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Dissociative

Dextromethorphan

Also called DXM, DMO, DM, Dex, Robitussin, Delsym, DexAlone, Duract

Original Wikipedia articleen.wikipedia.org/wiki/Dextromethorphan revision used (24 October 2026)

Why a "revision used" link? Anyone can edit Wikipedia at any time, so the article you open today may not say what it said when we read it. This link opens the exact version we read on 24 October 2026, frozen as it was. It is the only way to check that every quote on this page matches its source word for word. Newer versions may correct or change things. When we re-check this page against a newer version, the edit log records it. How we cite

Common dose · Oral200–400 mg PW
Onset30–120 minutes PW
Total8–12 hours PW
After-effects4–24 hours PW

Dosage

When sources disagree, both rows are shown as published. Nothing is averaged or merged.

Oral

SourceThresholdLightCommonStrongHeavy
PsychonautWiki75 mg PW100–200 mg PW200–400 mg PW400–700 mg PW700 mg+ PW
TripSit–1.5–2.5 mg/kg TS2.5–7.5 mg/kg TS7.5–15 mg/kg TS15–20 mg/kg TS

NOTE: See http://dxm.tripsit.me for mg/lb doses, among other things. Deaths have been reported at 25mg/kg TS

TripSit dose text

TripSit's factsheet also states its doses as text.

Oral First-Plateau: 1.5-2.5mg/kg Second-Plateau: 2.5-7.5mg/kg Third-Plateau: 7.5-15mg/kg Fourth: 15-20mg/kg | NOTE: See http://dxm.tripsit.me for mg/lb doses, among other things. Deaths have been reported at 25mg/kg TS

What dose are you on? (self-reported, unverified)
Read this first. These numbers come from anonymous visitors typing in a box. Nobody checks them. People misjudge, mistype, troll, or take untested products of unknown strength. They are not a dose guide and never override the sourced table above. They exist only so the sourced ranges can be compared with what people say they take. If you are deciding what to take, use the sourced table, start low, and read the risks section.
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Duration

Route · sourceOnsetCome-upPeakOffsetTotalAfter-effects
Oral · PsychonautWiki30–120 minutes PW60–120 minutes PW3–6 hours PW2–4 hours PW8–12 hours PW4–24 hours PW

TripSit factsheet

Onset
20-60 minutes TS
Duration
6-8 hours TS
Aftereffects
1-12 hours TS

Mixing

Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.

Backed by medical journals

  • Dangerous Antihistamines - Many H1 antagonists, including antihistamines such Benadryl or terfenadine, as well as many antipsychotics, can slow down the metabolism of DXM due to their inhibition of CYP2D6, leading to possible death.[21] PW
  • Unsafe Bupropion - Bupropion is a potent inhibitor of CYP2D6, the enzyme primarily responsible for breaking down DXM. This can lead to different and prolonged effects due to excessive accumulation of DXM in the bloodstream. Recreationally mixing Bupropion with DXM can lower the seizure threshold, heighten anxiety/paranoia and increase the potential of tachycardia among other symptoms. Information on this interaction within recreational doses is overall lesser-known and is to be advised against.[22][23] PW
  • Uncertain Cannabis - CBD is known to be an inhibitor of the CYP2D6 enzyme, which normally breaks down DXM to Dextorphan. This can lead to unexpected effects.[24] PW

