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Summary sheet: Dichloropane
Chemical Nomenclature
Common names Dichloropane, RTI-111
Substitutive name (−)-2β-Carbomethoxy-3β-(3,4-dichlorophenyl)tropane
Systematic name Methyl (2S,3S)-3-(3,4-dichlorophenyl)-8-methyl-8-azabicyclo[3.2.1]octane-2-carboxylate
Class Membership
Psychoactive class Stimulant
Chemical class Phenyltropane
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.

Threshold 2.5 mg
Light 2.5 - 7.5 mg
Common 7.5 - 20 mg
Strong 20 - 50 mg
Heavy 50 mg +
Total 40 - 75 minutes
Onset 15 - 60 seconds
Come up 15 - 60 seconds
Peak 15 - 30 minutes
Offset 20 - 40 minutes

Threshold 3 mg
Light 10 - 20 mg
Common 20 - 40 mg
Strong 40 - 60 mg
Heavy 60 mg +
Total 2 - 4 hours
Onset 15 - 30 minutes
Come up 15 - 30 minutes
Peak 60 - 90 minutes
Offset 60 - 90 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.


Dichloropane (also known as RTI-111 or O-401) is a novel stimulant substance of the phenyltropane class.[1] Its effects include stimulation, thought acceleration, appetite suppression and euphoria. It is structurally related to cocaine and shares many of its effects, although it notably lacks its local anesthetic properties.

Dichloropane has been shown to have a slower onset and longer duration of action compared to cocaine in animal studies.[2] Anecdotal reports characterize it as having the basic stimulant qualities of cocaine but without as much euphoria, more protracted comedown, and less general enjoyability.

Dichloropane first appeared on the research chemical market around 2010. It is among to the first cocaine analog to be made available (in limited quantities) on the online research chemical market.

Very little is known about the pharmacology, metabolism, and toxicity of dichloropane. It is highly advised to use harm reduction practices if using this substance.



This chemistry section is incomplete.

You can help by adding to it.

Dichloropane is a derivative of 3-phenyltropane.[2] Methylecgonidine as the direct precursor to this compound[3]. It is produced as a hydrochloride salt in its powdered form.

Dichloropane is structurally similar to cocaine, atropine and hyoscine, as it contains a tropane ring. The tropane ring of RTI-111 is substituted with a carbomethoxy group, also found in cocaine. RTI-111 differs from cocaine by its other addition, a dichlorinated phenyl ring. The phenyl ring of RTI-111 is substituted at R3 and R4 with chlorine groups. The phenyl ring of RTI-111 is attached directly to its tropane ring while in cocaine a carboxylate group bridges the two rings.


The most extensively studied effect of dichloropane on the central nervous system is the blockade of the serotonin, dopamine, and norepinephrine transporter.[1] This substance acts as a triple reuptake inhibitor and prevents monoamine neurotransmitters from being recycled, causing excessive amounts to build up in the synapse, or junction between neurons. The result is an enhanced and prolonged post-synaptic effect of monoaminergic signaling at receptors on the receiving neuron. It is this sudden flood of neurotransmitters in the synapses of various brain regions that is thought to cause dichloropane's effects.[1]

Transporter binding profiles of tropane stimulants[4][5]
IC50 (nM)
Cocaine 89 ± 4.8 3298 ± 293 1045 ± 89
Dichloropane 0.79 ± 0.09 17.96 ± 0.85 3.13 ± 0.36
Troparil 23 ± 5 920 ± 73 1962 ± 61

Compared to cocaine, dichloropane has a higher relative affinity for both the serotonin and norepinephrine transporters over the dopamine transporter, which is in part suspected to be responsible for the differences in its subjective effects.

Subjective effects

The general head space of dichloropane is described by many as one of moderate to extreme mental stimulation, increased focus, sociability and euphoria.

Unlike cocaine, dichloropane is reported to produce a minimal rush component combined with a substantially longer come-up, protracted comedown and overall duration. This may render it less compulsive than cocaine for some users, but with a proportionally harder offset.

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

Cognitive effects

After effects
Aftereffects (3).svg

Experience reports

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

Additional experience reports can be found here: KTD Official Experience Report - RTI-111 (AKA Dichloropane) Trial III

Toxicity and harm potential

The toxicity and long-term health effects of recreational dichloropane use has not been studied in any scientific context and the exact toxic dosage is unknown. This is because dichloropane has very little history of human usage. In terms of neurotoxicity (as defined by the damage or death of cells in the brain in response to over-excitation or reactive oxidation caused by drugs), it is reasonable to assume that like other stimulants which work principally through reuptake inhibition (e.g. cocaine), dichloropane should not exhibit these effects unlike certain other substances such as methamphetamine, which have suspected mechanisms of direct neurotoxicity. The extended use or abuse of dichloropane, however, is likely to cause both short and down-term down regulation of the receptors of the major neurotransmitter (monoamine) systems it interacts with. However, this still remains a subject of active inquiry.

