Dextropropoxyphene is an opioid analgesic patented in 1955 and manufactured by Eli Lilly and Company. It is an optical isomer of levopropoxyphene. It is intended to treat mild pain and also has antitussive (cough suppressant) and local anesthetic effects. The drug has been taken off the market in Europe and the United States due to concerns of fatal overdoses and heart arrhythmias. It is still available in Australia, albeit with restrictions after an application by its manufacturer to review its proposed banning. Its onset of analgesia (pain relief) is said to be 20–30 minutes and peak effects are seen about 1.5–2.0 hours after oral administration.
Dextropropoxyphene is sometimes combined with paracetamol (acetaminophen). Trade names include Darvocet-N, Di-Gesic, and Darvon with APAP (for dextropropoxyphene and paracetamol). The British approved name (i.e. the generic name of the active ingredient) of the paracetamol/dextropropoxyphene preparation is co-proxamol (sold under a variety of brand names); however, it has been withdrawn since 2007, and is no longer available to new patients, with exceptions. The paracetamol combinations are known as Capadex or Di-Gesic in Australia, Lentogesic in South Africa, and Di-Antalvic in France (unlike co-proxamol, which is an approved name, these are all brand names).
Safety at a Glance
High Risk- It is strongly recommended that one use harm reduction practices when using this drug.
- Serotonin syndrome risk
- Toxicity: Dextropropoxyphene has a high toxicity relative to dose. As with all opioids, long-term effects can vary but can incl...
- Dangerous with: 3-Cl-PCP, 3-HO-PCE, 3-HO-PCP, 3-MeO-PCE (+43 more)
- Overdose risk: fatal heart arrhythmias, and it is discouraged to take in very heavy doses or several days in a r...
If someone is in crisis, call 911 or Poison Control: 1-800-222-1222
Dosage
oral
Duration
oral
Total: 2.5 hrs – 10.9 hrsHow It Feels
Dextropropoxyphene is an opioid of modest ambitions. Its onset unfolds over forty-five minutes to an hour, arriving not with any particular fanfare but with a quiet, almost apologetic warmth that settles into the body like a lukewarm bath. The first signs are easy to miss: a faint relaxation in the jaw, a subtle easing of whatever minor aches had been occupying your attention. There is no rush, no wave, no moment of dramatic transition -- just a slow, incremental softening of the body's baseline discomfort.
At its peak, dextropropoxyphene delivers a mild but genuine comfort. The warmth is present but thin, spread across the body in an even layer that lacks the depth and intensity of stronger opioids. There is a gentle drowsiness, a pulling-down of the eyelids that suggests sleep without insisting upon it. The emotional landscape shifts subtly toward contentment -- worries recede slightly, irritations lose their edge, and there is a modest sense of well-being that, while far from euphoric, represents a genuine improvement over baseline. Conversation flows a touch more easily. The body relaxes into its seat with a quiet gratitude.
Physically, the experience is unremarkable by opioid standards. There may be mild nausea, a faint dizziness that passes quickly, and a slight constriction of the pupils. The opioid itch is largely absent or so faint as to be ignorable. Breathing remains essentially normal. The body feels slightly heavy but not immobilized -- you can move through the world with reasonable functionality, though there is a preference for stillness, for letting gravity do its work. Pain relief is present but limited, adequate for mild to moderate discomfort but insufficient for anything more demanding.
The duration stretches to four or five hours, though the peak itself is shorter, lasting perhaps two hours before beginning its gentle decline. The plateau has a flat, undramatic quality -- the experience holds steady without intensifying, a reliable but unspectacular companion. There is something almost forgettable about the peak, a quality of quiet competence that does its job without calling attention to itself.
The offset mirrors the onset in its gentleness. The warmth recedes gradually, so slowly that the return to baseline feels more like a natural transition than a loss. There is no crash, no rebound discomfort. A mild residual drowsiness may linger for an hour or two, and sleep comes easily if pursued. The overall impression is of a compound that operates within narrow parameters -- effective within its range, unpretentious, and fundamentally gentle.