Other documented combinations

  • Dangerous ΑMT PW
  • Dangerous PCP - Due to PCP's unique pharmacology affecting dopamine levels this may cause cardiovascular complications. PW
  • Dangerous MDMA - High risk of serotonin syndrome due to the fact that both MDMA and DXM are both serotonergic substances. PW
  • Dangerous Alcohol - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Additionally CNS depression can lead to difficulty breathing. Avoid on anything higher than 1st plateau. PW
  • Dangerous GHB - Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. This combination is hard to predict PW
  • Dangerous GBL - Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. This combination is hard to predict PW
  • Dangerous Opioids - Both substances can, with heavy doses, cause respiratory depression, and additionally, extremely heavy doses of both may be hepatotoxic. Additionally, use of NMDA antagonists such as dextromethorphan can lower tolerance to and potentiate opioids, increasing their effects. PW
  • Dangerous Tramadol- Both substances can, with heavy doses, cause respiratory depression and if heavy doses are taken both may be hepatotoxic. Additionally, if one takes DXM, their tolerance of opiates goes down slightly, thus causing additional synergistic effects. PW
  • Dangerous MAOIs - High risk of serotonin syndrome. PW
  • Dangerous SSRIs - High risk of serotonin syndrome. PW
  • Unsafe DOx - The DOx class as psychedelic stimulants have the potential to mask the effects of DXM and could lead to redosing to an unsafe level. DXM can also potentiate DOx resulting in an unpleasantly intense experience. DOx are also very physically stimulating and can cause heart rate and blood pressure problems especially since both substances have a very long duration. PW
  • Unsafe 25x-NBOMe PW
  • Unsafe 2C-T-x - As most 2C-T-x's are MAOIs this can potentially lead to serotonin syndrome, among other dangerous effects. PW
  • Unsafe 5-MeO-xxT - Little information exists about this combination. PW
  • Unsafe Amphetamines - Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues. PW
  • Unsafe Cocaine - Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues. PW
  • Uncertain Benzodiazepines - Small doses of benzodiazepines can end a bad trip, however, both substances potentiate the ataxia and sedation caused by the other. This can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. PW

TripSit combination chart

TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.

Dangerous

alcohol TSamt TSghb/gbl TSmaois TSmdma TSmephedrone[25–31] TSopioids TSpcp TSssris TStramadol TS

Unsafe

2c-t-x TS5-meo-xxt TSamphetamines TScocaine TSdox TSmxe[32–36] TSnbomes TS

Caution

benzodiazepines TScaffeine[37][38][39] TS

Low Risk & Synergy

2c-x TScannabis TSdmt TSketamine[40–45] TSlsd TSmescaline TSmushrooms TSnitrous TS

Risks and toxicity

The toxicity and long-term health effects of recreational DXM use in humans has not been studied in any scientific context and the exact toxic dosage is unknown. PW

Anecdotal evidence suggests that there do not seem to be any negative health effects attributed to simply trying DXM at low to moderate doses by itself and using it sparingly, however, many DXM users report that waiting a week between their respective plateaus before doing DXM again (one week after first plat., two weeks after 2nd plat., etc.) can potentially prevent or minimize severe damage to the kidneys and many other organs including the heart and liver due to an excess of assorted toxic chemicals in the blood stream after DXM use. This 1-4 week period gives your body time to filter out these chemicals and help get you back to baseline levels to where its safe to do again. Some more heavy users of DXM report that these chemicals can build up heavily over time if you do not follow these guidelines, which could mean waiting longer to do again after more heavy use between short periods. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption. PW

Despite early speculation that DXM may cause neurotoxicity and Olney's lesions, it has not been shown to cause this effect in animals, However, many chronic users report significant issues with memory, attention, and mood that persist for many months after stopping usage. In rats, oral administration of dextromethorphan did not cause neurotoxic effects in laboratory tests. Oral administration of dextromethorphan repeatedly during adolescence, however, has been shown to impair learning in those rats during adulthood.[46–49] PW

It is strongly advised to use harm reduction practices if using this substance. PW

Dependence and abuse potential

As with other dissociatives, DXM produces dependence with chronic use and has moderate abuse potential. When dependence has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. PW

A formal survey of dextromethorphan users showed that more than half of users reported experience of the following withdrawal symptoms individually for the first week after long-term/addictive dextromethorphan use: fatigue, apathy, flashbacks, and constipation. Over a quarter reported insomnia, nightmares, inability to feel pleasure, impaired memory, attention deficit and decreased libido. Rarer side effects included panic attacks, impaired learning, tremor, yellowing of the skin, hives and muscle pain. Frequent and long-term usage at very high doses could lead to toxic psychosis and other permanent psychological problems.[50][51] PW

