APICA

(Redirected from SDB-001)
Summary sheet: APICA
APICA
APICA.svg
Chemical Nomenclature
Common names APICA, SDB-001, 2NE1
Substitutive name APICA
Systematic name N-(1-Adamantyl)-1-pentyl-1H-indole-3-carboxamide
Class Membership
Psychoactive class Cannabinoid
Chemical class Indolecarboxamide
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.


⇣ Smoked
Dosage
Threshold < 0.5 mg
Light 0.5 - 1.5 mg
Common 1.5 - 2 mg
Strong 2 - 4 mg
Heavy 4 mg +
Duration
Total 30 - 60 minutes
Onset 0 - 20 seconds
Peak 10 - 30 minutes
Offset 5 - 10 minutes
After effects 15 - 35 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.

Interactions


APICA (also known as SDB-001, and 2NE1) is a novel synthetic cannabinoid that produces modified cannabis-like effects when administered. It has been shown to act as a potent agonist for the CB1 and CB2 cannabinoid receptors.[1]

The name "2NE1" appears to be a reference to the South Korean all-girl K-Pop group,[2] a naming convention shared by the closely related chemical AKB48. In 2011, the two chemicals were first identified in Japan as a mixture in a product sold under the name "Fragrance Powder".[3] APICA has since been available for sale as a grey-area research chemical through online vendors.

Synthetic cannabinoids are commonly smoked or vaporized to achieve a quick onset of effects and rapid offset. There is little information available about the use of APICA via other routes of administration, although as with other synthetic cannabinoids it could be expected to be orally active when dissolved in a lipid, which may significantly extend its duration. It is insoluble in water, but dissolves in ethanol and lipids.[citation needed]

Unlike cannabis, the chronic abuse of synthetic cannabinoids has been associated with multiple deaths and more dangerous side effects and toxicity in general. Therefore, it is strongly discouraged to take this substance for extended periods of time or in excessive doses. Thorough independent research and harm reduction practices are strongly advised if choosing to use this substance.

Chemistry

APICA, or N-(1-adamantyl)-1-pentyl-1H-indole-3-carboxamide, is a synthetic indole cannabinoid. Like many synthetic cannabinoids, it can be considered to be composed of four linked structures: core, bridge, head, and tail.[4] In APICA, the core indole group is substituted at R1 with a pentyl chain tail and at R3 with a carboxamide bridge linking to an adamantyl head.

APICA can be considered an analog of both AKB48, which features an indazole in place of APICA's indole group, and STS-135, in which the pentyl tail is further substituted with a terminal fluorine.

Pharmacology

APICA acts as a full agonist of the cannabinoid receptors, with similar potency at both CB1 and CB2. In vivo experiments measuring the response of rats to APICA and similar drugs found that APICA had a similar potency to Δ9-THC and around a third the potency of JWH-018. In comparison to these other cannabinoids, APICA appeared to elicit a longer duration of effect. Caution should be exercised in interpreting studies using animals, however, as effects may differ significantly in humans.[5]

Pharmacological studies have reported EC50 values of 6.89 ± 0.11nM at CB1 and 7.54 ± 0.11nM at CB2.[1] It is likely that APICA shares many of the in vivo properties of Δ9-THC. However, the role of these interactions and how they result in the cannabinoid high has yet to be scientifically validated.

In vivo metabolic studies on APICA have shown that the drug is fully metabolized with none of the original compound detectable in urine. The major metabolites were mono- or dihydroxylated on the adamantyl ring system and monohydroxylated on the pentyl chain.[6]

