PPAP (phenylpropylaminopentane)

updated

PPAP (phenylpropylaminopentane) is a deprenyl-derived research compound sold for energy, focus and performance. Its published pharmacology is rat and animal tissue work from 1992 to 2006, largely from the group that developed it, and no controlled human study exists: a PubMed search on 10 October 2026 found no abstract reporting PPAP given to a person. Sellers describe limited human characterization, but no human data were found.

Catecholaminergic activity enhancer (deprenyl-derived)

  • The PPAP racemate is PubChem CID 10262369, C14H23N, molecular weight 205.34; the (-)-enantiomer used in the research is a separate record, CID 51529346.
  • In rats, PPAP facilitated learning and retention, antagonized tetrabenazine-induced depression and was very effective in the forced swimming test, with substantially less stereotyped behavior than amphetamine or methamphetamine.
  • In two breeds of Wistar rats, (-)PPAP fully antagonized tetrabenazine-induced learning depression in the high-performing breed and was ineffective in the low-performing breed at the dose tested.
  • A PubMed search on 10 October 2026 returned 11 records dated 1992 to 2016, and no abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control.
  • DailyMed returned no labels for phenylpropylaminopentane on 10 October 2026, and ClinicalTrials.gov returned no studies.
  • A racemic or unspecified vendor product is not the studied material, because (-)PPAP was much more potent than (+)PPAP in one test.

What is PPAP, and what is its regulatory status?

PPAP (phenylpropylaminopentane) is a deprenyl-derived research compound. The research used the (-)-enantiomer, so a racemic or unspecified vendor product is not the studied material, and no label, application or registered study exists.

The racemate (1-phenyl-N-propylpentan-2-amine) is PubChem CID 10262369, C14H23N, molecular weight 205.34, CAS 119485-94-8. The (-)-enantiomer, (2R)-1-phenyl-N-propylpentan-2-amine, is a separate record, CID 51529346, CAS 784118-64-5. The research reviewed used (-)PPAP, and in one test (-)PPAP was much more potent than (+)PPAP, so a racemic or unspecified vendor product is not the studied material. No public record ties any vendor material to either entry.

A 1990 paper uses the abbreviation (-)PPAP for a different molecule, a sigma binding site ligand. That is not phenylpropylaminopentane, a search on PPAP alone will mix the two, and the paper is not used here as evidence about this compound.

DailyMed returned no labels for phenylpropylaminopentane on 10 October 2026, and an openFDA Drugs@FDA query returned no match. ClinicalTrials.gov queries for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane and PPAP deprenyl-derived returned no studies. A 2016 review from Budapest on the catecholaminergic activity enhancer concept says that presently deprenyl is the only available drug of that kind, which places PPAP as a research compound. Status outside the United States is not covered here.

PubChem: PPAP racemate and (-)-enantiomer identity

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 51529346, (2R)-1-phenyl-N-propylpentan-2-amine; the racemate is CID 10262369.

The racemate (1-phenyl-N-propylpentan-2-amine) is PubChem CID 10262369, C14H23N, 205.34 g/mol, CAS 119485-94-8. The (-)-enantiomer, (2R)-1-phenyl-N-propylpentan-2-amine, is a separate record, CID 51529346, CAS 784118-64-5. The research reviewed used (-)PPAP, and in one test (-)PPAP was much more potent than (+)PPAP.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule; racemate and R-enantiomer
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. A racemic or unspecified vendor product is not the studied material, and no public record ties any vendor material to either entry.

Read the original source
Different compound with the same acronym; not evidence about this compound

Chemical identity record

Glennon RA et al. Pharmacol Biochem Behav. 1990;37(3):557-9. PMID 1965044.

A 1990 paper describes (-)PPAP as R(-)-N-(3-phenyl-n-propyl)-1-phenyl-2-aminopropane, a sigma binding site ligand. That is not phenylpropylaminopentane, and a search on PPAP alone will mix the two.

Participants / model
Different compound; not a population for this page
Treatment
Not applicable
Follow-up
Not applicable
Study design
Identity disambiguation; the paper concerns a different compound
Funding
not stated in the source

Listed only to separate two molecules that share an acronym. It is not cited as evidence about phenylpropylaminopentane.

Read the original source
No label, no application, no registered study; deprenyl the only drug of its kind

Regulatory record

Miklya I. Mol Psychiatry. 2016;21(11):1499-1503. PMID 27480491.

