BPAP (benzofuranylpropylaminopentane)

updated

BPAP (benzofuranylpropylaminopentane) is a deprenyl-derived research compound. It is sold for dopaminergic and noradrenergic enhancement and neuroprotection at extremely low doses. The acronym is also bisphenol AP, a plastics chemical, and bilevel positive airway pressure, a breathing treatment. Its published work is rat and isolated-tissue pharmacology, mostly from the group that developed it, and no controlled human study exists: a PubMed query on 10 October 2026 returned 32 records, and none reports BPAP given to a person.

Catecholaminergic activity enhancer (deprenyl-derived)

  • BPAP here is benzofuranylpropylaminopentane (racemate PubChem CID 9859674, R-(-) enantiomer CID 9816303); the same acronym names bisphenol AP, a plastics chemical (CID 623849), and bilevel positive airway pressure.
  • In isolated rat brain regions release of dopamine, noradrenaline and serotonin rose significantly at 10^-12 to 10^-14 M, and an acute 0.1 microg/kg subcutaneous injection in rats enhanced monoamine neuron activity 30 minutes later.
  • The dose-response is bell shaped: 0.0005 mg/kg subcutaneously raised locus coeruleus noradrenaline release from 4.7 to 15.4 nmol/g in rats, while 0.05 mg/kg gave no difference from control.
  • In HEK 293 cells expressing human transporters (-)BPAP inhibited dopamine, norepinephrine and serotonin uptake with IC50 values of 42, 52 and 640 nM.
  • Neuroprotection is shown only in cell culture: the racemate protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 to 10^-15 M, and no record tests (-)BPAP in a lesion model in a living animal.
  • A lifespan study from the developing group found longer lifespan in male Wistar rats, while a later study in aged, experienced Long-Evans rats found BPAP could not improve cognitive performance or prolong lifespan.

What is BPAP, and what is its regulatory status?

BPAP here means benzofuranylpropylaminopentane, a deprenyl-derived research compound, usually the R-(-) enantiomer. The acronym is also bisphenol AP, a plastics chemical, and bilevel positive airway pressure, a breathing treatment. No label, application or registered study exists for the compound.

The acronym does not resolve to this compound. PubChem returns CID 623849 for the name BPAP, which is bisphenol AP (C20H18O2, 290.4 g/mol, CAS 1571-75-1), a plastics chemical. In medicine BPAP means bilevel positive airway pressure: a PubMed query on the acronym forms returned 397 records, the top-ranked ones on sleep apnea and ventilation, and ClinicalTrials.gov returns noninvasive ventilation studies for BPAP. Neither is the compound on this page.

The studied molecule is benzofuranylpropylaminopentane, 1-(1-benzofuran-2-yl)-N-propylpentan-2-amine. The racemate is PubChem CID 9859674, C16H23NO, 245.36 g/mol, with no CAS number among its listed synonyms. The R-(-) enantiomer, (2R)-1-(1-benzofuran-2-yl)-N-propylpentan-2-amine, is CID 9816303, CAS 260550-89-8, with the synonyms R-(-)-BPAP and FPFS-1169 free base. Most work used the R-(-) enantiomer as the hydrochloride, written (-)BPAP, and a 2001 paper reports its beta-amyloid result for the racemate, written (+/-)BPAP. One 2004 abstract uses the codes R-FPFS-1169 and R-FPFS-1180 for compounds compared with their S-enantiomers, and what that code denotes is not settled here.

A vial labeled BPAP cannot be tied to either CID by the name alone, and no public record ties any vendor material to the studied compound. On 10 October 2026 DailyMed returned no label for benzofuranylpropylaminopentane or for BPAP, an openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for propylaminopentane, benzofuranylpropylaminopentane and catecholaminergic activity enhancer returned no studies. The query for the acronym forms returned 10 records, all noninvasive ventilation, asthma, sleep apnea or unrelated studies. A 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP as a research compound. Status outside the United States is not covered here.

PubChem: BPAP racemate and R-(-) enantiomer identity, and the acronym collisions

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 9816303, (2R)-1-(1-benzofuran-2-yl)-N-propylpentan-2-amine; the racemate is CID 9859674.

The acronym does not resolve to this compound: PubChem returns CID 623849 for the name BPAP, which is bisphenol AP (C20H18O2, 290.4 g/mol, CAS 1571-75-1), a plastics chemical, and in medicine BPAP means bilevel positive airway pressure (a PubMed query on the acronym forms returned 397 records, the top-ranked ones on sleep apnea and ventilation). The studied molecule is benzofuranylpropylaminopentane, 1-(1-benzofuran-2-yl)-N-propylpentan-2-amine. The racemate is CID 9859674, C16H23NO, 245.36 g/mol, with no CAS number among its listed synonyms. The R-(-) enantiomer is CID 9816303, CAS 260550-89-8, with the synonyms R-(-)-BPAP and FPFS-1169 free base. Most work used the R-(-) enantiomer as the hydrochloride, written (-)BPAP, and a 2001 paper reports its beta-amyloid result for the racemate, written (+/-)BPAP. One 2004 abstract uses the codes R-FPFS-1169 and R-FPFS-1180 for compounds compared with their S-enantiomers.

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

Identity record only. A vial labeled BPAP cannot be tied to either CID by the name alone, and no public record ties any vendor material to the studied compound. What the FPFS code denotes in the 2004 abstract is not settled.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for benzofuranylpropylaminopentane, BPAP, propylaminopentane and catecholaminergic activity enhancer, run 10 October 2026.

DailyMed returned no label for benzofuranylpropylaminopentane or for BPAP, the openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for propylaminopentane, benzofuranylpropylaminopentane and catecholaminergic activity enhancer returned no studies. The query for the acronym forms returned 10 records, all noninvasive ventilation, asthma, sleep apnea or unrelated studies. A 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP 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
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records only.

Read the original source

What did the rat and tissue studies find?

In rats and isolated rat brain tissue, (-)BPAP enhanced release of dopamine, noradrenaline and serotonin at extremely low doses and concentrations, with a bell-shaped dose-response, and at much higher doses it increased locomotor activity. All of it is animal and tissue work, mostly from the group that developed the compound, and no controlled human study exists.

The founding paper comes from the group that developed the compound. (-)BPAP was selected out of 65 newly synthesized compounds as a potential follower of (-)deprenyl. It enhanced impulse-propagation-mediated release of [3H]noradrenaline and [3H]dopamine at 0.18 micromol per liter and of [3H]serotonin at 36 nmol per liter from isolated rat brain stem. In isolated discrete rat brain regions release rose significantly at 10^-12 to 10^-14 M. In rats, catecholaminergic and serotoninergic neuron activity was significantly enhanced 30 minutes after an acute 0.1 microg/kg subcutaneous injection, and in the shuttle box (-)BPAP was about 130 times more potent than (-)deprenyl at antagonizing tetrabenazine-induced inhibition of performance.

The dose-response is bell shaped, so the extremely low dose wording is dose-specific. In rats, 0.0005 mg/kg subcutaneously raised the noradrenaline released from isolated locus coeruleus 30 minutes later from 4.7 +/- 0.10 to 15.4 +/- 0.55 nmol/g wet weight (P < 0.001), while a hundred times higher dose, 0.05 mg/kg, gave 4.3 +/- 0.25 nmol/g, no different from control. Ex vivo, locus coeruleus release was enhanced from 10^-16 M with a peak at 10^-13 M, 10^-10 M was ineffective, and a second effective range ran from 10^-8 M with a peak at 10^-6 M. Later abstracts from the same group name 0.0001 mg/kg as the specific enhancer dose and 0.05 mg/kg as the non-specific dose in rats.

A Japanese group reported that (-)BPAP potentiated locomotor activity in non-habituated rats dose-dependently at 0.3 to 10 mg/kg and reversed reserpine-induced hypolocomotion at 1 to 3 mg/kg, and that the D1 antagonist SCH 23390 attenuated both, which the authors read as dopaminergic mediation. A companion paper gives the route as subcutaneous at 0.3 and 1 mg/kg in normal rats and reports an L-DOPA-sparing effect. By arithmetic, 0.3 mg/kg is 3,000 times the 0.0001 mg/kg specific dose.