Tolerance to many of the effects of DXM develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). PW

DXM produces cross-tolerance with all dissociatives, meaning that after the consumption of DXM all dissociatives will have a reduced effect. PW

Additionally, some users report an irreversible, permanent tolerance to DXM, which develops over a long period of time and is thought to correlate with the number of doses a person has ingested throughout their lifetime. Some users claim that there is a "50 trip limit", after which the rewarding and unique effects of DXM are said to disappear permanently. The reason for this is unknown, although it may be indicative of neurotoxicity. PW

Tolerance

Long-term dextromethorphan (DXM) abuse may result in a permanent irreversible tolerance due to several different mechanisms. PW

DXM is an NMDA receptor antagonist that blocks the inhibitory effects of glutamate in the brain. With repeated use, the body compensates for this blockade by increasing glutamate production. This leads to the rapid development of tolerance to DXM. PW⚠ PsychonautWiki itself has flagged this text: citation needed.

Chronic DXM abuse leads to neuroadaptations, including changes in neurons and synapses. These adaptive changes result in altered brain function that reduces the effects of DXM. PW⚠ PsychonautWiki itself has flagged this text: citation needed.

DXM exerts its effects by blocking NMDA receptors. Long-term abuse can lead to the downregulation of these receptors, meaning they are decreased in number. Reduced receptors result in diminished responsiveness to DXM. PW⚠ PsychonautWiki itself has flagged this text: citation needed.

DXM is metabolized in the liver. Chronic abuse can induce metabolic enzymes, which accelerate DXM breakdown. PW

Overdose

Anecdotal evidence suggests that the risk of DXM overdose becomes significant at roughly 15mg/kg to 20mg/kg, or roughly 1000mg - 1500mg in a 70kg person. DXM overdose can have a wide range of effects, including delusions, hallucinations, psychosis, confusion, panic attacks, mania, sedation and severe balance issues, sometimes very inappropriate or violent behavior, increased heart rate, nystagmus and amnesia. PW⚠ PsychonautWiki itself has flagged this text: citation needed.

More serious side effects include anesthesia, respiratory depression, dangerously high fever, risk of accidental injury, self-harm and seizures. Seizures are created possibly due to hyponatremia and a general lowering of the seizure threshold. They are reported above the 900-1000mg dose range. It is possible that DXM may also affect other levels like potassium, vitamins or blood sugar further contributing to seizures and other health problems in a linear fashion in terms of severity and duration.[52] PW⚠ PsychonautWiki itself has flagged this text: citation needed.

It is also believed that extremely high and repeated doses lead to serotonin syndrome. PW⚠ PsychonautWiki itself has flagged this text: citation needed.

One should not disrupt a person undergoing this experience as their delusions may cause them to respond with violence. Care should be taken as to not let the user get injured, and medical attention, or at the very least, medical surveillance should be sought to prevent severe respiratory depression, choking or organ damage. PW

Death from DXM toxicity is rare, although most overdose cases do cite life-threatening complications, typically extremely elevated heart rate and blood pressure, urinary retention and rhabdomylosis. Fever and seizures can lead to brain cell death.[53] PW

Testing

Awaiting sourceReagent reactions and test kit guidance from a harm reduction testing service.

Effects

Awaiting sourceSubjective and physical effects from PsychonautWiki or TripSit.

