Talk:PPAP

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It may contain incorrect information, particularly with respect to dosage, duration, subjective effects, toxicity and other risks.

PPAP
Phenylpropylaminopentane.svg
Chemical Nomenclature
Common names PPAP, Phenylpropylaminopentane
Substitutive name N,α-dipropylphenethylamine
Systematic name (-)-1-Phenyl-2-propylaminopentane
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.



Oral
Dosage
Threshold 10 mg
Light 10 - 30 mg
Common 30 - 50 mg
Strong 50 - 100 mg
Heavy 100 mg +
Duration
Total 4 - 7 hours
Onset 30 - 60 minutes
Come up 10 - 30 minutes
Peak 2 - 3 hours
Offset 2 - 5 hours









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


(-)-1-Phenyl-2-propylaminopentane (also known as (-)-PPAP and N,α-dipropylphenethylamine) is a stimulant of the substituted phenethylamine class and a derivative of Selegiline.[1] It is mainly considered as a nootropic and research chemical.

PPAP is classified as a monoaminergic activity enhancer that stimulates the impulse propagation mediated transmitter release of the neurotransmitters dopamine, norepinephrine and serotonin in the brain. Unlike stimulants such as amphetamine, which release a flood of monoamine neurotransmitters in an uncontrolled manner, PPAP instead only increases the amount of neurotransmitters that get released when a neuron is stimulated by receiving an impulse from a neighbouring neuron. Both amphetamine and (-)-PPAP promote the release of monoamines and deuteramines, however while amphetamine causes neurons to dump neurotransmitter stores into the synapse regardless of external input, PPAP does not influence the pattern of neurotransmitter release and instead releases a larger amount of neurotransmitters than normal.[2]

Clinical trials of PPAP indicate a low toxicity and a lack of typical stimulant-related side effects. The preferred daily dosage was described as being between 10 mg to 150 mg, with a particular suitability at 30 mg.[3] The long-term risks of PPAP intake have yet to be studied in detail.

Subjective effects

In comparison to traditional stimulants such as amphetamine, this compound induces an experience which is far less forceful, recreational and euphoric. Although in comparison to modafinil it is usually considered to be more mood-lifting and energetic. Unlike for most other stimulants, the expressiveness of PPAP effects are somehow dependent on set and setting due to it's unique pharmacological activity.

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These 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 of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects
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Toxicity and harm potential

The toxicity and long-term health effects of recreational PPAP use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because PPAP has very little history of human usage. Anecdotal evidence from people who have tried PPAP 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).

The LD50 of PPAP in rats is 270 mg/kg p.o.[3]

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

Tolerance and addiction potential

The chronic use of PPAP can be considered as mildly addictive with a low potential for abuse. It may be capable of causing psychological dependence among certain users due to it's nature to potentiate effects of other stimulants.

Tolerance to many of the effects of PPAP develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. Anecdotal evidence from people who have tried PPAP within the community suggest that tolerance develops less rapidly than most of other stimulants (amphetamine, caffeine).

Dangerous interactions

Although many psychoactive substances are reasonably safe to use on their own, they can quickly become dangerous or even life-threatening when taken with other substances. The following lists some known dangerous combinations, but cannot be guaranteed to include all of them. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume. Some interactions listed have been sourced from TripSit.

  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other amphetamines.
  • Cocaine - This combination may increase strain on the heart.
  • Stimulants - PPAP can be potentially dangerous in combination with other stimulants as it can increase one's heart rate and blood pressure to dangerous levels.
  • 25x-NBOMe & 25x-NBOH - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be strictly avoided due to DXM's effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Tramadol lowers the seizure threshold.[4] Combinations with stimulants may further increase this risk.
  • 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.[5]
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other stimulants.

Legal status

  • United States: PPAP has no schedule assigned to it in the U.S., making it unregulated and therefore legally available for anyone in the country to buy, possess and use.
  • United Kingdom: It is illegal to produce, supply, or import this drug under the Psychoactive Substance Act, which came into effect on May 26th, 2016.[6]

See also

External links

References

  1. Knoll J, Knoll B, Török Z, Timár J, Yasar S (March–April 1992). "The pharmacology of 1-phenyl-2-propylamino-pentane (PPAP), a deprenyl-derived new spectrum psychostimulant". Archives internationales de Pharmacodynamie et de Thérapie (316): 5–29. PMID 1356324. 
  2. Joseph Knoll; Ildikó Miklya; Berta Knoll; Raissa Markó; Károly Kelemen (February 1996). "(−)Deprenyl and (−)1-phenyl-2-propylaminopentane, [(−) PPAP] act primarily as potent stimulants of action potential — transmitter release coupling in the catecholaminergic neurons". Life Sciences. 58 (10): 817–827. doi:10.1016/0024-3205(96)00014-8. PMID 8602114. 
  3. 3.0 3.1 Knoll J, Knoll B, Török Z, Timár J, Yasar S. (1992). The pharmacology of 1-phenyl-2-propylamino-pentane (PPAP), a deprenyl-derived new spectrum psychostimulant., Arch Int Pharmacodyn Ther, 316:5-29.
  4. Talaie, H., Panahandeh, R., Fayaznouri, M. R., Asadi, Z., & Abdollahi, M. (2009). Dose-independent occurrence of seizure with tramadol. Journal of Medical Toxicology, 5(2), 63-67. https://doi.org/10.1007/BF03161089
  5. 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
  6. Psychoactive Substances Act 2016 (Legislation.gov.uk) | http://www.legislation.gov.uk/ukpga/2016/2/contents/enacted