Trip killer

{{See also|Trazodone#Antagonism of serotonergic psychedelics}}

Serotonergic psychedelics, such as psilocybin (found in psilocybin mushrooms), lysergic acid diethylamide (LSD), mescaline (found in peyote cactii), and dimethyltryptamine (DMT) (found in ayahuasca), mediate their hallucinogenic effects by acting as agonists of the serotonin 5-HT_2A receptor.{{Cite journal |vauthors=Nichols DE |date=April 2016 |title=Psychedelics |journal=Pharmacol Rev |volume=68 |issue=2 |pages=264–355 |doi=10.1124/pr.115.011478 |pmc=4813425 |pmid=26841800}}{{Cite book |vauthors=Nichols DE |date=2018 |title=Chemistry and Structure-Activity Relationships of Psychedelics |series=Current Topics in Behavioral Neurosciences |volume=36 |pages=1–43 |doi=10.1007/7854_2017_475 |pmid=28401524|isbn=978-3-662-55878-2 }} As a result, serotonin 5-HT_2A receptor antagonists would theoretically be expected to block the hallucinogenic effects of serotonergic psychedelics. Accordingly, the serotonin 5-HT_2A receptor antagonists ketanserin, an antihypertensive agent, and risperidone, an antipsychotic, have been shown to block the effects of serotonergic psychedelics in clinical studies.{{Cite journal |vauthors=Canal CE |date=2018 |title=Serotonergic Psychedelics: Experimental Approaches for Assessing Mechanisms of Action |journal=Handb Exp Pharmacol |series=Handbook of Experimental Pharmacology |volume=252 |pages=227–260 |doi=10.1007/164_2018_107 |isbn=978-3-030-10560-0 |pmc=6136989 |pmid=29532180 |quote=Reports from clinical trials conclude that the psychedelic effects of psilocybin and LSD are mediated by 5-HT2A receptors, because they are blocked by ketanserin (40 mg, P.O.), typically viewed as a selective 5-HT2A antagonist (Kometer et al. 2012; Kraehenmann et al. 2017; Preller et al. 2017; Quednow et al. 2012). Haloperidol, typically viewed as a selective dopamine D2 antagonist, is much less effective than ketanserin at blocking psilocybin's effects, but risperidone, an antipsychotic with combined D2/5-HT2 activity, is as effective as ketanserin (Vollenweider et al. 1998).}}{{Cite journal |vauthors=Holze F, Singh N, Liechti ME, D'Souza DC |date=May 2024 |title=Serotonergic Psychedelics: A Comparative Review of Efficacy, Safety, Pharmacokinetics, and Binding Profile |journal=Biol Psychiatry Cogn Neurosci Neuroimaging |volume=9 |issue=5 |pages=472–489 |doi=10.1016/j.bpsc.2024.01.007|pmid=38301886 |doi-access=free }} This includes the effects of psilocybin,{{Cite journal |vauthors=Vollenweider FX, Vollenweider-Scherpenhuyzen MF, Bäbler A, Vogel H, Hell D |date=December 1998 |title=Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action |journal=NeuroReport |volume=9 |issue=17 |pages=3897–3902 |doi=10.1097/00001756-199812010-00024 |pmid=9875725}}{{Cite journal |vauthors=Carter OL, Hasler F, Pettigrew JD, Wallis GM, Liu GB, Vollenweider FX |date=December 2007 |title=Psilocybin links binocular rivalry switch rate to attention and subjective arousal levels in humans |journal=Psychopharmacology (Berl) |volume=195 |issue=3 |pages=415–424 |doi=10.1007/s00213-007-0930-9 |pmid=17874073|url=http://doc.rero.ch/record/315131/files/213_2007_Article_930.pdf }}{{Cite journal |vauthors=Quednow BB, Kometer M, Geyer MA, Vollenweider FX |date=February 2012 |title=Psilocybin-induced deficits in automatic and controlled inhibition are attenuated by ketanserin in healthy human volunteers |journal=Neuropsychopharmacology |volume=37 |issue=3 |pages=630–640 |doi=10.1038/npp.2011.228 |pmc=3260978 |pmid=21956447}} LSD,{{Cite journal |vauthors=Holze F, Vizeli P, Ley L, Müller F, Dolder P, Stocker M, Duthaler U, Varghese N, Eckert A, Borgwardt S, Liechti ME |date=February 2021 |title=Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects |journal=Neuropsychopharmacology |volume=46 |issue=3 |pages=537–544 |doi=10.1038/s41386-020-00883-6 |pmc=8027607 |pmid=33059356}}{{Cite journal |vauthors=Becker AM, Klaiber A, Holze F, Istampoulouoglou I, Duthaler U, Varghese N, Eckert A, Liechti ME |date=February 2023 |title=Ketanserin Reverses the Acute Response to LSD in a Randomized, Double-Blind, Placebo-Controlled, Crossover Study in Healthy Participants |journal=Int J Neuropsychopharmacol |volume=26 |issue=2 |pages=97–106 |doi=10.1093/ijnp/pyac075 |pmid=36342343 |pmc=9926053}} mescaline,{{Cite journal |vauthors=Klaiber A, Schmid Y, Becker AM, Straumann I, Erne L, Jelusic A, Thomann J, Luethi D, Liechti ME |date=September 2024 |title=Acute dose-dependent effects of mescaline in a double-blind placebo-controlled study in healthy subjects |journal=Transl Psychiatry |volume=14 |issue=1 |pages=395 |doi=10.1038/s41398-024-03116-2 |pmc=11442856 |pmid=39349427}} and ayahuasca.{{Cite journal |vauthors=Valle M, Maqueda AE, Rabella M, Rodríguez-Pujadas A, Antonijoan RM, Romero S, Alonso JF, Mañanas MÀ, Barker S, Friedlander P, Feilding A, Riba J |date=July 2016 |title=Inhibition of alpha oscillations through serotonin-2A receptor activation underlies the visual effects of ayahuasca in humans |journal=Eur Neuropsychopharmacol |volume=26 |issue=7 |pages=1161–1175 |doi=10.1016/j.euroneuro.2016.03.012 |pmid=27039035|hdl=2117/101863 |hdl-access=free }} Ketanserin is under formal clinical investigation as a "neutralizer" or "off-switch" for psychedelics.{{cite web | last=Hallifax | first=James | title=New MindMed Study Shortens Trip with "LSD-Neutralizer" | website=Microdose | date=30 November 2022 | url=https://microdose.buzz/news/new-mindmed-study-can-shorten-an-lsd-trip/ | access-date=12 May 2025}}{{cite web | title=LSD "off-switch" developed by psychedelic pharmaceutical company | website=New Atlas | date=27 April 2020 | url=https://newatlas.com/science/lsd-off-switch-mindmed-liechti-psychedelic-science/ | access-date=12 May 2025}}{{cite web | title=Delving into the Latest Updates on Ketanserin with Synapse | website=Synapse | date=8 May 2025 | url=https://synapse.patsnap.com/drug/58c17006f00e495d96118ae65436560a | access-date=12 May 2025}} The more selective serotonin 5-HT_2A receptor antagonist pimavanserin is also being studied as a blocker of the effects of psychedelics.{{cite web | title=Psilocybin Mechanism of Action (MOA) | website=ClinicalTrials.gov | url=https://clinicaltrials.gov/study/NCT06592833 | access-date=13 November 2024}}