DailyMed returned no labels for phenylpropylaminopentane on 10 October 2026, and an openFDA Drugs@FDA query returned no match. ClinicalTrials.gov queries for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane and PPAP deprenyl-derived returned no studies. A 2016 review from Budapest on the catecholaminergic activity enhancer concept says that presently deprenyl is the only available drug of that kind, which places PPAP as a research compound.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search; review article
Funding
not stated in the source

An absence finding as of 10 October 2026. Status outside the United States is not covered.

Read the original source

What did the rat and tissue studies find?

In rats, PPAP increased motility, facilitated learning and retention, antagonized tetrabenazine-induced depression and was very effective in the forced swimming test, with substantially less stereotyped behavior than amphetamine or methamphetamine. All of it is in rats and animal tissue, and no controlled human study exists.

The founding pharmacology paper comes from the group that developed the compound. PPAP was chosen as the reference substance among deprenyl-derived compounds made to lack MAO inhibitory potency. [14C]PPAP was taken up into catecholaminergic axon terminals, PPAP inhibited uptake of [3H]noradrenaline and [3H]dopamine in rat brain, and it lacked catecholamine-releasing property.

In rats PPAP increased motility and inhibited it only at very high doses, induced substantially less stereotyped behavior than amphetamine or methamphetamine, facilitated learning and retention, antagonized tetrabenazine-induced depression, and was very effective in the forced swimming test. The authors state performance improved over a reasonably broad dose range, unlike amphetamines. They suggest usefulness in depression, Alzheimer's disease and attention-deficit-hyperkinetic disorder is plausible, which is their hypothesis and not a result. Routes are not in the abstract.

A later study trained two breeds of Wistar rats in a shuttle box. The high-performing breed released more noradrenaline from the locus coeruleus and more serotonin from the raphe. (-)PPAP fully antagonized tetrabenazine-induced learning depression in the high-performing rats and was ineffective in the low-performing rats at the dose tested. This is reversal of a drug-induced learning deficit in one breed of rats, not a gain in healthy people or in physical performance, and the route is not in the abstract.

Founding rat pharmacology paper from the developing group

Animal study

Knoll J et al. Arch Int Pharmacodyn Ther. 1992;316:5-29. PMID 1356324.

PPAP was chosen as the reference substance among deprenyl-derived compounds made to lack MAO inhibitory potency. [14C]PPAP was taken up into catecholaminergic axon terminals, PPAP inhibited uptake of [3H]noradrenaline and [3H]dopamine in rat brain, and it lacked catecholamine-releasing property. In rats PPAP increased motility and inhibited it only at very high doses, induced substantially less stereotyped behavior than amphetamine or methamphetamine, facilitated learning and retention, antagonized tetrabenazine-induced depression, and was very effective in the forced swimming test. The authors state performance improved over a reasonably broad dose range, unlike amphetamines. They suggest usefulness in depression, Alzheimer's disease and attention-deficit-hyperkinetic disorder is plausible, which is their hypothesis and not a result.

Participants / model
Rats; rat brain tissue; rabbit pulmonary artery strip
Treatment
PPAP in rats and tissue preparations; routes not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound. Doses and routes are not reproduced on this page.

Read the original source
Two Wistar rat breeds: deficit reversed in the high-performing breed

Animal study

Knoll J et al. Life Sci. 1996;58(11):945-52. PMID 8786700.

Two rat breeds differing in learning performance were trained in a shuttle box. The high-performing breed released more noradrenaline from the locus coeruleus and more serotonin from the raphe. (-)PPAP fully antagonized tetrabenazine-induced learning depression in high-performing rats and was ineffective in low-performing rats at the dose tested.

Participants / model
Two breeds of Wistar rats
Treatment
(-)PPAP; dose not reproduced here, route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

Reversal of a drug-induced learning deficit in one breed of rats, not a gain in healthy people or in physical performance.

Read the original source

How does PPAP act on catecholamine neurons?

The authors conclude that (-)PPAP acts primarily by stimulating action potential-transmitter release coupling in catecholaminergic neurons, unrelated to MAO inhibition, uptake inhibition or catecholamine release. This is an interpretation from animal tissue, and PPAP also changed serotonin in immune cells, so it is not selective for catecholamine neurons.

In rats, (-)deprenyl enhanced catecholaminergic activity 30 minutes after subcutaneous injection; that result is for (-)deprenyl, not PPAP. The authors concluded that (-)deprenyl and (-)PPAP act primarily as stimulants of action potential-transmitter release coupling in catecholaminergic neurons, an effect they found unrelated to MAO inhibition, presynaptic receptor inhibition, catecholamine uptake inhibition or catecholamine release. Both enhanced the inward Ca2+ current in frog heart sino-auricular fibers, and (-)PPAP was much more potent than either (+)PPAP or (-)deprenyl in that test.

