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| Targets |
FPFS-1169 enhances the activity of the monoamine neurotransmitters noradrenalin, dopamine and serotonin in certain brain areas and it can generally be considered to produce stimulant effects. It is part of the group of monoaminergic activity enhancers (MAE), which increase the amount of monoamines secreted into the synaptic cleft, but do not lead to a continuous release without proper stimulation by a neuron as is the case with most amphetamines.
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| ln Vitro |
- Upregulation of Neurotrophin and Receptor Expression in Mesencephalic Slices:
- Reference [1]: In rat embryonic mesencephalic slice cultures (embryonic day 14), treatment with R-(-)-BPAP (FPFS-1169) at concentrations of 10 nM and 1 μM for 48 hours significantly upregulated the expression of neurotrophins and their receptors. Specifically: 1) Brain-derived neurotrophic factor (BDNF) mRNA levels (detected via RT-PCR) increased by 1.8-fold (10 nM) and 2.5-fold (1 μM) compared to the vehicle control; 2) Neurotrophin-3 (NT-3) mRNA levels increased by 1.6-fold (10 nM) and 2.1-fold (1 μM); 3) Protein expression of TrkB (BDNF receptor) and TrkC (NT-3 receptor) (detected via immunohistochemistry) was enhanced by 1.5-fold (10 nM) and 2.0-fold (1 μM) in dopaminergic neurons (identified by tyrosine hydroxylase staining). No significant changes were observed in nerve growth factor (NGF) or TrkA (NGF receptor) expression [1]
- Neuroprotective Effect Against Dopaminergic Neurotoxin-Induced Apoptosis: - Reference [2]: In human dopaminergic neuroblastoma SH-SY5Y cells, R-(-)-BPAP (FPFS-1169) (1–10 μM) exhibited dose-dependent neuroprotection against apoptosis induced by N-methyl(R)salsolinol (NM(R)S, 100 μM, an endogenous dopaminergic neurotoxin). Key results included: 1) Cell viability (assessed via MTT assay) was reduced to 45% by NM(R)S alone, but increased to 65% (1 μM R-(-)-BPAP), 78% (5 μM), and 85% (10 μM) with co-treatment; 2) Caspase-3 activity (a marker of apoptosis, detected via colorimetric assay) was elevated 3.2-fold by NM(R)S, but reduced to 2.1-fold (1 μM), 1.6-fold (5 μM), and 1.2-fold (10 μM) with R-(-)-BPAP; 3) The percentage of apoptotic cells (detected via Annexin V-FITC/PI double staining and flow cytometry) decreased from 42% (NM(R)S alone) to 28% (1 μM), 18% (5 μM), and 12% (10 μM) with R-(-)-BPAP co-treatment [2] |
| ln Vivo |
In ex vivo experiments, when an isolated brain region was soaked in an organ bath containing BPAP, the release of noradrenaline was significantly enhanced at 10−16 M BPAP, reached a peak effect at 10−13 M, but 10−10 M BPAP was ineffective. A significant enhancer effect was detected also in the high concentration range from 10−8 M, the peak effect was reached at 10−6 M concentration and 10−5 M BPAP was ineffective. BPAP enhanced in the low concentration range the performance of dopaminergic and serotoninergic neurons with a peak effect at 10−13 and 10−12 M concentration, respectively. The results suggest that high and low affinity ‘enhancer’ receptors may exist in the brain. BPAP also inhibited the noradrenaline release usually induced by the compound tyramine. Thus, BPAP may block tyramine-induced adverse effects such as hypertensive crisis. It was also found in the same study that BPAP is not only catecholaminergic and serotonergic activity enhancer, but also a norepinephrine and dopamine reuptake inhibitor (NDRI) and a weak serotonin reuptake inhibitor (SRI). Expermientally, these properties lead to an increased movement urge in rats when administered with 1-3 mg/kg of BPAP. This dose was also able to counter the movement depressing properties of the drug reserpine. Furthermore, although antiparkinsonian agents, such as apomorphine and amantadine, failed to improve reserpineinduced ptosis, BPAP HCl significantly improved ptosis.[3]
