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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: Dihydrocodeine
Chemical Nomenclature
Common names Dihydrocodeine
Systematic name 4,5-alpha-epoxy-3-methoxy-17-methylmorphinan-6-ol
Class Membership
Psychoactive class Opioid
Chemical class Morphinan
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.

Threshold 20 mg
Light 50 - 100 mg
Common 100 - 150 mg
Strong 150 - 200 mg
Heavy 200 mg +
Total 3 - 4 hours
Onset 30 - 45 minutes

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.


Dihydrocodeine is a semi-synthetic morphinan opioid analgesic prescribed for pain, or as an antitussive (either alone or compounded with paracetamol or aspirin). It was developed in Germany in 1908 and first marketed in 1911.[2]

Dihydrocodeine is also known as Drocode, Paracodeine and Parzone. Its many brand names include Synalgos DC, Panlor DC, Panlor SS, Contugesic, Bron Tablet, New Bron Solution-ACE, Pabron S Gold W Tablets, Huscode, Drocode, Paracodin,[3] Codidol, Dehace, Didor Continus, Dicogesic, Codhydrine, Dekacodin, DHC,[3] DH-Codeine, Didrate, Dihydrin, Hydrocodin, Makatussin, Nadeine, Novicodin, Rapacodin, Paramol, Remedeine, Dico and DF-118.

Dihydrocodeine is available as tablets, solutions, elixirs, and other oral forms. In some countries, the drug is available as an injectable solution for deep subcutaneous and intra-muscular administration. As with codeine, intravenous administration should be avoided as it could result in anaphylaxis and dangerous pulmonary edema. Dihydrocodeine is available in suppository form on prescription.[citation needed]

Dihydrocodeine is used as an alternative or adjunct to codeine and is similar in chemical structure. Dihydrocodeine is generally considered to have up to twice as strong analgesic effects as codeine.[4] It is also noteworthy that Dihydrocodeine has no ceiling effect unlike codeine (considered to be around 200-600mg/day) [5], meaning with Dihydrocodeine you can, theoretically, achieve more euphoria the higher the dose, which codeine can’t due to the so-called ceiling effect.


Dihydrocodeine, or 4,5-alpha-epoxy-3-methoxy-17-methylmorphinan-6-ol, is an opioid of the morphinan class. Dihydrocodeine and other molecules of this class contain a polycyclic core of three benzene rings fused in a zig-zag pattern called a phenanthrene. A fourth nitrogen containing ring is fused to the phenanthrene at R9 and R13 with the nitrogen member looking at R17 of the combined structure. This structure is called morphinan.

Dihydrocodeine, along with other morphinans, contains an ether bridge between two of its rings, connecting R4 and R5 through an oxygen group. It also contains a hydroxy group (OH-) bound at R6 and a methyl group located on the nitrogen atom at R17. On the same ring containing the hydroxy group, codeine contains a double bond, which dihydrocodeine lacks. This results in a much more stable chemical structure and also affects its metabolism.

Dihydrocodeine can be synthesized from morphine by reduction of the 7,8-double bond. It readily converts to dihydromorphine with high yields (>95%) which can be methylated to create dihydrocodeine. Dihydrocodeine is analogous to the other morphinans including codeine, heroin, ethylmorphine, hydrocodone, and oxycodone.


Dihydrocodeine exerts its 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.[citation needed]

Dihydrocodeine is metabolized via CYP2D6 to the active metabolite dihydromorphine, which has a potency similar to morphine. Other weakly active metabolites include nordihydrocodeine (which is formed via CYP3A4) and dihydrocodeine-6-glucuronide.[6] Although dihydrocodeine does have extremely active metabolites in the form of dihydromorphine and dihydromorphine-6-glucuronide, these metabolites are produced in such a small amount that they do not have clinically important effects.[7]

Binding affinities (Ki)[8]

  • Mu opioid agonist - 325 nM
  • Kappa opioid agonist - 14242 nM
  • Delta opioid agonist - 5905 nM

Dihydrocodeine itself is a weak ligand for the opioid receptors however its main active metabolite - dihydromorphine and one of its metabolites - dihydromorphine-6-O-glucuronide show much stronger agonistic effects.[8]

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

Visual 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

Dihydrocodeine has a low toxicity relative to dose. As with all opiates, long-term effects can vary but can include diminished libido, apathy and memory loss. Some people may also have an allergic reaction to dihydrocodeine, such as the swelling of skin and rashes. It is also potentially lethal when mixed with depressants like alcohol or benzodiazepines.

