Talk:Clobenzorex - PsychonautWiki

Talk:Clobenzorex

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Summary sheet: Clobenzorex
Clobenzorex
Clobenzorex.svg
Chemical Nomenclature
Common names Clobenzorex, Greenies, Asenlix, Itravil, Finedal, Rexigen
Substitutive name N-(2-Chlorobenzyl)amphetamine
Systematic name (+)-N-[(2-Chlorophenyl)methyl]-α-methylbenzeneethanamine
Class Membership
Psychoactive class Stimulant
Chemical class Amphetamine
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 x%[1]
Threshold 30 mg
Light 60 - 90 mg
Common 120 - 150 mg
Strong 180 - 210 mg
Heavy 240 mg +
Duration
Total 7 - 15 hours
Onset x - y minutes
Come up x - y minutes
Peak x - y hours
Offset x - y hours
After effects x - y 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

Clobenzorex (also known as 2'-chlorobenzylamphetamine or clobenzorex hydrochloride when under the brand names Asenlix, Itravil, Finedal, and Rexigen) is a stimulant substance of the amphetamine class. It is an N-alkylated amphetamine prodrug that primarily metabolizes into 4-hydroxyclobenzorex; however it also metabolizes into d-amphetamine (dextroamphetamine) in small amounts.[2] The drug is legally distributed in Mexico as an appetite suppressant.[3] Like other amphetamine derivatives, clobenzorex produces its effects by promoting the release of neurotransmitters dopamine and norepinephrine in the brain.

History and culture

 

This History and culture section is a stub.

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

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Chemistry

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Pharmacology

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Pharmacokinetics

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Pharmacodynamics

Amphetamine is a full agonist of the trace amine-associated receptor 1 (TAAR1), which is a key regulator of common and trace brain monoamines such as dopamine, serotonin and noradrenaline.[4][5][6] The agonism of this set of receptors results in the release of increased concentrations of dopamine, serotonin and noradrenaline in the synaptic cleft. This leads to cognitive and physical stimulation within the user.

d-amphetamine's affinity for the TAAR1 receptor is twice that of l-amphetamine.[7] As a result, d-amphetamine produces three to four times as much central nervous system (CNS) stimulation as l-amphetamine. l-amphetamine, on the other hand, has stronger cardiovascular and peripheral effects.

Conversion rate

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Subjective effects

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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
 

Cognitive effects
 

Auditory effects
 

  • If applicable, a brief paragraph summary of the substance's auditory effects may be included here. You may select from a list of auditory effects to add below here.

After effects
 

  • If applicable, a brief paragraph summary of the substance's aftereffects may be included here. You may select from a list of aftereffects to add below here.

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

In rodents and primates, sufficiently high doses of amphetamine cause dopaminergic neurotoxicity, or damage to dopamine neurons, which is characterized by reduced transporter and receptor function. There is no evidence that amphetamine is directly neurotoxic in humans. However, large doses of amphetamine may cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine.

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

Tolerance and addiction potential

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Overdose

A severe amphetamine overdose can result in a stimulant psychosis that may involve a variety of symptoms, such as paranoia, delusions, and hallucinations, including the infamous Shadow people. A Cochrane Collaboration review on treatment for amphetamine, dextroamphetamine, and methamphetamine psychosis states that about 5–15% of users fail to recover completely. According to the same review, there is at least one trial that shows antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis. Psychosis very rarely arises from therapeutic use. The combination of prolonged use of high doses combined with sleep deprivation significantly increases the risk of stimulant psychosis.

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 - Drinking alcohol on stimulants is considered risky because it reduces the sedative effects of the alcohol that the body uses to gauge drunkenness. This often leads to excessive drinking with greatly reduced inhibitions, increasing the risk of liver damage and increased dehydration. The effects of stimulants will also allow one to drink past a point where they might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel the alcohol and the stimulant less.
  • GHB/GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the depressant effects of the GHB/GBL may overcome the user and cause respiratory arrest.
  • Opioids - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
  • Cocaine - The rewarding effects of cocaine are mediated by DAT inhibition, and an increase of exocytosis of dopamine through the cell membrane. Amphetamine reverses the direction of DAT and the direction vesicular transports within the cell by a pH mediated mechanism of displacement, thus excludes the regular mechanism of dopamine release through means of exocytosis because the effects Na+/K+ ATPase are inhibited. You will find cardiac effects with the combination of cocaine and amphetamine due to a SERT mediated mechanism from the subsequent activation of 5-HT2B, which is an effect of serotonin-related valvulopathy. Amphetamines generally cause hypertension in models of abuse, and this combination can increase the chances of syncope due to turbulent blood flow during valve operation. The rewarding mechanisms of cocaine are reversed by administration of amphetamine.[8][9]
  • Cannabis - Stimulants increase anxiety levels and the risk of thought loops and paranoia which can lead to negative experiences.
  • Caffeine - This combination of stimulants is generally considered unnecessary and may increase strain on the heart, as well as potentially causing anxiety and physical discomfort.
  • Tramadol - Tramadol and stimulants both increase the risk of seizures.
  • DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these substances have led to more serious heart issues.
  • Ketamine - Combining amphetamine and ketamine may result in psychoses that resemble schizophrenia, but not worse than the psychoses produced by either substance alone, but this is debatable. This is due to amphetamines ability to attenuated the disruption of working memory caused by ketamine. Amphetamine alone may result in grandiosity, paranoia, or somatic delusions with little to no effect on negative symptoms. Ketamine, however, will result in thought disorders, disruption of executive functioning, and delusions due to a modification of conception. These mechanisms are due to an increase of dopaminergic activity in the mesolimbic pathway caused by amphetamine due to its pharmacology effecting dopamine, and due to a disruption of dopaminergic functioning in the mesocortical pathways via NMDA antagonism effects of ketamine. Combining the two, you may expect mainly thought disorder along with positive symptoms.[10]
  • PCP - Increases risk of tachycardia, hypertension, and manic states.
  • Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
  • Psychedelics (e.g. LSD, mescaline, psilocybin) - Increases risk of anxiety, paranoia, and thought loops.
    • 25x-NBOMe - Amphetamines and NBOMes both provide considerable stimulation that when combined they can result in tachycardia, hypertension, vasoconstriction and, in extreme cases, heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics as they can lead to unpleasant thought loops. NBOMes are known to cause seizures and stimulants can increase this risk.
    • 2C-T-x - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
    • 5-MeO-xxT - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
    • DOx
  • aMT - aMT has MAOI properties which may interact unfavorably with amphetamines.
  • MAOIs - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with amphetamine can lead to hypertensive crises.