Other potent serotonin 5-HT_2A receptor antagonists that may block or reduce the effects of serotonergic psychedelics besides the above-listed drugs include other antipsychotics like quetiapine, olanzapine, aripiprazole, and pipamperone, antidepressants like trazodone, mirtazapine, mianserin, nefazodone, and etoperidone, and the antimigraine agent pizotifen, among others.{{cite journal | vauthors = Fradet M, Kelly CM, Donnelly AJ, Suppes T | title = Psilocybin and hallucinogenic mushrooms | journal = CNS Spectr | volume = 29 | issue = 6 | pages = 611–632 | date = December 2024 | pmid = 39789676 | doi = 10.1017/S1092852924002487 | url = | doi-access = free }} The typical antipsychotic chlorpromazine, which has significant but less-potent serotonin 5-HT_2A receptor antagonism than many other antipsychotics, has shown incomplete and inconsistent effects in reversing psychedelic effects in clinical studies,{{cite book | vauthors = Brimblecombe RW, Pinder RM | chapter = Indolealkylamines and Related Compounds | pages = 98–144 | title = Hallucinogenic Agents | date = 1975 | publisher = Wright-Scientechnica | location = Bristol | isbn = 978-0-85608-011-1 | oclc = 2176880 | ol = OL4850660M | url = https://bitnest.netfirms.com/external/Books/978-0-85608-011-1 | quote=Chlorpromazine is the recommended treatment for those 'bad trips' (Consroe, 1973), although it is not a complete antagonist and can exacerbate the symptoms of other drugs which may be present in illicit samples of LSD or be mistaken for LSD. Usually, the dose is 25-50 mg. intramuscularly, repeated every 30 minutes until the situation is under control.}} while the typical antipsychotic haloperidol, which is a dopamine D₂ receptor antagonist but not a significant serotonin 5-HT_2A receptor antagonist, is ineffective and has actually been found to increase anxiety and dysphoria in the setting of psychedelic experiences.{{Cite journal |vauthors=Halberstadt AL |date=January 2015 |title=Recent advances in the neuropsychopharmacology of serotonergic hallucinogens |journal=Behav Brain Res |volume=277 |pages=99–120 |doi=10.1016/j.bbr.2014.07.016 |pmc=4642895 |pmid=25036425}}{{cite journal | vauthors = Holze F, Liechti ME, Müller F | title = Pharmacological Properties of Psychedelics with a Special Focus on Potential Harms | journal = Current Topics in Behavioral Neurosciences | series = Curr Top Behav Neurosci | volume = | issue = | pages = | date = July 2024 | pmid = 39080236 | doi = 10.1007/7854_2024_510 | url = }} In spite of variably acting as serotonin 5-HT_2A receptor antagonists, tricyclic antidepressants (TCAs), including desipramine, imipramine, and clomipramine, have paradoxically been reported to potentiate the effects of serotonergic psychedelics rather than diminish them, albeit based on very limited data.

Cyproheptadine, a non-selective serotonin receptor antagonist including of the serotonin 5-HT_2A receptor, is used as an antidote in the treatment of serotonin syndrome (serotonin toxicity) caused by serotonergic drugs, including the toxicity of serotonergic psychedelics like the NBOMe drugs.{{cite journal | vauthors = Scotton WJ, Hill LJ, Williams AC, Barnes NM | title = Serotonin Syndrome: Pathophysiology, Clinical Features, Management, and Potential Future Directions | journal = Int J Tryptophan Res | volume = 12 | issue = | pages = 1178646919873925 | date = 2019 | pmid = 31523132 | pmc = 6734608 | doi = 10.1177/1178646919873925 | url = }}{{cite journal | vauthors = Ordak M, Zmysłowska A, Bielski M, Rybak D, Tomaszewska M, Wyszomierska K, Kmiec A, Garlicka N, Zalewska M, Zalewski M, Nasierowski T, Muszynska E, Bujalska-Zadrozny M | title = Pharmacotherapy of Patients Taking New Psychoactive Substances: A Systematic Review and Analysis of Case Reports | journal = Front Psychiatry | volume = 12 | issue = | pages = 669921 | date = 2021 | pmid = 33967865 | pmc = 8102790 | doi = 10.3389/fpsyt.2021.669921 | doi-access = free | url = }}{{cite journal | last1=Jacobs | first1=Elizabeth T | last2=Akers | first2=Katherine G | last3=Vohra | first3=Varun | last4=King | first4=Andrew M | title=Cyproheptadine for Serotonin Toxicity: an Updated Systematic Review and Grading of Evidence | journal=Current Emergency and Hospital Medicine Reports | publisher=Springer Science and Business Media LLC | volume=8 | issue=4 | date=10 October 2020 | issn=2167-4884 | doi=10.1007/s40138-020-00222-5 | pages=151–159}} Certain other serotonin receptor antagonists, like chlorpromazine, have also been used for such purposes.{{cite journal | vauthors = Chiew AL, Isbister GK | title = [Not Available] | language = French | journal = Br J Clin Pharmacol | volume = 91| issue = 3| pages = 654–661| date = June 2024 | pmid = 38926083 | doi = 10.1111/bcp.16152 | url = | doi-access = free | pmc = 11862804 }}