The founding paper had reported that PPAP inhibited uptake of noradrenaline and dopamine in rat brain and lacked a catecholamine-releasing property. The later mechanism paper concludes that the primary action is unrelated to uptake inhibition. Both readings come from animal tissue work, and the pharmacology rests largely on the group that developed the compound.

PPAP is not selective for catecholamine neurons in animals. In peritoneal cells of young female animals, species not stated in the abstract, PPAP significantly increased the serotonin level 30 minutes after treatment at 6 weeks of age, while deprenyl did not. Three weeks after treatment at weaning, PPAP moderately but significantly raised serotonin in monocytes, granulocytes and mast cells, while deprenyl drastically lowered it. The authors say the two molecules have different effects on immune cells independent of MAO-B inhibition. The abstract gives no dose or route.

Mechanism work in rat tissue and frog heart fibers

Animal study

Knoll J et al. Life Sci. 1996;58(10):817-27. PMID 8602114.

In rats, (-)deprenyl enhanced catecholaminergic activity 30 minutes after subcutaneous injection. The authors concluded that (-)deprenyl and (-)PPAP act primarily as stimulants of action potential-transmitter release coupling in catecholaminergic neurons, an effect they found unrelated to MAO inhibition, presynaptic receptor inhibition, catecholamine uptake inhibition or catecholamine release. Both enhanced the inward Ca2+ current in frog heart sino-auricular fibers, and (-)PPAP was much more potent than either (+)PPAP or (-)deprenyl in that test.

Participants / model
Rats; isolated rat brain stem; frog heart fibers
Treatment
Subcutaneous (-)deprenyl in rats; (-)PPAP and (-)deprenyl in tissue preparations
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

The rat injection result is for (-)deprenyl, not PPAP. Animal tissue only, and the conclusion is the authors' interpretation.

Read the original source
Founding rat pharmacology paper from the developing group

Animal study

Knoll J et al. Arch Int Pharmacodyn Ther. 1992;316:5-29. PMID 1356324.

PPAP was chosen as the reference substance among deprenyl-derived compounds made to lack MAO inhibitory potency. [14C]PPAP was taken up into catecholaminergic axon terminals, PPAP inhibited uptake of [3H]noradrenaline and [3H]dopamine in rat brain, and it lacked catecholamine-releasing property. In rats PPAP increased motility and inhibited it only at very high doses, induced substantially less stereotyped behavior than amphetamine or methamphetamine, facilitated learning and retention, antagonized tetrabenazine-induced depression, and was very effective in the forced swimming test. The authors state performance improved over a reasonably broad dose range, unlike amphetamines. They suggest usefulness in depression, Alzheimer's disease and attention-deficit-hyperkinetic disorder is plausible, which is their hypothesis and not a result.

Participants / model
Rats; rat brain tissue; rabbit pulmonary artery strip
Treatment
PPAP in rats and tissue preparations; routes not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound. Doses and routes are not reproduced on this page.

Read the original source
Peritoneal immune cells: PPAP raised serotonin, deprenyl did not

Animal study

Csaba G et al. Cell Biochem Funct. 2006;24(1):49-53. PMID 15584092.

In peritoneal cells of young female animals (species not stated in the abstract), PPAP significantly increased the serotonin level 30 minutes after treatment at 6 weeks of age, while deprenyl did not. Three weeks after treatment at weaning PPAP moderately but significantly raised serotonin in monocytes, granulocytes and mast cells, while deprenyl drastically lowered it. The authors say the two molecules have different effects on immune cells independent of MAO-B inhibition.

Participants / model
Peritoneal immune cells of young female animals, species not stated in the abstract
Treatment
PPAP and deprenyl; dose and route not stated in the abstract
Follow-up
30 minutes and 3 weeks after treatment
Study design
Original preclinical study
Funding
not stated in the source

Shows PPAP is not selective for catecholamine neurons in animals. The abstract gives no dose or route.

Read the original source

Has PPAP been tested in people?

No. A PubMed search on 10 October 2026 returned 11 records dated 1992 to 2016, and no abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control. ClinicalTrials.gov returned no studies.

A PubMed search on 10 October 2026 for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane or 1-phenyl-2-propylamino-pentane returned 11 records dated 1992 to 2016. Titles were read for all 11 and abstracts for those on PPAP itself; the rest concern deprenyl, BPAP, phenylethylamine, or a rat analysis of why alpha-tocopherol failed in the DATATOP trial.