Other animal results are not tied to the supplier claim. In mice, acute but not chronic (-)BPAP shortened forced-swim immobility, and chronic but not acute treatment ameliorated impaired social interaction after forced swimming, an effect suppressed by dopamine receptor antagonists. In olfactory bulbectomized rats, chronic treatment improved social interaction, prepulse inhibition and tone-cue fear learning without changing locomotion. In rats trained to self-administer methamphetamine, repeated (-)BPAP during extinction and acute doses on test day attenuated cue-induced and priming-induced reinstatement without reinstating seeking or changing self-administration, and dopamine antagonists did not change the effect, so the abstract does not show dopamine receptor mediation. That is a relapse model and not a test of dopamine downregulation. In rats treated for 3 weeks at the specific doses, phosphorylated GluR1 and GluN2B rose, dark-phase corticosterone fell and anxiety-like behavior did not change significantly. Routes are not stated in most of these abstracts.

Founding paper from the developing group: release enhancement, beta-amyloid protection, shuttle box

Animal study

Knoll J et al. Br J Pharmacol. 1999;128(8):1723-32. PMID 10588928.

(-)BPAP was selected out of 65 newly synthesized compounds as a potential follower of (-)deprenyl. It enhanced impulse-propagation-mediated release of [3H]noradrenaline and [3H]dopamine at 0.18 micromol per liter and of [3H]serotonin at 36 nmol per liter from isolated rat brain stem. In isolated discrete rat brain regions (dopamine from striatum, substantia nigra and tuberculum olfactorium, noradrenaline from locus coeruleus, serotonin from raphe) release rose significantly at 10^-12 to 10^-14 M. It protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 M. In rats, catecholaminergic and serotoninergic neuron activity was significantly enhanced 30 minutes after an acute 0.1 microg/kg subcutaneous injection, and in the shuttle box (-)BPAP was about 130 times more potent than (-)deprenyl at antagonizing tetrabenazine-induced inhibition of performance.

Participants / model
Isolated rat brain stem and brain regions; cultured hippocampal neurons (species not stated in the abstract); rats
Treatment
(-)BPAP in tissue and cell preparations; 0.1 microg/kg by subcutaneous injection in rats
Follow-up
Neuron activity measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound.

Read the original source
Rats: 0.0005 mg/kg raised release, 0.05 mg/kg did not (bell-shaped)

Animal study

Knoll J et al. Life Sci. 2002;71(18):2137-44. PMID 12204771.

In rats, 0.0005 mg/kg subcutaneously raised the noradrenaline released from isolated locus coeruleus 30 minutes later from 4.7 +/- 0.10 to 15.4 +/- 0.55 nmol/g wet weight (P < 0.001), while a hundred times higher dose, 0.05 mg/kg, gave 4.3 +/- 0.25 nmol/g, no different from control. Ex vivo, locus coeruleus release was enhanced from 10^-16 M with a peak at 10^-13 M, 10^-10 M was ineffective, and a second effective range ran from 10^-8 M with a peak at 10^-6 M. Dopaminergic and serotoninergic neurons peaked at 10^-13 and 10^-12 M. The authors suggest the trace amine receptors as the site of action. Later abstracts from the same group name 0.0001 mg/kg as the specific enhancer dose and 0.05 mg/kg as the non-specific dose in rats.

Participants / model
Rats; isolated rat locus coeruleus, striatum and raphe tissue
Treatment
Subcutaneous injection, 0.0005 and 0.05 mg/kg; tissue baths
Follow-up
Release measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

The dose-response is bell shaped, so the extremely low dose claim is dose-specific.

Read the original source
Locomotor activity at higher doses; uptake inhibition at nanomolar concentrations; TAAR1

Animal study

Shimazu S et al. Eur J Pharmacol. 2001;421(3):181-9. PMID 11516435.

A Japanese group reported that (-)BPAP potentiated locomotor activity in non-habituated rats dose-dependently at 0.3 to 10 mg/kg and reversed reserpine-induced hypolocomotion at 1 to 3 mg/kg, and that the D1 antagonist SCH 23390 attenuated both, which the authors read as dopaminergic mediation. A companion paper (PMID 12527038) gives the route as subcutaneous at 0.3 and 1 mg/kg in normal rats and reports an L-DOPA-sparing effect. In HEK 293 cells expressing human transporters, (-)BPAP inhibited [3H]dopamine, norepinephrine and serotonin uptake with IC50 values of 42 +/- 9, 52 +/- 19 and 640 +/- 120 nM. In rat brain synaptosomes it did not potentiate tyramine-induced norepinephrine release and inhibited it, which the authors say may block tyramine-induced hypertensive crisis (PMID 14659999). A 2022 rat striatal slice paper reports (-)BPAP potentiated vesicular dopamine release through TAAR1 and did not induce non-vesicular release; its conflict statement names support from Fujimoto Pharmaceutical Corporation, Osaka (PMID 35955676).

Participants / model
Rats; HEK 293 cells expressing human DAT, NET and SERT; rat brain synaptosomes and striatal slices
Treatment
Subcutaneous injection in rats; cell and tissue preparations
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

By arithmetic, 0.3 mg/kg is 3,000 times the 0.0001 mg/kg specific dose. The tyramine result is a synaptosome result and the authors' inference, not a human safety finding.

Read the original source
Other animal behavior: forced swim, social interaction, methamphetamine reinstatement

Animal study

Hiranita T et al. Neuroscience. 2010;165(2):300-12. PMID 19883738.

In mice, acute but not chronic (-)BPAP shortened forced-swim immobility, and chronic but not acute treatment ameliorated impaired social interaction after forced swimming, an effect suppressed by dopamine receptor antagonists. In olfactory bulbectomized rats, chronic treatment improved social interaction, prepulse inhibition and tone-cue fear learning without changing locomotion (PMID 18243357). In rats trained to self-administer methamphetamine, repeated (-)BPAP during extinction and acute doses on test day attenuated cue-induced and priming-induced reinstatement without reinstating seeking or changing self-administration, and dopamine antagonists did not change the effect, so the abstract does not show dopamine receptor mediation. In rats treated for 3 weeks at the specific doses (0.0001 mg/kg BPAP), phosphorylated GluR1 and GluN2B rose, dark-phase corticosterone fell and anxiety-like behavior did not change significantly (PMID 31610214).

Participants / model
Mice; olfactory bulbectomized rats; rats self-administering methamphetamine; rats
Treatment
(-)BPAP; route not stated in most abstracts; dose not stated in the reinstatement abstract
Follow-up
Chronic and acute schedules; 3 weeks in the glutamate receptor study
Study design
Original preclinical studies
Funding
not stated in the source

The reinstatement work is a relapse model, not a test of dopamine downregulation.

Read the original source

How does BPAP act on monoamine neurons?

In isolated rat brain tissue (-)BPAP enhanced impulse-driven release of dopamine, noradrenaline and serotonin at extremely low concentrations, and its developers suggest trace amine receptors as the site of action. At nanomolar concentrations in human transporter cells it also inhibited dopamine, norepinephrine and serotonin uptake, so more than one action is involved.

The group that developed (-)BPAP describes it as an enhancer of impulse-propagation-mediated release of monoamines from nerve terminals, and suggests trace amine receptors as the site of action. Dopaminergic and serotoninergic neurons peaked at 10^-13 and 10^-12 M, and a second effective range for locus coeruleus release began at 10^-8 M.

At higher concentrations a different pharmacology appears. In HEK 293 cells expressing human transporters, (-)BPAP inhibited [3H]dopamine, norepinephrine and serotonin uptake with IC50 values of 42 +/- 9, 52 +/- 19 and 640 +/- 120 nM. In rat brain synaptosomes it did not potentiate tyramine-induced norepinephrine release and inhibited it, which the authors say may block tyramine-induced hypertensive crisis; that is a synaptosome result and the authors' inference, not a human safety finding. A 2022 rat striatal slice paper reports (-)BPAP potentiated vesicular dopamine release through TAAR1 and did not induce non-vesicular release, and its conflict statement names support from Fujimoto Pharmaceutical Corporation, Osaka.

In cultured cortical neurons the rescue of cell death by (-)BPAP involved sigma receptors, and in astrocytes it raised neurotrophin secretion, as described in the section on neuroprotection.

