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Death 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: Desomorphine
Chemical Nomenclature
Common names Desomorphine, "Krokodil", "Krok"
Substitutive name Dihydrodesoxymorphine
Systematic name 4,5-α-Epoxy-17-methylmorphinan-3-o
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 Common Heavy
10 - 10 - 15 - 20 - 30 mg
Light Strong
Threshold < 10 mg
Light 10 - 15 mg
Common 15 - 20 mg
Strong 20 - 30 mg
Heavy 30 mg +
Total 3 - 4 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.

Desomorphine (also known as Dihydrodesoxymorphine) is an opioid substance of the morphinan chemical class that produces analgesic, muscle-relaxing, sedative, and euphoric effects when administered. It is a structural analog of morphine and the psychoactive component of the mixture known as Krokodil (also known as Crocodile, Krok, or Croc).

Developed by Roche in the 1930s, desomorphine first saw use in Switzerland under the trade name Permonid.[2] It was described as having a fast onset, a short duration of action, relatively little nausea, and analgesic potency 8 to 10 times higher than morphine.[3][4][5] Concerns about its dependence and abuse potential stemming from these properties led it to fall out of clinical use.

Desomorphine first emerged in the Russian drug scene around 2003 under the term Krokodil.[6] The name is a reference to the scaly, green-black skin discoloration frequently noted in its users.[7] Its use and prevalence has been attributed to widespread availability of codeine tablets as inexpensive over-the-counter drugs, along with a simple production process that can be done in a kitchen laboratory using iodine, red phosphorus, paint thinner, and hydrochloric acid.[8]

The application of krokodil regularly induces immediate damage to blood vessels, muscles, and bone and can induce multiple organ failure.[8] These severe complications are, however, caused by the toxic byproducts of the home production process rather than desomorphine itself.[8]

It should be noted that the scientific coverage of Krokodil is lacking and most of the knowledge concerning krokodil is based on media coverage. A small number of cases involving krokodil use outside of Russia, including Germany and the United States, have been reported but have failed to be substantiated. As of 2018, the only confirmed reports of krokodil use are from Russia.

History and culture

Desomorphine was first synthesized and patented in the United States in 1932.[9][10] It was originally synthesized with the intention to create an alternative to morphine in terms of tolerance and addiction properties and improve the side effect profile.[11] However, desomorphine fell short of these expectations and showed an increased dependence potential compared with morphine.

Desomorphine was used in Switzerland and introduced to the Swiss market in 1940 by the company Hoffman-La Roche, under the registered trade name of Permonid. It was used predominantly for postoperative pain due to its fast onset of action and reduced the tendency to cause respiratory depression and nausea.[11][12] Toward the end of 1952, Permonid was withdrawn from the market. Notably, the production of Permonid was continued in Switzerland until 1981 due to the idiosyncratic analgesic needs of a single patient in Bern, Switzerland, who suffered from a rare disease.[8]

In Russia, krokodil is considered an inexpensive and highly addictive substitute for heroin.[13][14] Its name is derived from crocodile (krokodil in Russian) and refers to the scaly, green-black skin discoloration frequently noted in its users.[7] Krokodil is produced by synthesizing desomorphine from codeine and combining it with other low-cost, easily obtained additives.[14] These additives can include hydrochloric acid, red phosphorus (from matchbook striking surfaces), iodine, gasoline, and paint thinner and have been proposed to underly krokodil's severe skin and systemic effects.[7][14] This production process is similar to that used to make street methamphetamine.

Since 2003, the prevalence of krokodil use in Russia has been increasing rapidly, presumably as a consequence of its low cost and its high dependence potential.


Desomorphine, a benzylisoquinoline alkaloid, is an opioid of the morphinan class. Dorphine and other molecules of this class contain a polycyclic core of three benzene rings fused in a zig-zag pattern called 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.

Desomorphine (along with other morphinans) contains an ether bridge between two of its rings, connecting R4 and R5 through an oxygen group. It contains one hydroxy group (OH-), bound at R3, and a methyl group located on the nitrogen atom at R17. It chemically differs from morphine with regard to the absent secondary hydroxy group at R6 and the saturated double bond.


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This pharmacology section is incomplete.

You can help by adding to it.

Like other opiates, desomorphine exerts its effects by binding to and activating the μ-opioid receptor as an agonist. This occurs due to the way in which opioids functionally mimic the body's natural endorphins. Endorphins are responsible for analgesia (pain reduction), sleepiness, and feelings of pleasure and enjoyment. They can be released in response to pain, strenuous exercise, orgasm, or excitement.

This mimicking of natural endorphins results in the drug's euphoric, analgesic (pain relief), and anxiolytic (anti-anxiety) effects.

Subjective effects

This subjective effects section is a stub.