Adding human, patients, volunteers or clinical returned 3 records: a deprenyl review, the rat DATATOP analysis and a BPAP paper. Adding pharmacokinetic, metabolism, doping, toxicity or LD50 returned 10 records from the same cluster. No abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control.

PubMed: 11 records from 1992 to 2016, none reports PPAP given to a person

PubMed search record

PubMed search for phenylpropylaminopentane OR 1-phenyl-2-propylaminopentane OR 1-phenyl-2-propylamino-pentane, run 10 October 2026, with follow-up queries adding human terms and pharmacokinetic and toxicology terms.

A PubMed search on 10 October 2026 for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane or 1-phenyl-2-propylamino-pentane returned 11 records dated 1992 to 2016. Titles were read for all 11 and abstracts for those on PPAP itself; the rest concern deprenyl, BPAP, phenylethylamine, or a rat analysis of why alpha-tocopherol failed in the DATATOP trial. Adding human, patients, volunteers or clinical returned 3 records (a deprenyl review, the rat DATATOP analysis and a BPAP paper), and adding pharmacokinetic, metabolism, doping, toxicity or LD50 returned 10 records from the same cluster. No abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists. The supplier wording of limited human characterization overstates what exists, because no human data were found.

Read the original source
No label, no application, no registered study; deprenyl the only drug of its kind

Regulatory record

Miklya I. Mol Psychiatry. 2016;21(11):1499-1503. PMID 27480491.

DailyMed returned no labels for phenylpropylaminopentane on 10 October 2026, and an openFDA Drugs@FDA query returned no match. ClinicalTrials.gov queries for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane and PPAP deprenyl-derived returned no studies. A 2016 review from Budapest on the catecholaminergic activity enhancer concept says that presently deprenyl is the only available drug of that kind, which places PPAP as a research compound.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search; review article
Funding
not stated in the source

An absence finding as of 10 October 2026. Status outside the United States is not covered.

Read the original source

Does PPAP improve energy, focus and performance?

Only as rat pharmacology. PPAP increased motility, facilitated learning and retention, antagonized a drug-induced learning deficit in one breed of rats and was very effective in the forced swimming test. Sellers describe limited human characterization, but no human data were found.

Sellers market PPAP for energy, focus and performance, with limited human characterization. The rat studies measured motility, shuttle-box learning against a drug-induced deficit and forced swimming. None of these outcomes was measured in a person.

The phrase limited human characterization overstates what exists: no human data were found in the PubMed search of 10 October 2026. The learning result is reversal of a deficit caused by tetrabenazine in one breed of rats, not a gain in healthy people or in physical performance.

Founding rat pharmacology paper from the developing group

Animal study

Knoll J et al. Arch Int Pharmacodyn Ther. 1992;316:5-29. PMID 1356324.

PPAP was chosen as the reference substance among deprenyl-derived compounds made to lack MAO inhibitory potency. [14C]PPAP was taken up into catecholaminergic axon terminals, PPAP inhibited uptake of [3H]noradrenaline and [3H]dopamine in rat brain, and it lacked catecholamine-releasing property. In rats PPAP increased motility and inhibited it only at very high doses, induced substantially less stereotyped behavior than amphetamine or methamphetamine, facilitated learning and retention, antagonized tetrabenazine-induced depression, and was very effective in the forced swimming test. The authors state performance improved over a reasonably broad dose range, unlike amphetamines. They suggest usefulness in depression, Alzheimer's disease and attention-deficit-hyperkinetic disorder is plausible, which is their hypothesis and not a result.

Participants / model
Rats; rat brain tissue; rabbit pulmonary artery strip
Treatment
PPAP in rats and tissue preparations; routes not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound. Doses and routes are not reproduced on this page.

Read the original source
Two Wistar rat breeds: deficit reversed in the high-performing breed

Animal study

Knoll J et al. Life Sci. 1996;58(11):945-52. PMID 8786700.

Two rat breeds differing in learning performance were trained in a shuttle box. The high-performing breed released more noradrenaline from the locus coeruleus and more serotonin from the raphe. (-)PPAP fully antagonized tetrabenazine-induced learning depression in high-performing rats and was ineffective in low-performing rats at the dose tested.

Participants / model
Two breeds of Wistar rats
Treatment
(-)PPAP; dose not reproduced here, route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

Reversal of a drug-induced learning deficit in one breed of rats, not a gain in healthy people or in physical performance.

Read the original source
PubMed: 11 records from 1992 to 2016, none reports PPAP given to a person

PubMed search record

PubMed search for phenylpropylaminopentane OR 1-phenyl-2-propylaminopentane OR 1-phenyl-2-propylamino-pentane, run 10 October 2026, with follow-up queries adding human terms and pharmacokinetic and toxicology terms.