Due to its structural similarity to cocaine, it is worth noting that the most potentially harmful physical effects of dichloropane could not be neurological but cardiovascular. For example, severe cardiac adverse events, particularly sudden cardiac death, become a serious risk at high doses for cocaine due to cocaine's blocking effect on cardiac sodium channels, and it is possible that dichloropane may share this risk despite not having topical anesthetic activity.[6] Moreover, long-term cocaine usage may result in Cocaine-Related Cardiomyopathy. [7] It is as of yet unknown whether dichloropane presents similar risks, but it is reasonable to assume that it might, and thus should be approached with additional caution.

It is suspected that regular dichloropane insufflation can have extremely adverse effects on one's nostrils, nose and nasal cavities. These include a loss of the sense of smell, nosebleeds, difficulty swallowing, hoarseness, or a chronically runny nose.

Anecdotal evidence from people who have tried dichloropane within the community suggest 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 strongly recommended that one use harm reduction practices when using this substance.

Tolerance and addiction potential

As with other stimulants, the chronic use of dichloropane can be considered to have the potential to be moderately addictive with a high potential for abuse, though perhaps less so than that of cocaine, and is thus 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 dichloropane 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 2 - 4 days for the tolerance to be reduced to half and 1 - 1.5 weeks to be back at baseline (in the absence of further consumption). Dichloropane likely presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of dichloropane all stimulants will have a reduced effect.

Withdrawal symptoms

It is possible that after taking dichloropane on a regular or extended basis, some users will become addicted like they would to cocaine. When the drug is discontinued immediately, the user will experience what has come to be known as a "crash" along with a number of other withdrawal symptoms including paranoia, depression, anxiety, itching, mood swings, irritability, fatigue, insomnia, an intense craving for more of the drug, and, in some cases, nausea and vomiting. Some cocaine users also report having similar symptoms to schizophrenic patients and feel that their mind is scattered or incoherent. Some users also report a feeling of a crawling sensation on the skin also known as "coke bugs".

These symptoms can last for weeks or, in some cases, months. Even after most withdrawal symptoms dissipate most users feel the need to continue using the drug; this feeling can last for years and may peak during times of stress.


Due to its very brief history of human usage, little is known about dichloropane's ability to induce psychosis, although it is reasonable to assume it presents similar risks to that of cocaine and other dopaminergic stimulants when abused, typically for extended durations, in high doses and or for prolonged periods of time.

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.

  • Stimulants - When used in conjunction with other stimulants, the cardiovascular effects of cocaine such as increased heart rate become dangerously high. This is potentially fatal and severely increases the risk of cardiac arrest.
  • Depressants - When used in conjunction with depressants such as opioids and benzodiazepines, the cardiovascular effects of the two classes begin to conflict as one increases the heart rate while the other decreases it. This is potentially fatal and can result in an extremely irregular heart rate leading onto cardiac arrest.
  • Depressants - It is dangerous to combine alcohol, a depressant, with stimulants due to the risk of excessive intoxication. Stimulants decrease the sedative effect of alcohol which is the main factor most people consider when determining their level of intoxication. Once the stimulant wears off, the effects of alcohol will be significantly increased, leading to intensified disinhibition as well as respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • MDMA - The neurotoxic and potential cardiotoxic effects of MDMA may be increased when combined with dichloropane.
  • MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, and some antidepressants.[8]
  • Nicotine - Some dichloropane users find that consumption of tobacco products during dichloropane use enhances the euphoria because nicotine increases the levels of dopamine in the brain. This, however, may have undesirable consequences such as uncontrollable chain smoking during dichloropane use, in addition to the detrimental health effects and the additional strain on the cardiovascular system caused by tobacco.

Legal status


This legality section is a stub.

