Page last updated: 2024-12-08

phenserine

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Description

phenserine: a carbamate analog of physostigmine; a long-acting inhibitor of cholinesterase [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID192706
CHEMBL ID74926
SCHEMBL ID1537384
MeSH IDM0243599

Synonyms (53)

Synonym
(-)-eseroline phenylcarbamate
pyrrolo(2,3-b)indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, phenylcarbamate (ester), (3as-cis)-
bdbm10958
(-)-phenserine
chembl74926 ,
phenserine
(3as,8ar)-1,3a,8-trimethyl-1h,2h,3h,3ah,8h,8ah-pyrrolo[2,3-b]indol-5-yl n-phenylcarbamate
NCGC00163250-01
NCGC00163250-02
(3as,8ar)-1,3a,8-trimethyl-1,2,3,3a,8,8a-hexahydropyrrolo[2,3-b]indol-5-yl phenylcarbamate
101246-66-6
BRD-K46580984-001-01-0
[(3ar,8bs)-3,4,8b-trimethyl-2,3a-dihydro-1h-pyrrolo[2,3-b]indol-7-yl] n-phenylcarbamate
HMS3261J07
n-phenylcarbamoyl eseroline
pyrrolo(2,3-b)indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, 5-(n-phenylcarbamate), (3as,8ar)-
n-phenylcarbamoyleseroline
AKOS015967321
unii-sue285ug3s
sue285ug3s ,
phenserine (racemate) [mi]
n8142nv8um ,
(+/-)-phenserine
159652-53-6
phenserine, (+/-)-
pyrrolo(2,3-b)indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, phenylcarbamate (ester), cis-(+/-)-
unii-n8142nv8um
pyrrolo(2,3-b)indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, 5-(n-phenylcarbamate), (3ar,8as)-rel-
LP00523
DB04892
CCG-221827
buntanetap, (+/-)-
phenserine [mi]
buntanetap, (-)-
tox21_500523
NCGC00261208-01
SCHEMBL1537384
(3as,8ar)-1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethylpyrrolo[2,3-b]indol-5-ol 5-(n-phenylcarbamate)
mfcd00672748
J-000348
phenserine, >=98% (hplc), solid
pyrrolo[2,3-b]indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, 5-(n-phenylcarbamate), (3ar,8as)-
pyrrolo[2,3-b]indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, 5-(n-phenylcarbamate), (3as,8ar)-, (2r,3r)-2,3-dihydroxybutanedioate (1:1);pyrrolo[2,3-b]indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, 5-(n-phenylcarbamate), (3as,8ar)-, (2r,3r)
101246-66-6 (free base)
PBHFNBQPZCRWQP-QUCCMNQESA-N
HY-103374
CS-0027770
Q27095557
pyrrolo[2,3-b]indol-5-ol, 1,2,3,3a,8,8a-hexahydro-1,3a,8-trimethyl-, 5-(n-phenylcarbamate), (3as,8ar)-
SDCCGSBI-0633726.P001
NCGC00163250-05
MS-25129
DTXSID00906018

Research Excerpts

Overview

Phenserine is a reversible AChE inhibitor possessing neuroprotective and amyloid precursor protein lowering actions. Phenserine reached Phase III clinical trials for Alzheimer's Disease where it exhibited a wide safety margin.

ExcerptReferenceRelevance
"(-)-Phenserine is a reversible AChE inhibitor possessing neuroprotective and amyloid precursor protein lowering actions that reached Phase III clinical trials for Alzheimer's Disease where it exhibited a wide safety margin."( (-)-Phenserine attenuates soman-induced neuropathology.
Chen, C; Chen, J; Greig, NH; He, J; Iskandar, K; Jacobowitz, DM; Marini, AM; McDonough, JH; Pan, H; Piermartiri, T; Wu, W; Yu, QS, 2014
)
1.44
"Phenserine is a potentially attractive drug for Alzheimer's disease. "( Synthesis of phenserine analogues and evaluation of their cholinesterase inhibitory activities.
Higuchi, K; Kawasaki, T; Matsumoto, K; Narumi, F; Osada, Y; Satoh, M; Shinada, M; Tanaka, H; Yoshida, T, 2012
)
2.19
"Phenserine is a long-acting and selective inhibitor of acetylcholinesterase with a preferential brain uptake."( Maze learning in aged rats is enhanced by phenserine, a novel anticholinesterase.
Brossi, A; Greig, NH; Ikari, H; Ingram, DK; Patel, N; Pei, XF; Spangler, EL; Speer, D, 1995
)
1.28

Effects

ExcerptReferenceRelevance
"(-)-Phenserine has been discussed as possibly failing due to flawed methods and practices in development."( Fire in the ashes: can failed Alzheimer's disease drugs succeed with second chances?
Becker, RE; Greig, NH, 2013
)
0.87

Actions

ExcerptReferenceRelevance
"Phenserine was found to inhibit Electrophorus electricus AChE in a dose-dependent manner with an IC50 value of 0.013 µM. "( Computational and Kinetic Studies of Acetylcholine Esterase Inhibition by Phenserine.
Damanhouri, GA; Tabrez, S, 2019
)
2.19

Treatment

Phenserine was associated with an improvement in cognition and an increase in rCMRglc. Phenserine treatment resulted in decreased secretion of soluble betaAPP and Abeta into the conditioned media of human neuroblastoma cells without cellular toxicity.

