^abcKnoll J (2005). "Enhancer Regulation: A Neurochemical Approach to the Innate and Acquired Drives".The Brain and Its Self: A Neurochemical Concept of the Innate and Acquired Drives. Berlin/Heidelberg: Springer-Verlag. pp. 25–94.doi:10.1007/3-540-27434-0_4.ISBN978-3-540-23969-7.Fig. 3.10. The chemical structure and pharmacological spectrum of tryptamine and two of its most representative synthetic derivatives. Taken from Knoll (2001). [Fig. 3.10.: IPAP has the enhancer effect, has no releasing effect, and is a weak MAO-A inhibitor similarly to BPAP.]
^abcdefghiYoneda F, Moto T, Sakae M, Ohde H, Knoll B, Miklya I, et al. (May 2001). "Structure-activity studies leading to (-)1-(benzofuran-2-yl)-2-propylaminopentane, ((-)BPAP), a highly potent, selective enhancer of the impulse propagation mediated release of catecholamines and serotonin in the brain".Bioorg Med Chem.9 (5):1197–1212.doi:10.1016/s0968-0896(01)00002-5.PMID11377178.Group 4. Indolyl, benzothienyl and benzofuryl derivatives of PPAP (Table 4). The indol-3-yl analogue of PPAP (IPAP, 7a) and its (—) and (+)enantiomers ((—)IPAP and (+ )IPAP) (see Table 5) were used as reference substances for the indol analogues of PPAP. (—)IPAP was about 5 times more potent than PPAP in the shuttle box experiment. [...] IPAP was less potent than PPAP. [...] (-)BPAP, the most potent member of the group, was about 100 times more potent than PPAP in the shuttle box experiment. [...] The two most effective substances, (—)IPAP and (—)BPAP enhanced the release of dopamine from the striatum, substantia nigra and tuberculum olfactorium, noradrenaline from the locus coeruleus and serotonin from the raphe in 0.5 and 0.1 gg kg (1.78 and 0.36 nmol kg), respectively (Table 7). The release of dopamine from the substantia nigra of rats treated for 3 weeks with (—)IPAP or (—)BPAP demonstrates that the compounds enhanced significantly the release of dopamine in rats treated with low or high doses, while the release of noradrenaline from the locus coeruleus and serotonin from the raphe was significantly increased only in rats treated with a low dose of (—)IPAP or (—)BPAP. In the case of serotonin, high dose treatment even inhibited the release of the transmitter. [...] (—)PPAP was about twice as potent as (—)deprenyl in [antagonism of tetrabenazine in the shuttle box test]. Of the newly synthesized compounds, NPAP was as active as PPAP, the further order of potency was as follows: IPAP < MPAP < BPAP. [...] (—)BPAP, was [...] about 130 times more potent than (—)deprenyl. [...] [Plus tables]
^abcdefghijHarsing LG, Knoll J, Miklya I (August 2022)."Enhancer Regulation of Dopaminergic Neurochemical Transmission in the Striatum".Int J Mol Sci.23 (15): 8543.doi:10.3390/ijms23158543.PMC9369307.PMID35955676.Figure 1. The chemical structure [...] and enhancer substances (PPAP, IPAP, BPAP). [...] The most well-characterized member of the enhancers is (—)BPAP [...] besides PPAP and IPAP (Figure 1). In the case of PPAP, IPAP, and BPAP, the negative enantiomers (R configurations) proved to be biologically more active [29]. [...] Although compounds shown in Figure 1 can be derived from phenylethylamine or other trace amines, there are differences in the ring or the attached alkylamine side chains. A phenyl ring can be found in the structure of (—)PPAP and (±)methamphetamine, whereas there are indole or benzofuran ring in (—)IPAP or (—)BPAP, respectively. [...] (—)IPAP exerts its major effect on serotonergic transmission, whereas (—)BPAP shows approximatively equal potency on both biogenic amine transmissions [26]. [...] Compounds ((—)PPAP, (—)IPAP, (—)BPAP) (Figure 1) that contain 2-propyl- aminopentane moiety are selective enhancers of the impulse propagation mediated-release of catecholamines or serotonin, but leave MAO activity practically unchanged [25]. [...] The enhancer compounds (—)PPAP, (—)IPAP; and (—)BPAP were without effect on non-vesicular [3H]dopamine release. [...] Figure 3B demonstrates that the enhancer compounds (—)PPAP, (—)IPAP, and (—)BPAP, which all contain propyl group substitutions on the nitrogen and carbon atoms but with various rings attached (phenyl, indole, and benzofuran) to the side chain, do not possess releasing ability [...]
^abHarsing LG, Timar J, Miklya I (August 2023)."Striking Neurochemical and Behavioral Differences in the Mode of Action of Selegiline and Rasagiline".Int J Mol Sci.24 (17) 13334.doi:10.3390/ijms241713334.PMC10487936.PMID37686140.Compounds exhibiting these unique pharmacological actions are designated as catecholaminergic activity enhancer (CAE) drugs, and the most widely investigated compounds of this series are (−)PPAP ((−)-1-phenyl-2-propylaminopentane, Figure 1), and its indole (−)IPAP ((−)-1-(indol-3-yl)-2-propylaminopentane), and benzofuran ((−)BPAP ((R)-(−)-1-(benzofuran-2-yl)-2-propylaminopentane) analogs [14]. [...] Previous investigations of other members of the N,α,-dipropylarylethylamine series ((−)PPAP, (−)IPAP) indicated that the catecholamine activity enhancer effect is not related to MAO inhibition [13,14].
^abShimazu S, Miklya I (May 2004). "Pharmacological studies with endogenous enhancer substances: beta-phenylethylamine, tryptamine, and their synthetic derivatives".Progress in Neuro-Psychopharmacology & Biological Psychiatry.28 (3):421–427.doi:10.1016/j.pnpbp.2003.11.016.PMID15093948.S2CID37564231.
^abKnoll J (August 2003). "Enhancer regulation/endogenous and synthetic enhancer compounds: a neurochemical concept of the innate and acquired drives".Neurochemical Research.28 (8):1275–1297.doi:10.1023/a:1024224311289.PMID12834268.
^abGaszner P, Miklya I (January 2006). "Major depression and the synthetic enhancer substances, (-)-deprenyl and R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane".Progress in Neuro-Psychopharmacology & Biological Psychiatry.30 (1):5–14.doi:10.1016/j.pnpbp.2005.06.004.PMID16023777.S2CID26570703.