Non-hallucinogenic partial agonists of the serotonin 5-HT_2A receptor with sufficiently low intrinsic activity, such as 2-bromo-LSD (bromolysergide; BOL-148) and lisuride, are effective in blocking the hallucinogenic-related effects of psychedelics in animals and/or humans as well.{{cite journal | vauthors = Lewis V, Bonniwell EM, Lanham JK, Ghaffari A, Sheshbaradaran H, Cao AB, Calkins MM, Bautista-Carro MA, Arsenault E, Telfer A, Taghavi-Abkuh FF, Malcolm NJ, El Sayegh F, Abizaid A, Schmid Y, Morton K, Halberstadt AL, Aguilar-Valles A, McCorvy JD | title = A non-hallucinogenic LSD analog with therapeutic potential for mood disorders | journal = Cell Rep | volume = 42 | issue = 3 | pages = 112203 | date = March 2023 | pmid = 36884348 | pmc = 10112881 | doi = 10.1016/j.celrep.2023.112203 | url = }}{{cite journal | vauthors = Glatfelter GC, Pottie E, Partilla JS, Stove CP, Baumann MH | title = Comparative Pharmacological Effects of Lisuride and Lysergic Acid Diethylamide Revisited | journal = ACS Pharmacol Transl Sci | volume = 7 | issue = 3 | pages = 641–653 | date = March 2024 | pmid = 38481684 | doi = 10.1021/acsptsci.3c00192 | pmc = 10928901 | url = }} However, it has been argued that lisuride may actually be a psychedelic or hallucinogen itself at sufficiently high doses in humans.{{cite journal | vauthors = Kehler J, Lindskov MS | title = Are the LSD-analogs lisuride and ergotamine examples of non-hallucinogenic serotonin 5-HT2A receptor agonists? | journal = Journal of Psychopharmacology | pages = 2698811251330741 | date = May 2025 | pmid = 40322975 | doi = 10.1177/02698811251330741 }}

Serotonergic psychedelics are being developed as novel treatments for psychiatric disorders and other conditions such as depression.{{cite journal | vauthors = McClure-Begley TD, Roth BL | title = The promises and perils of psychedelic pharmacology for psychiatry | journal = Nat Rev Drug Discov | volume = 21 | issue = 6 | pages = 463–473 | date = June 2022 | pmid = 35301459 | doi = 10.1038/s41573-022-00421-7 | url = https://cdr.lib.unc.edu/downloads/jw827p78p}}{{cite journal | vauthors = Rhee TG, Davoudian PA, Sanacora G, Wilkinson ST | title = Psychedelic renaissance: Revitalized potential therapies for psychiatric disorders | journal = Drug Discov Today | volume = 28 | issue = 12 | pages = 103818 | date = December 2023 | pmid = 37925136 | doi = 10.1016/j.drudis.2023.103818 | url = }}{{cite book | last1=Nutt | first1=D. J. | last2=Peill | first2=J. M. | last3=Weiss | first3=B. | last4=Godfrey | first4=K. | last5=Carhart-Harris | first5=R. L. | last6=Erritzoe | first6=D. | title=Emerging Neurobiology of Antidepressant Treatments | chapter=Psilocybin and Other Classic Psychedelics in Depression | journal=Current Topics in Behavioral Neurosciences | publisher=Springer International Publishing | publication-place=Cham | volume=66 | date=2023 | isbn=978-3-031-66355-0 | doi=10.1007/7854_2023_451 | url=https://link.springer.com/10.1007/7854_2023_451 | access-date=12 May 2025 | pages=149–174 | pmid=37955822 | quote=5.1 Duration of Trip for Psychedelics: Why Does This Matter? [...] There are profound differences in the duration of action of serotonin psychedelics. LSD and mescaline are long lasting with effects for up to a day and so; often requiring overnight stays in clinical studies. Oral Psilocybin lasts approximately 4–6 h. Other psychedelics, like DMT (i.v. or smoked/intranasal) or 5-MEO-DMT (i.v./im/intranasal) can produce very short altered experiences (just 5–10 min). A key question is: are each equally effective for depression? If short acting psychedelics such as DMT and 5-MEO-DMT prove just as effective for treating depression, this would offer a cost-benefit when compared to longer lasting psychedelics such as psilocybin or LSD. [...] An alternative approach, being considered by some companies, is utilising a 5-HT2A receptor antagonist such as ketanserin (Becker et al. 2023) which can terminate an LSD trip after a given time, so shortening the treatment period in the clinic. Going forward, if psychedelics are integrated into health services; cost-benefit analyses will be crucial in delivering them as a viable treatment option. Overall, a shortened experience with similar antidepressant effects will be favourable.}} A practical limitation in terms of clinical use of many major psychedelics, for instance psilocybin, LSD, and mescaline, is their long durations of action (4–12{{nbsp}}hours), which may require a whole day of clinical monitoring.{{cite journal | vauthors = Ramaekers JG, Reckweg JT, Mason NL | title = Benefits and Challenges of Ultra-Fast, Short-Acting Psychedelics in the Treatment of Depression | journal = Am J Psychiatry | volume = 182 | issue = 1 | pages = 33–46 | date = January 2025 | pmid = 39741439 | doi = 10.1176/appi.ajp.20230890 | url = }}{{cite journal | vauthors = Ramaekers JG | title = Less is more? Antidepressant effects of short-acting psychedelics | journal = Neuropsychopharmacology | volume = 50 | issue = 6 | pages = 875–876 | date = May 2025 | pmid = 40258989 | doi = 10.1038/s41386-025-02103-5 | pmc = 12032289 | pmc-embargo-date = May 1, 2026 | url = }} In relation to this, shorter-acting psychedelics, like DMT, 5-MeO-DMT (mebufotenin), and bretisilocin (5-fluoro-MET; GM-2505), are also being investigated for potential therapeutic use.{{cite web | last=Peplow | first=Mark | title=Should Next-Generation Psychedelics Skip the Trip? | website=Scientific American | date=22 June 2024 | url=https://www.scientificamerican.com/article/should-next-generation-psychedelics-skip-the-trip/ | access-date=20 February 2025 | archive-url=https://archive.today/20240626183623/https://www.scientificamerican.com/article/should-next-generation-psychedelics-skip-the-trip/ | archive-date = 26 June 2024 | quote=But the psychoactive effects of [psychedelics] pose some major challenges. [...] And patients typically need close supervision for many hours while under the influence of the drugs, making it burdensome, expensive and impractical for many patients. To avoid these problems, some companies are tweaking psychedelic drugs to induce shorter or milder ‘trips’ that will not require such intensive patient oversight from clinicians. [...] Gilgamesh is also working on GM-2505, a 5-HT2A agonist that is structurally related to psilocybin and DMT. GM-2505 completed a phase 1 trial late last year and should enter phase 2 for major depressive disorder this year. Its psychedelic effect lasts 60 to 90 minutes — long enough for patients to “explore the altered state of consciousness that might be needed for long-term durable efficacy,” Krugel says, yet within a timeframe that is manageable for healthcare systems. [...]}} However, an alternative approach that is being investigated is use of serotonin 5-HT_2A receptor antagonists like ketanserin as trip killers to shorten the experiences of psychedelics.{{cite journal | last1=Aday | first1=Jacob S. | last2=Barnett | first2=Brian S. | last3=Grossman | first3=Dan | last4=Murnane | first4=Kevin S. | last5=Nichols | first5=Charles D. | last6=Hendricks | first6=Peter S. | title=Psychedelic Commercialization: A Wide-Spanning Overview of the Emerging Psychedelic Industry | journal=Psychedelic Medicine | volume=1 | issue=3 | date=1 September 2023 | issn=2831-4425 | pmid=40046566 | pmc=11661494 | doi=10.1089/psymed.2023.0013 | pages=150–165 | quote=Recent work supported by MindMed demonstrated that ketanserin is able to shorten the duration of LSD’s mind-altering effects while preserving LSD-induced elevations of brain-derived neurotrophic factor, a marker of neuroplasticity, suggesting the possibility that LSDinduced therapeutic effects might be retained despite the psychedelic experience being prematurely aborted.84 [...] Many of the formulation and chemical strategies target shortening the duration of action of psychedelics to promote patient compliance, reduce clinical utilization costs, and enhance their fit to the payment system of our current model of care. [...] Further, at present, very little is known about best practices for psychedelic-assisted psychotherapy, including the quantity and types of therapeutic support needed to maximize safety and efficacy, and companies are forced to navigate the tension between providing adequate support to participants while minimizing costs. One of the greatest costs will undoubtedly be therapist/monitor time, leading some companies to invest in researching and/or developing short-acting psychedelic compounds that theoretically reduce the amount of therapist time needed, or leading them to minimize the support offered in their trials (e.g., MindMed’s LSD for generalized anxiety disorder study87).}} In a clinical trial, ketanserin given 1{{nbsp}}hour after LSD shortened its duration from 8.5{{nbsp}}hours to 3.5{{nbsp}}hours (by ~60%). It did not modify the pharmacokinetics of LSD, and its side effects, such as nasal congestion, were minimal.