A PubMed search on 10 October 2026 for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane or 1-phenyl-2-propylamino-pentane returned 11 records dated 1992 to 2016. Titles were read for all 11 and abstracts for those on PPAP itself; the rest concern deprenyl, BPAP, phenylethylamine, or a rat analysis of why alpha-tocopherol failed in the DATATOP trial. Adding human, patients, volunteers or clinical returned 3 records (a deprenyl review, the rat DATATOP analysis and a BPAP paper), and adding pharmacokinetic, metabolism, doping, toxicity or LD50 returned 10 records from the same cluster. No abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists. The supplier wording of limited human characterization overstates what exists, because no human data were found.

Read the original source

What is known about the safety of PPAP?

No human safety, pharmacokinetic or toxicology data exist for PPAP in the records reviewed. The rat work reports less stereotyped behavior than amphetamine, which is a behavioral finding and not a safety assessment, and the identity of vendor material is not established.

No abstract reports PPAP given to a person, so no human adverse event, tolerability or interaction information exists. No abstract reports its pharmacokinetics, metabolism, toxicity or detection in doping control, and no toxicology result of any kind appears in the records reviewed.

The rat work states that PPAP inhibited motility only at very high doses and induced substantially less stereotyped behavior than amphetamine or methamphetamine. These are behavioral findings in rats and not a safety assessment. PPAP also changed serotonin content in immune cells of young female animals, which shows it is not selective for catecholamine neurons.

Product identity is a separate concern. The research used the (-)-enantiomer, which was much more potent than (+)PPAP in one test, and a racemic or unspecified vendor product is not the studied material. Whether any vendor product is racemic, (-)PPAP or something else is unknown.

PubMed: 11 records from 1992 to 2016, none reports PPAP given to a person

PubMed search record

PubMed search for phenylpropylaminopentane OR 1-phenyl-2-propylaminopentane OR 1-phenyl-2-propylamino-pentane, run 10 October 2026, with follow-up queries adding human terms and pharmacokinetic and toxicology terms.

A PubMed search on 10 October 2026 for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane or 1-phenyl-2-propylamino-pentane returned 11 records dated 1992 to 2016. Titles were read for all 11 and abstracts for those on PPAP itself; the rest concern deprenyl, BPAP, phenylethylamine, or a rat analysis of why alpha-tocopherol failed in the DATATOP trial. Adding human, patients, volunteers or clinical returned 3 records (a deprenyl review, the rat DATATOP analysis and a BPAP paper), and adding pharmacokinetic, metabolism, doping, toxicity or LD50 returned 10 records from the same cluster. No abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists. The supplier wording of limited human characterization overstates what exists, because no human data were found.

Read the original source
Founding rat pharmacology paper from the developing group

Animal study

Knoll J et al. Arch Int Pharmacodyn Ther. 1992;316:5-29. PMID 1356324.

PPAP was chosen as the reference substance among deprenyl-derived compounds made to lack MAO inhibitory potency. [14C]PPAP was taken up into catecholaminergic axon terminals, PPAP inhibited uptake of [3H]noradrenaline and [3H]dopamine in rat brain, and it lacked catecholamine-releasing property. In rats PPAP increased motility and inhibited it only at very high doses, induced substantially less stereotyped behavior than amphetamine or methamphetamine, facilitated learning and retention, antagonized tetrabenazine-induced depression, and was very effective in the forced swimming test. The authors state performance improved over a reasonably broad dose range, unlike amphetamines. They suggest usefulness in depression, Alzheimer's disease and attention-deficit-hyperkinetic disorder is plausible, which is their hypothesis and not a result.

Participants / model
Rats; rat brain tissue; rabbit pulmonary artery strip
Treatment
PPAP in rats and tissue preparations; routes not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound. Doses and routes are not reproduced on this page.

Read the original source
Peritoneal immune cells: PPAP raised serotonin, deprenyl did not

Animal study

Csaba G et al. Cell Biochem Funct. 2006;24(1):49-53. PMID 15584092.

In peritoneal cells of young female animals (species not stated in the abstract), PPAP significantly increased the serotonin level 30 minutes after treatment at 6 weeks of age, while deprenyl did not. Three weeks after treatment at weaning PPAP moderately but significantly raised serotonin in monocytes, granulocytes and mast cells, while deprenyl drastically lowered it. The authors say the two molecules have different effects on immune cells independent of MAO-B inhibition.