Subjective Effects
The effects listed below are based on the Subjective Effect Index (SEI), an open research literature based on anecdotal reports and personal analyses. They should be viewed with a healthy degree of skepticism. 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.
Physical Effects
Physical(21)
- Appetite suppression— A distinct decrease in hunger and desire to eat, ranging from reduced interest in food to complete d...
- Constipation— A slowing or cessation of bowel movements resulting in difficulty passing stool, commonly caused by ...
- Cough suppression— A decreased desire and need to cough, medically known as antitussive action, which can also allow in...
- Decreased libido— Decreased libido is a diminished interest in and desire for sexual activity, commonly caused by subs...
- Diarrhea— Diarrhea is the occurrence of frequent, loose, or watery bowel movements as a side effect of certain...
- Difficulty urinating— Difficulty urinating, also known as urinary retention, is the experience of being unable to easily p...
- Dizziness— A sensation of spinning, swaying, or lightheadedness that impairs balance and spatial orientation, o...
- Headache— A painful sensation of pressure, throbbing, or aching in the head that can range from a dull backgro...
- Increased heart rate— A noticeable acceleration of heartbeat that can range from a subtle awareness of one's pulse to a fo...
- Itchiness— A persistent, diffuse urge to scratch the skin that arises without any external irritant, most commo...
- Motor control loss— A distinct decrease in the ability to control one's physical body with precision, balance, and coord...
- Nausea— An uncomfortable sensation of queasiness and stomach discomfort that may or may not lead to vomiting...
- Orgasm suppression— Orgasm suppression (anorgasmia) is the difficulty or complete inability to achieve orgasm despite ad...
- Pain relief— A suppression of negative physical sensations such as aches and pains, ranging from dulled awareness...
- Physical euphoria— An intensely pleasurable bodily sensation that can manifest as waves of warmth, tingling electricity...
- Pupil constriction— A visible narrowing of the pupil diameter (miosis) that reduces the size of the dark center of the e...
- Respiratory depression— A dangerous slowing and shallowing of breathing that can progress from barely noticeable reductions ...
- Sedation— A state of deep physical and mental calming that manifests as a progressive desire to remain still, ...
- Seizure— Uncontrolled brain electrical activity causing convulsions and loss of consciousness -- a life-threa...
- Serotonin syndrome— Serotonin syndrome is a potentially fatal medical emergency caused by excessive serotonergic activit...
- Spontaneous physical movements— Spontaneous physical movements are involuntary, seemingly random yet patterned body movements — twit...
Cognitive & Perceptual Effects
Cognitive(9)
- Amnesia— A complete or partial inability to form new memories or recall existing ones during and after substa...
- Anxiety— Intense feelings of apprehension, worry, and dread that can range from a subtle background unease to...
- Anxiety suppression— A partial to complete suppression of anxiety and general unease, producing a calm, relaxed mental st...
- Cognitive euphoria— A cognitive and emotional state of intense well-being, elation, happiness, and joy that manifests as...
- Compulsive redosing— An overwhelming, difficult-to-resist urge to continuously take more of a substance in order to maint...
- Confusion— An impairment of abstract thinking marked by a persistent inability to grasp or comprehend concepts ...
- Depression— A persistent state of low mood, emotional numbness, hopelessness, and diminished interest or pleasur...
- Dream potentiation— Enhanced dream vividness, complexity, and recall, often occurring as REM rebound after discontinuing...
- Sleepiness— A progressive onset of drowsiness, heaviness, and the desire to sleep that pulls the individual towa...
Pharmacology
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. 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.
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 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.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.
As with other opioids,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.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,3 - 71 - 2 weeks to be back at baseline (in the absence of further consumption). Dextropropoxyphene presents cross-tolerance with Cross-all other opioids, meaning that after the consumption of dextropropoxyphene all opioids will have a reduced effect.
