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BioAssay: AID 743234

Fluorescence-based cell-based late stage dose response assay to identify antagonists of the human trace amine associated receptor 1 (TAAR1)

Name: Fluorescence-based cell-based late stage dose response assay to identify antagonists of the human trace amine associated receptor 1 (TAAR1). ..more
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 Tested Compounds
 Tested Compounds
All(10)
 
 
Active(7)
 
 
Inactive(3)
 
 
 Tested Substances
 Tested Substances
All(10)
 
 
Active(7)
 
 
Inactive(3)
 
 
AID: 743234
Data Source: The Scripps Research Institute Molecular Screening Center (TAAR1_ANT_FLUO8_1536_3XIC50 MDRUN)
BioAssay Type: Confirmatory, Concentration-Response Relationship Observed
Depositor Category: NIH Molecular Libraries Probe Production Network
Deposit Date: 2013-12-18
Hold-until Date: 2014-12-18
Modify Date: 2014-12-18

Data Table ( Complete ):           View Active Data    View All Data
Target
BioActive Compounds: 7
Related Experiments
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AIDNameTypeComment
624466Fluorescence-based cell-based primary high throughput screening assay to identify antagonists of the human trace amine associated receptor 1 (TAAR1)Screeningdepositor-specified cross reference: Primary screen (TAAR1 antagonists in singlicate)
624475Summary of the probe development effort to identify antagonists of the human trace amine associated receptor 1 (TAAR1)Summarydepositor-specified cross reference: Summary (TAAR1 antagonists)
651780Counterscreen for antagonists of the human trace amine associated receptor 1 (hTAAR1): Fluorescence-based cell-based high throughput screening assay to identify nonselective antagonistsScreeningdepositor-specified cross reference: Counterscreen(nonselective Ga16 antagonists in triplicate)
651785Fluorescence-based cell-based primary high throughput confirmation assay to identify antagonists of the human trace amine associated receptor 1 (TAAR1)Screeningdepositor-specified cross reference: Confirmation screen(TAAR1 antagonists in triplicate)
651953Counterscreen for antagonists of the human trace amine associated receptor 1 (hTAAR1): Fluorescence-based cell-based high throughput screening assay to identify nonselective Ga16 agonistsScreeningdepositor-specified cross reference: Counterscreen (nonselective Ga16 agonists that may cause an antagonist response in a dual screening
651955Counterscreen for antagonists of the human trace amine associated receptor 1 (hTAAR1): Fluorescence-based cell-based high throughput screening assay to identify TAAR1 AgonistsScreeningdepositor-specified cross reference: Counterscreen(TAAR1 agonists that also are TAAR1 antagonists in the dual screening mode in triplicat
686986Counterscreen for antagonists of the human trace amine associated receptor 1 (hTAAR1): Fluorescence-based cell-based high throughput dose response assay to identify TAAR1 AgonistsConfirmatorydepositor-specified cross reference: Dose Response counterscreen (TAAR1 agonist in triplicate)
686987Counterscreen for antagonists of the human trace amine associated receptor 1 (hTAAR1): Fluorescence-based cell-based high throughput dose response assay to identify nonselective Ga16 antagonistsConfirmatorydepositor-specified cross reference: Dose Response counterscreen (nonselective Ga16 antagonist in triplicate)
686989Counterscreen for antagonists of the human trace amine associated receptor 1 (TAAR1): Fluorescence-based cell-based high throughput dose reponse assay to identify nonselective Ga16 agonistsConfirmatorydepositor-specified cross reference: Dose Response counterscreen (nonselective Ga16 agonists that may cause an antagonist response in a d
686994Fluorescence-based cell-based high throughput dose response assay to identify antagonists of the human trace amine associated receptor 1 (TAAR1)Confirmatorydepositor-specified cross reference: Dose Response assay (TAAR1 antagonists in triplicate)
743235Counterscreen for antagonists of the human trace amine associated receptor 1 (hTAAR1): Fluorescence-based cell-based late stage dose response assay to identify TAAR1 AgonistsConfirmatorysame project related to Summary assay
743236Counterscreen for antagonists of the human trace amine associated receptor 1 (TAAR1): Fluorescence-based cell-based late state dose reponse assay to identify nonselective Ga16 agonistsConfirmatorysame project related to Summary assay
743237Counterscreen for antagonists of the human trace amine associated receptor 1 (hTAAR1): Fluorescence-based cell-based late stage dose response assay to identify nonselective Ga16 antagonistsConfirmatorysame project related to Summary assay
743489On Hold
743492On Hold
743493On Hold
743495On Hold
1053182On Hold
1117265On Hold
Description:
Source (MLPCN Center Name): The Scripps Research Institute Molecular Screening Center (SRIMSC)
Affiliation: RTI International
Assay Provider: Brian P. Gilmour, RTI International
Network: Molecular Library Probe Production Centers Network (MLPCN)
Grant Proposal Number: 1R21NS064780-01A1
Grant Proposal PI: Brian P. Gilmour, RTI International
External Assay ID: TAAR1_ANT_FLUO8_1536_3XIC50 MDRUN