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| Cell Assay |
- Mesencephalic Slice Culture and Neurotrophin Detection:
- Reference [1]: Rat embryos (embryonic day 14) were dissected to isolate mesencephalic tissues, which were cut into 300-μm-thick slices using a vibratome. Slices were cultured in serum-free medium at 37°C in a 5% CO₂ incubator for 24 hours to stabilize. Then, R-(-)-BPAP (FPFS-1169) was added to the medium at final concentrations of 10 nM and 1 μM, with vehicle (medium containing 0.1% DMSO) as the control. After 48 hours of incubation, slices were collected for: 1) RT-PCR: Total RNA was extracted, reverse-transcribed to cDNA, and amplified using primers for BDNF, NT-3, NGF, TrkB, TrkC, and TrkA; GAPDH was used as an internal control. 2) Immunohistochemistry: Slices were fixed with 4% paraformaldehyde, permeabilized, and incubated with primary antibodies against TrkB, TrkC, and tyrosine hydroxylase (TH, a dopaminergic neuron marker), followed by fluorescent secondary antibodies. Fluorescence intensity was quantified using image analysis software [1]
- SH-SY5Y Cell Apoptosis Assay: - Reference [2]: SH-SY5Y cells were seeded in 96-well plates (for MTT assay) or 6-well plates (for caspase-3 and Annexin V assays) at a density of 5×10³ cells/well (96-well) or 2×10⁵ cells/well (6-well) and cultured in DMEM/F12 medium containing 10% fetal bovine serum at 37°C in a 5% CO₂ incubator for 24 hours. Cells were pre-treated with R-(-)-BPAP (FPFS-1169) (1, 5, 10 μM) for 1 hour, then co-treated with NM(R)S (100 μM) for 24 hours. Vehicle (medium containing 0.1% DMSO) and NM(R)S alone groups were included as controls. After treatment: 1) MTT assay: MTT solution was added to 96-well plates, incubated for 4 hours, formazan crystals were dissolved, and absorbance was measured at 570 nm. 2) Caspase-3 assay: Cells were lysed, caspase-3 substrate was added to the lysate, and absorbance was measured at 405 nm to quantify enzyme activity. 3) Annexin V assay: Cells were harvested, stained with Annexin V-FITC and PI, and analyzed via flow cytometry to count apoptotic cells [2] |
| ADME/Pharmacokinetics |
In rats, BPAP is mainly excreted in urine, with a small amount also excreted in feces. Its biological half-life is about 5.6 hours, so almost all BPAP is excreted within 3 days after administration. Conclusion: BPAP is structurally closely related to currently used drugs, especially the monoamine oxidase inhibitor selegiline. However, BPAP has a variety of additional pharmacological effects on the neurotransmitter system. It affects neurotransmitters such as norepinephrine, dopamine and serotonin, and usually leads to enhanced activity of related neurons. Through this mechanism, BPAP may be used in the study of depression and Parkinson's disease. In addition, studies have shown that BPAP can improve neuronal survival, and one study even confirmed that it can prolong the life of rats. Although there is a lot of interesting preclinical data, there are currently no reports of clinical trials of BPAP. Therefore, its metabolic characteristics have not been studied. [3]
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| Toxicity/Toxicokinetics |
Data on in vitro/in vivo toxicity (e.g., LD50, hepatotoxicity/nephrotoxicity), drug interactions, or plasma protein binding of BPAP (FPFS-1169) were not reported in references [1] and [2]. In cell/section experiments, concentrations of up to 1 μM (section culture) and 10 μM (SH-SY5Y cells) of R-(-)-BPAP did not cause significant cytotoxicity (e.g., no decrease in cell viability was observed in the untreated group), but no formal toxicity assessment was performed [1][2].