As such, it is still in progress and may contain incomplete or wrong information.

You can help by expanding it.

Due to a lack of anecdotal reports using high purity desomorphine, the following effects are extrapolated from early clinical reports and inferences based on its relation to codeine and morphine. Desomorphine is considered to be powerfully euphoric opiate analgesia, with a fast onset and shorter duration that can encourage compulsive usage.

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.

Physical effects

Cognitive effects

Visual effects

Toxicity and harm potential

Toxicity of desomorphine

Like most opioids, unadulterated desomorphine does not cause many long-term complications other than dependence and constipation.[15] Outside of the extremely powerful addiction and physical dependence potential, the harmful or toxic aspects of desomorphine usage are exclusively associated with not taking appropriate precautions in regards to its administration, overdosing and using impure products derived from low-quality black-market self-manufacture.

Animal studies comparing pure desomorphine to morphine showed it to have increased toxicity, more potent relief of pain, higher levels of sedation, decreased respiration, and increased digestive activity

Heavy dosages of desomorphine can result in respiratory depression, leading to fatal or dangerous levels of anoxia (oxygen deprivation). This occurs because the breathing reflex is suppressed by agonism of µ-opioid receptors proportional to the dosage consumed.

Desomorphine can also cause nausea and vomiting; a significant number of deaths attributed to opioid overdose are caused by aspiration of vomit by an unconscious victim. This is when an unconscious or semi-conscious user who is lying on their back vomits into their mouth and unknowingly suffocates. It can be prevented by ensuring that one is lying on their side with their head tilted downwards so that the airways cannot be blocked in the event of vomiting while unconscious (also known as the recovery position).

Toxicity of "krokodil"

Illicitly produced desomorphine is typically far from pure and often contains large amounts of toxic substances as a result of being "cooked" and used without any significant effort to remove the byproducts and leftovers from synthesis. Injecting any such mixture can cause serious damage to the skin, blood vessels, bone, and muscles, sometimes requiring limb amputation in long-term users.[16]

Causes of this damage include iodine, phosphorus, and leftover solvents like gasoline and paint-thinner that are not adequately removed after synthesis. Strong acids and bases such as hydrochloric acid and sodium hydroxide are also employed without measuring pH of the final solution. Failure to remove insoluble fillers and binding aids from the codeine tablets used as starting material, as well as co-administration with pharmaceuticals such as tropicamide[14] and tianeptine[17], are also cited as possible contributors to the high toxicity observed in users.

The frequent occurrence of tissue damage and infection among illicit users are what gained the drug its nickname of the "flesh-eating drug." The pure form of the drug itself does not cause this damage. Despite the severe health impacts and short survival times commonly reported, there are also rarer cases of krokodil users more skilled in the manufacturing process who have used the drug for many years without experiencing the tissue damage associated with the impure "street" product.

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

Tolerance and addiction potential

As with other opiate-based painkillers, the chronic use of desomorphine can be considered extremely addictive and is capable of causing both physical and psychological dependence. When physical dependence has developed, withdrawal symptoms may occur if a person suddenly stops their usage.

Tolerance to many of the effects of desomorphine develops with prolonged use, including therapeutic effects. This results in users having to administer increasingly large doses to achieve the same effects. The rate at which this occurs develops at different rates for different effects with tolerance to the euphoric effects growing most quickly.


Depending on drug interactions and numerous other factors, death from overdose can take anywhere from several minutes to several hours. Death usually occurs due to lack of oxygen resulting from the lack of breathing. Many fatalities reported as opiate overdoses are probably caused by interactions with other depressants such as alcohol or benzodiazepines.[18] It should also be noted that since opiates can cause nausea and vomiting, a significant number of deaths attributed to opiate overdose are caused by aspiration of vomit by an unconscious person.

The risk of fatal opioid overdoses rise sharply after a period of cessation and relapse, largely because of reduced tolerance.[19] To account for this lack of tolerance, it is safer to only dose a fraction of one's usual dosage if relapsing. It has also been found that the environment one is in can play a role in opioid tolerance. In one scientific study, rats with the same history of heroin administration were significantly more likely to die after receiving their dose in an environment not associated with the drug in contrast to a familiar environment.[20]

Opiate overdose is usually treated with an opioid antagonist, such as naloxone (Narcan). This reverses the effects of opioids like desomorphine and causes an immediate return of consciousness but may result in withdrawal symptoms. The half-life of naloxone is shorter than most opioids, so it may have to be administered multiple times until the body has metabolized the opioid.

Dangerous interactions

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.