ExcerptReferenceRelevance
"Phenserine treatment increased cortical synaptophysin levels in younger mice, while decreased interleukin-1β and increased monocyte chemoattractant protein-1 and tumor necrosis factor-alpha levels were detected in the cortices of older mice."( Age-dependent neuroplasticity mechanisms in Alzheimer Tg2576 mice following modulation of brain amyloid-β levels.
Gonzalez, D; Greig, NH; Lilja, AM; Marutle, A; Mustafiz, T; Nordberg, A; Röjdner, J; Storelli, E; Thomé, CM; Unger-Lithner, C, 2013
)
1.11
"Phenserine treatment was associated with an improvement in cognition and an increase in rCMRglc."( Effect of phenserine treatment on brain functional activity and amyloid in Alzheimer's disease.
Almkvist, O; Andreasen, N; Blennow, K; Engler, H; Forsberg, A; Hagman, G; Kadir, A; Långström, B; Lärksäter, M; Nordberg, A; Wall, A; Winblad, B; Zetterberg, H, 2008
)
2.19
"Phenserine treatment resulted in decreased secretion of soluble betaAPP and Abeta into the conditioned media of human neuroblastoma cells without cellular toxicity."( Phenserine regulates translation of beta -amyloid precursor protein mRNA by a putative interleukin-1 responsive element, a target for drug development.
Brossi, A; Ge, YW; Greig, NH; Lahiri, DK; Rogers, J; Sambamurti, K; Shaw, KT; Utsuki, T; Yu, QS, 2001
)
2.47

Pharmacokinetics

ExcerptReferenceRelevance
" Its long duration of action, coupled with its short pharmacokinetic half-life, reduces dosing frequency, decreases body drug exposure and minimizes the dependence of drug action on the individual variations of drug metabolism commonly found in the elderly."( The experimental Alzheimer drug phenserine: preclinical pharmacokinetics and pharmacodynamics.
Brossi, A; De Micheli, E; Deutsch, J; Greig, NH; Holloway, HW; Ingram, DK; Lahiri, DK; Perry, TA; Soncrant, TT; Utsuki, T; Yu, QS, 2000
)
0.59
" The Cmax and AUC(0-24) of phenserine increased with dose, but neither were dose-proportional."( Anticholinesterase and pharmacokinetic profile of phenserine in healthy elderly human subjects.
Brownell, L; Burford, RG; Canfield, CJ; Comer, P; Flanagan, DR; Greig, NH; Holloway, HW; Ruckle, J, 2005
)
0.88
"Posiphen single and multiple ascending dose phase 1 randomised, double blind, placebo-controlled safety, tolerance, pharmacokinetic studies were undertaken in a total of 120 healthy volunteers to define a dose that was then used in a small non-randomised study of five MCI subjects, used as their own controls, to define target engagement."( Posiphen as a candidate drug to lower CSF amyloid precursor protein, amyloid-β peptide and τ levels: target engagement, tolerability and pharmacokinetics in humans.
Chang, MY; Greig, NH; John, V; Maccecchini, ML; Pan, C; Zetterberg, H, 2012
)
0.38
" Pharmacodynamic analyses of ChEIs provide paradoxical observations."( Pharmacodynamics of cholinesterase inhibitors suggests add-on therapy with a low-dose carbamylating inhibitor in patients on long-term treatment with rapidly reversible inhibitors.
Darreh-Shori, T; Hosseini, SM; Nordberg, A, 2014
)
0.4

Bioavailability

ExcerptReferenceRelevance
" doses provided an estimate of oral bioavailability of 100%."( The experimental Alzheimer drug phenserine: preclinical pharmacokinetics and pharmacodynamics.
Brossi, A; De Micheli, E; Deutsch, J; Greig, NH; Holloway, HW; Ingram, DK; Lahiri, DK; Perry, TA; Soncrant, TT; Utsuki, T; Yu, QS, 2000
)
0.59
" Like many oral drugs, bioavailability and plasma concentrations of PST are regulated by hepatic and gastrointestinal first-pass effects."( Preclinical investigation of the topical administration of phenserine: transdermal flux, cholinesterase inhibition, and cognitive efficacy.
Greig, NH; Holloway, HW; Ingram, DK; Irie, T; Irikura, M; Mamczarz, J; Moriuchi, H; Spangler, EL; Uchimura, N; Utsuki, T; Yu, QS, 2007
)
0.58

Dosage Studied

(-)-Phenserine mitigated OGD/PR-induced SH-SY5Y cell death, providing an inverted U-shaped dose-response relationship between concentration and survival. These actions translated into amelioration of spatial and visual memory impairments in a mouse model of mild TBI.

