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Fatal overdose may occur when opiates are combined with other depressants such as benzodiazepines, barbiturates, gabapentinoids, thienodiazepines, alcohol or other GABAergic substances.[1]

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

Summary sheet: Dextropropoxyphene
Chemical Nomenclature
Common names Dextropropoxyphene, Propoxyphene, Darvon
Systematic name [(2S,3R)-4-(dimethylamino)-3-methyl-1,2-diphenylbutan-2-yl] propanoate
Class Membership
Psychoactive class Opioid
Chemical class Phenylpropylamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Bioavailability 40%
Threshold 15 mg
Light 30 - 65 mg
Common 65 - 100 mg
Strong 100 - 200 mg
Heavy 200 mg +
Onset 20 - 30 minutes
Peak 1 - 4 hours
After effects 1 - 6 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Serotonin releasers

Dextropropoxyphene (also known as Propoxyphene and Darvon) is a synthetic opioid of the phenylpropylamine chemical class. Like other substances in its class, particularly tapentadol and tramadol, it produces mild euphoric, analgesic, sedative and antitussive effects when administered (typically orally, but sometimes intravenous or rectally).[citation needed] Notably, it is reported to produce significantly less euphoria in comparison to other opioids.[citation needed]

Dextropropoxyphene was first patented in 1955 and subsequently manufactured by Eli Lilly and Company.[citation needed]

Due to its euphoric and analgesic effects, dextropropoxyphene is known to be habit forming, albeit not to the same extent as other opioids such as morphine or heroin.[citation needed] Notably, dextropropoxyphene is also known to cause seizures and potentially fatal cardiac arrhythmia at high doses[citation needed], which are not able to be reversed by naloxone.[citation needed]

Today, dextropropoxyphene is rarely encountered on the streets and is sometimes obtained by prescription from a compounding pharmacy.[citation needed] It is strongly recommended that one research this substance's toxicity and use proper harm reduction practices if choosing to use this substance.


Dextropropoxyphene is similar in structure to tapentadol. While tapentadol has an ethyl substitution on the gamma-carbon, dextropropoxyphene instead has both benzyl and propionyl substitutions. Dextropropoxyphene also contains a benzene ring in place of the phenol ring found in tapentadol. The empirical formula of dextropropoxyphene is C22H29NO2 and has a molar mass of 339.471 grams per mole.


Opioids produce their effects by binding to and activating the μ-opioid receptor. This occurs because opioids structurally mimic endogenous endorphins which are naturally found within the body and also work upon the μ-opioid receptor set. The way in which opioids structurally mimic these natural endorphins results in their euphoria, pain relief and anxiolytic effects. This is because endorphins are responsible for reducing pain, causing sleepiness, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or general excitement.

Unlike most opioids, dextropropoxyphene is also a weak serotonin reuptake inhibitor as well as a potent nicotinic acetylcholine antagonist[2]. Dextropropoxyphene has a bioavailability of about 40% and is metabolized by the cytochrome P450 3A4 enzyme. The optical isomer of dextropropoxyphene, levopropoxyphene has no analgesic activity but retains antitussive effects.

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects

Cognitive effects

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Dextropropoxyphene has a high toxicity relative to dose. As with all opioids, long-term effects can vary but can include diminished libido, apathy and memory loss. It is also potentially lethal when mixed with depressants like alcohol or benzodiazepines and generally has a wider range of substances which it is dangerous to combine with in comparison to other opioids. Dextropropoxyphene is known to lower the seizure threshold. It should not be taken during benzodiazepine withdrawals as this can potentially cause seizures. Dextropropoxyphene is known to cause potentially fatal heart arrhythmias, and it is discouraged to take in very heavy doses or several days in a row.

It is strongly recommended that one use harm reduction practices when using this drug.

Tolerance and addiction potential

As with other opioids, the chronic use of dextropropoxyphene can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal symptoms may occur if a person suddenly stops their usage.

Tolerance to many of the effects of dextropropoxyphene develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. 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). Dextropropoxyphene presents cross-tolerance with all other opioids, meaning that after the consumption of dextropropoxyphene all opioids will have a reduced effect.

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • 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. Memory blackouts are likely
  • Stimulants - Stimulants increase respiration rate which allows for a higher dose of opiates than would otherwise be used. If the stimulant wears off first then the opiate may overcome the user and cause respiratory arrest.
  • Benzodiazepines - Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position blackouts/memory loss likely.
  • DXM - Generally considered to be toxic. CNS depression, difficulty breathing, heart issues, and liver toxicity have been observed. Additionally if one takes DXM, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.
  • GHB/GBL - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position
  • Ketamine - Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.
  • MAOIs - Coadministration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases.
  • MXE - MXE can potentiate the effects of opioids but also increases the risk of respiratory depression and organ toxicity.
  • Nitrous - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are common.
  • PCP - PCP may reduce opioid tolerance, increasing the risk of overdose.
  • Tramadol - Increased risk of seizures. Tramadol itself is known to induce seizures and it may have additive effects on seizure threshold with other opioids. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.
  • Grapefruit - While grapefruit is not psychoactive, it may affect the metabolism of certain opioids. Tramadol, oxycodone, and fentanyl are all primarily metabolized by the enzyme CYP3A4, which is potently inhibited by grapefruit juice[3]. This may cause the drug to take longer to clear from the body. it may increase toxicity with repeated doses. Methadone may also be affected[3]. Codeine and hydrocodone are metabolized by CYP2D6. People who are on medicines that inhibit CYP2D6, or that lack the enzyme due to a genetic mutation will not respond to codeine as it can not be metabolized into its active product: morphine.

Serotonin syndrome risk

Combinations with the following substances can cause dangerously high serotonin levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.

Legal status

  • Germany: Dextropropoxyphene is controlled under BtMG Anlage II, making it illegal to manufacture, import, possess, sell, or transfer it without a license.[5]
  • Russia: Dextropropoxyphene is a Schedule II controlled substance.[6]
  • Switzerland: Dextropropoxyphene is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted. Some preparations containing Dextropropoxyphene are included in Verzechnis C, while certain ones are excluded.[7]
  • United Kingdom: Dextropropoxyphene is a Class C, Schedule 2 or Schedule 5 substance depending on the dose.[8]
  • United States: Dextropropoxyphene is a Schedule II or Schedule IV Controlled Substance depending on the dosage and other ingredients.[9] Dextropropoxyphene has been withdrawn in the United States and is no longer available through prescription, although it is possible some compounding pharmacies may still carry it.

See also

External links