Rats: 0.0005 mg/kg raised release, 0.05 mg/kg did not (bell-shaped)

Animal study

Knoll J et al. Life Sci. 2002;71(18):2137-44. PMID 12204771.

In rats, 0.0005 mg/kg subcutaneously raised the noradrenaline released from isolated locus coeruleus 30 minutes later from 4.7 +/- 0.10 to 15.4 +/- 0.55 nmol/g wet weight (P < 0.001), while a hundred times higher dose, 0.05 mg/kg, gave 4.3 +/- 0.25 nmol/g, no different from control. Ex vivo, locus coeruleus release was enhanced from 10^-16 M with a peak at 10^-13 M, 10^-10 M was ineffective, and a second effective range ran from 10^-8 M with a peak at 10^-6 M. Dopaminergic and serotoninergic neurons peaked at 10^-13 and 10^-12 M. The authors suggest the trace amine receptors as the site of action. Later abstracts from the same group name 0.0001 mg/kg as the specific enhancer dose and 0.05 mg/kg as the non-specific dose in rats.

Participants / model
Rats; isolated rat locus coeruleus, striatum and raphe tissue
Treatment
Subcutaneous injection, 0.0005 and 0.05 mg/kg; tissue baths
Follow-up
Release measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

The dose-response is bell shaped, so the extremely low dose claim is dose-specific.

Read the original source
Locomotor activity at higher doses; uptake inhibition at nanomolar concentrations; TAAR1

Animal study

Shimazu S et al. Eur J Pharmacol. 2001;421(3):181-9. PMID 11516435.

A Japanese group reported that (-)BPAP potentiated locomotor activity in non-habituated rats dose-dependently at 0.3 to 10 mg/kg and reversed reserpine-induced hypolocomotion at 1 to 3 mg/kg, and that the D1 antagonist SCH 23390 attenuated both, which the authors read as dopaminergic mediation. A companion paper (PMID 12527038) gives the route as subcutaneous at 0.3 and 1 mg/kg in normal rats and reports an L-DOPA-sparing effect. In HEK 293 cells expressing human transporters, (-)BPAP inhibited [3H]dopamine, norepinephrine and serotonin uptake with IC50 values of 42 +/- 9, 52 +/- 19 and 640 +/- 120 nM. In rat brain synaptosomes it did not potentiate tyramine-induced norepinephrine release and inhibited it, which the authors say may block tyramine-induced hypertensive crisis (PMID 14659999). A 2022 rat striatal slice paper reports (-)BPAP potentiated vesicular dopamine release through TAAR1 and did not induce non-vesicular release; its conflict statement names support from Fujimoto Pharmaceutical Corporation, Osaka (PMID 35955676).

Participants / model
Rats; HEK 293 cells expressing human DAT, NET and SERT; rat brain synaptosomes and striatal slices
Treatment
Subcutaneous injection in rats; cell and tissue preparations
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

By arithmetic, 0.3 mg/kg is 3,000 times the 0.0001 mg/kg specific dose. The tyramine result is a synaptosome result and the authors' inference, not a human safety finding.

Read the original source
Cell culture only: beta-amyloid protection, sigma receptors, astrocyte neurotrophins

Cell study

Yoneda F et al. Bioorg Med Chem. 2001;9(5):1197-212. PMID 11377178.

The racemate (+/-)BPAP protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 to 10^-15 M. In serum-free cortical neuron cultures (-)BPAP rescued cell death through sigma receptors, blocked by BD1063, with weak displacement of [3H]pentazocine binding (PMID 11100977; concentration not in the abstract). In cultured mouse astrocytes, (-)BPAP raised NGF, BDNF and GDNF secretion, up to 120, two and seven times control at 0.35 mM for 24 hours as the abstract states (PMID 12147307). A companion paper found minimum effective concentrations of 5 x 10^-5, 1 x 10^-5 and 1 x 10^-6 M for NGF, BDNF and GDNF, a bell-shaped curve peaking at 1 x 10^-4 M for NGF, and no effect at fM to pM concentrations (PMID 12679194), roughly ten orders of magnitude above the 10^-14 M neuroprotection figure. In rat mesencephalic slice cultures R-(-)-BPAP raised BDNF and trkB mRNA at 48 hours (PMID 16079507). A human neuroblastoma SH-SY5Y paper (PMID 15102525) reports anti-apoptotic effects of BPAP analogues, but its abstract says levorotatory compounds did not prevent the mitochondrial permeability transition.

Participants / model
Cultured hippocampal and cortical neurons; mouse astrocytes; rat mesencephalic slices; human SH-SY5Y cells
Treatment
Cell and slice culture, in vitro
Follow-up
24 hours and 48 hours in the neurotrophin studies; not stated for the others
Study design
Original preclinical studies
Funding
not stated in the source

The 0.35 mM figure in the astrocyte abstract looks inconsistent with the lower concentrations in its companion paper, and the discrepancy is unresolved. The SH-SY5Y paper is not used as evidence for (-)BPAP. None of the 32 records reviewed tests (-)BPAP in a lesion or injury model for neuroprotection in a living animal.

Read the original source

Does BPAP protect neurons?

Only in cell culture. The racemate protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 to 10^-15 M, and (-)BPAP raised neurotrophin secretion in astrocytes at concentrations about ten orders of magnitude higher. None of the 32 records reviewed tests (-)BPAP in a lesion or injury model for neuroprotection in a living animal.

The racemate (+/-)BPAP protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 to 10^-15 M. In serum-free cortical neuron cultures (-)BPAP rescued cell death through sigma receptors, blocked by BD1063, with weak displacement of [3H]pentazocine binding; the concentration is not in the abstract.

In cultured mouse astrocytes, (-)BPAP raised NGF, BDNF and GDNF secretion, up to 120, two and seven times control at 0.35 mM for 24 hours as the abstract states. A companion paper found minimum effective concentrations of 5 x 10^-5, 1 x 10^-5 and 1 x 10^-6 M for NGF, BDNF and GDNF, a bell-shaped curve peaking at 1 x 10^-4 M for NGF, and no effect at fM to pM concentrations, roughly ten orders of magnitude above the 10^-14 M neuroprotection figure. The 0.35 mM figure looks inconsistent with the lower concentrations in the companion paper, and the discrepancy is unresolved. In rat mesencephalic slice cultures R-(-)-BPAP raised BDNF and trkB mRNA at 48 hours.

A human neuroblastoma SH-SY5Y paper reports anti-apoptotic effects of BPAP analogues, but its abstract says levorotatory compounds did not prevent the mitochondrial permeability transition, so it is not used as evidence for (-)BPAP. The extremely low concentration holds for the beta-amyloid result and not for the astrocyte neurotrophin result.

Cell culture only: beta-amyloid protection, sigma receptors, astrocyte neurotrophins

Cell study

Yoneda F et al. Bioorg Med Chem. 2001;9(5):1197-212. PMID 11377178.

The racemate (+/-)BPAP protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 to 10^-15 M. In serum-free cortical neuron cultures (-)BPAP rescued cell death through sigma receptors, blocked by BD1063, with weak displacement of [3H]pentazocine binding (PMID 11100977; concentration not in the abstract). In cultured mouse astrocytes, (-)BPAP raised NGF, BDNF and GDNF secretion, up to 120, two and seven times control at 0.35 mM for 24 hours as the abstract states (PMID 12147307). A companion paper found minimum effective concentrations of 5 x 10^-5, 1 x 10^-5 and 1 x 10^-6 M for NGF, BDNF and GDNF, a bell-shaped curve peaking at 1 x 10^-4 M for NGF, and no effect at fM to pM concentrations (PMID 12679194), roughly ten orders of magnitude above the 10^-14 M neuroprotection figure. In rat mesencephalic slice cultures R-(-)-BPAP raised BDNF and trkB mRNA at 48 hours (PMID 16079507). A human neuroblastoma SH-SY5Y paper (PMID 15102525) reports anti-apoptotic effects of BPAP analogues, but its abstract says levorotatory compounds did not prevent the mitochondrial permeability transition.