Benzodiazepines, such as diazepam and alprazolam, are sometimes used to manage the effects of serotonergic psychedelics, including clinically.{{Cite book |last1=Halpern |first1=John H. |title=Addiction Medicine |last2=Suzuki |first2=Joji |last3=Huertas |first3=Pedro E. |last4=Passie |first4=Torsten |publisher=Springer New York |year=2010 |isbn=978-1-4419-0337-2 |publication-place=New York, NY |pages=1083–1098 |chapter=Hallucinogens |doi=10.1007/978-1-4419-0338-9_54}} They act as positive allosteric modulators of the GABA_A receptor, and do not specifically antagonize hallucinogenic effects (i.e., are not antidotes), but instead have anxiolytic, sedative, and memory-impairing effects that can lessen the negative effects of psychedelic experiences.{{Cite journal |vauthors=Olsen RW |date=July 2018 |title=GABAA receptor: Positive and negative allosteric modulators |journal=Neuropharmacology |volume=136 |issue=Pt A |pages=10–22 |doi=10.1016/j.neuropharm.2018.01.036 |pmc=6027637 |pmid=29407219}} Alcohol, which is also a GABA_A receptor positive allosteric modulator with similar effects, has been used for such purposes as well.

Besides serotonin 5-HT_2A receptor antagonists, chronic use of other serotonergic drugs may also diminish the effects of serotonergic psychedelics. Examples include serotonin 5-HT_1A receptor agonists like buspirone, serotonin reuptake inhibitors such as selective serotonin reuptake inhibitors (SSRIs) like fluoxetine, paroxetine, and sertraline and serotonin–norepinephrine reuptake inhibitors (SNRIs) like venlafaxine, duloxetine, and milnacipran, and monoamine oxidase inhibitors (MAOIs) such as phenelzine, tranylcypromine, and moclobemide. Buspirone, a partial agonist of the serotonin 5-HT_1A receptor, has specifically been found to markedly attenuate the visual and certain other effects of psilocybin, although it did not completely block the hallucinogenic effects of psilocybin.{{cite journal | vauthors = Brandt SD, Kavanagh PV, Twamley B, Westphal F, Elliott SP, Wallach J, Stratford A, Klein LM, McCorvy JD, Nichols DE, Halberstadt AL | title = Return of the lysergamides. Part IV: Analytical and pharmacological characterization of lysergic acid morpholide (LSM-775) | journal = Drug Test Anal | volume = 10 | issue = 2 | pages = 310–322 | date = February 2018 | pmid = 28585392 | pmc = 6230476 | doi = 10.1002/dta.2222 | url = | quote = Additionally, pretreatment with the 5‐HT1A agonist buspirone (20 mg p.o.) markedly attenuates the visual effects of psilocybin in human volunteers.59 Although buspirone failed to completely block the hallucinogenic effects of psilocybin, the limited inhibition is not necessarily surprising because buspirone is a low efficacy 5‐HT1A partial agonist.60 The level of 5‐HT1A activation produced by buspirone may not be sufficient to completely counteract the stimulation of 5‐HT2A receptors by psilocin (the active metabolite of psilocybin). Another consideration is that psilocin acts as a 5‐HT1A agonist.30 If 5‐HT1A activation by psilocin buffers its hallucinogenic effects similar to DMT58 then competition between psilocin and a weaker partial agonist such as buspirone would limit attenuation of the hallucinogenic response.}}{{cite journal | vauthors = Pokorny T, Preller KH, Kraehenmann R, Vollenweider FX | title = Modulatory effect of the 5-HT1A agonist buspirone and the mixed non-hallucinogenic 5-HT1A/2A agonist ergotamine on psilocybin-induced psychedelic experience | journal = Eur Neuropsychopharmacol | volume = 26 | issue = 4 | pages = 756–766 | date = April 2016 | pmid = 26875114 | doi = 10.1016/j.euroneuro.2016.01.005 | url = }} The reduced effects of psychedelics in the case of concomitant drugs that elevate serotonin levels may be due to desensitization of serotonin 5-HT_2A receptors. In contrast to earlier studies however, other more recent studies have found that SSRIs like escitalopram may not diminish the hallucinogenic effects of psychedelics like psilocybin and DMT.{{cite journal | vauthors = James E, Joel Z, Attwooll V, Benway T, Good M, Tziras G, Routledge C, Macek T | title=ACNP 63rd Annual Meeting: Poster Abstracts P1-P304: P160. SPL026 (DMT Fumarate) in Combination With Selective Serotonin Reuptake Inhibitors (SSRIs) for Patients With Major Depressive Disorder | journal=Neuropsychopharmacology | volume=49 | issue=S1 | date=2024 | issn=0893-133X | pmid=39643633 | pmc=11627186 | doi=10.1038/s41386-024-02011-0 | doi-access=free | pages=65–235 (155–156) | url=https://www.nature.com/articles/s41386-024-02011-0.pdf | access-date=31 January 2025}} Instead, in one study, escitalopram resulted in greater mystical experience, emotional breakthrough, and ego dissolution scores with DMT than in people not on escitalopram.