ExcerptRelevanceReference
" Studies were carried out in control animals and after dosing with phenserine, a selective centrally active AChE inhibitor; neostigmine, a peripheral cholinesterase inhibitor; and a combination of the two drugs."( Simplified methods for in vivo measurement of acetylcholinesterase activity in rodent brain.
Kilbourn, MR; Sherman, PS; Snyder, SE, 1999
)
0.54
" Constant infusion of physostigmine at a dosage of 250 microg/kg/min produced an identical increase in radioligand binding."( Acetylcholinesterase inhibition increases in vivo N-(2-[18F]fluoroethyl)-4-piperidyl benzilate binding to muscarinic acetylcholine receptors.
Kilbourn, MR; Sherman, PS; Skaddan, MB; Snyder, SE, 2001
)
0.31
" Its long duration of action, coupled with its short pharmacokinetic half-life, reduces dosing frequency, decreases body drug exposure and minimizes the dependence of drug action on the individual variations of drug metabolism commonly found in the elderly."( The experimental Alzheimer drug phenserine: preclinical pharmacokinetics and pharmacodynamics.
Brossi, A; De Micheli, E; Deutsch, J; Greig, NH; Holloway, HW; Ingram, DK; Lahiri, DK; Perry, TA; Soncrant, TT; Utsuki, T; Yu, QS, 2000
)
0.59
" Particular benefits over oral therapies might include avoiding first-pass metabolic effects and improved dosing compliance."( Preclinical investigation of the topical administration of phenserine: transdermal flux, cholinesterase inhibition, and cognitive efficacy.
Greig, NH; Holloway, HW; Ingram, DK; Irie, T; Irikura, M; Mamczarz, J; Moriuchi, H; Spangler, EL; Uchimura, N; Utsuki, T; Yu, QS, 2007
)
0.58
" Phenserine is also unique because of differing actions of its enantiomers: (-)-phenserine is the active enantiomer for inhibition of AChE, whereas (+)-phenserine ('posiphen') has weak activity as an AChE inhibitor and can be dosed much higher."( Phenserine.
Klein, J, 2007
)
2.69
" These actions translated into amelioration of spatial and visual memory impairments in a mouse model of closed head mild TBI (mTBI) two days following cessation of clinically translatable dosing with phenserine (2."( Cognitive Impairments Induced by Concussive Mild Traumatic Brain Injury in Mouse Are Ameliorated by Treatment with Phenserine via Multiple Non-Cholinergic and Cholinergic Mechanisms.
Barak, S; Becker, KG; Becker, RE; Fukui, K; Greig, NH; Hoffer, BJ; Holloway, HW; Lehrmann, E; Li, Y; Luo, Y; Perez, E; Pick, CG; Rubovitch, V; Tamargo, IA; Tweedie, D; Van Praag, H; Wood, WH; Yu, QS; Zhang, Y, 2016
)
0.83
" (-)-Phenserine mitigated OGD/PR-induced SH-SY5Y cell death, providing an inverted U-shaped dose-response relationship between concentration and survival."( (-)-Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury.
Becker, RE; Chang, CF; Chen, KY; Chen, YH; Chiang, YH; Greig, NH; Kang, SJ; Lai, JH; Luo, Y; Wu, JC, 2017
)
1.53
" We hence developed an extended controlled release formulation of (-)-phenserine to provide individualized dosing and stable therapeutic brain concentrations, to pharmacologically interrogate PPCD as a drug development target."( (-)-Phenserine and Inhibiting Pre-Programmed Cell Death: In Pursuit of a Novel Intervention for Alzheimer's Disease.
Aarsland, D; Ballard, C; Becker, RE; Bledsoe, J; Ferrucci, L; Flanagan, D; Govindarajan, R; Greig, NH; Kapogiannis, D; Lahiri, DK; Majercik, S; Sano, M; Schneider, LS, 2018
)
1.27
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (21)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
thioredoxin reductaseRattus norvegicus (Norway rat)Potency1.25890.100020.879379.4328AID588453
USP1 protein, partialHomo sapiens (human)Potency79.43280.031637.5844354.8130AID504865
GLS proteinHomo sapiens (human)Potency1.12200.35487.935539.8107AID624146
TDP1 proteinHomo sapiens (human)Potency6.15900.000811.382244.6684AID686978; AID686979
Microtubule-associated protein tauHomo sapiens (human)Potency31.62280.180013.557439.8107AID1460; AID1468
aldehyde dehydrogenase 1 family, member A1Homo sapiens (human)Potency11.22020.011212.4002100.0000AID1030
regulator of G-protein signaling 4Homo sapiens (human)Potency37.68580.531815.435837.6858AID504845
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency19.39980.001530.607315,848.9004AID1224820; AID1224821
arylsulfatase AHomo sapiens (human)Potency6.01201.069113.955137.9330AID720538
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency24.71820.035520.977089.1251AID504332
hexokinase-4 isoform 1Homo sapiens (human)Potency0.35482.511913.800328.1838AID743205
NPC intracellular cholesterol transporter 1 precursorHomo sapiens (human)Potency9.20000.01262.451825.0177AID485313
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency47.39350.354828.065989.1251AID504847
chromobox protein homolog 1Homo sapiens (human)Potency100.00000.006026.168889.1251AID488953
glucokinase regulatory proteinHomo sapiens (human)Potency0.35482.511913.800328.1838AID743205
survival motor neuron protein isoform dHomo sapiens (human)Potency17.78280.125912.234435.4813AID1458
ATP-dependent phosphofructokinaseTrypanosoma brucei brucei TREU927Potency4.77550.060110.745337.9330AID485368
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
AcetylcholinesteraseElectrophorus electricus (electric eel)IC50 (µMol)0.35000.00000.94539.9400AID30999
CholinesteraseHomo sapiens (human)IC50 (µMol)1.04770.00001.559910.0000AID1796572; AID1796574; AID1820979; AID1916836
AcetylcholinesteraseHomo sapiens (human)IC50 (µMol)0.48370.00000.933210.0000AID1796572; AID1796574; AID1820943; AID1916835; AID241692; AID31501; AID31504; AID511766
AcetylcholinesteraseRattus norvegicus (Norway rat)IC50 (µMol)0.01190.00020.52597.2000AID465959
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (25)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processCholinesteraseHomo sapiens (human)
learningCholinesteraseHomo sapiens (human)
negative regulation of cell population proliferationCholinesteraseHomo sapiens (human)
neuroblast differentiationCholinesteraseHomo sapiens (human)
peptide hormone processingCholinesteraseHomo sapiens (human)
response to alkaloidCholinesteraseHomo sapiens (human)
cocaine metabolic processCholinesteraseHomo sapiens (human)
negative regulation of synaptic transmissionCholinesteraseHomo sapiens (human)
response to glucocorticoidCholinesteraseHomo sapiens (human)
response to folic acidCholinesteraseHomo sapiens (human)
choline metabolic processCholinesteraseHomo sapiens (human)
acetylcholine catabolic processCholinesteraseHomo sapiens (human)
acetylcholine catabolic process in synaptic cleftAcetylcholinesteraseHomo sapiens (human)
regulation of receptor recyclingAcetylcholinesteraseHomo sapiens (human)
osteoblast developmentAcetylcholinesteraseHomo sapiens (human)
acetylcholine catabolic processAcetylcholinesteraseHomo sapiens (human)
cell adhesionAcetylcholinesteraseHomo sapiens (human)
nervous system developmentAcetylcholinesteraseHomo sapiens (human)
synapse assemblyAcetylcholinesteraseHomo sapiens (human)
receptor internalizationAcetylcholinesteraseHomo sapiens (human)
negative regulation of synaptic transmission, cholinergicAcetylcholinesteraseHomo sapiens (human)
amyloid precursor protein metabolic processAcetylcholinesteraseHomo sapiens (human)
positive regulation of protein secretionAcetylcholinesteraseHomo sapiens (human)
retina development in camera-type eyeAcetylcholinesteraseHomo sapiens (human)
acetylcholine receptor signaling pathwayAcetylcholinesteraseHomo sapiens (human)
positive regulation of cold-induced thermogenesisAcetylcholinesteraseHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (15)

