This article requires proofreading.
As such, it may contain incorrect grammar, spelling, or punctuation.
|Summary sheet: Dextropropoxyphene|
|Common names||Dextropropoxyphene, propoxyphene, Darvon|
|Systematic name||[(2S,3R)-4-(dimethylamino)-3-methyl-1,2-diphenylbutan-2-yl] propanoate|
|Routes of Administration|
Dextropropoxyphene (also known as Propoxyphene and Darvon) is a synthetic opioid of the propionate 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). Notably, it is reported to produce significantly less euphoria in comparison to other opioids.
Dextropropoxyphene was first patented in 1955 and subsequently manufactured by Eli Lilly and Company.
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. Notably, dextropropoxyphene is also known to cause seizures and potentially fatal cardiac arrhythmia at high doses, which are not able to be reversed by naloxone.
Today, dextropropoxyphene is rarely encountered on the streets and is sometimes obtained by prescription from a compounding pharmacy. 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. 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.
The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.
The general sensation of dextropropoxyphene can be described as one of euphoria, relaxation, anxiety suppression and pain relief.
- Pain relief - This effect is less intense than that of other opioids such as morphine and fentanyl.
- Physical euphoria - This particular substance can be considered as less intense in its physical euphoria when compared with that of morphine or diacetylmorphine (heroin). The sensation itself can be described as extreme feelings of intense physical comfort, warmth, love and bliss.
- Respiratory depression - At low to moderate doses, this effect results in the sensation that the breath is slowed down mildly to moderately, but does not cause noticeable impairment. At high doses and overdoses, opioid-induced respiratory depression can result in a shortness of breath, abnormal breathing patterns, semi-consciousness, or unconsciousness. Severe overdoses can result in a coma or death without immediate medical attention.
- Cough suppression
- Difficulty urinating
- Pupil constriction
- Decreased libido
- Appetite suppression
- Dizziness - Dextropropoxyphene causes dizziness at a higher rate than other opioids.
- Orgasm suppression
- Cognitive euphoria - This particular substance can be considered as less intense in its cognitive euphoria when compared with that of morphine or diacetylmorphine (heroin). The sensation itself can be described as powerful and overwhelming feeling of emotional bliss, contentment, and happiness.
- Anxiety suppression
- Compulsive redosing
- Confusion - Dextropropoxyphene may cause confusion at a higher rate than other opioids.
- Dream potentiation
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.
Although many psychoactive substances are safe to use on their own, they can become dangerous or even life-threatening when taken with other substances. The list below contains some potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses but still increase the possibility of injury of death. Independent research should always be conducted to ensure that a combination of two or more substances is safe before consumption.
- Depressants (1,4-Butanediol, 2M2B, alcohol, benzodiazepines, barbiturates, GHB/GBL, methaqualone, opioids) - This combination potentiates the muscle relaxation, amnesia, sedation, and respiratory depression caused by one another. At higher doses, it can lead to a sudden, unexpected loss of consciousness along with a dangerous amount of depressed respiration. There is also an increased risk of vomiting while unconsciousness and dying from the resulting suffocation. If nausea or vomiting occurs before a loss of consciousness, users should attempt to fall asleep in the recovery position or have a friend move them into it.
- Stimulants - It can be dangerous to combine depressants with stimulants due to the risk of accidental excessive intoxication. Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.
- Dissociatives - This combination can unpredictably potentiate the amnesia, sedation, motor control loss and delusions that can be caused by each other. It may also result in a sudden loss of consciousness accompanied by a dangerous degree of respiratory depression. If nausea or vomiting occurs before consciousness is lost, users should attempt to fall asleep in the recovery position or have a friend move them into it.
- Psychedelics - Dextropropoxyphene is known to lower seizure threshold and psychedelics also cause occasional seizures.
- Cocaine - Cocaine and dextropropoxyphene both block sodium ion channels, which may increase cardiotoxicity and lead to possible cardiac death.
Serotonin syndrome risk
- MAOIs such as syrian rue, banisteriopsis caapi, 2C-T-2, 2C-T-7, αMT, and some antidepressants
- Serotonin releasers such as MDMA, 4-FA, methylone and αMT
- Selective serotonin re-uptake inhibitors (SSRIs)
- Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as tramadol and DXM
- 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.
- United Kingdom - Dextropropoxyphene is a Class C, Schedule 2 or Schedule 5 substance depending on the dose.
- Risks of Combining Depressants (Tripsit) | https://tripsit.me/combining-depressants/
- Blockade of Rat α3β4 Nicotinic Receptor Function by Methadone, Its Metabolites, and Structural Analogs | http://jpet.aspetjournals.org/content/299/1/366.abstract
- Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210
- DEA Controlled Drugs | https://www.deadiversion.usdoj.gov/schedules/orangebook/e_cs_sched.pdf
- Home Office Controlled Drugs | https://www.gov.uk/government/publications/controlled-drugs-list--2/list-of-most-commonly-encountered-drugs-currently-controlled-under-the-misuse-of-drugs-legislation