Talk:Glaucine

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]

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]

Glaucine is a sedative-psychedelic. The psychedelic effects perceived from glaucine are in fact from interaction of 5-HT_2A 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]

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 ☠.

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:

• Erowid Experience Vaults: Glaucine

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]

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

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.

• Responsible use

• Glaucine (Wikipedia)