Processvia Protein(s)Taxonomy
amyloid-beta bindingCholinesteraseHomo sapiens (human)
catalytic activityCholinesteraseHomo sapiens (human)
acetylcholinesterase activityCholinesteraseHomo sapiens (human)
cholinesterase activityCholinesteraseHomo sapiens (human)
protein bindingCholinesteraseHomo sapiens (human)
hydrolase activity, acting on ester bondsCholinesteraseHomo sapiens (human)
enzyme bindingCholinesteraseHomo sapiens (human)
choline bindingCholinesteraseHomo sapiens (human)
identical protein bindingCholinesteraseHomo sapiens (human)
amyloid-beta bindingAcetylcholinesteraseHomo sapiens (human)
acetylcholinesterase activityAcetylcholinesteraseHomo sapiens (human)
cholinesterase activityAcetylcholinesteraseHomo sapiens (human)
protein bindingAcetylcholinesteraseHomo sapiens (human)
collagen bindingAcetylcholinesteraseHomo sapiens (human)
hydrolase activityAcetylcholinesteraseHomo sapiens (human)
serine hydrolase activityAcetylcholinesteraseHomo sapiens (human)
acetylcholine bindingAcetylcholinesteraseHomo sapiens (human)
protein homodimerization activityAcetylcholinesteraseHomo sapiens (human)
laminin bindingAcetylcholinesteraseHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (16)

Processvia Protein(s)Taxonomy
extracellular regionCholinesteraseHomo sapiens (human)
nuclear envelope lumenCholinesteraseHomo sapiens (human)
endoplasmic reticulum lumenCholinesteraseHomo sapiens (human)
blood microparticleCholinesteraseHomo sapiens (human)
plasma membraneCholinesteraseHomo sapiens (human)
extracellular spaceCholinesteraseHomo sapiens (human)
extracellular regionAcetylcholinesteraseHomo sapiens (human)
basement membraneAcetylcholinesteraseHomo sapiens (human)
extracellular spaceAcetylcholinesteraseHomo sapiens (human)
nucleusAcetylcholinesteraseHomo sapiens (human)
Golgi apparatusAcetylcholinesteraseHomo sapiens (human)
plasma membraneAcetylcholinesteraseHomo sapiens (human)
cell surfaceAcetylcholinesteraseHomo sapiens (human)
membraneAcetylcholinesteraseHomo sapiens (human)
neuromuscular junctionAcetylcholinesteraseHomo sapiens (human)
synaptic cleftAcetylcholinesteraseHomo sapiens (human)
synapseAcetylcholinesteraseHomo sapiens (human)
perinuclear region of cytoplasmAcetylcholinesteraseHomo sapiens (human)
side of membraneAcetylcholinesteraseHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (46)