Legal status


This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

  • United States: Desomorphine is a Schedule I substance in the United States. It is illegal to manufacture, buy, possess, or distribute without a DEA license.[citation needed]

See also

External links


  • Gahr, M., Freudenmann, R. W., Hiemke, C., Gunst, I. M., Connemann, B. J., & Schönfeldt-Lecuona, C. (2012). Desomorphine goes “crocodile”. Journal of Addictive Diseases, 31(4), 407-412.


  1. Risks of Combining Depressants (Tripsit) |
  2. Hackenthal E. Desomorphin. Hintergrund. (Desomorphine Background). In: Hagers Handbuch der Pharmazeutischen Praxis (Hager′s compendium of pharmaceutical practice). vol 4, 5th ed. Berlin: NOVOSTI, 1998.
  3. Sargent L, May E. Agonists-antagonists derived from desomorphine and metopon. J Med Chem 1970; 13:1061–3.
  4. Janssen P. A review of the chemical features associated with strong morphine-like activity. Br J Anaesthesia 1962; 34:260–8.
  5. Bognar R, Makleit S. Neue Methode für die Vorbereitung von dihydro-6-desoxymorphine (A new method for the preparation of dihydro-6-desoxymorphinan). Arzneimittelforschung 1958; 6:323–5.
  6. Russian News & Information Agency NOVOSTI. Desomorphin. Hintergrund (Desomorphine. Background). (accessed December 20, 2011).
  7. 7.0 7.1 7.2 Grund, Jean-Paul C.; Latypov, Alisher; Harris, Magdalena (2013). "Breaking worse: The emergence of krokodil and excessive injuries among people who inject drugs in Eurasia". International Journal of Drug Policy. 24 (4): 265–274. doi:10.1016/j.drugpo.2013.04.007. ISSN 0955-3959. 
  8. 8.0 8.1 8.2 8.3 Gahr, Maximilian; Freudenmann, Roland W.; Hiemke, Christoph; Gunst, Ingo M.; Connemann, Bernhard J.; Schönfeldt-Lecuona, Carlos (2012). "Desomorphine Goes "Crocodile"". Journal of Addictive Diseases. 31 (4): 407–412. doi:10.1080/10550887.2012.735570. ISSN 1055-0887. 
  9. US Patent 1980972. Lyndon Frederick Small. Morphine derivates and processes. Published July 19, 1934. Issued November 13, 1934.
  10. Small L, Yuen K, Eilers L. The catalytic hydrogenation of the halogenomorphides: dihydrodesoxymorphine-D. J Am Chem Soc 1933; 55:3863–70.
  11. 11.0 11.1 Eddy N, Howes H. Studies of morphine, codeine and their derivatives x.desoxymorphine-c, desoxycodeine-c and their hydrogenated derivatives. Journal of Pharmacology and Experimental Therapeutics 1935; 55:257–267.
  12. Hackenthal E. Desomorphin. Hintergrund. (Desomorphine Background). In: Hagers Handbuch der Pharmazeutischen Praxis (Hager′s compendium of pharmaceutical practice). vol 4, 5th ed. Berlin: NOVOSTI, 1998.
  13. Alves, Emanuele Amorim; Grund, Jean-Paul Cornelis; Afonso, Carlos Manuel; Netto, Annibal Duarte Pereira; Carvalho, Félix; Dinis-Oliveira, Ricardo Jorge (2015). "The harmful chemistry behind krokodil (desomorphine) synthesis and mechanisms of toxicity". Forensic Science International. 249: 207–213. doi:10.1016/j.forsciint.2015.02.001. ISSN 0379-0738. 
  14. 14.0 14.1 14.2 14.3 Shelton, Megan; Ramirez-Fort, Marigdalia K.; Lee, Kachiu C.; Ladizinski, Barry (2015). "Krokodil". JAMA Dermatology. 151 (1): 32. doi:10.1001/jamadermatol.2014.1025. ISSN 2168-6068. 
  15. Merck Manual of Home Health Handbook – 2nd edition, 2003, p. 2097
  16. Katselou, M; Papoutsis, I; Nikolaou, P; Spiliopoulou, C; Athanaselis, S (May 2014). "A "Krokodil" emerges from the murky waters of addiction. Abuse trends of an old drug". Life Sciences. 102 (2): 81–87. PMID 24650492.
  17. Haskin, A., Kim, N., & Aguh, C. (2016). A new drug with a nasty bite: A case of krokodil-induced skin necrosis in an intravenous drug user. JAAD Case Reports, 2(2), 174.
  18. Darke S, Zador D (1996). "Fatal heroin 'overdose': a review". Addiction. 91 (12): 1765–1772. PMID 8997759.
  19. Why Heroin Relapse Often Ends In Death - Lauren F Friedman (Business Insider) |
  20. Siegel, S., Hinson, R., Krank, M., & McCully, J. (1982). Heroin “overdose” death: contribution of drug-associated environmental cues. Science, 216(4544), 436–437.