Although MAOIs can diminish the effects of serotonergic psychedelics, it must be noted that some serotonergic psychedelics, such as DMT, are highly susceptible substrates for monoamine oxidase (MAO), and hence can simultaneously be greatly potentiated by MAOIs (as in ayahuasca).{{cite journal | last1=Egger | first1=Klemens | last2=Aicher | first2=Helena D. | last3=Cumming | first3=Paul | last4=Scheidegger | first4=Milan | title=Neurobiological research on N,N-dimethyltryptamine (DMT) and its potentiation by monoamine oxidase (MAO) inhibition: from ayahuasca to synthetic combinations of DMT and MAO inhibitors | journal=Cellular and Molecular Life Sciences | publisher=Springer Science and Business Media LLC | volume=81 | issue=1 | date=10 September 2024 | issn=1420-682X | doi=10.1007/s00018-024-05353-6 | doi-access=free | page=395| pmid=39254764 | pmc=11387584 }} The 2C drugs, such as 2C-B, 2C-I, and 2C-E, are also notable substrates of both MAO-A and MAO-B, and may likewise be greatly potentiated by MAOIs.{{cite journal | vauthors = Dean BV, Stellpflug SJ, Burnett AM, Engebretsen KM | title = 2C or not 2C: phenethylamine designer drug review | journal = J Med Toxicol | volume = 9 | issue = 2 | pages = 172–178 | date = June 2013 | pmid = 23494844 | pmc = 3657019 | doi = 10.1007/s13181-013-0295-x | url = }}{{cite journal | vauthors = Theobald DS, Maurer HH | title = Identification of monoamine oxidase and cytochrome P450 isoenzymes involved in the deamination of phenethylamine-derived designer drugs (2C-series) | journal = Biochem Pharmacol | volume = 73 | issue = 2 | pages = 287–297 | date = January 2007 | pmid = 17067556 | doi = 10.1016/j.bcp.2006.09.022 | url = }}

High-dose nicotinic acid (niacin, a B₃ vitamer) was reported to reduce and block the effects of LSD in one early clinical study.{{Cite book |last=Murphree |first=Henry |title=Research Advances in Alcohol and Drug Problems |publisher=Springer US |year=1983 |isbn=978-1-4613-3628-0 |publication-place=Boston, MA |pages=175–205 |chapter=The Pharmacology of Hallucinogens |doi=10.1007/978-1-4613-3626-6_5 |quote=In older work, various steroids (Bergen et al., 1960) including progesterone (Krus et al., 1961) were reported to be effective antagonists. This has not been replicated. In other early work, some compounds initially reported to be effective were not found to be so by other workers. These include azacyclonal (Fabing, 1955) and niacin (Agnew and Hoffer, 1955).}}{{Cite journal |vauthors=Agnew N, Hoffer A |date=January 1955 |title=Nicotinic acid modified lysergic acid diethylamide psychosis |journal=J Ment Sci |volume=101 |issue=422 |pages=12–27 |doi=10.1192/bjp.101.422.12 |pmid=14368207}} However, a subsequent clinical study attempting to replicate the findings found that it was not effective for this purpose. Azacyclonol, a claimed ataractive (i.e., non-antipsychotic hallucination-suppressing medication) that is no longer marketed, likewise seems to be ineffective. Other non-serotonergic drugs that may block or reduce the effects of serotonergic psychedelics based on animal studies include AMPA receptor antagonists, metabotropic glutamate mGlu₂ and mGlu₃ receptor agonists, μ-opioid receptor agonists, and adenosine A₁ receptor agonists.{{cite book | vauthors = Marek GJ, Schoepp DD | chapter = Cortical influences of serotonin and glutamate on layer V pyramidal neurons | title = 5-HT Interaction with Other Neurotransmitters: Experimental Evidence and Therapeutic Relevance - Part B | journal = Prog Brain Res | series = Progress in Brain Research | volume = 261 | issue = | pages = 341–378 | date = 2021 | pmid = 33785135 | doi = 10.1016/bs.pbr.2020.11.002 | isbn = 978-0-444-64258-5 | url = }}{{cite journal | vauthors = Marek GJ | title = Behavioral evidence for mu-opioid and 5-HT2A receptor interactions | journal = Eur J Pharmacol | volume = 474 | issue = 1 | pages = 77–83 | date = August 2003 | pmid = 12909198 | doi = 10.1016/s0014-2999(03)01971-x | url = }}

Some drugs that have been reported to potentiate rather than inhibit the effects of serotonergic psychedelics include lithium, reserpine, pindolol, and methysergide. Pindolol, a beta blocker and serotonin 5-HT_1A receptor antagonist, has been reported to potentiate the hallucinogenic effects of DMT by 2- to 3-fold in humans.{{cite journal | vauthors = Strassman RJ | title = Human psychopharmacology of N,N-dimethyltryptamine | journal = Behav Brain Res | volume = 73 | issue = 1–2 | pages = 121–124 | date = 1996 | pmid = 8788488 | doi = 10.1016/0166-4328(96)00081-2 | url = }} A high rate of seizures has been reported with the combination of lithium and psychedelics.{{cite journal | vauthors = Nayak SM, Gukasyan N, Barrett FS, Erowid E, Erowid F, Griffiths RR | title = Classic Psychedelic Coadministration with Lithium, but Not Lamotrigine, is Associated with Seizures: An Analysis of Online Psychedelic Experience Reports | journal = Pharmacopsychiatry | volume = 54 | issue = 5 | pages = 240–245 | date = September 2021 | pmid = 34348413 | doi = 10.1055/a-1524-2794 | url = https://www.thieme-connect.com/products/ejournals/pdf/10.1055/a-1524-2794.pdf}}