Assay IDTitleYearJournalArticle
AID251372Reduction in Amyloid-beta precursor protein levels in Human SK-N-SH cells at 10 uM2005Journal of medicinal chemistry, Feb-24, Volume: 48, Issue:4
Novel anticholinesterases based on the molecular skeletons of furobenzofuran and methanobenzodioxepine.
AID465960Inhibition of rat plasma BChE by Ellman's method2010Bioorganic & medicinal chemistry letters, Mar-01, Volume: 20, Issue:5
Synthesis of physostigmine analogues and evaluation of their anticholinesterase activities.
AID44456Inhibitory activity against Butyrylcholinesterase in cortex1990Journal of medicinal chemistry, Sep, Volume: 33, Issue:9
Alfred Burger award address. Bioactive alkaloids. 4. Results of recent investigations with colchicine and physostigmine.
AID511766Inhibition of human AChE by Ellmans test2010Journal of medicinal chemistry, Sep-09, Volume: 53, Issue:17
Novel carbamates as orally active acetylcholinesterase inhibitors found to improve scopolamine-induced cognition impairment: pharmacophore-based virtual screening, synthesis, and pharmacology.
AID1820943Inhibition of AChE (unknown origin)2022European journal of medicinal chemistry, Feb-05, Volume: 229Design, synthesis, and biological evaluation of carbamate derivatives of N-salicyloyl tryptamine as multifunctional agents for the treatment of Alzheimer's disease.
AID31504Inhibitory activity against Acetylcholinesterase in erythrocyte1990Journal of medicinal chemistry, Sep, Volume: 33, Issue:9
Alfred Burger award address. Bioactive alkaloids. 4. Results of recent investigations with colchicine and physostigmine.
AID241692Inhibitory concentration against human erythrocyte Acetylcholinesterase2005Journal of medicinal chemistry, Feb-24, Volume: 48, Issue:4
Novel anticholinesterases based on the molecular skeletons of furobenzofuran and methanobenzodioxepine.
AID468443Inhibition of human FAAH at 1 uM2009Bioorganic & medicinal chemistry letters, Dec-01, Volume: 19, Issue:23
Mining biologically-active molecules for inhibitors of fatty acid amide hydrolase (FAAH): identification of phenmedipham and amperozide as FAAH inhibitors.
AID1820979Inhibition of BuChE (unknown origin)2022European journal of medicinal chemistry, Feb-05, Volume: 229Design, synthesis, and biological evaluation of carbamate derivatives of N-salicyloyl tryptamine as multifunctional agents for the treatment of Alzheimer's disease.
AID1916836Inhibition of BChE (unknown origin)2022European journal of medicinal chemistry, Oct-05, Volume: 240Recent advance on carbamate-based cholinesterase inhibitors as potential multifunctional agents against Alzheimer's disease.
AID465961Selectivity ratio of IC50 for rat plasma BChE to IC50 for rat brain AChE2010Bioorganic & medicinal chemistry letters, Mar-01, Volume: 20, Issue:5
Synthesis of physostigmine analogues and evaluation of their anticholinesterase activities.
AID1916835Inhibition of AChE (unknown origin)2022European journal of medicinal chemistry, Oct-05, Volume: 240Recent advance on carbamate-based cholinesterase inhibitors as potential multifunctional agents against Alzheimer's disease.
AID44293In vitro inhibition of human plasma butyrylcholinesterase.2001Journal of medicinal chemistry, Nov-22, Volume: 44, Issue:24
Methyl analogues of the experimental Alzheimer drug phenserine: synthesis and structure/activity relationships for acetyl- and butyrylcholinesterase inhibitory action.
AID241560Inhibitory concentration against human plasma Butyrylcholinesterase2005Journal of medicinal chemistry, Feb-24, Volume: 48, Issue:4
Novel anticholinesterases based on the molecular skeletons of furobenzofuran and methanobenzodioxepine.
AID1916838Selectivity index, ratio of IC50 for AChE (unknown origin) to BChE (unknown origin)2022European journal of medicinal chemistry, Oct-05, Volume: 240Recent advance on carbamate-based cholinesterase inhibitors as potential multifunctional agents against Alzheimer's disease.
AID30999Inhibitory activity against Acetylcholinesterase in electric eel1990Journal of medicinal chemistry, Sep, Volume: 33, Issue:9
Alfred Burger award address. Bioactive alkaloids. 4. Results of recent investigations with colchicine and physostigmine.
AID31501In vitro inhibition of human erythrocyte acetylcholinesterase.2001Journal of medicinal chemistry, Nov-22, Volume: 44, Issue:24
Methyl analogues of the experimental Alzheimer drug phenserine: synthesis and structure/activity relationships for acetyl- and butyrylcholinesterase inhibitory action.
AID44457Inhibitory activity against Butyrylcholinesterase in plasma1990Journal of medicinal chemistry, Sep, Volume: 33, Issue:9
Alfred Burger award address. Bioactive alkaloids. 4. Results of recent investigations with colchicine and physostigmine.
AID31503Inhibitory activity against Acetylcholinesterase in cortex1990Journal of medicinal chemistry, Sep, Volume: 33, Issue:9
Alfred Burger award address. Bioactive alkaloids. 4. Results of recent investigations with colchicine and physostigmine.
AID465959Inhibition of rat brain AChE by Ellman's method2010Bioorganic & medicinal chemistry letters, Mar-01, Volume: 20, Issue:5
Synthesis of physostigmine analogues and evaluation of their anticholinesterase activities.
AID1347410qHTS for inhibitors of adenylyl cyclases using a fission yeast platform: a pilot screen against the NCATS LOPAC library2019Cellular signalling, 08, Volume: 60A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.
AID1347405qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS LOPAC collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347057CD47-SIRPalpha protein protein interaction - LANCE assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID588349qHTS for Inhibitors of ATXN expression: Validation of Cytotoxic Assay
AID1347050Natriuretic polypeptide receptor (hNpr2) antagonism - Pilot subtype selectivity assay2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID504836Inducers of the Endoplasmic Reticulum Stress Response (ERSR) in human glioma: Validation2002The Journal of biological chemistry, Apr-19, Volume: 277, Issue:16
Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347049Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot screen2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347059CD47-SIRPalpha protein protein interaction - Alpha assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347045Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot counterscreen GloSensor control cell line2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347058CD47-SIRPalpha protein protein interaction - HTRF assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID588378qHTS for Inhibitors of ATXN expression: Validation
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347151Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1508628Confirmatory qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1508627Counterscreen qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: GLuc-NoTag assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1508629Cell Viability qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1796574Cholinesterase Inhibition Assay from Article 10.1021/jm010080x: \\Methyl analogues of the experimental Alzheimer drug phenserine: synthesis and structure/activity relationships for acetyl- and butyrylcholinesterase inhibitory action.\\2001Journal of medicinal chemistry, Nov-22, Volume: 44, Issue:24
Methyl analogues of the experimental Alzheimer drug phenserine: synthesis and structure/activity relationships for acetyl- and butyrylcholinesterase inhibitory action.
AID1796572Cholinesterase Inhibition Assay from Article 10.1021/jm010491d: \\Anticholinesterase activity of compounds related to geneserine tautomers. N-Oxides and 1,2-oxazines.\\2002Journal of medicinal chemistry, Aug-15, Volume: 45, Issue:17
Anticholinesterase activity of compounds related to geneserine tautomers. N-Oxides and 1,2-oxazines.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (87)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's10 (11.49)18.2507
2000's32 (36.78)29.6817
2010's34 (39.08)24.3611
2020's11 (12.64)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 29.39