Name: Fluorescence-based cell-based late stage dose response assay to identify antagonists of the human trace amine associated receptor 1 (TAAR1).

Description:

Heterotrimeric G-protein coupled receptors (GPCRs) are major targets for disease therapeutics, due in part to their broad tissue distribution, structural diversity, varied modes of action, and disease-associated mutations (1-4). TAAR1 (trace amine associated receptor 1) is a G protein-coupled receptor activated by trace amines. Trace amines (TA) such as Beta-phenethylamine (Beta-PEA), p-tyramine (TYR), octopamine, and tryptamine are endogenous amine compounds that account for less than 1% of the biogenic amines in most brain regions (5), and exert pharmacological actions in humans (6,7). In addition to binding Beta-PEA and TYR, rat TAAR1 is also activated by dopamine, octopamine, tryptamine, amphetamine, and lysergic acid (8-10). TAs are of particular interest because they have been shown to modulate the activity of neurotransmitters such as dopamine (11-13) and gamma-amino butyric acid (14-16) and alterations in their brain levels are associated with schizophrenia (17-19) and depression (20, 21). Their potential to modulate dopaminergic activity suggests that they may play a role in the efficacy of L-DOPA in treating Parkinson disease4 and addiction (13). In humans, only TAAR1 has been shown to be activated by Beta-PEA and TYR, resulting in increased cyclic adenosine monophosphate (cAMP) accumulation through coupling to Gs (9, 10). Endogenous hTAAR1 activity is predominantly coupled to G-alpha-s and the accumulation of cAMP. The variety of compounds potentially acting at this receptor makes it attractive to assume that hTAAR1 is involved in a variety of integrated CNS processes such as mood and cognition. As a result, hTAAR1 is an interesting target for the development of ligands to probe the role of this receptor in CNS function and disease. For this project, the assay provider has created a cell line expressing the hTAAR1 in a parent cell line (RD-HGA16 cells, Molecular Devices) that stably over expresses the promiscuous G-protein, G-alpha-16, thereby coupling hTAAR1 activation to mobilization of internal calcium stores. Because TAs may be involved in modulating a variety of behaviors including mood, cognition, and addiction, it is of interest to discover novel ligands for TAAR1 to probe the role TAs play in brain function (22, 23).

References:

1. Pan, H.L., Wu, Z.Z., Zhou, H.Y., Chen, S.R., Zhang, H.M., and Li, D.P., Modulation of pain transmission by G-protein-coupled receptors. Pharmacol Ther, 2008. 117(1): p. 141-61.
2. Lagerstrom, M.C. and Schioth, H.B., Structural diversity of G protein-coupled receptors and significance for drug discovery. Nat Rev Drug Discov, 2008. 7(4): p. 339-57.
3. Thompson, M.D., Cole, D.E., and Jose, P.A., Pharmacogenomics of G protein-coupled receptor signaling: insights from health and disease. Methods Mol Biol, 2008. 448: p. 77-107.
4. Bosier, B. and Hermans, E., Versatility of GPCR recognition by drugs: from biological implications to therapeutic relevance. Trends Pharmacol Sci, 2007. 28(8): p. 438-46.
5. Bunzow JR, Sonders MS, Arttamangkul S, Harrison LM, Zhang G, Quigley DI, Darland T, Suchland KL, Pasumamula S, Kennedy JL, Olson SB, Magenis RE, Amara SG, Grandy DK. Amphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptor. Mol Pharmacol. 2001 Dec;60(6):1181-8.
6. Premont RT, Gainetdinov RR, Caron MG: Following the trace of elusive amines. Proc Natl Acad Sci U S A 2001;98:9474-9475.
7. Branchek TA, Blackburn TP: Trace amine receptors as targets for novel therapeutics: legend, myth and fact. Curr Opin Pharmacol 2003;3:90-97.
8. Borowsky B, Adham N, Jones KA, Raddatz R, Artymyshyn R, Ogozalek KL, et al: Trace amines: identification of a family of mammalian G protein-coupled receptors. Proc Natl Acad Sci U S A 2001;98:8966-8971.
9. Bunzow JR, Sonders MS, Arttamangkul S, Harrison LM, Zhang G, Quigley DI, et al: Amphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptor. Mol Pharmacol 2001;60:1181-1188.
10. Lindemann L, Ebeling M, Kratochwil NA, Bunzow JR, Grandy DK, Hoener MC: Trace amine-associated receptors form structurally and functionally distinct subfamilies of novel G protein-coupled receptors. Genomics 2005;85:372-385.
11. Jones RS: Specific enhancement of neuronal responses to catecholamine by p-tyramine. J Neurosci Res 1981;6:49-61.
12. Mercuri NB, Bernardi G: The "magic" of L-dopa: why is it the gold standard Parkinson's disease therapy? Trends Pharmacol Sci 2005;26:341-344.
13. Miller GM, Verrico CD, Jassen A, Konar M, Yang H, Panas H, et al: Primate trace amine receptor 1 modulation by the dopamine transporter. J Pharmacol Exp Ther 2005;313:983-994.
14. Dourish CT, Cooper SJ: Pharmacology of beta-phenylethylamine induced seizures in mice. Prog Neuropsychopharmacol Biol Psychiatry 1983;7:787-790.
15. Berretta N, Giustizieri M, Bernardi G, Mercuri NB: Trace amines reduce GABA(B) receptor-mediated presynaptic inhibition at GABAergic synapses of the rat substantia nigra pars compacta. Brain Res 2005;1062:175-178.
16. Federici M, Geracitano R, Tozzi A, Longone P, Di Angelantonio S, Bengtson CP, et al: Trace amines depress GABA B response in dopaminergic neurons by inhibiting G-betagamma-gated inwardly rectifying potassium channels. Mol Pharmacol 2005;67:1283-1290.
17. Boulton AA: Some aspects of basic psychopharmacology: the trace amines. Prog Neuropsychopharmacol Biol Psychiatry 1982;6:563-570.
18. Anderson GM, Gerner RH, Cohen DJ, Fairbanks L: Central tryptamine turnover in depression, schizophrenia, and anorexia: measurement of indoleacetic acid in cerebrospinal fluid. Biol Psychiatry 1984;19: 1427-1435.
19. Duan J, Martinez M, Sanders AR, Hou C, Saitou N, Kitano T, et al: Polymorphisms in the trace amine receptor 4 (TRAR4) gene on chromosome 6q23.2 are associated with susceptibility to schizophrenia. Am J Hum Genet 2004;75:624-638.
20. Davis BA, Boulton AA: The trace amines and their acidic metabolites in depression-an overview. Prog Neuropsychopharmacol Biol Psychiatry 1994;18:17-45.
21. Baker GB, Coutts RT, Greenshaw AJ: Neurochemical and metabolic aspects of antidepressants: an overview. J Psychiatry Neurosci 2000; 25:481-496.
22. Navarro HA, Gilmour BP, Lewin AH. A rapid functional assay for the human trace amine-associated receptor 1 based on the mobilization of internal calcium. J Biomol Screen. 2006 Sep;11(6):688-93. Epub 2006 Jul 10.
23. Bradaia A, Trube G, Stalder H, Norcross RD, Ozmen L, Wettstein JG, Pinard A, Buchy D, Gassmann M, Hoener MC, Bettler B. The selective antagonist EPPTB reveals TAAR1-mediated regulatory mechanisms in dopaminergic neurons of the mesolimbic system. Proc Natl Acad Sci U S A. 2009 Nov 24;106(47):20081-6.