Serotonin syndrome risk
Germany:** Dextropropoxyphene is controlled under BtMG Anlage II, making it illegal to manufacture, import, possess, sell, or transfer it without a license.
Russia:** Dextropropoxyphene is a Schedule II controlled substance.
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.
United Kingdom:** Dextropropoxyphene is a Class C, Schedule 2 or Schedule 5 substance depending on the dose.
United States:** Dextropropoxyphene is a Schedule II or Schedule IV Controlled Substance depending on the dosage and other ingredients. 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.
Responsible use
Opioid
Tapentadol
Dextropropoxyphene (Wikipedia)
Detection Methods
Standard Drug Panel Inclusion
Dextropropoxyphene (Propoxyphene) is a synthetic opioid that is not detected on standard 5-panel immunoassay drug screens. Some older 10-panel drug screens included a propoxyphene-specific channel, though this has become less common after the drug was withdrawn from many markets due to safety concerns. Standard opiate immunoassays target the morphine backbone structure, and synthetic opioids lack this structural motif. Detection of Dextropropoxyphene (Propoxyphene) requires either an expanded panel with a specific immunoassay channel or confirmatory instrumental analysis.
Urine Detection
Dextropropoxyphene (Propoxyphene) and its metabolites can be detected in urine for approximately 2 to 4 days after a single dose, though this varies with dose, frequency of use, and individual metabolism. Synthetic opioids undergo extensive hepatic metabolism, primarily via cytochrome P450 enzymes, producing metabolites that are excreted renally. The metabolite profile is specific to Dextropropoxyphene (Propoxyphene) and does not overlap with morphine-class metabolites used as markers in standard opiate screens.
Blood and Saliva Detection
Blood concentrations of Dextropropoxyphene (Propoxyphene) are typically detectable for 12 to 48 hours, depending on the half-life and dose administered. Oral fluid testing can detect Dextropropoxyphene (Propoxyphene) for a similar window. Blood testing is most commonly used in emergency department settings, postmortem toxicology, and driving-under-the-influence investigations.
Hair Follicle Detection
Hair follicle testing can detect Dextropropoxyphene (Propoxyphene) for up to 90 days. However, synthetic opioids are not always included in standard hair testing panels. Specialized forensic or clinical laboratories may offer expanded panels that include Dextropropoxyphene (Propoxyphene), but this must be specifically requested. LC-MS/MS with appropriate reference standards is required.
Confirmatory Testing
Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is the definitive method for identifying Dextropropoxyphene (Propoxyphene) in biological specimens. GC-MS is also effective for many synthetic opioids. These instrumental methods provide the specificity needed to distinguish Dextropropoxyphene (Propoxyphene) from other opioids and from endogenous compounds. Quantitative analysis can determine concentrations relevant to therapeutic monitoring, compliance testing, or forensic investigation.
Reagent Testing
Reagent testing for Dextropropoxyphene (Propoxyphene) depends on its specific chemical structure. Marquis reagent may produce little or no reaction, which is itself informative as it distinguishes synthetic opioids from morphine-class opiates (which turn purple). Mecke reagent may show a faint color change. Fentanyl-specific test strips are available for harm reduction purposes but their cross-reactivity with non-fentanyl synthetic opioids varies. Mass spectrometry remains the only reliable identification method.