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be moderate demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index29.39 (24.57)
Research Supply Index4.55 (2.92)
Research Growth Index4.82 (4.65)
Search Engine Demand Index35.06 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (29.39)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials6 (6.82%)5.53%
Reviews12 (13.64%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other70 (79.55%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (5)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Randomized, Double-Blind, Placebo-Controlled, Dose-Ranging, Multicenter Study of Buntanetap in Participants With Mild to Moderate Alzheimer's Disease [NCT05686044]Phase 2/Phase 3320 participants (Anticipated)Interventional2023-04-01Active, not recruiting
A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Ascending Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics (PK) and Pharmacodynamic (PD) Effects of Posiphen® in Subjects With Early Alzheimer's Disease (AD) [NCT02925650]Phase 1/Phase 218 participants (Actual)Interventional2017-03-02Completed
A 6-month Prospective, Randomized, Double-blind, Placebo-controlled Clinical Trial Investigating the Efficacy, Safety, and Tolerability of Two Different Doses of Buntanetap or Placebo in Patients With Early Parkinson's Disease [NCT05357989]Phase 3523 participants (Actual)Interventional2022-08-03Completed
An Open-Label, Two-Stage Study to Evaluate the Pharmacokinetics and Pharmacodynamics of POSIPHEN® in Plasma and CSF After a 10-Day Treatment Period in Subjects With Amnestic Mild Cognitive Impairment [NCT01072812]Phase 15 participants (Actual)Interventional2010-02-28Terminated(stopped due to Business decision based on funding)
A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Dose-Finding Study to Evaluate the Safety, Tolerability, Pharmacokinetic and Pharmacodynamic Effects of Posiphen® in Subjects With Early Alzheimer's Disease (AD) or Early Parkinson's Disease (PD [NCT04524351]Phase 1/Phase 275 participants (Actual)Interventional2020-08-14Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT02925650 (11) [back to overview]Assessment of Cognitive Effects
NCT02925650 (11) [back to overview]Assessment of Mental Status Effects
NCT02925650 (11) [back to overview]Assessment of Neuropsychiatric Effects
NCT02925650 (11) [back to overview]Feasibility of CSF Catheter Study With SILK™ Technology to Evaluate %CSF Samples With Enough Volume for Testing
NCT02925650 (11) [back to overview]Feasibility of CSF Catheter Study With SILK™ Technology to Evaluate Rates of Enrollment
NCT02925650 (11) [back to overview]Fractional Synthesis Rate of Aβ40 in CSF Using the SILK™ Technique With Multiple Doses of Posiphen
NCT02925650 (11) [back to overview]Feasibility of CSF Catheter Study With SILK™ Technology to Evaluate Research Satisfaction
NCT02925650 (11) [back to overview]Pharmacodynamic and PK-PD Effects on CSF Alzheimer's Disease Biomarkers
NCT02925650 (11) [back to overview]Safety and Tolerability of Multiple Ascending Doses of Posiphen: Reports of Adverse Events or Study Discontinuations
NCT02925650 (11) [back to overview]The Levels of Posiphen and Its Metabolites Will be Determined in Cerebrospinal Fluid (CSF)
NCT02925650 (11) [back to overview]The Levels of Posiphen and Its Metabolites Will be Determined in Plasma
NCT04524351 (2) [back to overview]Concentration of Posiphen in Plasma
NCT04524351 (2) [back to overview]Percentage of Participants With Treatment-Emergent Adverse Events

Assessment of Cognitive Effects

The short-term effects of Posiphen on cognition were measured using the The Alzheimer's Disease Assessment Scale-Cognitive 12 (ADAS-Cog12). The ADAS-Cog is a structured scale that evaluates memory (word recall, word recognition), reasoning, language (naming, comprehension), orientation, ideational praxis and constructional praxis. The test is scored in terms of errors, with higher scores reflecting poorer performance and greater impairment. Total ADAS-Cog12 scores can range from 0 to 80, with lower scores being better and higher scores being worse. Results of the ADAS-Cog12 for this trial are reported as a raw change score, calculated as the change between the total scores at two evaluation time points (Baseline, Pre-Confinement Visit) with negative scores being better and positive scores being worse. (NCT02925650)
Timeframe: ADAS-Cog12 was administered at Baseline and at the Pre-Confinement Visit 1-3 days prior to the Confinement Visit. This confinement visit occurred following 21-23 days of treatment with either Posiphen or placebo, also allowing a +/- 2-day visit window.