Participants / model
Cultured hippocampal and cortical neurons; mouse astrocytes; rat mesencephalic slices; human SH-SY5Y cells
Treatment
Cell and slice culture, in vitro
Follow-up
24 hours and 48 hours in the neurotrophin studies; not stated for the others
Study design
Original preclinical studies
Funding
not stated in the source

The 0.35 mM figure in the astrocyte abstract looks inconsistent with the lower concentrations in its companion paper, and the discrepancy is unresolved. The SH-SY5Y paper is not used as evidence for (-)BPAP. None of the 32 records reviewed tests (-)BPAP in a lesion or injury model for neuroprotection in a living animal.

Read the original source
PubMed, 10 October 2026: 32 records from 1999 to 2025, none gives BPAP to a person

PubMed search record

PubMed search run 10 October 2026: benzofuran*[tiab] AND (propylaminopentane[tiab] OR propylpentan*[tiab] OR BPAP[tiab]), with a follow-up query adding human, humans, patients, volunteers, clinical, trial or trials.

The search returned 32 records dated 1999 to 2025, and abstracts were read for all 32. Adding human, humans, patients, volunteers, clinical, trial or trials returned 15 of them, all read, and none reports (-)BPAP given to a person: the human terms matched human cell lines and transporter clones, a deprenyl-trial analysis in rats, and reviews. Two 2004 to 2006 review abstracts express hope for a role in treatment-resistant depression, and a 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP as a research compound. No controlled human trial exists in the records reviewed.

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 or unindexed work exists. Whether any vendor product is the R-(-) enantiomer, the racemate or something else is unknown.

Read the original source

Did BPAP change lifespan or aging in rats?

The results conflict. The developing group reported longer lifespan in male Wistar rats, and a later study in aged, experienced Long-Evans rats found BPAP could not improve cognitive performance or prolong lifespan. Both are rat studies, and neither is in people.

In groups of male Wistar rats (N=40 as stated), subcutaneous (-)BPAP three times weekly from the 10th week until death at 0.0001 or 0.05 mg/kg extended lifespan significantly over saline (P < 0.02), and 18-month-old rats on 0.0001 mg/kg were as good learners as 3-month-old saline rats. That study is from the group that developed the compound.

In aged, experienced male Long-Evans rats followed from 27 months to death, with half treated with BPAP, BPAP could not improve cognitive performance or prolong lifespan. The average lifespan of the population was 36 months, and the authors suggest a ceiling effect from dietary restriction and lifelong cognitive engagement. One author of that study is also on the founding papers, and the abstract gives no dose or route.

A 2017 paper from the developing group reports that 20 of 40 saline-treated rats developed a fibromyxosarcoma versus 8 of 40 at 0.0001 mg/kg BPAP (P < 0.001) and 7 of 40 at 0.05 mg/kg (P < 0.01), with no direct cytotoxicity of BPAP on human medulloblastoma cell lines.

Rat aging studies: longer lifespan in one study, none in a later study

Animal study

Ernyey AJ et al. Geroscience. 2024;46(1):417-429. PMID 37306892.

In groups of male Wistar rats (N=40 as stated), subcutaneous (-)BPAP three times weekly from the 10th week until death at 0.0001 or 0.05 mg/kg extended lifespan significantly over saline (P < 0.02), and 18-month-old rats on 0.0001 mg/kg were as good learners as 3-month-old saline rats (PMID 27777099, from the developing group). In aged, experienced male Long-Evans rats followed from 27 months to death, with half treated with BPAP, BPAP could not improve cognitive performance or prolong lifespan; the average lifespan of the population was 36 months, and the authors suggest a ceiling effect from dietary restriction and lifelong cognitive engagement. A 2017 paper from the developing group reports that 20 of 40 saline-treated rats developed a fibromyxosarcoma versus 8 of 40 at 0.0001 mg/kg BPAP (P < 0.001) and 7 of 40 at 0.05 mg/kg (P < 0.01), with no direct cytotoxicity of BPAP on human medulloblastoma cell lines (PMID 28623006).

Participants / model
Male Wistar rats; aged male Long-Evans rats; human medulloblastoma cell lines
Treatment
Subcutaneous injection three times weekly (Wistar); route and dose not stated for Long-Evans
Follow-up
From the 10th week until death (Wistar); from 27 months to death (Long-Evans)
Study design
Original preclinical studies
Funding
not stated in the source

One positive result from the developing group and one negative result in a later study. One author of the negative study is also on the founding papers. Rat data only.

Read the original source

Does BPAP work at extremely low doses?

As rat and isolated-tissue pharmacology, yes for monoamine release at 0.0001 to 0.0005 mg/kg subcutaneously, with a bell-shaped curve. Neuroprotection is shown only in cell culture, and nothing in the records reviewed shows any of it in people.

Sellers describe dopaminergic and noradrenergic enhancement and neuroprotection at extremely low doses. Enhancement of dopamine, noradrenaline and serotonin release is supported as rat and isolated-tissue pharmacology at 0.0001 to 0.0005 mg/kg subcutaneously, and as an uptake-inhibiting and release-modulating action at higher doses.

The low dose wording is dose-specific, because the dose-response is bell shaped and a dose 100 times higher gave no difference from control in one measure. Neuroprotection is supported only in cell culture, and the extremely low concentration applies to the beta-amyloid result and not to the astrocyte neurotrophin result. None of the 32 records reviewed tests it in a lesion model in a living animal.

No human data exist. A PubMed query on 10 October 2026 for benzofuran-containing records with propylaminopentane, propylpentane or BPAP returned 32 records dated 1999 to 2025, abstracts were read for all 32, and none reports (-)BPAP given to a person. Adding human, humans, patients, volunteers, clinical, trial or trials returned 15 of them, and the human terms matched human cell lines and transporter clones, a deprenyl-trial analysis in rats, and reviews. Two review abstracts from 2004 to 2006 express hope for a role in treatment-resistant depression, which is an opinion and not a result.

Founding paper from the developing group: release enhancement, beta-amyloid protection, shuttle box

Animal study

Knoll J et al. Br J Pharmacol. 1999;128(8):1723-32. PMID 10588928.

(-)BPAP was selected out of 65 newly synthesized compounds as a potential follower of (-)deprenyl. It enhanced impulse-propagation-mediated release of [3H]noradrenaline and [3H]dopamine at 0.18 micromol per liter and of [3H]serotonin at 36 nmol per liter from isolated rat brain stem. In isolated discrete rat brain regions (dopamine from striatum, substantia nigra and tuberculum olfactorium, noradrenaline from locus coeruleus, serotonin from raphe) release rose significantly at 10^-12 to 10^-14 M. It protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 M. In rats, catecholaminergic and serotoninergic neuron activity was significantly enhanced 30 minutes after an acute 0.1 microg/kg subcutaneous injection, and in the shuttle box (-)BPAP was about 130 times more potent than (-)deprenyl at antagonizing tetrabenazine-induced inhibition of performance.

Participants / model
Isolated rat brain stem and brain regions; cultured hippocampal neurons (species not stated in the abstract); rats
Treatment
(-)BPAP in tissue and cell preparations; 0.1 microg/kg by subcutaneous injection in rats
Follow-up
Neuron activity measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound.

Read the original source
Rats: 0.0005 mg/kg raised release, 0.05 mg/kg did not (bell-shaped)

Animal study

Knoll J et al. Life Sci. 2002;71(18):2137-44. PMID 12204771.

In rats, 0.0005 mg/kg subcutaneously raised the noradrenaline released from isolated locus coeruleus 30 minutes later from 4.7 +/- 0.10 to 15.4 +/- 0.55 nmol/g wet weight (P < 0.001), while a hundred times higher dose, 0.05 mg/kg, gave 4.3 +/- 0.25 nmol/g, no different from control. Ex vivo, locus coeruleus release was enhanced from 10^-16 M with a peak at 10^-13 M, 10^-10 M was ineffective, and a second effective range ran from 10^-8 M with a peak at 10^-6 M. Dopaminergic and serotoninergic neurons peaked at 10^-13 and 10^-12 M. The authors suggest the trace amine receptors as the site of action. Later abstracts from the same group name 0.0001 mg/kg as the specific enhancer dose and 0.05 mg/kg as the non-specific dose in rats.

