Tenocyclidine (TCP, thienylcyclohexylpiperidine, C15H23NS) is an analog of phencyclidine (PCP) with a similar chemical structure. PCP was discovered in 1956 and soon became a popular street drug due to its dissociative properties. At least 14 derivatives of PCP were sold for non-medical and illicit use from the late 1960s until the 1990s.1
Drugs that lead to a dissociative effect cause a person to feel detached from their surroundings. They may have a distortion of sights and sounds, experience rapid swings of their emotions, and have feelings that seem real but are not, according to the National Institute of Drug Abuse (NIDA).
Other dissociative agents of abuse include the general anesthetic agent ketamine and the non-prescription cough suppressant dextromethorphan (DXM). These agents may be used legitimately in medicine and research, but also have found a place as drugs of abuse accessed via the street, on the Internet, or unknowingly consumed in an illegally purchased drug. Abusers often consume excessively high doses of these drugs to achieve their "high".
Tenocyclidine (TCP) was originally patented by Parke Davis in the late 1950s. Chemically, substituting PCP’s benzene ring for thiophene results in TCP, as reported in patent documents. TCP is in a chemical class known as arylcyclohexylamines. Arylcyclohexylamines have a long history of being illegally manufactured for illicit sale, and includes many dissociative drugs.
Drugs of abuse with dissociative properties lead to mind-altering effects by interfering with the actions of the chemical glutamate at N-methyl-D-aspartate (NMDA) receptors in the brain, and are referred to as N-methyl-D-aspartate (NMDA) receptor (NMDAR) antagonists.
Some reports also suggest that TCP has dopamine reuptake inhibitor activity. Dopamine is a neurotransmitter responsible for the euphoria and “rush” associated with many abused drugs.
TCP was originally evaluated in 1960 by Parke Davis as an intravenous (IV) anesthetic, as it appeared to display similar activity to PCP. However, research on TCP as a commercial drug for anesthesia was abandoned by Parke Davis due to psychiatric side effects such as emergence delirium.1
A radiolabelled form of TCP has been used for research into NMDA receptors because it has a high affinity for binding at the phencyclidine site. NMDA receptors may play a role in central nervous system diseases such as depression or schizophrenia.2
Case reports describe TCP as being slightly more potent than PCP by weight, with a longer duration.1 However, other reports state it is “considerably more potent”.3
The US Drug Enforcement Agency (DEA) placed TCP into Schedule I of the Controlled Substances Act in August of 1975. TCP was entered into Schedule I as it was considered an agent without legitimate medical use and of high abuse potential. In 1989, another related TCP analog, TCPy, was also placed into Schedule I.1,4
TCP is not classified as a narcotic by the DEA and is not structurally related.
The dissociatives properties of TCP can result in psychostimulant and hallucinogenic effects often sought after by users of these illicit drugs. In the 1970’s there were reports of TCP found in street samples in Los Angeles, California and in Hawaii; however, by 1975, TCP and PCP use were reported in 25 states. In 1980, it was reported that TCP was sold on the streets as a white powder, but it has also been sold as tablets and on plant matter.1
Online drug forums, many of which have been shut down by the DEA or FDA, are frequently used as chat boards for discussion or development of drugs of abuse. Street sale and abuse of TCP, particularly in recent times, is not frequently cited. However, street use of phencyclidine (PCP) in the U.S. may be on rise today after a decline seen in the late 1980s and 1990s.1
- As a dissociative, tenocyclidine’s psychotomimetic effects are probably similar to phencyclidine (PCP).
- Dissociatives most likely create the “high” due to alterations in glutamate at NMDA receptors, and possible alterations of the neurotransmitter dopamine.
- Glutamate also plays a role in learning, memory, emotion, and the perception of pain (the latter via activation of pain-regulating cells outside of the brain).
- PCP also alters the actions of dopamine, a neurotransmitter responsible for the euphoria and “rush” associated with many abused drugs.5,6
General Effects of Dissociative Drugs*
|Low to Moderate Doses||Higher Doses|
|Feeling numb, tremors||Hallucinations (hearing and visual)|
|Disorientation, confused state, loss of coordination||Memory loss|
|Alterations in sensory perception of light, sound, shapes, time, and body image||Physical changes in blood pressure, heart rate, breathing rate, and body temperature, which may be dangerous|
|Hallucinations (hearing and visual); Feeling separated from self and environment; sense of floating||Psychological distress such as anxiety, extreme panic, fear, paranoia, exaggerated strength, aggressiveness|
|Elevated blood pressure, heart rate, breathing rate, and body temperature||Respiratory arrest (stopped breathing), possible death if combined with alcohol or other drugs with central nervous system action.|
*Adapted from National Institute of Drug Abuse (5); dissociative drugs include agents such as phencyclidine (PCP), dextromethorphan (DMX) or tenocyclidine (TCP)
The National Institute of Drug Abuse (NIDA) notes that the magnitude of these effects can depend on the amount of the drug taken and can be unpredictable. Effects may begin within minutes of ingestion and persist for several hours, although some users report feeling the drug’s effects for days.
The NIDA also notes that dissociative drugs such as PCP, in moderate to high doses, can cause a user to have seizures or severe muscle contractions, become aggressive or violent, or even experience psychotic symptoms similar to schizophrenia. Specific references to TCP are not mentioned, but may be similar based on similar pharmacology.5
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- Morris, H. and Wallach, J. (2014), From PCP to MXE: a comprehensive review of the non-medical use of dissociative drugs. Drug Test. Analysis, 6: 614–632. Accessed July 20, 2021. doi: 10.1002/dta.1620
- Zhou Q, Sheng M. NMDA receptors in nervous system diseases. Neuropharmacology. 2013 Nov;74:69-75. doi: 10.1016/j.neuropharm.2013.03.030. Epub 2013 Apr 11. PMID: 23583930. Accessed July 20, 2021
- Drug Bank Version 5.0. Canadian Institutes of Health Research. Accessed June 25, 2019 at https://www.drugbank.ca/drugs/DB01520#identification
- Drugs of Abuse. Drug Enforcement Administration (DEA). 2020 Edition: A DEA Resource Guide. Accessed July 20, 2021 at https://www.dea.gov/sites/default/files/2020-04/Drugs%20of%20Abuse%202020-Web%20Version-508%20compliant-4-24-20_0.pdf
- What Are the Effects of Common Dissociative Drugs on the Brain and Body?. National Institute on Drug Abuse (NIDA). https://www.drugabuse.gov/publications/research-reports/hallucinogens-dissociative-drugs/what-are-effects-common-dissociative-drugs-brain-body. June 2, 2020 Accessed July 20, 2021.
- What Are Hallucinogens and Dissociative Drugs? National Institute on Drug Abuse (NIDA). https://www.drugabuse.gov/publications/research-reports/hallucinogens-dissociative-drugs/what-are-hallucinogens. April 9, 2020. Accessed July 20, 2021
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