Warning
This is an unofficial archive of PsychonautWiki as of 2025-08-11T15:14:44Z. Content on this page may be outdated, incomplete, or inaccurate. Please refer to the original page for the most up-to-date information.

Talk:Dichloropane

From PsychonautWiki Archive
Revision as of 18:07, 22 October 2016 by >Unity (Created page with "{{SubstanceBox/Dichloropane}} {| |- |- | ''Summary sheet: Dichloropane'' |} '''Dichloropane''' ('''RTI-111''') is a synthetic stimulant drug of th...")
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to navigation Jump to search
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.


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




Insufflated
Dosage
Threshold 3 mg
Light 10 - 20 mg
Common 20 - 40 mg
Strong 40 - 60 mg
Heavy 60 mg +
Duration
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.

Interactions
Summary sheet: Dichloropane

Dichloropane (RTI-111) is a synthetic stimulant drug of the phenyltropane class.[1] It is structurally similar to cocaine and is classed as a stimulant and an appetite suppressant. In animal studies, dichloropane had a slower onset and longer duration of action compared to cocaine[2]. It is thought to be the first cocaine/tropane analogue to be made available on the consumer research chemical market, first appearing in 2016.

Chemistry

Dichloropane is a derivative of 3-phenyltropane[3]. Methylecgonidine as the direct precursor to this compound[4]. It is produced as a hydrochloride salt in its powdered form.

Pharmacology

The most extensively studied effect of dichloropane on the central nervous system is the blockade of the serotonin, dopamine, and norepinephrine transporter. 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.[5] It is this sudden flood of neurotransmitters that is thought to cause dichloropane's effects.

Notably, dichloropane has a relatively higher affinity for the serotonin transporter than cocaine, which could be responsible for the differences in its effects.[6]

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects will rarely (if ever) occur all at once, but heavier dosages will increase the chances and are more likely to induce a full range of effects.

Physical effects

Cognitive effects

The cognitive effects of dichloropane can be broken down into several components which progressively intensify proportional to dosage. The general head space of dichloropane is described by many as one of moderate to extreme mental stimulation, increased focus, sociability and euphoria. It contains a large number of typical stimulant cognitive effects. Although negative side effects are usually mild at low to moderate dosages, they become increasingly likely to manifest themselves with higher amounts or extended usage. This particularly holds true during the offset of the experience.

The most prominent of these cognitive effects generally include:

After effects

The effects which occur during the offset of a stimulant experience generally feel negative and uncomfortable in comparison to the effects which occurred during its peak. This is often referred to as a "comedown" and occurs because of neurotransmitter depletion. Its effects commonly include:

Some users have observed that the comedown from dichloropane is far more pronounced than that of cocaine, even at common dosages, perhaps as a result of its increased duration and greater activity on the serotonin system.

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. Its extended use or abuse does, however, is likely to cause short-term down regulation of the receptors of the neurotransmitter systems it interacts with. However, this remains a subject of speculation.

Due to its structural similarity to cocaine, it is worth noting that the most potentially harmful physical effects of cocaine appear to be not neurological but cardiovascular. Severe cardiac adverse events, particularly sudden cardiac death, become a serious risk at high doses due to cocaine's blocking effect on cardiac sodium channels.[7] Moreover, long-term cocaine usage may result in Cocaine-Related Cardiomyopathy. [8] It is as of yet unknown whether dichloropane presents similar risks, but it is reasonable to assume that it might.

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 drug 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 drug.

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 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). Dichloropane likely presents cross-tolerance with [[Cross-tolerance::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 cocaine, 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.

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.
  • ]] - 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.[9]
  • 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.

Psychosis

Due to its novelty, little is known about dichloropane's ability to induce psychosis, although it is reasonable to assume it presents similar risks to that of cocaine when abused.

  • USA: 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

References

  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. 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
  4. 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
  5. 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
  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. 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
  8. http://emedicine.medscape.com/article/152535-overview#a2
  9. 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.