Interactions
| Substance | Status | Note |
|---|---|---|
| 3-Cl-PCP | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| 3-HO-PCE | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| 3-HO-PCP | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| 3-MeO-PCE | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| 3-MeO-PCMo | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| 3-MeO-PCP | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| 4-MeO-PCP | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Alcohol | Dangerous | — |
| Atropa belladonna | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Benzodiazepines | Dangerous | — |
| Cake | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| Datura | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Deschloroetizolam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Deschloroketamine | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Desomorphine | Dangerous | Compounding respiratory depression and overdose risk |
| Diclazepam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Diphenhydramine | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Diphenidine | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Ephenidine | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Eszopiclone | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| Etizolam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Flubromazepam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Flubromazolam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Flunitrazepam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Flunitrazolam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Gaboxadol | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| GBL | Dangerous | — |
| GHB | Dangerous | — |
| Harmala alkaloid | Dangerous | Risk of serotonin syndrome and severe respiratory depression; potentially fatal |
| HXE | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Inhalants | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Ketamine | Dangerous | — |
| Lorazepam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Memantine | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Mephenaqualone | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| Metizolam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| Midazolam | Dangerous | Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths |
| MXiPr | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Naloxone | Dangerous | Compounding respiratory depression and overdose risk |
| Nicotine | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| Nifoxipam | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| O-PCE | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| PCE | Dangerous | Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration |
| Peganum harmala | Dangerous | Risk of serotonin syndrome and severe respiratory depression; potentially fatal |
| Pentobarbital | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| Phenobarbital | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| SAMe | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| 3-FMA | Caution | Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off |
| 4-MMC | Caution | Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off |
| 8-Chlorotheophylline | Caution | Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off |
| Adrafinil | Caution | Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off |
| Benzydamine | Caution | Stimulants mask opioid sedation, increasing overdose risk when the stimulant wears off |
| Nitrous | Uncertain | — |
| PCP | Uncertain | — |
| 1,3-Butanediol | Low Risk & No Synergy | No significant pharmacological interaction; opioids may slightly dull the psychedelic experience |
| 25E-NBOH | Low Risk & No Synergy | No significant pharmacological interaction; opioids may slightly dull the psychedelic experience |
| 2C-T | Low Risk & No Synergy | No significant pharmacological interaction; opioids may slightly dull the psychedelic experience |
History
Dextropropoxyphene belongs to the opioid class of substances, which has a history spanning thousands of years from the ancient use of opium poppy to modern synthetic and semi-synthetic analogues.
The isolation of morphine from opium in 1804 by Friedrich Sertürner marked the beginning of modern opioid pharmacology. Subsequent developments included the synthesis of heroin (diacetylmorphine) in 1874, the development of numerous semi-synthetic and fully synthetic opioids throughout the 20th century, and the identification of endogenous opioid receptors and peptides in the 1970s.
The opioid crisis of the early 21st century, driven largely by overprescription of pharmaceutical opioids and the subsequent emergence of illicit fentanyl and its analogues, represents one of the most significant public health challenges in modern history. This crisis has fundamentally reshaped discussions around opioid prescribing, addiction treatment, and harm reduction policy.
Dextropropoxyphene exists within this complex pharmacological and social context, with its history shaped by its development, clinical utility, and the broader dynamics of opioid use and regulation.
Harm Reduction
It is strongly recommended that one use harm reduction practices when using this drug.
As with other opioids,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.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,3 - 71 - 2 weeks to be back at baseline (in the absence of further consumption). Dextropropoxyphene presents cross-tolerance with Cross-all other opioids, meaning that after the consumption of dextropropoxyphene all opioids will have a reduced effect.
Serotonin syndrome risk
Germany:** Dextropropoxyphene is controlled under BtMG Anlage II, making it illegal to manufacture, import, possess, sell, or transfer it without a license.
Russia:** Dextropropoxyphene is a Schedule II controlled substance.
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.
United Kingdom:** Dextropropoxyphene is a Class C, Schedule 2 or Schedule 5 substance depending on the dose.
United States:** Dextropropoxyphene is a Schedule II or Schedule IV Controlled Substance depending on the dosage and other
Toxicity & Safety
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. 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. 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.
MAOIs - Such as banisteriopsis caapi, syrian rue, phenelzine, selegiline, and moclobemide.
Serotonin releasers - Such as MDMA, 4-FA, methamphetamine, methylone and αMT.
SSRIs - Such as citalopram and sertraline
SNRIs - Such as tramadol and venlafaxine
Addiction Potential
moderately addictive with a high potential for abuse
Overdose Information
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.