Overview

Dextromethorphan (also known as robo, dex, DM, and DXM) is a dissociative substance of the morphinan class. It is the primary active ingredient in many common over-the-counter (OTC) cold and cough medicines. When exceeding approved doses, DXM produces dissociative effects similar to those of ketamine and phencyclidine (PCP). It acts as a noncompetitive NMDA receptor antagonist.[1] PW

Commonly found in certain over the counter cough medicines. Has dissociative effects similar to ketamine or MXE, though also shares properties with opioids and alcohol. Make sure DXM is the only active ingredient in the preparation.[2–9] TS

Dextromethorphan is a cough suppressant used in many cough and cold medicines. In 2022, the US Food and Drug Administration (FDA) approved the combination dextromethorphan/bupropion to serve as a rapid-acting antidepressant in people with major depressive disorder.[10][11] WP⚠ The source has a footnote here that is not shown.⚠ The source gives a pronunciation guide here that is not shown.

It is in the morphinan class of medications with dissociative and stimulant properties (at lower doses). Dextromethorphan does not have a significant affinity for the mu-opioid receptor activity typical of morphinan compounds and exerts its therapeutic effects through several other receptors. In its pure form, dextromethorphan occurs as a white powder.[12][13] WP

When exceeding approved dosages, dextromethorphan acts as a dissociative hallucinogen. It has multiple mechanisms of action, including actions as a nonselective serotonin–norepinephrine reuptake inhibitor and a sigma-1 receptor agonist. Dextromethorphan and its major metabolite dextrorphan also block the NMDA receptor at high doses, producing effects similar to those of other dissociative anesthetics such as ketamine, nitrous oxide, and phencyclidine.[14][15][16] WP

It was patented in 1949 and approved for medical use in 1953. In 2023, the combination with promethazine was the 252nd most commonly prescribed medication in the United States, with more than 1 million prescriptions; and the combination with brompheniramine and pseudoephedrine was the 281st most commonly prescribed medication in the United States, with more than 700,000 prescriptions.[17–20] WP

History

History

The racemic parent compound racemorphan was first described in a Swiss and US patent application from Hoffmann-La Roche in 1946 and 1947, respectively; a patent was granted in 1950. A resolution of the two isomers of racemorphan with tartaric acid was published in 1952, and dextromethorphan was successfully tested in 1954 as part of US Navy and CIA-funded research on nonaddictive substitutes for codeine. Dextromethorphan was approved by the FDA in 1958 as an over-the-counter antitussive. As had been initially hoped, dextromethorphan was a solution for some of the problems associated with the use of codeine phosphate as a cough suppressant, such as sedation and opiate dependence, but like the dissociative anesthetics phencyclidine and ketamine, dextromethorphan later became associated with nonmedical use.[54][55][56] WP

During the 1960s and 1970s, dextromethorphan became available in an over-the-counter tablet form by the brand name Romilar. In 1973, Romilar was taken off the shelves after a burst in sales because of frequent misuse. A few years later, products with an unpleasant taste were introduced (such as Vicks-44, and Dextrotussion), but later the same manufacturers began producing products with a better taste. The advent of widespread internet access in the 1990s allowed users to rapidly disseminate information about dextromethorphan, and online discussion groups formed around use and acquisition of the drug. As early as 1996, dextromethorphan hydrobromide powder could be purchased in bulk from online retailers, allowing users to avoid consuming dextromethorphan in syrup preparations.[54][56] WP

FDA panels considered moving dextromethorphan to prescription status due to its potential for abuse, but voted against the recommendation in September 2010, citing lack of evidence that making it prescription-only would curb abuse. Some states have restricted the sale of dextromethorphan to adults or put other restrictions on its purchase in place, similar to those for pseudoephedrine. As of 1 January 2012, dextromethorphan is prohibited for sale to minors in the State of California and in the State of Oregon as of 1 January 2018, except with a doctor's prescription. Several other states have also begun regulating sales of dextromethorphan to minors.[57][58] WP