Participants / model
Peritoneal immune cells of young female animals, species not stated in the abstract
Treatment
PPAP and deprenyl; dose and route not stated in the abstract
Follow-up
30 minutes and 3 weeks after treatment
Study design
Original preclinical study
Funding
not stated in the source

Shows PPAP is not selective for catecholamine neurons in animals. The abstract gives no dose or route.

Read the original source
PubChem: PPAP racemate and (-)-enantiomer identity

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 51529346, (2R)-1-phenyl-N-propylpentan-2-amine; the racemate is CID 10262369.

The racemate (1-phenyl-N-propylpentan-2-amine) is PubChem CID 10262369, C14H23N, 205.34 g/mol, CAS 119485-94-8. The (-)-enantiomer, (2R)-1-phenyl-N-propylpentan-2-amine, is a separate record, CID 51529346, CAS 784118-64-5. The research reviewed used (-)PPAP, and in one test (-)PPAP was much more potent than (+)PPAP.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule; racemate and R-enantiomer
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. A racemic or unspecified vendor product is not the studied material, and no public record ties any vendor material to either entry.

Read the original source

Why does PPAP sit in C tier?

PPAP has internally coherent rat pharmacology and no failed trial or documented harm in the records reviewed, but the data come from one research tradition and include no human, pharmacokinetic or toxicology data at all.

The rat pharmacology is internally coherent: indirect catecholaminergic enhancement without MAO inhibition or catecholamine release, a broad dose range, and learning and forced swimming effects. Nothing in the records reviewed shows a failed trial or documented harm, and the supplier claim is worded cautiously.

The data are thin in the C sense. They come from one research tradition, with work from 1992 to 2006 and no independent replication in the records reviewed, and there are no human, pharmacokinetic or toxicology data at all.

Founding rat pharmacology paper from the developing group

Animal study

Knoll J et al. Arch Int Pharmacodyn Ther. 1992;316:5-29. PMID 1356324.

PPAP was chosen as the reference substance among deprenyl-derived compounds made to lack MAO inhibitory potency. [14C]PPAP was taken up into catecholaminergic axon terminals, PPAP inhibited uptake of [3H]noradrenaline and [3H]dopamine in rat brain, and it lacked catecholamine-releasing property. In rats PPAP increased motility and inhibited it only at very high doses, induced substantially less stereotyped behavior than amphetamine or methamphetamine, facilitated learning and retention, antagonized tetrabenazine-induced depression, and was very effective in the forced swimming test. The authors state performance improved over a reasonably broad dose range, unlike amphetamines. They suggest usefulness in depression, Alzheimer's disease and attention-deficit-hyperkinetic disorder is plausible, which is their hypothesis and not a result.

Participants / model
Rats; rat brain tissue; rabbit pulmonary artery strip
Treatment
PPAP in rats and tissue preparations; routes not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound. Doses and routes are not reproduced on this page.

Read the original source
Mechanism work in rat tissue and frog heart fibers

Animal study

Knoll J et al. Life Sci. 1996;58(10):817-27. PMID 8602114.

In rats, (-)deprenyl enhanced catecholaminergic activity 30 minutes after subcutaneous injection. The authors concluded that (-)deprenyl and (-)PPAP act primarily as stimulants of action potential-transmitter release coupling in catecholaminergic neurons, an effect they found unrelated to MAO inhibition, presynaptic receptor inhibition, catecholamine uptake inhibition or catecholamine release. Both enhanced the inward Ca2+ current in frog heart sino-auricular fibers, and (-)PPAP was much more potent than either (+)PPAP or (-)deprenyl in that test.

Participants / model
Rats; isolated rat brain stem; frog heart fibers
Treatment
Subcutaneous (-)deprenyl in rats; (-)PPAP and (-)deprenyl in tissue preparations
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

The rat injection result is for (-)deprenyl, not PPAP. Animal tissue only, and the conclusion is the authors' interpretation.

Read the original source
Two Wistar rat breeds: deficit reversed in the high-performing breed

Animal study

Knoll J et al. Life Sci. 1996;58(11):945-52. PMID 8786700.

Two rat breeds differing in learning performance were trained in a shuttle box. The high-performing breed released more noradrenaline from the locus coeruleus and more serotonin from the raphe. (-)PPAP fully antagonized tetrabenazine-induced learning depression in high-performing rats and was ineffective in low-performing rats at the dose tested.

Participants / model
Two breeds of Wistar rats
Treatment
(-)PPAP; dose not reproduced here, route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

Reversal of a drug-induced learning deficit in one breed of rats, not a gain in healthy people or in physical performance.