Participants / model
Rats; isolated rat locus coeruleus, striatum and raphe tissue
Treatment
Subcutaneous injection, 0.0005 and 0.05 mg/kg; tissue baths
Follow-up
Release measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

The dose-response is bell shaped, so the extremely low dose claim is dose-specific.

Read the original source
Cell culture only: beta-amyloid protection, sigma receptors, astrocyte neurotrophins

Cell study

Yoneda F et al. Bioorg Med Chem. 2001;9(5):1197-212. PMID 11377178.

The racemate (+/-)BPAP protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 to 10^-15 M. In serum-free cortical neuron cultures (-)BPAP rescued cell death through sigma receptors, blocked by BD1063, with weak displacement of [3H]pentazocine binding (PMID 11100977; concentration not in the abstract). In cultured mouse astrocytes, (-)BPAP raised NGF, BDNF and GDNF secretion, up to 120, two and seven times control at 0.35 mM for 24 hours as the abstract states (PMID 12147307). A companion paper found minimum effective concentrations of 5 x 10^-5, 1 x 10^-5 and 1 x 10^-6 M for NGF, BDNF and GDNF, a bell-shaped curve peaking at 1 x 10^-4 M for NGF, and no effect at fM to pM concentrations (PMID 12679194), roughly ten orders of magnitude above the 10^-14 M neuroprotection figure. In rat mesencephalic slice cultures R-(-)-BPAP raised BDNF and trkB mRNA at 48 hours (PMID 16079507). A human neuroblastoma SH-SY5Y paper (PMID 15102525) reports anti-apoptotic effects of BPAP analogues, but its abstract says levorotatory compounds did not prevent the mitochondrial permeability transition.

Participants / model
Cultured hippocampal and cortical neurons; mouse astrocytes; rat mesencephalic slices; human SH-SY5Y cells
Treatment
Cell and slice culture, in vitro
Follow-up
24 hours and 48 hours in the neurotrophin studies; not stated for the others
Study design
Original preclinical studies
Funding
not stated in the source

The 0.35 mM figure in the astrocyte abstract looks inconsistent with the lower concentrations in its companion paper, and the discrepancy is unresolved. The SH-SY5Y paper is not used as evidence for (-)BPAP. None of the 32 records reviewed tests (-)BPAP in a lesion or injury model for neuroprotection in a living animal.

Read the original source
PubMed, 10 October 2026: 32 records from 1999 to 2025, none gives BPAP to a person

PubMed search record

PubMed search run 10 October 2026: benzofuran*[tiab] AND (propylaminopentane[tiab] OR propylpentan*[tiab] OR BPAP[tiab]), with a follow-up query adding human, humans, patients, volunteers, clinical, trial or trials.

The search returned 32 records dated 1999 to 2025, and abstracts were read for all 32. Adding human, humans, patients, volunteers, clinical, trial or trials returned 15 of them, all read, and none reports (-)BPAP given to a person: the human terms matched human cell lines and transporter clones, a deprenyl-trial analysis in rats, and reviews. Two 2004 to 2006 review abstracts express hope for a role in treatment-resistant depression, and a 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP as a research compound. No controlled human trial exists in the records reviewed.

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 or unindexed work exists. Whether any vendor product is the R-(-) enantiomer, the racemate or something else is unknown.

Read the original source

What is known about the safety of BPAP?

No human safety, pharmacokinetic or toxicology data exist for BPAP. In rats, radioactivity from labeled (-)BPAP was well absorbed after oral, intraperitoneal and subcutaneous dosing and eliminated mainly in urine, but no LD50, repeat-dose, genotoxicity or safety pharmacology study appears in the 32 records reviewed, and the identity of vendor material is not established.

No record reports BPAP given to a person, so no human adverse event, tolerability or interaction information exists.

After radiolabeled (-)BPAP-14C in rats, radioactivity was well absorbed after intraperitoneal, subcutaneous and oral treatment, peaked at 30 to 60 minutes, showed a second peak at 4 hours that the authors read as enterohepatic circulation, entered nine brain regions with a peak at 30 minutes after subcutaneous dosing, and was eliminated mainly in urine, with more than 90% recovered in excreta over 72 hours and a t1/2 beta of 5.5 to 5.8 hours. These figures are for total radioactivity and not parent compound, and they are rat data.

A 2020 mouse paper says BPAP has low toxicity while giving no toxicity figures in its abstract; it reports that in a lung adenocarcinoma xenograft model a low and a high dose both inhibited tumor growth, with the low dose activating MAPK and Akt/mTOR signaling and the high dose inhibiting it. A 2006 review abstract credits (-)BPAP with unusual safeness and tolerability and gives no data. No LD50, repeat-dose, genotoxicity or safety pharmacology study appears in the 32 records reviewed.

Product identity is a separate concern. Whether any vendor product is the R-(-) enantiomer, the racemate or something else is unknown, and the acronym is shared with bisphenol AP and with a breathing treatment.

Rat pharmacokinetics of radioactivity; no toxicology

Animal study

Magyar K et al. Eur J Drug Metab Pharmacokinet. 2002;27(3):157-61. PMID 12365195.

After radiolabeled (-)BPAP-14C, radioactivity was well absorbed after intraperitoneal, subcutaneous and oral treatment, peaked at 30 to 60 minutes, showed a second peak at 4 hours that the authors read as enterohepatic circulation, entered nine brain regions with a peak at 30 minutes after subcutaneous dosing, and was eliminated mainly in urine, with more than 90% recovered in excreta over 72 hours and a t1/2 beta of 5.5 to 5.8 hours. A 2020 mouse paper (PMID 30734151) says BPAP has low toxicity while giving no toxicity figures in its abstract; it reports that in a lung adenocarcinoma xenograft model both a low and a high dose inhibited tumor growth, with the low dose activating MAPK and Akt/mTOR signaling and the high dose inhibiting it. A 2006 review abstract (PMID 16023777) credits (-)BPAP with unusual safeness and tolerability and gives no data.

Participants / model
Rats; mice with lung adenocarcinoma xenografts
Treatment
Radiolabeled (-)BPAP-14C by intraperitoneal, subcutaneous and oral routes; dose not stated in the abstract
Follow-up
Radioactivity followed over 72 hours
Study design
Original preclinical studies; review abstract
Funding
not stated in the source

The figures are for total radioactivity, not parent compound, and they are rat data. No LD50, repeat-dose, genotoxicity or safety pharmacology study appears in the 32 records reviewed.

Read the original source
PubMed, 10 October 2026: 32 records from 1999 to 2025, none gives BPAP to a person

PubMed search record

PubMed search run 10 October 2026: benzofuran*[tiab] AND (propylaminopentane[tiab] OR propylpentan*[tiab] OR BPAP[tiab]), with a follow-up query adding human, humans, patients, volunteers, clinical, trial or trials.

The search returned 32 records dated 1999 to 2025, and abstracts were read for all 32. Adding human, humans, patients, volunteers, clinical, trial or trials returned 15 of them, all read, and none reports (-)BPAP given to a person: the human terms matched human cell lines and transporter clones, a deprenyl-trial analysis in rats, and reviews. Two 2004 to 2006 review abstracts express hope for a role in treatment-resistant depression, and a 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP as a research compound. No controlled human trial exists in the records reviewed.

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 or unindexed work exists. Whether any vendor product is the R-(-) enantiomer, the racemate or something else is unknown.

Read the original source
Locomotor activity at higher doses; uptake inhibition at nanomolar concentrations; TAAR1

Animal study

Shimazu S et al. Eur J Pharmacol. 2001;421(3):181-9. PMID 11516435.

A Japanese group reported that (-)BPAP potentiated locomotor activity in non-habituated rats dose-dependently at 0.3 to 10 mg/kg and reversed reserpine-induced hypolocomotion at 1 to 3 mg/kg, and that the D1 antagonist SCH 23390 attenuated both, which the authors read as dopaminergic mediation. A companion paper (PMID 12527038) gives the route as subcutaneous at 0.3 and 1 mg/kg in normal rats and reports an L-DOPA-sparing effect. In HEK 293 cells expressing human transporters, (-)BPAP inhibited [3H]dopamine, norepinephrine and serotonin uptake with IC50 values of 42 +/- 9, 52 +/- 19 and 640 +/- 120 nM. In rat brain synaptosomes it did not potentiate tyramine-induced norepinephrine release and inhibited it, which the authors say may block tyramine-induced hypertensive crisis (PMID 14659999). A 2022 rat striatal slice paper reports (-)BPAP potentiated vesicular dopamine release through TAAR1 and did not induce non-vesicular release; its conflict statement names support from Fujimoto Pharmaceutical Corporation, Osaka (PMID 35955676).

