., 2017). However, the latter assumption should be taken with caution, as some compounds (e.g., fenfluramine) that substitute for MDMA in rats do not produce MDMA-like empathogenic effects in humans (Schechter, 1988).". 
  102. ↑ "Serotonergic Psychedelics: Experimental Approaches for Assessing Mechanisms of Action". Handb Exp Pharmacol. Handbook of Experimental Pharmacology 252: 227–260. 2018. doi:10.1007/164_2018_107. ISBN 978-3-030-10560-0. PMID 29532180. "Recent studies employing drug discrimination in rats show that novel psychedelics including 25I-, 25B-, and 25C-NBOMe, and 5-MeO-DALT fully substitute for DOM; interestingly, the NBOMe drugs also substitute for MDMA, but 5-MeO-DALT does not (Gatch et al. 2017).". 
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  110. ↑ Shulgin, Alexander T. (1990). "History of MDMA". Ecstasy: The Clinical, Pharmacological and Neurotoxicological Effects of the Drug MDMA. Topics in the Neurosciences. 9. Boston, MA: Springer US. pp. 1–20. doi:10.1007/978-1-4613-1485-1_1. ISBN 978-1-4612-8799-5. http://link.springer.com/10.1007/978-1-4613-1485-1_1. Retrieved 15 May 2025. 
  111. ↑ "An exploration of the history and controversies surrounding MDMA and MDA". J Psychoactive Drugs 33 (3): 213–221. 2001. doi:10.1080/02791072.2001.10400568. PMID 11718314. 
  112. ↑ Colman, Andrew M. (2015) (in en). Dictionary of Psychology - Oxford Reference. doi:10.1093/acref/9780199657681.001.0001. ISBN 978-0-19-965768-1. 

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