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
 

    • Spontaneous physical sensations - The "body high" of APICA can be described as a sharp, uncomfortable, all-encompassing, and electric tingling sensation that spreads over the body after initial ingestion. It maintains a consistent presence that quickly rises with the onset and hits its limit once the peak has been reached before immediately dissipating.
    • Motor control loss - This substance causes a partial to moderate suppression of motor control which intensifies proportional to dose, but rarely results in a complete inability to walk and perform basic movements.
    • Appetite enhancement - As with many other cannabinoids, APICA causes an increase in appetite[7], known colloquially as "the munchies" in popular American and United Kingdom culture. Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food.[8] This is thought to be due to the way in which endocannabinoids in the hypothalamus activate cannabinoid receptors that are responsible for maintaining food intake.[8]
    • Pain relief - Cannabinoids have been clinically demonstrated to provide pain relief via agonism of cannabinoid receptors CB1 and CB2, which extends to synthetic cannabinoid receptor agonists.[9][10]
    • Perception of bodily heaviness or Perception of bodily lightness
    • Changes in felt gravity
    • Dehydration
    • Dry mouth - This is known colloquially as "cotton mouth" in popular American and United Kingdom culture.
    • Vasodilation[citation needed]

Cognitive effects
 

Auditory effects
 

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:


Toxicity and harm potential

Further information: Synthetic cannabinoid § Toxicity and harm potential, and Research chemicals § Toxicity and harm potential

The toxicity and long-term health effects of recreational APICA use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because APICA has very little history of human usage. Anecdotal evidence from people who have tried APICA within the community suggests that there do not seem to be any negative health effects attributed to simply trying this substance at low to moderate doses by itself and using it sparingly (but nothing can be completely guaranteed).

It is advised that those with severe pre-existing mental conditions should not ingest these substances due to the way they strongly amplify one's current state of mind and emotions. Also, as with THC and cannabis, prolonged usage of synthetic cannabinoids including APICA may increase one's disposition to mental illness and psychosis,[11] particularly in vulnerable individuals with risk factors for psychotic illnesses (like a past or family history of schizophrenia).[12][13][14]

As synthetic cannabinoids are active in the milligram range (with below 5mg being a common dose), it is important to use proper precautions when dosing to avoid a negative experience and injury to oneself or others.

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

Tolerance and addiction potential

As with other synthetic cannabinoids, the chronic use of APICA 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 effects may occur if a person suddenly stops their usage.

Tolerance to many of the effects of APICA develops with prolonged and repeated use. 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). APICA presents cross-tolerance with all cannabinoids, meaning that after the consumption of APICA all cannabinoids will have a reduced effect.

Overdose

It has been reported that overdose on this substance will cause physical discomfort including heart palpitations, vertigo and sedation at much lower than dangerous doses, usually causing the user to suffer large amounts of anxiety and paranoia, or to fall asleep.[citation needed]

Legal status

 

This legality section is a stub.

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

  • China: As of October 2015 APICA is a controlled substance in China.[15]
  • Germany: APICA is controlled under Anlage II BtMG (Narcotics Act, Schedule II)[16] as of December 13, 2014.[17] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[18]
  • Switzerland: APICA is a controlled substance specifically named under Verzeichnis E.[19]
  • United Kingdom: APICA is a Class B controlled substance under the third-generation synthetic cannabinoids generic definition, which came into effect on December 14, 2016 and is illegal to possess, produce, supply, or import. [20]