In Indonesia, the National Agency of Drug and Food Control (BPOM-RI) prohibited single-component dextromethorphan drug sales with or without prescription. Indonesia is the only country that makes single-component dextromethorphan illegal over the counter and by prescription and violators may be prosecuted by law. National Anti-Narcotics Agency (BNN RI) has threatened to revoke pharmacies' and drug stores' licenses if they still stock dextromethorphan, and will notify the police for criminal prosecution. As a result of this regulation, 130 medications have been withdrawn from the market, but those containing multicomponent dextromethorphan can still be sold over the counter.[59–62] WP

Pharmacology

Pharmacodynamics

Dextromethorphan has been found to possess the following actions (<1 μM) using rat tissues:[78][84] WP

  • Uncompetitive antagonist of the NMDA receptor via the MK-801/PCP (phencyclidine) site[84] WP
  • SERT (Serotonin transporter) and NET (norepinephrine transporter) blocker (cf. serotonin–norepinephrine reuptake inhibitor)[78][84] WP
  • Sigma σ₁ receptor agonist[78][84] WP
  • Negative allosteric modulator of nicotinic acetylcholine receptors[78][84] WP
  • Ligand of the serotonin 5-HT1B/1D, histamine H₁, α₂-adrenergic, and muscarinic acetylcholine receptors[78][84] WP

Dextromethorphan is a prodrug of dextrorphan, which is the actual mediator of most of its dissociative effects through acting as a more potent NMDA receptor antagonist than dextromethorphan itself. What role, if any, (+)-3-methoxymorphinan, dextromethorphan's other major metabolite, plays in its effects is not entirely clear.[85][86] WP

Pharmacokinetics

Following oral administration, dextromethorphan is rapidly absorbed from the gastrointestinal tract, where it enters the bloodstream and crosses the blood–brain barrier. WP⚠ Wikipedia itself has flagged this text: citation needed.

At therapeutic doses, dextromethorphan acts centrally (meaning that it acts on the brain) as opposed to locally (on the respiratory tract). It elevates the threshold for coughing, without inhibiting ciliary activity. Dextromethorphan is rapidly absorbed from the gastrointestinal tract and converted into the active metabolite dextrorphan in the liver by the cytochrome P450 enzyme CYP2D6. The average dose necessary for effective antitussive therapy is between 10 and 45 mg, depending on the individual. The International Society for the Study of Cough recommends "an adequate first dose of medication is 60 mg in the adult and repeat dosing should be infrequent rather than qds recommended."[87] WP

Dextromethorphan has an elimination half-life of approximately four hours in individuals with an extensive metabolizer phenotype; this is increased to approximately 13 hours when dextromethorphan is given in combination with quinidine. The duration of action after oral administration is about three to eight hours for dextromethorphan hydrobromide, and 10 to 12 hours for dextromethorphan polistirex. Around one in ten of the Caucasian population has little or no CYP2D6 enzyme activity, leading to long-lived high drug levels.[12][87] WP⚠ Wikipedia itself has flagged this text: citation needed.

Metabolism

The first pass through the hepatic portal vein results in some of the drug being metabolized by O-demethylation into an active metabolite of dextromethorphan called dextrorphan, the 3-hydroxy derivative of dextromethorphan. The therapeutic activity of dextromethorphan is believed to be caused by both the drug and this metabolite. Dextromethorphan also undergoes N-demethylation (to 3-methoxymorphinan or MEM), and partial conjugation with glucuronic acid and sulfate ions. Hours after dextromethorphan therapy, (in humans) the metabolites (+)-3-hydroxy-N-methylmorphinan and (+)-3-morphinan and traces of the unchanged drug are detectable in the urine.[88][89] WP

A major metabolic catalyst involved is the cytochrome P450 enzyme known as 2D6, or CYP2D6. A significant portion of the population has a functional deficiency in this enzyme and are known as poor CYP2D6 metabolizers. O-demethylation of dextromethorphan to dextrorphan contributes to at least 80% of the dextrorphan formed during dextromethorphan metabolism. As CYP2D6 is a major metabolic pathway in the inactivation of dextromethorphan, the duration of action and effects of dextromethorphan can be increased by as much as three times in such poor metabolizers. In one study on 252 Americans, 84.3% were found to be "fast" (extensive) metabolizers, 6.8% to be "intermediate" metabolizers, and 8.8% were "slow" metabolizers of dextromethorphan. A number of alleles for CYP2D6 are known, including several completely inactive variants. The distribution of alleles is uneven amongst ethnic groups.[88][90][91] WP