As with other opioids,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.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,3 - 71 - 2 weeks to be back at baseline (in the absence of further consumption). Dextropropoxyphene presents cross-tolerance with Cross-all other opioids, meaning that after the consumption of dextropropoxyphene all opioids will have a reduced effect.
Serotonin syndrome risk
Germany:** Dextropropoxyphene is controlled under BtMG Anlage II, making it illegal to manufacture, import, possess, sell, or transfer it without a license.
Russia:** Dextropropoxyphene is a Schedule II controlled substance.
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.
United Kingdom:** Dextropropoxyphene is a Class C, Schedule 2 or Schedule 5 substance depending on the dose.
Dangerous Interactions
The combinations listed below may be life-threatening. Independent research should always be conducted to ensure safety when combining substances.
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Severe respiratory depression risk; leading cause of polydrug overdose
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Compounding respiratory depression and overdose risk
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Severe respiratory depression risk; leading cause of polydrug overdose
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Severe respiratory depression risk; leading cause of polydrug overdose
Risk of serotonin syndrome and severe respiratory depression; potentially fatal
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Severe respiratory depression risk; leading cause of polydrug overdose
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Severe respiratory depression; this combination is the leading cause of prescription drug overdose deaths
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Compounding respiratory depression and overdose risk
Severe respiratory depression risk; leading cause of polydrug overdose
Severe respiratory depression risk; leading cause of polydrug overdose
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Both cause respiratory depression and unconsciousness; vomiting while dissociated risks aspiration
Risk of serotonin syndrome and severe respiratory depression; potentially fatal
Severe respiratory depression risk; leading cause of polydrug overdose
Severe respiratory depression risk; leading cause of polydrug overdose
Severe respiratory depression risk; leading cause of polydrug overdose
Tolerance
| Full | develops with prolonged and repeated use |
| Half | 3 - 7 days |
| Zero | 1 - 2 weeks |
Cross-tolerances
Legal Status
Germany:** Dextropropoxyphene is controlled under BtMG Anlage II, making it illegal to manufacture, import, possess, sell, or transfer it without a license.
Russia:** Dextropropoxyphene is a Schedule II controlled substance.
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.
United Kingdom:** Dextropropoxyphene is a Class C, Schedule 2 or Schedule 5 substance depending on the dose.
United States:** Dextropropoxyphene is a Schedule II or Schedule IV Controlled Substance depending on the dosage and other ingredients. 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.
Responsible use
Opioid
Tapentadol
Dextropropoxyphene (Wikipedia)
Experience Reports (1)
Tips (5)
Never combine Dextropropoxyphene with benzodiazepines, alcohol, gabapentinoids, or other depressants. This dramatically increases respiratory depression risk. The majority of opioid overdose deaths involve a second depressant.
Opioid tolerance and cross-tolerance are complex with Dextropropoxyphene. Switching between different opioids requires careful dose conversion. Do not assume equivalent effects at standard conversion ratios; start lower than calculated.
ALWAYS have naloxone (Narcan) on hand when using Dextropropoxyphene. It reverses opioid overdose and is available over the counter in many places. Make sure someone nearby knows how to administer it. This is non-negotiable.
The highest risk of fatal overdose from Dextropropoxyphene comes after a tolerance break, whether from rehab, jail, hospital, or even a few days of abstinence. Your old dose can kill you. Always start at a fraction of your previous dose.
In most US states, Good Samaritan laws protect you from drug charges if you call 911 for an overdose. Never hesitate to call emergency services. A legal charge is infinitely preferable to a death.
See Also
References (4)
- Opioid receptors — Pasternak & Pan Annual Review of Pharmacology (2013)paper
- PubChem: Dextropropoxyphene
PubChem compound page for Dextropropoxyphene (CID: 10100)
pubchem - Dextropropoxyphene - TripSit Factsheet
TripSit factsheet for Dextropropoxyphene
tripsit - Dextropropoxyphene - Wikipedia
Wikipedia article on Dextropropoxyphene
wikipedia