Keywords:

MDRUN, late stage, powders, purchased, SAR, medchem, dose response, mood, cognition, addiction, ANT, INH, FLIPR, TAAR1, hTAAR1, MGC126874, MGC138399, RP11-295F4.9, TA1, TAR1, TRAR1, receptor, taR-1, trace amine receptor, trace amine-associated receptor 1, GPCR, Fluo-8, FLUO8, RD-HGA, RD-HGA16, cells, cell-based, CHO, dye, calcium, kinetic, fluorescence, antagonist, antagonism, inhibitor, inhibit, decrease, HTS, high throughput screen, 1536, Scripps Florida, The Scripps Research Institute Molecular Screening Center, SRIMSC, Molecular Libraries Probe Production Centers Network, MLPCN.
Protocol
Assay Overview:
The purpose of this assay is to determine dose response curves for available powder samples of compounds identified as active in a set of previous experiments entitled, "Fluorescence-based cell-based primary high throughput dose response assay to identify antagonists of the human trace amine associated receptor 1 (TAAR1)"(AID 686994). This assay allows TAAR1 to signal predominantly through calcium mobilization by stably expressing TAAR1 in the RD-HGA16 cell line. The RD-HGA16 cell line is a CHO cell-derived cell line that stably expresses Ga16. Ga16 has been shown to couple many GPCRs to calcium mobilization regardless of their endogenous signaling mechanisms. In other words, this cell line permits the coupling of non-Gq-coupled G-protein-coupled receptors to the mobilization of internal calcium. In this assay the CHO-Ga16 cell line is incubated with a fluorescent, cell permeable calcium indicator dye (Fluo-8). The dye serves to monitor levels of intracellular calcium. Test compounds are then added to the cells, followed by the addition of the TAAR1 agonist Beta-PEA. As designed, compounds that act as TAAR1 antagonists will decrease calcium mobilization, resulting in decreased relative fluorescence of the indicator dye, and decreased well fluorescence. The compounds are tested at 29.9uM with a 10 point, 1:3 dilution series in triplicate.
Protocol Summary:
The TAAR1-HGA16 cell line was routinely cultured in T-175 sq cm flasks at 37 C and 95% relative humidity (RH). The growth media consisted of Ham's F-12 Nutrient Media (F-12) supplemented with 10% v/v heat-inactivated qualified fetal bovine serum, 20 mM HEPES, 400 ug/mL Geneticin, 200 ug/mL Hygromycin and 1X antibiotic mix (penicillin and streptomycin).
The day before the assay 750 cells in 3 uL of growth media, lacking Geneticin and Hygromycin, were seeded into each well of 1536 well microtiter plates and allowed to incubate at 37 C, 5% CO2, and 95 % RH for 17-24 hours. Next, 2 uL of the fluorogenic Fluo-8 intracellular calcium indicator mixture (prepared according to the manufacturer's protocol) was added to each well. Plates were then incubated for 75 minutes at 37 C, 5% CO2, and 95 % RH, followed by 30 minute incubation at room temperature. Then, 30 nL of 100% DMSO was added to each well and incubated at room temperature for 5 minutes. Then, 15 nL of test compound in DMSO were dispensed to appropriate wells. The assay was started by performing a basal read of plate fluorescence (470-495 nm excitation and 515-575 nm emission) for 5 seconds on the FLIPR Tetra (Molecular Devices). Then a real time fluorescence measurement was immediately performed for the remaining 140 seconds of the assay. Then, a basal read of plate fluorescence for 5 seconds on the FLIPR Tetra prior to all wells being treated with EC80 of PEA in DMSO. Then a real time fluorescence measurement was immediately performed for the remaining 140 seconds of the assay (this is the read for the antagonist mode).
Hits for this assay were determined according to the following mathematical expression:
Ratio = I_Max / I_Min
Where:
I_Max represents the maximum measured fluorescence emission intensity over the 140 second read for the antagonist mode and;
I_Min represents the minimum (basal) measured fluorescence emission intensity before EC80 of PEA was added.
The percent inhibition was calculated from the median ratio as follows:
%_Inhibition = ( 1 - ( Ratio Test_Compound - Median_Ratio_High_Control ) / ( Median_Ratio_Low_Control - Median_Ratio_High_Control ) ) ) * 100
Where:
Test_Compound is defined as wells containing test compound.
High_Control is defined as wells containing DMSO.
Low_Control is defined as wells containing PEA (EC80) and DMSO.