A large number of medications are potent inhibitors of CYP2D6. Some types of medications known to inhibit CYP2D6 include certain SSRIs and tricyclic antidepressants, some antipsychotics, and the commonly available antihistamine diphenhydramine. Therefore, the potential for interactions exists between dextromethorphan and medications that inhibit this enzyme, particularly in slow metabolizers. WP

Dextromethorphan is also metabolized by CYP3A4. N-demethylation is primarily accomplished by CYP3A4, contributing to at least 90% of the MEM formed as a primary metabolite of dextromethorphan.[88] WP

A number of other CYP enzymes are implicated as minor pathways of dextromethorphan metabolism. CYP2D6 is more effective than CYP3A4 at N-demethylation of dextromethorphan, but since the average individual has a much lower CYP2D6 content in the liver compared to CYP3A4, most N-demethylation of dextromethorphan is catalyzed by CYP3A4.[88] WP

Receptor binding · Wikipedia

Dextromethorphan and metabolite

SiteDXM (Dextromethorphan)DXO (Dextrorphan)Species
NMDA (N-Methyl-D-aspartate receptor) (PCP)2120–8945486–906Rat[12][78][79][80] WP
σ₁142–652118–481Rat[12][78][79][80] WP
σ₂11060–2286411325–15582Rat[12][78][79][80] WP
MOR (μ-Opioid receptor)1280; ND (No data)420; 1000+Rat; Human[12][78–81] WP
DOR (δ-Opioid receptor)1150034700Rat[12][78][79][80] WP
KOR (κ-Opioid receptor)70005950Rat[12][78][79][80] WP
SERT (Serotonin transporter)23–40401–484Rat[12][78][79][80] WP
NET (Norepinephrine transporter)240+340+Rat[12][78][79][80] WP
DAT (Dopamine transporter)1000+1000+Rat[12][78][79][80] WP
5-HT1A1000+1000+Rat[12][78][79][80] WP
5-HT1B/1D61% at 1 μM54% at 1 μMRat[12][78][79][80] WP
5-HT2A1000+1000+Rat[12][78][79][80] WP
α₁1000+1000+Rat[12][78][79][80] WP
α₂60% at 1 μM1000+Rat[12][78][79][80] WP
β1000+35% at 1 μMRat[12][78][79][80] WP
D₂1000+1000+Rat[12][78][79][80] WP
H₁1000+95% at 1 μMRat[12][78][79][80] WP
mAChRs (Muscarinic acetylcholine receptors)1000+100% at 1 μMRat[12][78][79][80] WP
nAChRs (Nicotinic acetylcholine receptors)700–8900 (IC₅₀)1300–29600 (IC₅₀)Rat[12][78][79][80] WP
VDSCs (Voltage-dependent sodium channels)50000+ (IC₅₀)ND (No data)Rat[12][78][79][80][82][83] WP

Chemistry

Formula
C18H25NO PC
CAS number
125-71-3 PC
Molar mass (g/mol)
271.4 PC
IUPAC name (computed by PubChem)
(1S,9S,10S)-4-methoxy-17-methyl-17-azatetracyclo[7.5.3.01,10.02,7]heptadeca-2(7),3,5-triene PC
SMILES
CN1CC[C@@]23CCCC[C@@H]2[C@@H]1CC4=C3C=C(C=C4)OC PC
InChIKey
MKXZASYAUGDDCJ-NJAFHUGGSA-N PC
PubChem CID
5360696