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

  • Germany: Dichloropane is not a controlled substance under the BtMG[9] (Narcotics Act) or the NpSG[10] (New Psychoactive Substances Act). Technically it would fall under the definition of a medicine by §2 AMG (Medicines Act) because it induces a pharmacological effect.[11] By a decision of the European Court of Justice, this definition was declared ineffective because it was not compatible with EU law.[12] Dichloropane can be considered unregulated.
  • Switzerland: Dichloropane is a controlled substance specifically named under Verzeichnis E.[13]
  • Turkey: Dichloropane is a classed as drug and is illegal to possess, produce, supply, or import.[14]
  • United States: Dichloropane may be considered to be an analogue of cocaine under the Federal Analogue Act. The Federal Analogue Act, 21 U.S.C. § 813, is a section of the United States Controlled Substances Act, allowing any chemical "substantially similar" to an illegal drug (in Schedule I or II) to be treated as if it were also in Schedule I or II, but only if it is intended for human consumption.[citation needed]

See also

External links


  1. 1.0 1.1 1.2 Carroll, F. I., Blough, B. E., Nie, Z., Kuhar, M. J., Howell, L. L., Navarro, H. A. (1 April 2005). "Synthesis and Monoamine Transporter Binding Properties of 3β-(3',4'-Disubstituted phenyl)tropane-2β-carboxylic Acid Methyl Esters". Journal of Medicinal Chemistry. 48 (8): 2767–2771. doi:10.1021/jm040185a. ISSN 0022-2623. 
  2. 2.0 2.1 Ranaldi, R., Anderson, K. G., Ivy Carroll, F., Woolverton, W. L. (1 December 2000). "Reinforcing and discriminative stimulus effects of RTI 111, a 3-phenyltropane analog, in rhesus monkeys: interaction with methamphetamine". Psychopharmacology. 153 (1): 103–110. doi:10.1007/s002130000602. ISSN 1432-2072. 
  3. Carroll, F. I., Mascarella, S. W., Kuzemko, M. A., Gao, Y., Abraham, P., Lewin, A. H., Boja, J. W., Kuhar, M. J. (September 1994). "Synthesis, Ligand Binding, and QSAR (CoMFA and Classical) Study of 3.beta.-(3'-Substituted phenyl)-, 3.beta.-(4'-Substituted phenyl)-, and 3.beta.-(3',4'-Disubstituted phenyl)tropane-2.beta.-carboxylic Acid Methyl Esters". Journal of Medicinal Chemistry. 37 (18): 2865–2873. doi:10.1021/jm00044a007. ISSN 0022-2623. 
  4. Carroll, F. I., Kotian, P., Dehghani, A., Gray, J. L., Kuzemko, M. A., Parham, K. A., Abraham, P., Lewin, A. H., Boja, J. W., Kuhar, M. J. (January 1995). "Cocaine and 3.beta.-(4'-Substituted phenyl)tropane-2.beta.-carboxylic Acid Ester and Amide Analogs. New High-Affinity and Selective Compounds for the Dopamine Transporter". Journal of Medicinal Chemistry. 38 (2): 379–388. doi:10.1021/jm00002a020. ISSN 0022-2623. 
  5. Carroll, F. I., Blough, B. E., Nie, Z., Kuhar, M. J., Howell, L. L., Navarro, H. A. (1 April 2005). "Synthesis and Monoamine Transporter Binding Properties of 3β-(3',4'-Disubstituted phenyl)tropane-2β-carboxylic Acid Methyl Esters". Journal of Medicinal Chemistry. 48 (8): 2767–2771. doi:10.1021/jm040185a. ISSN 0022-2623. 
  6. O’Leary, M. E., Hancox, J. C. (28 January 2010). "Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias: Voltage-gated ion channels and cocaine-induced arrhythmia". British Journal of Clinical Pharmacology. 69 (5): 427–442. doi:10.1111/j.1365-2125.2010.03629.x. ISSN 0306-5251. 
  7. "Cocaine-Related Cardiomyopathy: Overview, Cardiac Effects of Cocaine, Epidemiology". 16 October 2021. 
  8. Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210Freely accessible. eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647. 
  9. "BtMG - Gesetz über den Verkehr mit Betäubungsmitteln" (in German). Bundesamt für Justiz [Federal Office of Justice]. Retrieved December 10, 2019. 
  10. "NpSG - Neue-psychoaktive-Stoffe-Gesetz" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 10, 2019. 
  11. "§ 2 AMG" (in German). Bundesamt für Justiz [Federal Office of Justice]. Retrieved December 10, 2019. 
  12. Prof. Dr. Helmut Pollähne (July 11, 2014). "Cannabinoide Kräutermischungen vor dem EuGH: Legal Highs bleiben legal" [Cannabinoid herbal mixtures at the ECJ: Legal highs stay legal] (in German). LTO. Retrieved December 28, 2019. 
  13. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  14. "Cumhurbaşkanı Kararı: Karar Sayısı: 1335" (PDF). Resmî Gazete, Sayı: 30837 (in Turkish). Başbakanlık Mevzuatı Geliştirme ve Yayın Genel Müdürlüğü [General Directorate of Legislation Development and Publication] (published July 20, 2019). July 19, 2020.