See also

External links

References

  1. ↑ 1.0 1.1 Banister, S. D., Stuart, J., Kevin, R. C., Edington, A., Longworth, M., Wilkinson, S. M., Beinat, C., Buchanan, A. S., Hibbs, D. E., Glass, M., Connor, M., McGregor, I. S., Kassiou, M. (19 August 2015). "Effects of bioisosteric fluorine in synthetic cannabinoid designer drugs JWH-018, AM-2201, UR-144, XLR-11, PB-22, 5F-PB-22, APICA, and STS-135". ACS chemical neuroscience. 6 (8): 1445–1458. doi:10.1021/acschemneuro.5b00107. ISSN 1948-7193. 
  2. ↑ 2NE1, 2022 
  3. ↑ Uchiyama, N., Kawamura, M., Kikura-Hanajiri, R., Goda, Y. (July 2012). "Identification of two new-type synthetic cannabinoids, N-(1-adamantyl)-1-pentyl-1H-indole-3-carboxamide (APICA) and N-(1-adamantyl)-1-pentyl-1H-indazole-3-carboxamide (APINACA), and detection of five synthetic cannabinoids, AM-1220, AM-2233, AM-1241, CB-13 (CRA-13), and AM-1248, as designer drugs in illegal products". Forensic Toxicology. 30 (2): 114–125. doi:10.1007/s11419-012-0136-7. ISSN 1860-8965. 
  4. ↑ Synthetic cannabinoids in Europe 
  5. ↑ Banister, S. D., Wilkinson, S. M., Longworth, M., Stuart, J., Apetz, N., English, K., Brooker, L., Goebel, C., Hibbs, D. E., Glass, M., Connor, M., McGregor, I. S., Kassiou, M. (3 April 2013). "The Synthesis and Pharmacological Evaluation of Adamantane-Derived Indoles: Cannabimimetic Drugs of Abuse". ACS Chemical Neuroscience. 4 (7): 1081–1092. doi:10.1021/cn400035r. ISSN 1948-7193. 
  6. ↑ Sobolevsky, T., Prasolov, I., Rodchenkov, G. (February 2015). "Study on the phase I metabolism of novel synthetic cannabinoids, APICA and its fluorinated analogue". Drug Testing and Analysis. 7 (2): 131–142. doi:10.1002/dta.1756. ISSN 1942-7611. 
  7. ↑ Mechoulam, R., ed. (1986). Cannabinoids as therapeutic agents. CRC Press. ISBN 9780849357725. 
  8. ↑ 8.0 8.1 How Marijuana Works, 2001 
  9. ↑ Martín-Sánchez, E., Furukawa, T. A., Taylor, J., Martin, J. L. R. (November 2009). "Systematic Review and Meta-analysis of Cannabis Treatment for Chronic Pain". Pain Medicine. 10 (8): 1353–1368. doi:10.1111/j.1526-4637.2009.00703.x. ISSN 1526-2375. 
  10. ↑ Lynch, M. E., Campbell, F. (November 2011). "Cannabinoids for treatment of chronic non-cancer pain; a systematic review of randomized trials: Cannabinoids for pain". British Journal of Clinical Pharmacology. 72 (5): 735–744. doi:10.1111/j.1365-2125.2011.03970.x. ISSN 0306-5251. 
  11. ↑ 11.0 11.1 Arseneault, L., Cannon, M., Witton, J., Murray, R. M. (February 2004). "Causal association between cannabis and psychosis: examination of the evidence". The British Journal of Psychiatry. 184 (2): 110–117. doi:10.1192/bjp.184.2.110. ISSN 0007-1250. 
  12. ↑ 12.0 12.1 Every-Palmer, S. (September 2011). "Synthetic cannabinoid JWH-018 and psychosis: An explorative study". Drug and Alcohol Dependence. 117 (2–3): 152–157. doi:10.1016/j.drugalcdep.2011.01.012. ISSN 0376-8716. 
  13. ↑ 13.0 13.1 Schneir, A. B., Cullen, J., Ly, B. T. (1 March 2011). ""Spice" Girls: Synthetic Cannabinoid Intoxication". The Journal of Emergency Medicine. 40 (3): 296–299. doi:10.1016/j.jemermed.2010.10.014. ISSN 0736-4679. 
  14. ↑ 14.0 14.1 Vearrier, D., Osterhoudt, K. C. (June 2010). "A Teenager With Agitation: Higher Than She Should Have Climbed". Pediatric Emergency Care. 26 (6): 462–465. doi:10.1097/PEC.0b013e3181e4f416. ISSN 0749-5161. 
  15. ↑ 关于印发《非药用类麻醉药品和精神药品列管办法》的通知 | http://www.sfda.gov.cn/WS01/CL0056/130753.html
  16. ↑ "Anlage II BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 30, 2019. 
  17. ↑ "Achtundzwanzigste Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften" (PDF). Bundesgesetzblatt Jahrgang 2014 Teil I Nr. 57 (in German). Bundesanzeiger Verlag. December 12, 2014. pp. 1999–2002. Retrieved December 19, 2019. 
  18. ↑ "§ 29 BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019. 
  19. ↑ "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  20. ↑ The Misuse of Drugs Act 1971 (Amendment) Order 2016 


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