Recreational psychedelic users sometimes employ trip killers to abort psychedelic trips. The most commonly encountered putative trip killers in a 2024 online study of Reddit social media postings were the benzodiazepines alprazolam and diazepam, the antipsychotic quetiapine, the antidepressant trazodone, and alcohol.{{Cite journal |last=Davidson |first=Colin |date=14 February 2024 |title=Using "trip killers" to cut short bad drug trips is potentially dangerous. |url=https://go.gale.com/ps/i.do?p=HRCA&sw=w&v=2.1&it=r&id=GALE%7CA782593467&sid=googleScholar&linkaccess=abs&userGroupName=anon~65c6fefa&aty=open-web-entry |journal=The Conversation (UK Edition) |publisher=SyndiGate Media Inc. |pages=NA |access-date=3 October 2024}} Others used less frequently included the benzodiazepines lorazepam, clonazepam, and etizolam, the antipsychotic olanzapine, and the antidepressant mirtazapine, among others. While employed by recreational users for harm-reduction purposes, the use of trip killers to abort the effects of psychedelics is not fully characterized and could pose medical risks. In addition, doses of trip killers used by recreational psychedelic users may be non-optimal or excessive and increase risks.

Cannabinoid CB₁ receptor antagonists like rimonabant, drinabant, surinabant, and selonabant have been found to block or reduce the psychoactive effects of cannabinoids in clinical studies and could be useful as antidotes against cannabinoid toxicity.{{Cite journal |vauthors=Skolnick P, Crystal R |date=February 2020 |title=Cannabinoid1 (CB-1) receptor antagonists: a molecular approach to treating acute cannabinoid overdose |journal=J Neural Transm (Vienna) |volume=127 |issue=2 |pages=279–286 |doi=10.1007/s00702-019-02132-7 |pmc=7035232 |pmid=31893308}}{{Cite journal |last1=Bosquez-Berger |first1=Taryn |last2=Szanda |first2=Gergő |last3=Straiker |first3=Alex |date=30 August 2023 |title=Requiem for Rimonabant: Therapeutic Potential for Cannabinoid CB1 Receptor Antagonists after the Fall |journal=Drugs and Drug Candidates |volume=2 |issue=3 |pages=689–707 |doi=10.3390/ddc2030035 |issn=2813-2998 |doi-access=free}}{{cite journal | vauthors = Gorbenko AA, Heuberger JA, Juachon M, Klaassen E, Tagen M, Lawler JF, Schneeberger D, Cundy KC, Klumpers LE, Groeneveld GJ | title = CB1 Receptor Antagonist Selonabant (ANEB-001) Blocks Acute THC Effects in Healthy Volunteers: A Phase II Randomized Controlled Trial | journal = Clin Pharmacol Ther | volume = 117| issue = 5| pages = 1427–1436| date = February 2025 | pmid = 39898464 | doi = 10.1002/cpt.3581 | url = | doi-access = free | pmc = 11993283 }} Likewise, the hallucinogenic and other effects of κ-opioid receptor agonists like salvinorin A (found in Salvia divinorum), butorphanol, and pentazocine have been shown to be blocked by the non-selective opioid receptor antagonist naltrexone in clinical studies.{{Cite journal |vauthors=Clark SD, Abi-Dargham A |date=October 2019 |title=The Role of Dynorphin and the Kappa Opioid Receptor in the Symptomatology of Schizophrenia: A Review of the Evidence |journal=Biol Psychiatry |volume=86 |issue=7 |pages=502–511 |doi=10.1016/j.biopsych.2019.05.012 |pmid=31376930 |quote=Finally, in a double-blind study of 24 healthy volunteers, Maqueda et al. (27) found that salvinorin A produced both visual and auditory changes that could be blocked by the kappa, mu, and delta receptor antagonist naltrexone (Table 2).|doi-access=free }}{{Cite journal |vauthors=Maqueda AE, Valle M, Addy PH, Antonijoan RM, Puntes M, Coimbra J, Ballester MR, Garrido M, González M, Claramunt J, Barker S, Lomnicka I, Waguespack M, Johnson MW, Griffiths RR, Riba J |date=July 2016 |title=Naltrexone but Not Ketanserin Antagonizes the Subjective, Cardiovascular, and Neuroendocrine Effects of Salvinorin-A in Humans |journal=Int J Neuropsychopharmacol |volume=19 |issue=7 |pages=pyw016 |doi=10.1093/ijnp/pyw016 |pmc=4966277 |pmid=26874330}}{{Cite journal |vauthors=Walsh SL, Chausmer AE, Strain EC, Bigelow GE |date=January 2008 |title=Evaluation of the mu and kappa opioid actions of butorphanol in humans through differential naltrexone blockade |journal=Psychopharmacology (Berl) |volume=196 |issue=1 |pages=143–155 |doi=10.1007/s00213-007-0948-z |pmid=17909753 |pmc=2766188}}{{Cite journal |vauthors=Preston KL, Bigelow GE |date=February 1993 |title=Differential naltrexone antagonism of hydromorphone and pentazocine effects in human volunteers |journal=J Pharmacol Exp Ther |volume=264 |issue=2 |pages=813–823 |doi=10.1016/S0022-3565(25)10212-7 |pmid=7679737}} Although clinical management of antimuscarinic deliriant intoxication and poisoning, for instance due to scopolamine, is usually supportive, acetylcholinesterase inhibitors, such as physostigmine, have sometimes been used in this context as well.{{cite journal | vauthors = Shim KH, Kang MJ, Sharma N, An SS | title = Beauty of the beast: anticholinergic tropane alkaloids in therapeutics | journal = Nat Prod Bioprospect | volume = 12 | issue = 1 | pages = 33 | date = September 2022 | pmid = 36109439 | doi = 10.1007/s13659-022-00357-w | url = | quote = The treatment of TA poisoning including gastric emptying, use of activated charcoal (0.5 to 1 g/kg in children or 25 to 100 g in adults) to absorb the drug and benzodiazepines for managing agitation [157, 158]. Physostigmine (an AChE inhibitor) is recommended in the case when both PNS and CNS are afected by anticholinergic poisoning [159, 160]. In such cases, intravenous dose of physostigmine (0.02 mg/kg for children and 0.5 to 2 mg/ kg for adults) is recommended [159]. Physostigmine is helpful in restoring the level of consciousness to its baseline [157] which is diferent from sedative action of benzodiazepines.| pmc = 9478010 }}{{cite journal | vauthors = Bulut NS, Arpacıoğlu ZB | title = Acute onset psychosis with complex neurobehavioural symptomatology following the intramuscular injection of hyoscine butylbromide: a case report with an overview of the literature | journal = Eur J Hosp Pharm | volume = 29 | issue = 5 | pages = 294–297 | date = September 2022 | pmid = 33376193 | doi = 10.1136/ejhpharm-2020-002583 | url = | quote = The most crucial intervention in the treatment of anticholinergic intoxication is without doubt the discontinuation of the suspected agent. Hospitalisation may be necessary for the close monitoring of severe cases. While physostigmine is commonly used as a specific antidote for anticholinergic toxicity, benzodiazepines and antipsychotics can prove to be useful in managing agitation, hallucinations, and aggressive and self-mutilative behaviours as in our case.2| pmc = 9660700 }} Benzodiazepines and antipsychotics have also been used in such situations.