Interventionscore on a scale (Mean)
Active Treatment Arms-0.55
Placebo Arm-1.57

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Assessment of Mental Status Effects

The short-term effects of Posiphen on mental status will be measured using the Mini-Mental State Examination (MMSE). The MMSE is a brief, global cognitive measure that includes orientation, memory, attention, concentration, naming, writing, repetition, comprehension, and construction. The total score ranges from 0 (worst) to 30 (best performance). Results of the MMSE for this trial were reported as a raw change score, calculated as the change between the total scores at two evaluation time points (Baseline, Pre-Confinement Visit) and where negative values are worse and positive values are better. (NCT02925650)
Timeframe: MMSE was administered at Baseline and at the Pre-Confinement Visit 1-3 days prior to the Confinement Visit. This confinement visit occurred following 21-23 days of treatment with either Posiphen or placebo, while also allowing a +/- 2-day visit window.

Interventionscore on a scale (Mean)
Low Dose-1.4
Medium Dose1.2
High Dose-1
Placebo1.14

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Assessment of Neuropsychiatric Effects

The Neuropsychiatric Inventory (NPI) was used to measure the frequency and severity of neuropsychiatric symptoms. On this scale frequency ratings range from 0 (no symptoms) to 4 (very frequently, once or more per day or continuously). Severity ratings range from 0 (no severity) to 3 (severe). The score for each of 12 symptoms measured in the scale is the product of severity and frequency within that symptom. The total score for the NPI is the sum of all 12 symptom item scores, for a highest possible total score of 144 in individuals with maximal symptoms, and a lowest possible total score of zero (0) in fully asymptomatic individuals. Lower scores are better and higher scores indicate more neuropsychiatric symptoms. Results are calculated as the change between the total scores at two evaluation time points (Baseline, Pre-Confinement Visit) with negative scores being better and positive scores being worse. (NCT02925650)
Timeframe: NPI was administered at Baseline and at the Pre-Confinement Visit 1-3 days prior to the Confinement Visit. This confinement visit occurred following 21-23 days of treatment with either Posiphen or placebo, while also allowing a +/- 2-day visit window.

Interventionscore on a scale (Mean)
Low Dose-2.6
Medium Dose3.4
High Dose-9
Placebo-3.86

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Feasibility of CSF Catheter Study With SILK™ Technology to Evaluate %CSF Samples With Enough Volume for Testing

The % of cerebrospinal fluid samples with sufficient volume for testing will be determined across study participants during the SILK sampling procedure (NCT02925650)
Timeframe: Up to 25 days

Interventionpercentage of CSF samples (Number)
All Randomized Participants Who Completed 36 Hour Confinement Visit (n=15)81.75

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Feasibility of CSF Catheter Study With SILK™ Technology to Evaluate Rates of Enrollment

Feasibility of CSF Catheter Study with SILK™ Technology was determined by comparing the total number of participants enrolled, randomized and treated with study drug in the trial to the total number of participants who completed the CSF Catheter Study across all participating sites. (NCT02925650)
Timeframe: Up to 25 days

InterventionParticipants (Count of Participants)
Active Treatment Arms10
Placebo Arm5

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Fractional Synthesis Rate of Aβ40 in CSF Using the SILK™ Technique With Multiple Doses of Posiphen

The fractional synthesis rate (FSR) of Aβ40 was measured in the CSF using the SILK™ technique. FSR is a measure of the rate of Aβ synthesis in the brain. During 13C6-leucine infusion, 13C6-leucine is incorporated into newly synthesized proteins throughout the body, including the brain, in proportion to the available 13C6-leucine. This FSR is calculated as the rate of change of the ratio of 13C6-leucine-labeled Aβ proteins to unlabeled Aβ proteins in the lumbar CSF between 6 to 16 hours, normalized to the ratio of labeled to unlabeled leucine amino acid in plasma. It is reported as a fraction of 13C6-leucine-labeled to unlabeled Aβ proteins per hour. The ratio of Aβ in CSF containing 13C6-leucine to that containing unlabeled leucine is measured using mass spectrometry. (NCT02925650)
Timeframe: The confinement visit occurred following 21-23 days of treatment with either Posiphen or placebo, while also allowing a +/- 2-day visit window. CSF was collected between 6 and 16hrs during the confinement visit.