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References

  1. Journal / agency Siu, A., Drachtman, R. Dextromethorphan: a review of N-methyl-d-aspartate receptor antagonist in the management of pain. CNS drug reviews. 2007. doi:10.1111/j.1527-3458.2007.00006.x
  2. Journal / agency Dextromethorphan and its metabolite dextrorphan block alpha3beta4 neuronal nicotinic receptors
  3. Journal / agency Dextromethorphan potentiates the antinociceptive effects of morphine and the delta-opioid agonist SNC80 in squirrel monkeys
  4. Journal / agency Dextromethorphan psychosis, dependence and physical withdrawal
  5. Journal / agency Evaluation the effects of dextromethorphan and midazolam on morphine induced tolerance and dependence in mice
  6. Journal / agency Dextromethorphan as a potential rapid-acting antidepressant
  7. Journal / agency The treatment of heroin addicts with dextromethorphan: a double-blind comparison of dextromethorphan with chlorpromazine
  8. Journal / agency High doses of dextromethorphan, an NMDA antagonist, produce effects similar to classic hallucinogens
  9. Journal / agency Lack of efficacy of dextromethorphan in managing alcohol withdrawal: a preliminary report of a randomized, double-blind, placebo-controlled trial
  10. Journal / agency Dicpinigaitis, P. The Current and Emerging Treatment Landscape for Chronic Cough. The American Journal of Managed Care. 12 September 2022. doi:10.37765/ajmc.2022.89244 · PMID 36198074
  11. Journal / agency Majeed A, Xiong J, Teopiz KM, Ng J, Ho R, Rosenblat JD, Phan L, Cao B, McIntyre RS. Efficacy of dextromethorphan for the treatment of depression: a systematic review of preclinical and clinical trials. Expert Opinion on Emerging Drugs. March 2021. doi:10.1080/14728214.2021.1898588 · PMID 33682569
  12. Journal / agency Taylor CP, Traynelis SF, Siffert J, Pope LE, Matsumoto RR. Pharmacology of dextromethorphan: Relevance to dextromethorphan/quinidine (Nuedexta) clinical use. Pharmacology & Therapeutics. August 2016. doi:10.1016/j.pharmthera.2016.04.010 · PMID 27139517
  13. Other Reference Tables: Description and SolubilityD. 2 May 2006
  14. Journal / agency Schwartz AR, Pizon AF, Brooks DE. Dextromethorphan-induced serotonin syndrome. Clinical Toxicology. September 2008. doi:10.1080/15563650701668625 · PMID 19238739
  15. Journal / agency Shin EJ, Nah SY, Chae JS, Bing G, Shin SW, Yen TP, Baek IH, Kim WK, Maurice T, Nabeshima T, Kim HC. Dextromethorphan attenuates trimethyltin-induced neurotoxicity via sigma1 receptor activation in rats. Neurochemistry International. May 2007. doi:10.1016/j.neuint.2007.01.008 · PMID 17386960
  16. Journal / agency Shin EJ, Nah SY, Kim WK, Ko KH, Jhoo WK, Lim YK, Cha JY, Chen CF, Kim HC. The dextromethorphan analog dimemorfan attenuates kainate-induced seizures via sigma1 receptor activation: comparison with the effects of dextromethorphan. British Journal of Pharmacology. April 2005. doi:10.1038/sj.bjp.0705998 · PMID 15723099 · PMC1576070
  17. Other Fischer J, Ganellin CR. Analogue-based Drug Discovery. 2006
  18. Other The Top 300 of 2023
  19. Other Dextromethorphan; Promethazine Drug Usage Statistics, United States, 2014 - 2023
  20. Other Brompheniramine; Dextromethorphan; Pseudoephedrine Drug Usage Statistics, United States, 2014 - 2023
  21. Journal / agency Kintz, P., Mangin, P. Toxicological findings in a death involving dextromethorphan and terfenadine. The American Journal of Forensic Medicine and Pathology. December 1992. doi:10.1097/00000433-199212000-00018
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