Participants / model
Rats; HEK 293 cells expressing human DAT, NET and SERT; rat brain synaptosomes and striatal slices
Treatment
Subcutaneous injection in rats; cell and tissue preparations
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

By arithmetic, 0.3 mg/kg is 3,000 times the 0.0001 mg/kg specific dose. The tyramine result is a synaptosome result and the authors' inference, not a human safety finding.

Read the original source
PubChem: BPAP racemate and R-(-) enantiomer identity, and the acronym collisions

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 9816303, (2R)-1-(1-benzofuran-2-yl)-N-propylpentan-2-amine; the racemate is CID 9859674.

The acronym does not resolve to this compound: PubChem returns CID 623849 for the name BPAP, which is bisphenol AP (C20H18O2, 290.4 g/mol, CAS 1571-75-1), a plastics chemical, and in medicine BPAP means bilevel positive airway pressure (a PubMed query on the acronym forms returned 397 records, the top-ranked ones on sleep apnea and ventilation). The studied molecule is benzofuranylpropylaminopentane, 1-(1-benzofuran-2-yl)-N-propylpentan-2-amine. The racemate is CID 9859674, C16H23NO, 245.36 g/mol, with no CAS number among its listed synonyms. The R-(-) enantiomer is CID 9816303, CAS 260550-89-8, with the synonyms R-(-)-BPAP and FPFS-1169 free base. Most work used the R-(-) enantiomer as the hydrochloride, written (-)BPAP, and a 2001 paper reports its beta-amyloid result for the racemate, written (+/-)BPAP. One 2004 abstract uses the codes R-FPFS-1169 and R-FPFS-1180 for compounds compared with their S-enantiomers.

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

Identity record only. A vial labeled BPAP cannot be tied to either CID by the name alone, and no public record ties any vendor material to the studied compound. What the FPFS code denotes in the 2004 abstract is not settled.

Read the original source

Why does BPAP sit in C tier?

BPAP has detailed, internally coherent rat pharmacology and no failed human trial or documented harm in the records reviewed, but the data come from one research tradition, include one negative aging study and cell-only neuroprotection, and contain no human, human pharmacokinetic or toxicology data.

The rat pharmacology is detailed and internally coherent: release of dopamine, noradrenaline and serotonin from isolated brain tissue at picomolar to femtomolar concentrations, oral absorption in rats, and no harm or failed human trial in the records reviewed.

The data are thin in the C sense. They come from one research tradition, with the developing group on most papers and a pharmaceutical company named as supporting one study. The dose-response is bell shaped, so dose matters, a later aging study in aged rats was negative, neuroprotection is shown in cell culture only, and there is no human exposure, human pharmacokinetic or toxicology study.

Founding paper from the developing group: release enhancement, beta-amyloid protection, shuttle box

Animal study

Knoll J et al. Br J Pharmacol. 1999;128(8):1723-32. PMID 10588928.

(-)BPAP was selected out of 65 newly synthesized compounds as a potential follower of (-)deprenyl. It enhanced impulse-propagation-mediated release of [3H]noradrenaline and [3H]dopamine at 0.18 micromol per liter and of [3H]serotonin at 36 nmol per liter from isolated rat brain stem. In isolated discrete rat brain regions (dopamine from striatum, substantia nigra and tuberculum olfactorium, noradrenaline from locus coeruleus, serotonin from raphe) release rose significantly at 10^-12 to 10^-14 M. It protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 M. In rats, catecholaminergic and serotoninergic neuron activity was significantly enhanced 30 minutes after an acute 0.1 microg/kg subcutaneous injection, and in the shuttle box (-)BPAP was about 130 times more potent than (-)deprenyl at antagonizing tetrabenazine-induced inhibition of performance.

Participants / model
Isolated rat brain stem and brain regions; cultured hippocampal neurons (species not stated in the abstract); rats
Treatment
(-)BPAP in tissue and cell preparations; 0.1 microg/kg by subcutaneous injection in rats
Follow-up
Neuron activity measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound.

Read the original source
Rats: 0.0005 mg/kg raised release, 0.05 mg/kg did not (bell-shaped)

Animal study

Knoll J et al. Life Sci. 2002;71(18):2137-44. PMID 12204771.

In rats, 0.0005 mg/kg subcutaneously raised the noradrenaline released from isolated locus coeruleus 30 minutes later from 4.7 +/- 0.10 to 15.4 +/- 0.55 nmol/g wet weight (P < 0.001), while a hundred times higher dose, 0.05 mg/kg, gave 4.3 +/- 0.25 nmol/g, no different from control. Ex vivo, locus coeruleus release was enhanced from 10^-16 M with a peak at 10^-13 M, 10^-10 M was ineffective, and a second effective range ran from 10^-8 M with a peak at 10^-6 M. Dopaminergic and serotoninergic neurons peaked at 10^-13 and 10^-12 M. The authors suggest the trace amine receptors as the site of action. Later abstracts from the same group name 0.0001 mg/kg as the specific enhancer dose and 0.05 mg/kg as the non-specific dose in rats.

Participants / model
Rats; isolated rat locus coeruleus, striatum and raphe tissue
Treatment
Subcutaneous injection, 0.0005 and 0.05 mg/kg; tissue baths
Follow-up
Release measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

The dose-response is bell shaped, so the extremely low dose claim is dose-specific.

Read the original source
Rat aging studies: longer lifespan in one study, none in a later study

Animal study

Ernyey AJ et al. Geroscience. 2024;46(1):417-429. PMID 37306892.

In groups of male Wistar rats (N=40 as stated), subcutaneous (-)BPAP three times weekly from the 10th week until death at 0.0001 or 0.05 mg/kg extended lifespan significantly over saline (P < 0.02), and 18-month-old rats on 0.0001 mg/kg were as good learners as 3-month-old saline rats (PMID 27777099, from the developing group). In aged, experienced male Long-Evans rats followed from 27 months to death, with half treated with BPAP, BPAP could not improve cognitive performance or prolong lifespan; the average lifespan of the population was 36 months, and the authors suggest a ceiling effect from dietary restriction and lifelong cognitive engagement. A 2017 paper from the developing group reports that 20 of 40 saline-treated rats developed a fibromyxosarcoma versus 8 of 40 at 0.0001 mg/kg BPAP (P < 0.001) and 7 of 40 at 0.05 mg/kg (P < 0.01), with no direct cytotoxicity of BPAP on human medulloblastoma cell lines (PMID 28623006).

Participants / model
Male Wistar rats; aged male Long-Evans rats; human medulloblastoma cell lines
Treatment
Subcutaneous injection three times weekly (Wistar); route and dose not stated for Long-Evans
Follow-up
From the 10th week until death (Wistar); from 27 months to death (Long-Evans)
Study design
Original preclinical studies
Funding
not stated in the source

One positive result from the developing group and one negative result in a later study. One author of the negative study is also on the founding papers. Rat data only.

Read the original source
PubMed, 10 October 2026: 32 records from 1999 to 2025, none gives BPAP to a person

PubMed search record

PubMed search run 10 October 2026: benzofuran*[tiab] AND (propylaminopentane[tiab] OR propylpentan*[tiab] OR BPAP[tiab]), with a follow-up query adding human, humans, patients, volunteers, clinical, trial or trials.

The search returned 32 records dated 1999 to 2025, and abstracts were read for all 32. Adding human, humans, patients, volunteers, clinical, trial or trials returned 15 of them, all read, and none reports (-)BPAP given to a person: the human terms matched human cell lines and transporter clones, a deprenyl-trial analysis in rats, and reviews. Two 2004 to 2006 review abstracts express hope for a role in treatment-resistant depression, and a 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP as a research compound. No controlled human trial exists in the records reviewed.

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 or unindexed work exists. Whether any vendor product is the R-(-) enantiomer, the racemate or something else is unknown.