Interventionfraction labeled:unlabeled Aβ40 per hr (Mean)
Low Dose0.0405
Medium Dose0.0400
High Dose0.0206
Placebo0.0375

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Feasibility of CSF Catheter Study With SILK™ Technology to Evaluate Research Satisfaction

Research satisfaction will be evaluated by qualitative response to 14 questions asked to participants about their experience with the study procedures. Responses will be grouped and reported by common themes (NCT02925650)
Timeframe: Up to 25 days

Interventionpercentage of participants (Number)
"Rated Excellent for quality of tests and attention received during participation in the study.""Reported Almost all of my expectations have been met by the research program.""Reported Yes, definitely they would recommend this research program to a friend.""Reported Yes, definitely they would choose to participate again.""Reported Volunteering as what they liked best about the study.""Reported Time Commitment as what they liked least about the study.""Reported Yes, the 36 hour catheter procedure was done.""Reported No adverse events were associated with the 36hr catheter procedure.""Reported Excellent as the quality of the 36hr catheter procedure and attention they received.""Reported the catheter procedure was almost all of what I expected.""Reported they liked best was participating in cutting edge research and interacting with the team.""Reported Other as what they liked least about the 36hr catheter procedure.""Reported Other as what they would change about the 36hr catheter procedure."Reported they would change the number of visits.
All Randomized Participants94819487.53131100738067100477150

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Pharmacodynamic and PK-PD Effects on CSF Alzheimer's Disease Biomarkers

Aβ38, Aβ40, Aβ42, sAPPα, sAPPβ, and T-Tau were sampled at Screening and at the start of the confinement visit. Results of these measures were reported as a least square means, calculated as the change between the measured values at the start of the confinement visit and Screening in ng/mL. (NCT02925650)
Timeframe: CSF was sampled at Screening and at the start of the confinement visit, which occurred following 21-23 days of treatment with either Posiphen or placebo, while also allowing a +/- 2-day visit window.

,
Interventionng/mL (Least Squares Mean)
Aβ38Aβ40Aβ42sAPPαsAPPβTotal Tau
Active Treatment Arms0.3911.730.1076.4919.1186.4
Placebo Arm0.5933.130.211-3.5-28.653.7

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Safety and Tolerability of Multiple Ascending Doses of Posiphen: Reports of Adverse Events or Study Discontinuations

Number of adverse events or study discontinuations, broken down by dose arm (i.e. Low vs. Medium vs. High vs. Placebo), and further broken down by relatedness to Posiphen (Definitely Related, Probably Related, Possibly Related, Unlikely Related, Unrelated) (NCT02925650)
Timeframe: Up to 25 days

,,,
Interventionevents (Number)
Definitely RelatedProbably RelatedPossibly RelatedUnlikely RelatedUnrelatedTotal
High Dose000000
Low Dose0012912
Medium Dose01031115
Placebo0022610

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The Levels of Posiphen and Its Metabolites Will be Determined in Cerebrospinal Fluid (CSF)

Mean CSF concentrations of levels of posiphen tartrate, N1 desmethyl posiphen, and N8 desmethyl Posiphen metabolite were determined for each of the three dose cohorts (Low Dose, Medium Dose, High Dose) by a protein precipitation extraction method using a high performance liquid chromatographic mass spectrometric detection method, with a linear weighted regression to determine the concentrations. (NCT02925650)
Timeframe: The confinement visit occurred following 21-23 days of treatment with either Posiphen or placebo, while also allowing a +/- 2-day visit window. Plasma was collected at 0, 2, 4, 8, 12, 16, 20, and 24hrs during the confinement visit.

,,
Interventionng/mL (Mean)
PosiphenN1 metaboliteN8 metabolite
High Dose0.7100.15
Low Dose0.460.020.35
Medium Dose0.730.280.77

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The Levels of Posiphen and Its Metabolites Will be Determined in Plasma

Mean plasma concentrations of levels of posiphen tartrate, N1 desmethyl posiphen, and N8 desmethyl Posiphen metabolite were determined for each of the three dose cohorts (Low Dose, Medium Dose, High Dose) by a protein precipitation extraction method using a high performance liquid chromatographic mass spectrometric detection method, with a linear weighted regression to determine their concentrations. (NCT02925650)
Timeframe: The confinement visit occurred following 21-23 days of treatment with either Posiphen or placebo, while also allowing a +/- 2-day visit window. Plasma was collected at 0, 2, 4, 8, 12, 16, 20, and 24hrs during the confinement visit.

,,
Interventionng/mL (Mean)
PosiphenN1 metaboliteN8 metabolite
High Dose12.012.513.35
Low Dose7.161.292.25
Medium Dose9.513.025.04

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Concentration of Posiphen in Plasma

Maximum Plasma Concentration (Cmax) of Posiphen reported as ng/mL. (NCT04524351)
Timeframe: Samples collected over a 6 hour timeframe

Interventionng/mL (Mean)
Posiphen, 80mg (Parkinson's Participants)94.9
Posiphen, 40mg (Parkinson's Participants)40.2
Posiphen, 20mg (Parkinson's Participants)15.3
Posiphen, 10mg (Parkinson's Participants)2.0
Posiphen, 5mg (Parkinson's Participants)0.4
Posiphen, 80mg (Alzheimer's Participants)112.3

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Percentage of Participants With Treatment-Emergent Adverse Events

Percent of patients with AEs in the Posiphen treatment arms compared to the Placebo group (NCT04524351)
Timeframe: 25±2 days

InterventionParticipants (Count of Participants)
Posiphen, 80mg (Parkinson's Participants)3
Posiphen, 40mg (Parkinson's Participants)5
Posiphen, 20mg (Parkinson's Participants)4
Posiphen, 10mg (Parkinson's Participants)6
Posiphen, 5mg (Parkinson's Participants)1
Placebo (Parkinson's Participants)3
Placebo (Alzheimer's Participants)3
Posiphen, 80mg (Alzheimer's Participants)5

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