Read the original source
PubMed: 11 records from 1992 to 2016, none reports PPAP given to a person

PubMed search record

PubMed search for phenylpropylaminopentane OR 1-phenyl-2-propylaminopentane OR 1-phenyl-2-propylamino-pentane, run 10 October 2026, with follow-up queries adding human terms and pharmacokinetic and toxicology terms.

A PubMed search on 10 October 2026 for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane or 1-phenyl-2-propylamino-pentane returned 11 records dated 1992 to 2016. Titles were read for all 11 and abstracts for those on PPAP itself; the rest concern deprenyl, BPAP, phenylethylamine, or a rat analysis of why alpha-tocopherol failed in the DATATOP trial. Adding human, patients, volunteers or clinical returned 3 records (a deprenyl review, the rat DATATOP analysis and a BPAP paper), and adding pharmacokinetic, metabolism, doping, toxicity or LD50 returned 10 records from the same cluster. No abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists. The supplier wording of limited human characterization overstates what exists, because no human data were found.

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No label, no application, no registered study; deprenyl the only drug of its kind

Regulatory record

Miklya I. Mol Psychiatry. 2016;21(11):1499-1503. PMID 27480491.

DailyMed returned no labels for phenylpropylaminopentane on 10 October 2026, and an openFDA Drugs@FDA query returned no match. ClinicalTrials.gov queries for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane and PPAP deprenyl-derived returned no studies. A 2016 review from Budapest on the catecholaminergic activity enhancer concept says that presently deprenyl is the only available drug of that kind, which places PPAP as a research compound.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search; review article
Funding
not stated in the source

An absence finding as of 10 October 2026. Status outside the United States is not covered.

Read the original source

Studies and sources

PubChem: PPAP racemate and (-)-enantiomer identity

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 51529346, (2R)-1-phenyl-N-propylpentan-2-amine; the racemate is CID 10262369.

The racemate (1-phenyl-N-propylpentan-2-amine) is PubChem CID 10262369, C14H23N, 205.34 g/mol, CAS 119485-94-8. The (-)-enantiomer, (2R)-1-phenyl-N-propylpentan-2-amine, is a separate record, CID 51529346, CAS 784118-64-5. The research reviewed used (-)PPAP, and in one test (-)PPAP was much more potent than (+)PPAP.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule; racemate and R-enantiomer
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

Identity record only. A racemic or unspecified vendor product is not the studied material, and no public record ties any vendor material to either entry.

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Founding rat pharmacology paper from the developing group

Animal study

Knoll J et al. Arch Int Pharmacodyn Ther. 1992;316:5-29. PMID 1356324.

PPAP was chosen as the reference substance among deprenyl-derived compounds made to lack MAO inhibitory potency. [14C]PPAP was taken up into catecholaminergic axon terminals, PPAP inhibited uptake of [3H]noradrenaline and [3H]dopamine in rat brain, and it lacked catecholamine-releasing property. In rats PPAP increased motility and inhibited it only at very high doses, induced substantially less stereotyped behavior than amphetamine or methamphetamine, facilitated learning and retention, antagonized tetrabenazine-induced depression, and was very effective in the forced swimming test. The authors state performance improved over a reasonably broad dose range, unlike amphetamines. They suggest usefulness in depression, Alzheimer's disease and attention-deficit-hyperkinetic disorder is plausible, which is their hypothesis and not a result.

Participants / model
Rats; rat brain tissue; rabbit pulmonary artery strip
Treatment
PPAP in rats and tissue preparations; routes not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound. Doses and routes are not reproduced on this page.

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Mechanism work in rat tissue and frog heart fibers

Animal study

Knoll J et al. Life Sci. 1996;58(10):817-27. PMID 8602114.

In rats, (-)deprenyl enhanced catecholaminergic activity 30 minutes after subcutaneous injection. The authors concluded that (-)deprenyl and (-)PPAP act primarily as stimulants of action potential-transmitter release coupling in catecholaminergic neurons, an effect they found unrelated to MAO inhibition, presynaptic receptor inhibition, catecholamine uptake inhibition or catecholamine release. Both enhanced the inward Ca2+ current in frog heart sino-auricular fibers, and (-)PPAP was much more potent than either (+)PPAP or (-)deprenyl in that test.

Participants / model
Rats; isolated rat brain stem; frog heart fibers
Treatment
Subcutaneous (-)deprenyl in rats; (-)PPAP and (-)deprenyl in tissue preparations
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

The rat injection result is for (-)deprenyl, not PPAP. Animal tissue only, and the conclusion is the authors' interpretation.