Legal status

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  • Brazil: Clobenzorex is a Class A3 controlled prohibited psychotropic.[11]
  • Canada: Clobenzorex is not specifically listed in the CDSA, however due to structural similarities with norbenzphetamine, it is a Schedule I under item 19(17).[citation needed]
  • United Kingdom: Clobenzorex is a Class B controlled drug.[12]
  • United States: Clobenzorex is not scheduled and is unaffected by the Federal Analogue Act as a derivative of Benzphetamine.[13] Importation for personal use is lawful provided that is for use to treat a condition with no approved medications, unlawful marketing is not occurring in the U.S, not deemed hazardous to health for the treating the condition, and is verified as a continuation of a treatment plan that began in a foreign country.[14]

See also

External links

Literature

  • APA formatted reference

References

  1. ↑ APA formatted citation.
  2. ↑ https://books.google.com/books?id=8JsQgRO3QcwC&dq=Clobenzorex+metabolism&pg=PA430
  3. ↑ Young R, Darmani NA, Elder EL, Dumas D, Glennon RA (1997-02). "Clobenzorex: Evidence for Amphetamine-like Behavioral Actions". Pharmacology, Biochemistry, and Behavior. 56 (2): 311–316. doi:10.1016/s0091-3057(96)00329-2. PMID 9050090.  Unknown parameter |s2cid= ignored (help)
  4. ↑ Miller, G. M. (January 2011). "The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity". Journal of neurochemistry. 116 (2): 164–176. doi:10.1111/j.1471-4159.2010.07109.x. ISSN 0022-3042. 
  5. ↑ Drug banks amphetamine targets 
  6. ↑ TA1 receptor | http://www.iuphar-db.org/DATABASE/ObjectDisplayForward?objectId=364
  7. ↑ Lewin, A. H., Miller, G. M., Gilmour, B. (1 December 2011). "Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class". Bioorganic & medicinal chemistry. 19 (23): 7044–7048. doi:10.1016/j.bmc.2011.10.007. ISSN 0968-0896. 
  8. ↑ Greenwald, M. K., Lundahl, L. H., Steinmiller, C. L. (December 2010). "Sustained Release d-Amphetamine Reduces Cocaine but not 'Speedball'-Seeking in Buprenorphine-Maintained Volunteers: A Test of Dual-Agonist Pharmacotherapy for Cocaine/Heroin Polydrug Abusers". Neuropsychopharmacology. 35 (13): 2624–2637. doi:10.1038/npp.2010.175. ISSN 0893-133X. 
  9. ↑ Siciliano, C. A., Saha, K., Calipari, E. S., Fordahl, S. C., Chen, R., Khoshbouei, H., Jones, S. R. (10 January 2018). "Amphetamine Reverses Escalated Cocaine Intake via Restoration of Dopamine Transporter Conformation". The Journal of Neuroscience. 38 (2): 484–497. doi:10.1523/JNEUROSCI.2604-17.2017. ISSN 0270-6474. 
  10. ↑ Krystal, J. H., Perry, E. B., Gueorguieva, R., Belger, A., Madonick, S. H., Abi-Dargham, A., Cooper, T. B., MacDougall, L., Abi-Saab, W., D’Souza, D. C. (1 September 2005). "Comparative and Interactive Human Psychopharmacologic Effects of Ketamine and Amphetamine: Implications for Glutamatergic and Dopaminergic Model Psychoses and Cognitive Function". Archives of General Psychiatry. 62 (9): 985. doi:10.1001/archpsyc.62.9.985. ISSN 0003-990X. 
  11. ↑ Anvisa (2023-07-24). "RDC Nº 804 - Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial" [Collegiate Board Resolution No. 804 - Lists of Narcotic, Psychotropic, Precursor, and Other Substances under Special Control] (in Portuguese). Diário Oficial da União (published 2023-07-25). Archived from the original on 2023-08-27. Retrieved 2023-09-28.  Unknown parameter |url-status= ignored (help)
  12. ↑ "Misuse of Drugs Act 1971 (c. 38): SCHEDULE 2: Controlled Drugs". Office of Public Sector Information. Retrieved 2009-06-15. 
  13. ↑ Boos, Terrence (2023-04-06). "Clobenzorex Letter". Imgur. Archived from the original on 2023-07-11. Retrieved 2023-07-11. 
  14. ↑ "Is it legal for me to personally import drugs?". FDA.gov. Food and Drug Administration. 2021-06-28. Retrieved 2021-07-22. 


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