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 dihydrocodeine 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 dihydrocodeine 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). Dihydrocodeine presents cross-tolerance with all other opioids, meaning that after the consumption of dihydrocodeine 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
  • Amphetamines - 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.
  • Cocaine - 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 patient and cause respiratory arrest.
  • 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[10]. 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[10]. 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.

Legal status

  • Austria: Dihydrocodeine is legal for medical use under the AMG (Arzneimittelgesetz Österreich) and illegal when sold or possessed without a prescription under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Australia: Dihydrocodeine is a Schedule 3 medicine meaning it is available without prescription but is stored behind the counter at a pharmacy. Consultation with pharmacist is required for purchase. It is most commonly available as an oral liquid (Brand name Rikodeine) at a dose of 19mg/10mL in 100 or 200mL bottles.

[11] [12]

  • Germany: Dihydrocodeine is a controlled substance under Anlage III of the BtMG. It can only be prescribed on a narcotic prescription form. There is an exception for preperations, containing up to 2,5% or 100mg dihydrocodeine per unit, which can be prescripted on a regular prescription, if not prescripted to an alcohol or drug dependent person.[13]
  • Hong Kong: In Hong Kong, dihydrocodeine is regulated under Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals and for university research purposes. A pharmacist can dispense Dihydrocodeine when furnished with a doctors prescription. Anyone who supplies the substance without a prescription can be fined $10000 (HKD). The penalty for trafficking or manufacturing the substance is a $5,000,000 (HKD) fine and life imprisonment. Possession of the substance for consumption, without a licence from the Department of Health, is illegal and carries a $1,000,000 (HKD) fine and/or 7 years imprisonment.[citation needed]
  • Japan: In Japan, dihydrocodeine is available without a prescription; used in cough medicines such as New Bron Solution-ACE. Dihydrocodeine is used as an antitussive in many products as a Dextromethorphan alternative. Medicines in Japan which contain dihydrocodeine are coupled with caffeine to offset the sedative effects and discourage recreational use. Cough medicines containing dihydrocodeine are controlled similarly to dextromethorphan in the United States, in that its sale is strictly limited by purchase quantity and is restricted to persons 20 and older for purchase.[citation needed]
  • Russia: Dihydrocodeine is a Schedule II controlled substance.[14]
  • Sweden: Dihydrocodeine is a prescription only medication.[15]
  • Switzerland: Dihydrocodeine is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted. Some preparations containing dihydrocodeine are included in Verzechnis C, while certain ones are excluded.[16]
  • United Kingdom: In the United Kingdom, dihydrocodeine is a Class B drug; but, it is available over-the-counter in small amounts (less than 8 mg), when combined with paracetamol (see co-dydramol). Dihydrocodeine is listed in Schedule 5 of the Misuse of Drugs Regulations 2001 whereby it is exempt from prohibition on possession provided that it is in the form of a single preparation not being designed for injection and less than 100 mg (calculated as free base) or with a total concentration less than 2.5% (calculated as free base).[17] Illegal possession of dihydrocodeine can result in up to 5 years in prison and/or a fine.[18]
  • United States: In the USA, dihydrocodeine is a DEA Schedule II substance, although preparations containing small amounts of dihydrocodeine are classified as Schedule III or Schedule V, depending on the concentration of dihydrocodeine relative to other active constituents, such as paracetamol (acetaminophen). This scheduling is similar to the UK's. The DEA's ACSCN for dihydrocodeine free base and all salts is 9120. The 2013 annual aggregate manufacturing quota is 250 kilos.[citation needed]

