Talk:Glaucine - PsychonautWiki

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Summary sheet: Glaucine

Glaucine is a naturally occurring novel psychedelic substance of the aporphine class found in Glaucium Flavum.[1] Glaucine has one stereocenter, therefore it has two stereoisomers, where (S)-Glaucine is a 5-HT2A agonist and (R)-Glaucine is a 5-HT2 positive allosteric modulator.[2] Its psychedelic effects are believed to be produced by its interaction with serotonin receptors like most psychedelics do, but also has clinically significant interactions at D1[3] and α1[4] receptors as an antagonist, and inhibits MOA to a moderate degree.[5] Glaucine has a close relative found in Blue Lotus (Nymphaea nouchali) called apomorphine. It is both psychedelic as well as sedating, but the sedation is more similar to that of opioids than psilocybin, a generally sedating psychedelic. It is most commonly consumed orally.

Glaucine
Glaucine.svg
Chemical Nomenclature
Common names Glaucine
Substitutive name 1,2,9,10-tetramethoxy-aporphine
Systematic name (S)-1,2,9,10-tetramethoxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinoline
Class Membership
Psychoactive class Psychedelic / Depressant
Chemical class Aporphine
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.



Oral
Dosage
Bioavailability 17 - 48% [6]
Threshold 20 mg
Light 20 - 75 mg
Common 75 - 150 mg
Strong 150 - 180 mg
Heavy 180 mg +
Duration
Total 3 - 6 hours
Onset 20 - 45 minutes
Come up 30 - 60 minutes
Peak 1 - 3 hours
Offset 1 - 2 hours
After effects 3 - 8 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.

Interactions


Glaucine is rarely sold on the streets and almost exclusively distributed as a legal alternative to more common psychedelics, where it is commonly used for recreational and entheogenic purposes. It was and still is a very uncommon and unheard of substance with sparing experiences on the internet.

Due to its potent sedating effects as well as unknown toxicity profile, it is strongly recommended that one use proper harm reduction practices if choosing to use this substance.

History and culture

Glaucine was first described in 1839 by Probst, defined as an 'acrid alkaloid, and was first isolated by Richard Fischer in 1901.[7] It has been used used for millennia, where records back to the year 131 claim it was used for aches and sores as well as abscess' in present-day Turkey.[7] In an overview study in 2007, glaucine's antitussive effectiveness was confirmed along with its potent bronchodilation effects, but lacked the respiratory depression and habit-forming use associated with opioid antitussives.[8] Today, it is sold as an antitussive medicine in Iceland and eastern European countries, as well as being used off-label for asthma.[9] It has very few written experiences online, but the earliest found is from 2009.[10]

 

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Chemistry

Glaucine is an aporphine, meaning 'not morphine.' It is named this because despite similar structure to morphine, it is in fact not morphine. Aporphine is the parent compound of glaucine, where glaucine has methoxy groups substituted at the 1, 2, 9, and 10 positions. Glaucine has one stereocenter, meaning it has two stereoisomers. Both stereoisomers are found in nature, albeit in different plants.[11]

 

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Pharmacology

Glaucine is a sedative-psychedelic. The psychedelic effects perceived from glaucine are in fact from interaction of 5-HT2A receptors, but both stereoisomers of glaucine interact with the receptor differently. (S)-glaucine is an agonist of the receptor, the same action performed by psychedelics like LSD and mescaline, but (R)-glaucine is a positive allosteric modulator, meaning it boosts the signaling and activity at the receptor.[2] Its sedating effects are believed to come from its strong antagonism at α1 receptors, the same receptors that the stimulant caffeine agonizes.[4] D1 antagonism is common amongst aporphines such as apomorphine, and might be a cause of reduction in drug-seeking behaviors following administration such as seen with apomorphine.[12]

 

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Subjective effects

 
This subjective effects section is a stub.

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

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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
 

Visual effects
 

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Experience reports

There are currently 0 experience reports which describe the effects of this substance in our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Intragastrical administration of glaucine to rats in doses of 5, 25 and 75 mg/kg bodyweight daily for 3 months did not produce any detectable harm to any organ. It has also been concluded that it is not an allergen, mutagenic, or toxic to embryos.[13]

 

This toxicity and harm potential section is a stub.

As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it.
Note: Always conduct independent research and use harm reduction practices if using this substance.

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

Lethal dosage

Intraperitoneal LD50 in mice was found to be between 150-180mg/kg bodyweight. Intragastrical route was 510-610mg/kg bodyweight.[14]

Tolerance and addiction potential

Like other serotonergic psychedelics, glaucine has been found to not produce dependency with humans, even after prolonged use.[15]

Dangerous interactions

 

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As such, it may contain incomplete or invalid information. You can help by expanding upon or correcting it.

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.

  • Lithium: Lithium is commonly prescribed in the treatment of bipolar disorder; however, there is a large body of anecdotal evidence that suggests taking it with psychedelics can significantly increase the risk of psychosis and seizures. As a result, this combination should be strictly avoided.
  • Tramadol: Tramadol is well documented to lower the seizure threshold in individuals and psychedelics also has the potential to induce seizures in susceptible individuals.[16]
  • Deliriants (e.g. diphenhydramine, scopolamine): Deliriants should generally not be combined with other substances, but may have additional risks when taken with psychedelics. May increase the risk of anxiety, delusions, mania, psychosis, and serotonin syndrome.
  • Cannabis: Cannabis has a strong, volatile synergy with psychedelics. While often used to intensify or prolong psychedelic effects, the combination increases the risk of adverse psychological effects like anxiety, paranoia, panic attacks, and psychosis. Anecdotal reports often describe cannabis use as the triggering event for a bad trip or psychosis. Caution is advised.
  • Depressants (e.g. GHB, alprazolam, hydrocodone): While respiratory depression isn't a problem with glaucine alone, due to the nature of the drug reducing blood pressure and heart contraction force, adding depressants could dangerously amplify the effects of a depressed CNS, leading to dangerous bradycardia, low blood pressure, and asphyxiation. Caution is advised.
  • Stimulants: (e.g. amphetamine, methcathinone): Due to a moderate inhibition of MAO-B, stimulants in combination with glaucine will cause a massive spike in blood pressure leading to hypertensive crisis as well as prolonged and more intense effects of stimulants. This combination should be strictly avoided.
  • Tyramine: Any food with a high level of tyramine should be avoided for two weeks after use. MAO-B inhibition can lead to a buildup of tyramine in the body, leading to a hypertensive crisis.

Legal status

 

This legality section is a stub.

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See also

External links

References

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