Although trip killers exist for certain types of hallucinogens, antidotes do not exist for all types of hallucinogens, for instance NMDA receptor antagonist dissociatives like ketamine and phencyclidine (PCP).{{Cite journal |vauthors=Schep LJ, Slaughter RJ, Watts M, Mackenzie E, Gee P |date=June 2023 |title=The clinical toxicology of ketamine |journal=Clin Toxicol (Phila) |volume=61 |issue=6 |pages=415–428 |doi=10.1080/15563650.2023.2212125 |pmid=37267048}}{{Cite book |last1=Jenkins |first1=Amanda J. |title=Principles of Forensic Toxicology |last2=Gates |first2=Madeleine J. |publisher=Springer International Publishing |year=2020 |isbn=978-3-030-42916-4 |publication-place=Cham |pages=467–489 |chapter=Hallucinogens and Psychedelics |doi=10.1007/978-3-030-42917-1_26}} NMDA receptor agonists, which theoretically could reverse the effects of NMDA receptor antagonists, can produce excitotoxic neurotoxicity and convulsions, which restricts their potential medical use.{{Cite journal |vauthors=Gonda X |date=2012 |title=Basic pharmacology of NMDA receptors |journal=Curr Pharm Des |volume=18 |issue=12 |pages=1558–1567 |doi=10.2174/138161212799958521 |pmid=22280436}}{{Cite journal |vauthors=Rana V, Ghosh S, Bhatt A, Bisht D, Joshi G, Purohit P |date=2024 |title=N-Methyl-D-Aspartate (NMDA) Receptor Antagonists and their Pharmacological Implication: A Medicinal Chemistry-oriented Perspective Outline |journal=Curr Med Chem |volume=31 |issue=29 |pages=4725–4744 |doi=10.2174/0109298673288031240405061759|pmid=38638036 }}{{Cite journal |last1=Rothman |first1=Steven M. |last2=Olney |first2=John W. |year=1987 |title=Excitotoxity and the NMDA receptor |journal=Trends in Neurosciences |publisher=Elsevier BV |volume=10 |issue=7 |pages=299–302 |doi=10.1016/0166-2236(87)90177-9 |issn=0166-2236}} In any case, benzodiazepines can be useful in managing dissociative intoxication, but can also augment sedation and associated risks.{{cite journal | vauthors = Bey T, Patel A | title = Phencyclidine intoxication and adverse effects: a clinical and pharmacological review of an illicit drug | journal = Cal J Emerg Med | volume = 8 | issue = 1 | pages = 9–14 | date = February 2007 | pmid = 20440387 | pmc = 2859735 | doi = | url = }} As with NMDA receptor antagonists, there is no antidote for Amanita muscaria intoxication, in which the hallucinogenic GABA_A receptor agonist muscimol is the active constituent.{{cite journal | vauthors = Mitchel DH | title = Amanita mushroom poisoning | journal = Annu Rev Med | volume = 31 | issue = | pages = 51–57 | date = 1980 | pmid = 6772091 | doi = 10.1146/annurev.me.31.020180.000411 | url = }}{{cite journal | vauthors = Rampolli FI, Kamler P, Carnevale Carlino C, Bedussi F | title = The Deceptive Mushroom: Accidental Amanita muscaria Poisoning | journal = Eur J Case Rep Intern Med | volume = 8 | issue = 3 | pages = 002212 | date = 2021 | pmid = 33768066 | doi = 10.12890/2021_002212 | url = | pmc = 7977045 }}