For each test compound, percent inhibition was plotted against compound concentration. A four parameter equation describing a sigmoidal dose-response curve was then fitted with adjustable baseline using Assay Explorer software (Accelrys Inc). The reported IC50 values were generated from fitted curves by solving for the X-intercept value at the 50% activation level of the Y-intercept value. In cases where the highest concentration tested (i.e. 29.9 uM) did not result in greater than 50% activation, the IC50 was determined manually as greater than 29.9 uM.
PubChem Activity Outcome and Score:
Compounds with an IC50 greater than 10 uM were considered inactive. Compounds with an IC50 equal to or less than 10 uM were considered active.
Any compound with a percent activity value < 50% at all test concentrations was assigned an activity score of zero. Any compound with a percent activity value >= 50% at any test concentration was assigned an activity score greater than zero.
Activity score was then ranked by the potency of the compounds with fitted curves, with the most potent compounds assigned the highest activity scores.
The PubChem Activity Score range for active compounds is 100-0, and for inactive compounds 0-0.
List of Reagents:
RD-HGA Cell Line (Molecular Devices)
Agonist:PEA Control (Sigma, P6513)
Calcium sensitive dye: Fluo-8 No Wash Calcium Assay Kit; (AAT Bioquest, part 36316)
Growth media: Ham's F-12; 10% FBS, 20mM HEPES, 400 ug/mL G418, 200ug/ml Hygromycin
Assay media: Ham's F-12, 10% FBS, 20 mM HEPES
Assay plates: Corning black/clear 1536well FLIPR plate; (Corning, part 7338)
Probenecid: 250mM (pH 8.0); (Sigma P8761)
Ham's F-12 Nutrient Mixture (Invitrogen, part 11765-054)
Charcoal/Dextran-treated Feta Bovine Serum (Hyclone, part SH3006803HI)
Penicillin-Streptomycin(100X) (Invitrogen, 15070-063)
Hygromycin B (Invitrogen, part 10687-010)
Geneticin(R) Selective Antibiotic (Invitrogen, part 10131-027)
Detachin Cell Detachment Reagent (Genlantis, part T100100)
T-175 Flasks (Nunc, part 159910)
Comment
Due to the increasing size of the MLPCN compound library, this assay may have been run as two or more separate campaigns, each campaign testing a unique set of compounds. All data reported were normalized on a per-plate basis. Possible artifacts of this assay can include, but are not limited to: dust or lint located in or on wells of the microtiter plate, and compounds that modulate well fluorescence. All test compound concentrations reported above and below are nominal; the specific test concentration(s) for a particular compound may vary based upon the actual sample provided by the MLSMR.
Due to limitations in the amount of MLSMR compounds that could be selected for retesting, compounds that demonstrated selective activity in AID 624466 vs. other Fluo8 antagonist screening assays run at the SRIMSC were prioritized for testing in this assay. Compounds that were agonist hits in AID 624467 were also not selected for testing in this assay.
Categorized Comment - additional comments and annotations
From BioAssay Depositor:
Assay: CurveFit [1]: Equation: =( ( [Maximal Response] * [Concentration]^[Hill Slope] ) / ( [Inflection Point Concentration]^[Hill Slope] + [Concentration]^[Hill Slope] ) ) + [Baseline Response]
Assay: CurveFit [1]: Mask: Excluded Points
Assay: Dictionary: Version: 0.1
Result Definitions
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TIDNameDescriptionHistogramTypeUnit
OutcomeThe BioAssay activity outcomeOutcome
ScoreThe BioAssay activity ranking scoreInteger
1Qualifierinhibition Qualifier identifies if the resultant data IC50 came from a fitted curve or was determined manually to be less than or greater than its listed IC50 concentration.String
2IC50*The concentration at which 50 percent of the inhibition in the inhibitor assay is observed; (IC50) shown in micromolar.FloatμM
3LogIC50Log10 of the qualified IC50 (IC50) from the inhibitor assay in M concentrationFloat
4Maximal ResponseThe maximal or asymptotic response above the baseline as concentration increases without bound.Float
5Baseline ResponseAdjustable baseline of the curve fit, minimal response value.Float
6Inflection Point ConcentrationThe concentration value for the inflection point of the curve.FloatμM
7Chi SquareA measure for the 'goodness' of a fit. The chi-square test (Snedecor and Cochran, 1989) is used to test if a sample of data came from a population with a specific distribution.Float
8RsquareThis statistic measures how successful the fit explains the variation of the data; R-square is the square of the correlation between the response values and the predicted response values.Float