Read the original source
Rat pharmacokinetics of radioactivity; no toxicology

Animal study

Magyar K et al. Eur J Drug Metab Pharmacokinet. 2002;27(3):157-61. PMID 12365195.

After radiolabeled (-)BPAP-14C, radioactivity was well absorbed after intraperitoneal, subcutaneous and oral treatment, peaked at 30 to 60 minutes, showed a second peak at 4 hours that the authors read as enterohepatic circulation, entered nine brain regions with a peak at 30 minutes after subcutaneous dosing, and was eliminated mainly in urine, with more than 90% recovered in excreta over 72 hours and a t1/2 beta of 5.5 to 5.8 hours. A 2020 mouse paper (PMID 30734151) says BPAP has low toxicity while giving no toxicity figures in its abstract; it reports that in a lung adenocarcinoma xenograft model both a low and a high dose inhibited tumor growth, with the low dose activating MAPK and Akt/mTOR signaling and the high dose inhibiting it. A 2006 review abstract (PMID 16023777) credits (-)BPAP with unusual safeness and tolerability and gives no data.

Participants / model
Rats; mice with lung adenocarcinoma xenografts
Treatment
Radiolabeled (-)BPAP-14C by intraperitoneal, subcutaneous and oral routes; dose not stated in the abstract
Follow-up
Radioactivity followed over 72 hours
Study design
Original preclinical studies; review abstract
Funding
not stated in the source

The figures are for total radioactivity, not parent compound, and they are rat data. No LD50, repeat-dose, genotoxicity or safety pharmacology study appears in the 32 records reviewed.

Read the original source

Studies and sources

PubChem: BPAP racemate and R-(-) enantiomer identity, and the acronym collisions

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 9816303, (2R)-1-(1-benzofuran-2-yl)-N-propylpentan-2-amine; the racemate is CID 9859674.

The acronym does not resolve to this compound: PubChem returns CID 623849 for the name BPAP, which is bisphenol AP (C20H18O2, 290.4 g/mol, CAS 1571-75-1), a plastics chemical, and in medicine BPAP means bilevel positive airway pressure (a PubMed query on the acronym forms returned 397 records, the top-ranked ones on sleep apnea and ventilation). The studied molecule is benzofuranylpropylaminopentane, 1-(1-benzofuran-2-yl)-N-propylpentan-2-amine. The racemate is CID 9859674, C16H23NO, 245.36 g/mol, with no CAS number among its listed synonyms. The R-(-) enantiomer is CID 9816303, CAS 260550-89-8, with the synonyms R-(-)-BPAP and FPFS-1169 free base. Most work used the R-(-) enantiomer as the hydrochloride, written (-)BPAP, and a 2001 paper reports its beta-amyloid result for the racemate, written (+/-)BPAP. One 2004 abstract uses the codes R-FPFS-1169 and R-FPFS-1180 for compounds compared with their S-enantiomers.

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

Identity record only. A vial labeled BPAP cannot be tied to either CID by the name alone, and no public record ties any vendor material to the studied compound. What the FPFS code denotes in the 2004 abstract is not settled.

Read the original source
Founding paper from the developing group: release enhancement, beta-amyloid protection, shuttle box

Animal study

Knoll J et al. Br J Pharmacol. 1999;128(8):1723-32. PMID 10588928.

(-)BPAP was selected out of 65 newly synthesized compounds as a potential follower of (-)deprenyl. It enhanced impulse-propagation-mediated release of [3H]noradrenaline and [3H]dopamine at 0.18 micromol per liter and of [3H]serotonin at 36 nmol per liter from isolated rat brain stem. In isolated discrete rat brain regions (dopamine from striatum, substantia nigra and tuberculum olfactorium, noradrenaline from locus coeruleus, serotonin from raphe) release rose significantly at 10^-12 to 10^-14 M. It protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 M. In rats, catecholaminergic and serotoninergic neuron activity was significantly enhanced 30 minutes after an acute 0.1 microg/kg subcutaneous injection, and in the shuttle box (-)BPAP was about 130 times more potent than (-)deprenyl at antagonizing tetrabenazine-induced inhibition of performance.

Participants / model
Isolated rat brain stem and brain regions; cultured hippocampal neurons (species not stated in the abstract); rats
Treatment
(-)BPAP in tissue and cell preparations; 0.1 microg/kg by subcutaneous injection in rats
Follow-up
Neuron activity measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

From the group that developed the compound.

Read the original source
Rats: 0.0005 mg/kg raised release, 0.05 mg/kg did not (bell-shaped)

Animal study

Knoll J et al. Life Sci. 2002;71(18):2137-44. PMID 12204771.

In rats, 0.0005 mg/kg subcutaneously raised the noradrenaline released from isolated locus coeruleus 30 minutes later from 4.7 +/- 0.10 to 15.4 +/- 0.55 nmol/g wet weight (P < 0.001), while a hundred times higher dose, 0.05 mg/kg, gave 4.3 +/- 0.25 nmol/g, no different from control. Ex vivo, locus coeruleus release was enhanced from 10^-16 M with a peak at 10^-13 M, 10^-10 M was ineffective, and a second effective range ran from 10^-8 M with a peak at 10^-6 M. Dopaminergic and serotoninergic neurons peaked at 10^-13 and 10^-12 M. The authors suggest the trace amine receptors as the site of action. Later abstracts from the same group name 0.0001 mg/kg as the specific enhancer dose and 0.05 mg/kg as the non-specific dose in rats.

Participants / model
Rats; isolated rat locus coeruleus, striatum and raphe tissue
Treatment
Subcutaneous injection, 0.0005 and 0.05 mg/kg; tissue baths
Follow-up
Release measured 30 minutes after injection
Study design
Original preclinical study
Funding
not stated in the source

The dose-response is bell shaped, so the extremely low dose claim is dose-specific.

Read the original source
Locomotor activity at higher doses; uptake inhibition at nanomolar concentrations; TAAR1

Animal study

Shimazu S et al. Eur J Pharmacol. 2001;421(3):181-9. PMID 11516435.

A Japanese group reported that (-)BPAP potentiated locomotor activity in non-habituated rats dose-dependently at 0.3 to 10 mg/kg and reversed reserpine-induced hypolocomotion at 1 to 3 mg/kg, and that the D1 antagonist SCH 23390 attenuated both, which the authors read as dopaminergic mediation. A companion paper (PMID 12527038) gives the route as subcutaneous at 0.3 and 1 mg/kg in normal rats and reports an L-DOPA-sparing effect. In HEK 293 cells expressing human transporters, (-)BPAP inhibited [3H]dopamine, norepinephrine and serotonin uptake with IC50 values of 42 +/- 9, 52 +/- 19 and 640 +/- 120 nM. In rat brain synaptosomes it did not potentiate tyramine-induced norepinephrine release and inhibited it, which the authors say may block tyramine-induced hypertensive crisis (PMID 14659999). A 2022 rat striatal slice paper reports (-)BPAP potentiated vesicular dopamine release through TAAR1 and did not induce non-vesicular release; its conflict statement names support from Fujimoto Pharmaceutical Corporation, Osaka (PMID 35955676).

Participants / model
Rats; HEK 293 cells expressing human DAT, NET and SERT; rat brain synaptosomes and striatal slices
Treatment
Subcutaneous injection in rats; cell and tissue preparations
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

By arithmetic, 0.3 mg/kg is 3,000 times the 0.0001 mg/kg specific dose. The tyramine result is a synaptosome result and the authors' inference, not a human safety finding.

Read the original source
Other animal behavior: forced swim, social interaction, methamphetamine reinstatement

Animal study

Hiranita T et al. Neuroscience. 2010;165(2):300-12. PMID 19883738.

In mice, acute but not chronic (-)BPAP shortened forced-swim immobility, and chronic but not acute treatment ameliorated impaired social interaction after forced swimming, an effect suppressed by dopamine receptor antagonists. In olfactory bulbectomized rats, chronic treatment improved social interaction, prepulse inhibition and tone-cue fear learning without changing locomotion (PMID 18243357). In rats trained to self-administer methamphetamine, repeated (-)BPAP during extinction and acute doses on test day attenuated cue-induced and priming-induced reinstatement without reinstating seeking or changing self-administration, and dopamine antagonists did not change the effect, so the abstract does not show dopamine receptor mediation. In rats treated for 3 weeks at the specific doses (0.0001 mg/kg BPAP), phosphorylated GluR1 and GluN2B rose, dark-phase corticosterone fell and anxiety-like behavior did not change significantly (PMID 31610214).