Entactogens like MDMA and MDA are generally only mildly hallucinogenic at best, but use of "trip killers" to reverse the effects of these drugs has also been described. Entactogens act primarily as serotonin releasing agents that indirectly activate serotonin receptors and require entry into serotonergic neurons via the serotonin transporter (SERT) to induce their entactogenic effects. Serotonin reuptake inhibitors (SRIs), for instance selective serotonin reuptake inhibitors (SSRIs) like fluoxetine and citalopram and serotonin–norepinephrine reuptake inhibitors (SNRIs) like duloxetine, can markedly block or abolish the serotonin release induced by entactogens by preventing their transport into these neurons, and thus can strongly reduce most of their subjective effects in humans.{{cite book| vauthors = Halberstadt AL, Nichols DE |title=Handbook of the Behavioral Neurobiology of Serotonin|chapter=Serotonin and serotonin receptors in hallucinogen action|series=Handbook of Behavioral Neuroscience|volume=31|year=2020|pages=843–863|issn=1569-7339|doi=10.1016/B978-0-444-64125-0.00043-8|isbn=9780444641250|s2cid=241134396|quote=Pretreatment with the selective 5-HT reuptake inhibitors citalopram, fluoxetine, and paroxetine significantly attenuated most of the subjective effects of MDMA, consistent with the proposed involvement of carriermediated 5-HT release in the effects of MDMA (Farre et al., 2007; Liechti, Baumann, et al., 2000; Tancer & Johanson, 2007). Citalopram also inhibits the effect of MDMA on PPI (Liechti, Geyer, Hell, & Vollenweider, 2001). According to another report (Hysek, Simmler et al., 2012), the mixed SERT/NET inhibitor duloxetine robustly blocked most of the subjective response to MDMA, raising the possibility that NE release contributes to its effects. In a follow-up study, the selective NET inhibitor reboxetine significantly reduced the emotional excitation and feelings of stimulation produced by MDMA but did not alter its entactogenic or mood-elevating effects (Hysek et al., 2011). Therefore, although NE release contributes to the stimulant effects produced by MDMA, 5-HT release appears to be principally responsible for the unique entactogenic effects of the drug. [...] Several studies have examined the contribution of 5-HT and DA receptors to the effects of MDMA. Pretreatment with ketanserin produced some attenuation of the subjective effects of MDMA (Liechti, Saur, et al., 2000). However, the most significant reduction of MDMA effects by ketanserin occurred in the VR dimension of the APZ, indicating that 5-HT2A receptors are responsible for the effects of MDMA on perception. Ketanserin also blocked MDMA-induced impairment of performance on a verbal memory task (van Wel et al., 2011), but had no effect on the ability of MDMA to induce depersonalization and derealization (Puxty et al., 2017).}}{{cite journal | vauthors = Price CM, Feduccia AA, DeBonis K | title = Effects of Selective Serotonin Reuptake Inhibitor Use on 3,4-Methylenedioxymethamphetamine-Assisted Therapy for Posttraumatic Stress Disorder: A Review of the Evidence, Neurobiological Plausibility, and Clinical Significance | journal = J Clin Psychopharmacol | volume = 42 | issue = 5 | pages = 464–469 | date = 2022 | pmid = 36018231 | doi = 10.1097/JCP.0000000000001595 | url = https://escholarship.org/uc/item/0rw3v152| quote = Anecdotal reports for decades have suggested that current SSRI use can significantly dampen or abolish the subjective effects of MDMA and serotonergic hallucinogens,16–22 although this was not always observed.23 Controlled studies beginning in the 2000s began to shed further light on this phenomenon by examining the impact of SSRI and MDMA coadministration in healthy controls. The SSRIs citalopram, paroxetine, and fluoxetine were all shown to reduce most of the psychological effects of MDMA when given as pretreatment, either orally for 3 to 5 days24–26 or intravenously for 90 minutes27,28 before MDMA oral dosing. The psychological effects of MDMA that were attenuated by SSRIs included positive mood/euphoria, alterations in thought process and content, extraversion/self-confidence, and dissociative phenomena. Not all psychological effects of MDMA were attenuated by SSRIs, however; effects on emotional excitability, sensitivity, and anxiety remained even with SSRI pretreatment.25,29 Selective serotonin reuptake inhibitors also reduced the effects of MDMA on various physiological parameters, including increases in blood pressure, heart rate, temperature, and pupil diameter.24–29 [...] 9 Studies in animal models support the idea that such attenuation of MDMA's effects via acute SSRI pretreatment occurs primarily through blockage of the serotonin reuptake transporter (SERT). Serotonin reuptake transporter–knockout animals have a marked reduction in MDMA-mediated serotonin release and subsequent depletion and neurotoxicity.30,31 Pretreatment of rats with SSRIs similarly attenuated MDMA-mediated increases in extracellular serotonin and led to preservation of serotonin metabolite concentrations and SERT binding that is normally depleted by MDMA after 1 week.32–35 }}{{cite journal | vauthors = Liechti ME, Vollenweider FX | title = Which neuroreceptors mediate the subjective effects of MDMA in humans? A summary of mechanistic studies | journal = Hum Psychopharmacol | volume = 16 | issue = 8 | pages = 589–598 | date = December 2001 | pmid = 12404538 | doi = 10.1002/hup.348 | url = }} The serotonin 5-HT_2A receptor antagonist ketanserin has also been found to partially reduce some of the subjective effects of MDMA, particularly its perceptual effects, whereas the serotonin 5-HT_1A receptor antagonist pindolol was largely ineffective.{{cite journal | vauthors = Liechti ME, Saur MR, Gamma A, Hell D, Vollenweider FX | title = Psychological and physiological effects of MDMA ("Ecstasy") after pretreatment with the 5-HT(2) antagonist ketanserin in healthy humans | journal = Neuropsychopharmacology | volume = 23 | issue = 4 | pages = 396–404 | date = October 2000 | pmid = 10989266 | doi = 10.1016/S0893-133X(00)00126-3 | url = }}{{cite journal | vauthors = van Wel JH, Kuypers KP, Theunissen EL, Bosker WM, Bakker K, Ramaekers JG | title = Effects of acute MDMA intoxication on mood and impulsivity: role of the 5-HT2 and 5-HT1 receptors | journal = PLOS ONE | volume = 7 | issue = 7 | pages = e40187 | date = 2012 | pmid = 22808116 | pmc = 3393729 | doi = 10.1371/journal.pone.0040187 | doi-access = free | bibcode = 2012PLoSO...740187V | url = }} Non-selective serotonin receptor antagonists like cyproheptadine have been used in the clinical management of serotonin toxicity induced by MDMA, for instance in overdose or precipitated by drug interactions like with monoamine oxidase inhibitors (MAOIs).{{cite journal | vauthors = Rusyniak DE, Sprague JE | title = Toxin-induced hyperthermic syndromes | journal = Med Clin North Am | volume = 89 | issue = 6 | pages = 1277–1296 | date = November 2005 | pmid = 16227063 | doi = 10.1016/j.mcna.2005.06.002 | url = }}{{cite journal | vauthors = Doyle AJ, Meyer J, Breen K, Hunt BJ | title = N-Methyl-3,4-methylendioxymethamphetamine (MDMA)-related coagulopathy and rhabdomyolysis: A case series and literature review | journal = Res Pract Thromb Haemost | volume = 4 | issue = 5 | pages = 829–834 | date = July 2020 | pmid = 32685891 | pmc = 7354411 | doi = 10.1002/rth2.12360 | url = }}{{cite journal | last1=Krolikowski | first1=Allana M. | last2=Koyfman | first2=Alex | title=Methamphetamine and MDMA: 'Safe' drugs of abuse | journal=African Journal of Emergency Medicine | volume=4 | issue=1 | date=2014 | doi=10.1016/j.afjem.2013.01.005 | doi-access=free | pages=34–38}}

• Psychedelic drug § Interactions

{{Reflist}}

• [https://doubleblindmag.com/dangers-of-trip-killers/ Reddit Says Xanax Is the Best “Trip Killer,” But Is It Safe? - Double Blind Magazine]
• [https://psychedelicreview.com/how-to-stop-a-psychedelic-trip-the-promise-of-ketanserin/ How To Stop A Psychedelic Trip: The Promise of Ketanserin - Psychedelic Science Review (PSR)]
• [https://psychedelicreview.com/stopping-bad-lsd-trips-with-off-switch-technology/ Stopping Bad LSD Trips with “Off-Switch” Technology - Psychedelic Science Review (PSR)]
• [https://theconversation.com/using-trip-killers-to-cut-short-bad-drug-trips-is-potentially-dangerous-222527 Using ‘trip killers’ to cut short bad drug trips is potentially dangerous - The Conversation]

{{Recreational drug use}}

Category:Hallucinogen antidotes