See also

External links


  • Schmidt, H., Vormfelde, S. V., Klinder, K., Gundert-Remy, U., Gleiter, C. H., Skopp, G., Aderjan, R. and Fuhr, U. (2002), Affinities of Dihydrocodeine and its Metabolites to Opioid Receptors. Pharmacology & Toxicology, 91: 57–63. https://doi.org/10.1034/j.1600-0773.2002.910203.x
  • Koch T, Höllt V (2008). Role of receptor internalization in opioid tolerance and dependence. Pharmacol. Ther. 117 (2): 199–206. https://doi.org/10.1016/j.pharmthera.2007.10.003
  • Pert, C. B., Pasternak, G., & Snyder, S. H. (1973). Opiate Agonists and Antagonists Discriminated by Receptor Binding in Brain. Science, 182 (4119), 1359-1361. https://doi.org/10.1126/science.182.4119.1359
  • Friswell J, Phillips C, Holding J, Morgan CJ, Brandner B, Curran HV (2008). Acute effects of opioids on memory functions of healthy men and women. Psychopharmacology (Berl.). 198 (2): 243–50. https://doi.org/10.1007/s00213-008-1123-x.
  • Stefano GB, Ptáček R, Kuželová H, Kream RM (2012). Endogenous morphine: up-to-date review (2011). Folia Biol. (Praha). 58 (2): 49–56. PMID 22578954.


  1. Risks of Combining Depressants - TripSit 
  2. Stolerman, I. (31 July 2010). Encyclopedia of Psychopharmacology. Springer Science & Business Media. ISBN 9783540686989. 
  3. 3.0 3.1 Dihydrocodein - Wirkstoff & Medikamente, Gelbe Liste, 2019 
  4. ((Leppert W Dihydrocodeine as an opioid analgesic for the treatment of moderate to severe chronic pain Curr Drug Metab 2010 Jul;11(6):494-506 doi: 102174/138920010791636211 PMID: 20540693.  Vancouver style error: punctuation (help); Missing or empty |title= (help)
  5. ((Shiratsuchi T, Ogawa S [Weak opioids] Nihon Rinsho 2001 Sep;59(9):1795-9 Japanese PMID: 11554054.  Vancouver style error: punctuation (help); Missing or empty |title= (help)
  6. Kirkwood, L. C., Nation, R. L., Somogyi, A. A. (December 1997). "Characterization of the human cytochrome P450 enzymes involved in the metabolism of dihydrocodeine". British Journal of Clinical Pharmacology. 44 (6): 549–555. doi:10.1046/j.1365-2125.1997.t01-1-00626.x. ISSN 0306-5251. 
  7. Schmidt, H., Vormfelde, S. V., Walchner-Bonjean, M., Klinder, K., Freudenthaler, S., Gleiter, C. H., Gundert-Remy, U., Skopp, G., Aderjan, R., Fuhr, U. (March 2003). "The role of active metabolites in dihydrocodeine effects". International Journal of Clinical Pharmacology and Therapeutics. 41 (3): 95–106. doi:10.5414/cpp41095. ISSN 0946-1965. 
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  9. Dihydrocodeine Tablets 30mg - Patient Information Leaflet (PIL) - (emc) 
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  11. https://www.nps.org.au/medicine-finder/rikodeine-oral-liquid
  12. https://search.tga.gov.au/s/search.html?collection=tga-artg&profile=record&meta_i=10587
  13. Anlage III BtMG - Einzelnorm 
  14. Постановление Правительства РФ от 01.10.2012 N 1002 (ред. от 09.08.2019) 
  15. Läkemedelsverkets föreskrifter (LVFS 1997:12) om förteckningar över narkotika, konsoliderad version t.o.m. LVFS 2010:1
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  17. The Misuse of Drugs Regulations 2001 
  18. Misuse of Drugs Act 1971, s.5(2)