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Summary sheet: Dichloropane
Molecular structure of 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 Tropane
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 3 - 10 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 synthetic stimulant substance of the tropane chemical class.[1] It is structurally similar to cocaine and has stimulant and anorectic properties, although is notably absent of cocaine's anesthetic effects.

Dichloropane has been shown to have a slower onset and longer duration of action compared to cocaine in animal studies.[2]

Dichloropane first appeared in late 2016. It is thought to be the first cocaine analog to be made available (in limited quantities) on the online research chemical market. It is also the only batch of a purported cocaine analog to be independently verified by third-party lab analysis.[3]

This is significant because it marks a marked evolution in the synthetic production capacities of the web-based research chemical market. It had up until that point been considered a non-viable compound to produce, due to the difficulty and expense of its synthesis.

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



This chemistry section is incomplete.

You can help by adding to it.

RTI-111, or dichloropane, is a derivative of 3-phenyltropane[4]. Methylecgonidine as the direct precursor to this compound[5]. It is produced as a hydrochloride salt in its powdered form.

RTI-111 is structurally similar to cocaine, atropine and hyoscine, as it contains a tropane ring. The tropane ring of RTI-11 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.[6] 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.[7]

Notably, dichloropane has a higher relative affinity for the serotonin transporter over the dopamine transporter than cocaine, which is in part suspected to be responsible for the differences in its subjective effects.[8]

Subjective effects

Early explorers of this compound have remarked that dichloropane is a substance that seems to contain elements of both cocaine as well as serotonin-releasers like MDAI (potentially due to its known higher affinity for the serotonin reuptake transporter, which results in greater relative concentrations of serotonin compared to dopamine relative to cocaine) but in a way that fails to fully capture the unique effects of either. Unlike cocaine, it produces 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. The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include 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.[9] Moreover, long-term cocaine usage may result in Cocaine-Related Cardiomyopathy. [10] 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 cocaine 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

Although many psychoactive substances are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

  • 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, 2C-T-2, 2C-T-7, αMT, and some antidepressants.[11]
  • 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.



This legality section is a stub.

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

  • United States: Dichloropane may be considered to be an analog of cocaine, thus falling under the Federal Analog Act.The Federal Analog 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.

See also


  1. Synthesis and Monoamine Transporter Binding Properties of 3β-(3‘,4‘-Disubstituted phenyl)tropane-2β-carboxylic Acid Methyl Esters | http://pubs.acs.org/doi/abs/10.1021/jm040185a
  2. Reinforcing and discriminative stimulus effects of RTI 111, a 3-phenyltropane analog, in rhesus monkeys: interaction with methamphetamine | https://link.springer.com/article/10.1007/s002130000602
  3. https://www.reddit.com/r/DrugNerds/comments/58k2a0/rti111_dichloropane_gcms_report/ | RTI-111 (dichloropane) GC-MS report
  4. Reinforcing and discriminative stimulus effects of RTI 111, a 3-phenyltropane analog, in rhesus monkeys: interaction with methamphetamine | https://link.springer.com/article/10.1007/s002130000602
  5. Synthesis, Ligand Binding, and QSAR (CoMFA and Classical) Study of 3β-(3'-Substituted phenyl)-, 3β-(4'-Substituted phenyl)-, and 3β-(3',4'-Disubstituted phenyl)tropane-2β-carboxylic Acid Methyl Esters | http://pubs.acs.org/doi/abs/10.1021/jm00044a007
  6. Synthesis and Monoamine Transporter Binding Properties of 3β-(3‘,4‘-Disubstituted phenyl)tropane-2β-carboxylic Acid Methyl Esters | http://pubs.acs.org/doi/abs/10.1021/jm040185a
  7. Synthesis and Monoamine Transporter Binding Properties of 3β-(3‘,4‘-Disubstituted phenyl)tropane-2β-carboxylic Acid Methyl Esters | http://pubs.acs.org/doi/abs/10.1021/jm040185a
  8. Synthesis and Monoamine Transporter Binding Properties of 3β-(3‘,4‘-Disubstituted phenyl)tropane-2β-carboxylic Acid Methyl Esters | http://pubs.acs.org/doi/abs/10.1021/jm040185a
  9. Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias | http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2125.2010.03629.x/abstract
  10. http://emedicine.medscape.com/article/152535-overview#a2
  11. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210