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Two Wistar rat breeds: deficit reversed in the high-performing breed

Animal study

Knoll J et al. Life Sci. 1996;58(11):945-52. PMID 8786700.

Two rat breeds differing in learning performance were trained in a shuttle box. The high-performing breed released more noradrenaline from the locus coeruleus and more serotonin from the raphe. (-)PPAP fully antagonized tetrabenazine-induced learning depression in high-performing rats and was ineffective in low-performing rats at the dose tested.

Participants / model
Two breeds of Wistar rats
Treatment
(-)PPAP; dose not reproduced here, route not stated in the abstract
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

Reversal of a drug-induced learning deficit in one breed of rats, not a gain in healthy people or in physical performance.

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Different compound with the same acronym; not evidence about this compound

Chemical identity record

Glennon RA et al. Pharmacol Biochem Behav. 1990;37(3):557-9. PMID 1965044.

A 1990 paper describes (-)PPAP as R(-)-N-(3-phenyl-n-propyl)-1-phenyl-2-aminopropane, a sigma binding site ligand. That is not phenylpropylaminopentane, and a search on PPAP alone will mix the two.

Participants / model
Different compound; not a population for this page
Treatment
Not applicable
Follow-up
Not applicable
Study design
Identity disambiguation; the paper concerns a different compound
Funding
not stated in the source

Listed only to separate two molecules that share an acronym. It is not cited as evidence about phenylpropylaminopentane.

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Peritoneal immune cells: PPAP raised serotonin, deprenyl did not

Animal study

Csaba G et al. Cell Biochem Funct. 2006;24(1):49-53. PMID 15584092.

In peritoneal cells of young female animals (species not stated in the abstract), PPAP significantly increased the serotonin level 30 minutes after treatment at 6 weeks of age, while deprenyl did not. Three weeks after treatment at weaning PPAP moderately but significantly raised serotonin in monocytes, granulocytes and mast cells, while deprenyl drastically lowered it. The authors say the two molecules have different effects on immune cells independent of MAO-B inhibition.

Participants / model
Peritoneal immune cells of young female animals, species not stated in the abstract
Treatment
PPAP and deprenyl; dose and route not stated in the abstract
Follow-up
30 minutes and 3 weeks after treatment
Study design
Original preclinical study
Funding
not stated in the source

Shows PPAP is not selective for catecholamine neurons in animals. The abstract gives no dose or route.

Read the original source
No label, no application, no registered study; deprenyl the only drug of its kind

Regulatory record

Miklya I. Mol Psychiatry. 2016;21(11):1499-1503. PMID 27480491.

DailyMed returned no labels for phenylpropylaminopentane on 10 October 2026, and an openFDA Drugs@FDA query returned no match. ClinicalTrials.gov queries for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane and PPAP deprenyl-derived returned no studies. A 2016 review from Budapest on the catecholaminergic activity enhancer concept says that presently deprenyl is the only available drug of that kind, which places PPAP as a research compound.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated label, application and registry search; review article
Funding
not stated in the source

An absence finding as of 10 October 2026. Status outside the United States is not covered.

Read the original source
PubMed: 11 records from 1992 to 2016, none reports PPAP given to a person

PubMed search record

PubMed search for phenylpropylaminopentane OR 1-phenyl-2-propylaminopentane OR 1-phenyl-2-propylamino-pentane, run 10 October 2026, with follow-up queries adding human terms and pharmacokinetic and toxicology terms.

A PubMed search on 10 October 2026 for phenylpropylaminopentane, 1-phenyl-2-propylaminopentane or 1-phenyl-2-propylamino-pentane returned 11 records dated 1992 to 2016. Titles were read for all 11 and abstracts for those on PPAP itself; the rest concern deprenyl, BPAP, phenylethylamine, or a rat analysis of why alpha-tocopherol failed in the DATATOP trial. Adding human, patients, volunteers or clinical returned 3 records (a deprenyl review, the rat DATATOP analysis and a BPAP paper), and adding pharmacokinetic, metabolism, doping, toxicity or LD50 returned 10 records from the same cluster. No abstract reports PPAP given to a person, or its pharmacokinetics, metabolism, toxicity or detection in doping control.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Searches run on 10 October 2026
Study design
Dated literature search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists. The supplier wording of limited human characterization overstates what exists, because no human data were found.

Read the original source

Why is PPAP (phenylpropylaminopentane) in C tier?

C fits a research compound with internally coherent rat pharmacology, no failed trial or documented harm in the records reviewed, and a cautiously worded claim. The data are thin: one research tradition, work from 1992 to 2006 with no independent replication, and no human, pharmacokinetic or toxicology data at all.