Participants / model
Mice; olfactory bulbectomized rats; rats self-administering methamphetamine; rats
Treatment
(-)BPAP; route not stated in most abstracts; dose not stated in the reinstatement abstract
Follow-up
Chronic and acute schedules; 3 weeks in the glutamate receptor study
Study design
Original preclinical studies
Funding
not stated in the source

The reinstatement work is a relapse model, not a test of dopamine downregulation.

Read the original source
Cell culture only: beta-amyloid protection, sigma receptors, astrocyte neurotrophins

Cell study

Yoneda F et al. Bioorg Med Chem. 2001;9(5):1197-212. PMID 11377178.

The racemate (+/-)BPAP protected cultured hippocampal neurons from beta-amyloid toxicity at 10^-14 to 10^-15 M. In serum-free cortical neuron cultures (-)BPAP rescued cell death through sigma receptors, blocked by BD1063, with weak displacement of [3H]pentazocine binding (PMID 11100977; concentration not in the abstract). In cultured mouse astrocytes, (-)BPAP raised NGF, BDNF and GDNF secretion, up to 120, two and seven times control at 0.35 mM for 24 hours as the abstract states (PMID 12147307). A companion paper found minimum effective concentrations of 5 x 10^-5, 1 x 10^-5 and 1 x 10^-6 M for NGF, BDNF and GDNF, a bell-shaped curve peaking at 1 x 10^-4 M for NGF, and no effect at fM to pM concentrations (PMID 12679194), roughly ten orders of magnitude above the 10^-14 M neuroprotection figure. In rat mesencephalic slice cultures R-(-)-BPAP raised BDNF and trkB mRNA at 48 hours (PMID 16079507). A human neuroblastoma SH-SY5Y paper (PMID 15102525) reports anti-apoptotic effects of BPAP analogues, but its abstract says levorotatory compounds did not prevent the mitochondrial permeability transition.

Participants / model
Cultured hippocampal and cortical neurons; mouse astrocytes; rat mesencephalic slices; human SH-SY5Y cells
Treatment
Cell and slice culture, in vitro
Follow-up
24 hours and 48 hours in the neurotrophin studies; not stated for the others
Study design
Original preclinical studies
Funding
not stated in the source

The 0.35 mM figure in the astrocyte abstract looks inconsistent with the lower concentrations in its companion paper, and the discrepancy is unresolved. The SH-SY5Y paper is not used as evidence for (-)BPAP. None of the 32 records reviewed tests (-)BPAP in a lesion or injury model for neuroprotection in a living animal.

Read the original source
Rat aging studies: longer lifespan in one study, none in a later study

Animal study

Ernyey AJ et al. Geroscience. 2024;46(1):417-429. PMID 37306892.

In groups of male Wistar rats (N=40 as stated), subcutaneous (-)BPAP three times weekly from the 10th week until death at 0.0001 or 0.05 mg/kg extended lifespan significantly over saline (P < 0.02), and 18-month-old rats on 0.0001 mg/kg were as good learners as 3-month-old saline rats (PMID 27777099, from the developing group). In aged, experienced male Long-Evans rats followed from 27 months to death, with half treated with BPAP, BPAP could not improve cognitive performance or prolong lifespan; the average lifespan of the population was 36 months, and the authors suggest a ceiling effect from dietary restriction and lifelong cognitive engagement. A 2017 paper from the developing group reports that 20 of 40 saline-treated rats developed a fibromyxosarcoma versus 8 of 40 at 0.0001 mg/kg BPAP (P < 0.001) and 7 of 40 at 0.05 mg/kg (P < 0.01), with no direct cytotoxicity of BPAP on human medulloblastoma cell lines (PMID 28623006).

Participants / model
Male Wistar rats; aged male Long-Evans rats; human medulloblastoma cell lines
Treatment
Subcutaneous injection three times weekly (Wistar); route and dose not stated for Long-Evans
Follow-up
From the 10th week until death (Wistar); from 27 months to death (Long-Evans)
Study design
Original preclinical studies
Funding
not stated in the source

One positive result from the developing group and one negative result in a later study. One author of the negative study is also on the founding papers. Rat data only.

Read the original source
Rat pharmacokinetics of radioactivity; no toxicology

Animal study

Magyar K et al. Eur J Drug Metab Pharmacokinet. 2002;27(3):157-61. PMID 12365195.

After radiolabeled (-)BPAP-14C, radioactivity was well absorbed after intraperitoneal, subcutaneous and oral treatment, peaked at 30 to 60 minutes, showed a second peak at 4 hours that the authors read as enterohepatic circulation, entered nine brain regions with a peak at 30 minutes after subcutaneous dosing, and was eliminated mainly in urine, with more than 90% recovered in excreta over 72 hours and a t1/2 beta of 5.5 to 5.8 hours. A 2020 mouse paper (PMID 30734151) says BPAP has low toxicity while giving no toxicity figures in its abstract; it reports that in a lung adenocarcinoma xenograft model both a low and a high dose inhibited tumor growth, with the low dose activating MAPK and Akt/mTOR signaling and the high dose inhibiting it. A 2006 review abstract (PMID 16023777) credits (-)BPAP with unusual safeness and tolerability and gives no data.

Participants / model
Rats; mice with lung adenocarcinoma xenografts
Treatment
Radiolabeled (-)BPAP-14C by intraperitoneal, subcutaneous and oral routes; dose not stated in the abstract
Follow-up
Radioactivity followed over 72 hours
Study design
Original preclinical studies; review abstract
Funding
not stated in the source

The figures are for total radioactivity, not parent compound, and they are rat data. No LD50, repeat-dose, genotoxicity or safety pharmacology study appears in the 32 records reviewed.

Read the original source
PubMed, 10 October 2026: 32 records from 1999 to 2025, none gives BPAP to a person

PubMed search record

PubMed search run 10 October 2026: benzofuran*[tiab] AND (propylaminopentane[tiab] OR propylpentan*[tiab] OR BPAP[tiab]), with a follow-up query adding human, humans, patients, volunteers, clinical, trial or trials.

The search returned 32 records dated 1999 to 2025, and abstracts were read for all 32. Adding human, humans, patients, volunteers, clinical, trial or trials returned 15 of them, all read, and none reports (-)BPAP given to a person: the human terms matched human cell lines and transporter clones, a deprenyl-trial analysis in rats, and reviews. Two 2004 to 2006 review abstracts express hope for a role in treatment-resistant depression, and a 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP as a research compound. No controlled human trial exists in the records reviewed.

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 or unindexed work exists. Whether any vendor product is the R-(-) enantiomer, the racemate or something else is unknown.

Read the original source
Label and registry searches, 10 October 2026: no label, no match, no study

Regulatory record

U.S. Food and Drug Administration (DailyMed label search; openFDA Drugs@FDA query) and ClinicalTrials.gov. Searches for benzofuranylpropylaminopentane, BPAP, propylaminopentane and catecholaminergic activity enhancer, run 10 October 2026.

DailyMed returned no label for benzofuranylpropylaminopentane or for BPAP, the openFDA Drugs@FDA query returned no match, and ClinicalTrials.gov queries for propylaminopentane, benzofuranylpropylaminopentane and catecholaminergic activity enhancer returned no studies. The query for the acronym forms returned 10 records, all noninvasive ventilation, asthma, sleep apnea or unrelated studies. A 2016 review says presently deprenyl is the only available drug of this enhancer type, which places BPAP 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
Funding
not stated in the source

An absence finding as of 10 October 2026. It covers United States label, application and registry records only.

Read the original source

Why is BPAP (benzofuranylpropylaminopentane) in C tier?

C fits a research compound with detailed, internally coherent rat pharmacology, oral absorption in rats and no failed human trial or documented harm in the records reviewed. The data are thin: one research tradition, a bell-shaped dose-response, one negative aging study, neuroprotection in cell culture only, and no human, human pharmacokinetic or toxicology data.