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| References |
[1]. Effects of R-(-)-BPAP on the expressions of neurotrophins and their receptors in mesencephalic slices. Biol Pharm Bull. 2005 Aug;28(8):1524-6.
[2]. Neuroprotective function of R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane, [R-(-)-BPAP], against apoptosis induced by N-methyl(R)salsolinol, an endogenous dopaminergic neurotoxin, in human dopaminergic neuroblastoma SH-SY5Y cells. Life Sci. 2004 May 21;75(1):107-17. [3]. https://umbrellalabs.is/wp-content/uploads/2024/11/ULB-Article-03_2025-01-Benzofuranylpropylaminopentane-WM.pdf |
| Additional Infomation |
Chemical and Pharmacological Background: - Reference [2]: BPAP (FPFS-1169) is a synthetic benzofuran derivative whose R-(-)-enantiomer (R-(-)-BPAP) is the pharmacologically active form. It is classified as a potential neuroprotective agent, particularly for dopaminergic neurons—degenerative cells in Parkinson's disease (PD). Its neuroprotective effect is thought to be related to the inhibition of apoptosis pathways and the regulation of neurotrophic factor signaling, but the exact molecular mechanism (e.g., direct target binding) remains unclear [2]
- Relevance to Neurodegenerative Diseases: - Reference [1][2]: R-(-)-BPAP (FPFS-1169) upregulates BDNF/TrkB and NT-3/TrkC (reference [1]) and its protective effect against NM(R)S-induced dopaminergic cell death (reference [2]) suggests its potential to treat neurodegenerative diseases associated with dopaminergic dysfunction, such as Parkinson's disease. NM(R)S is an endogenous neurotoxin that accumulates in the brains of Parkinson's disease patients; therefore, the observed protective effect is closely related to the pathogenesis of Parkinson's disease. |
| Molecular Formula |
C16H24CLNO
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| Molecular Weight |
281.820863723755
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| Exact Mass |
281.154
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| Elemental Analysis |
C, 68.19; H, 8.58; Cl, 12.58; N, 4.97; O, 5.68
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| CAS # |
265130-22-1
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| Related CAS # |
260550-89-8;265130-22-1 (HCl);
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| PubChem CID |
11984587
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| Appearance |
Typically exists as solid at room temperature
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
2
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
19
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| Complexity |
231
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| Defined Atom Stereocenter Count |
1
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| SMILES |
CCC[C@H](CC1=CC2=CC=CC=C2O1)NCCC.Cl
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| InChi Key |
GKKNDWKXWAVGOK-PFEQFJNWSA-N
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| InChi Code |
InChI=1S/C16H23NO.ClH/c1-3-7-14(17-10-4-2)12-15-11-13-8-5-6-9-16(13)18-15;/h5-6,8-9,11,14,17H,3-4,7,10,12H2,1-2H3;1H/t14-;/m1./s1
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| Chemical Name |
(2R)-1-(1-benzofuran-2-yl)-N-propylpentan-2-amine;hydrochloride
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| Synonyms |
FPFS 1169; FPFS-1169 HCl; 265130-22-1; (–)-Benzofuranylpropylaminopentane; BPAP; 327MBZ3R13; (R)-(-)-Fpfs-1169; UNII-327MBZ3R13; FPFS-1169; 2-Benzofuranethanamine, N,alpha-dipropyl-, hydrochloride, (alphaR)-; 2-BENZOFURANETHANAMINE, N,.ALPHA.-DIPROPYL-, HYDROCHLORIDE, (.ALPHA.R)-; RefChem:201003; FPFS-1169 hydrochloride
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.5484 mL | 17.7418 mL | 35.4836 mL | |
| 5 mM | 0.7097 mL | 3.5484 mL | 7.0967 mL | |
| 10 mM | 0.3548 mL | 1.7742 mL | 3.5484 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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