9Number of DataPointsOverall number of data points of normalized percent inhibition that was used for calculations (includes all concentration points); in some cases a data point can be excluded as outlier.Integer
10Hill SlopeThe variable HillSlope describes the steepness of the curve. This variable is called the Hill slope, the slope factor, or the Hill coefficient. If it is positive, the curve increases as X increases. If it is negative, the curve decreases as X increases. A standard sigmoid dose-response curve (previous equation) has a Hill Slope of 1.0. When HillSlope is less than 1.0, the curve is more shallow. When HillSlope is greater than 1.0, the curve is steeper. The Hill slope has no units.Float
11Response RangeThe range of Y.Float
12Excluded PointsFlags to indicate which of the dose-response points were excluded from analysis. (1) means the point was excluded and (0) means the point was not excluded.String
13Inhibition at 0.0015 uM [1] (0.0015μM**)Value of % inhibition at 0.0015 uM compound concentration; replicate [1]Float%
14Inhibition at 0.0015 uM [2] (0.0015μM**)Value of % inhibition at 0.0015 uM compound concentration; replicate [2]Float%
15Inhibition at 0.0015 uM [3] (0.0015μM**)Value of % inhibition at 0.0015 uM compound concentration; replicate [3]Float%
16Inhibition at 0.0045 uM [1]String
17Inhibition at 0.0045 uM [2]String
18Inhibition at 0.0045 uM [3]String
19Inhibition at 0.014 uM [1] (0.014μM**)Value of % inhibition at 0.014 uM compound concentration; replicate [1]Float%
20Inhibition at 0.014 uM [2] (0.014μM**)Value of % inhibition at 0.014 uM compound concentration; replicate [2]Float%
21Inhibition at 0.014 uM [3] (0.014μM**)Value of % inhibition at 0.014 uM compound concentration; replicate [3]Float%
22Inhibition at 0.041 uM [1] (0.041μM**)Value of % inhibition at 0.041 uM compound concentration; replicate [1]Float%
23Inhibition at 0.041 uM [2] (0.041μM**)Value of % inhibition at 0.041 uM compound concentration; replicate [2]Float%
24Inhibition at 0.041 uM [3] (0.041μM**)Value of % inhibition at 0.041 uM compound concentration; replicate [3]Float%
25Inhibition at 0.12 uM [1] (0.12μM**)Value of % inhibition at 0.12 uM compound concentration; replicate [1]Float%
26Inhibition at 0.12 uM [2] (0.12μM**)Value of % inhibition at 0.12 uM compound concentration; replicate [2]Float%
27Inhibition at 0.12 uM [3] (0.12μM**)Value of % inhibition at 0.12 uM compound concentration; replicate [3]Float%
28Inhibition at 0.37 uM [1] (0.37μM**)Value of % inhibition at 0.37 uM compound concentration; replicate [1]Float%
29Inhibition at 0.37 uM [2] (0.37μM**)Value of % inhibition at 0.37 uM compound concentration; replicate [2]Float%
30Inhibition at 0.37 uM [3] (0.37μM**)Value of % inhibition at 0.37 uM compound concentration; replicate [3]Float%
31Inhibition at 1.1 uM [1] (1.1μM**)Value of % inhibition at 1.1 uM compound concentration; replicate [1]Float%
32Inhibition at 1.1 uM [2] (1.1μM**)Value of % inhibition at 1.1 uM compound concentration; replicate [2]Float%
33Inhibition at 1.1 uM [3] (1.1μM**)Value of % inhibition at 1.1 uM compound concentration; replicate [3]Float%
34Inhibition at 3.3 uM [1] (3.3μM**)Value of % inhibition at 3.3 uM compound concentration; replicate [1]Float%
35Inhibition at 3.3 uM [2] (3.3μM**)Value of % inhibition at 3.3 uM compound concentration; replicate [2]Float%
36Inhibition at 3.3 uM [3] (3.3μM**)Value of % inhibition at 3.3 uM compound concentration; replicate [3]Float%
37Inhibition at 10 uM [1] (10μM**)Value of % inhibition at 10 uM compound concentration; replicate [1]Float%
38Inhibition at 10 uM [2] (10μM**)Value of % inhibition at 10 uM compound concentration; replicate [2]Float%
39Inhibition at 10 uM [3] (10μM**)Value of % inhibition at 10 uM compound concentration; replicate [3]Float%
40Inhibition at 29.9 uM [1] (29.9μM**)Value of % inhibition at 29.9 uM compound concentration; replicate [1]Float%
41Inhibition at 29.9 uM [2] (29.9μM**)Value of % inhibition at 29.9 uM compound concentration; replicate [1]Float%
42Inhibition at 29.9 uM [3] (29.9μM**)Value of % inhibition at 29.9 uM compound concentration; replicate [3]Float%

* Activity Concentration. ** Test Concentration.
Additional Information
Grant Number: 1R21NS064780-01A1

Data Table (Concise)
Data Table ( Complete ):     View Active Data    View All Data
Classification
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