Name: Counterscreen for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS): Luminescence-based cell-based high throughput dose response assay to identify compounds that are cytotoxic to Jurkat human T lymphocyte cells. ..more
BioActive Compounds: 2
Depositor Specified Assays
| AID | Name | Type | Comment |
|---|---|---|---|
| 624268 | Luminescence-based biochemical primary high throughput screening assay to identify inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS) | screening | Primary screen (MetRS inhibitors in singlicate) |
| 624282 | Summary of the probe development efforts to identify inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS) | summary | Summary (MetRS inhibitors) |
| 624412 | Luminescence-based biochemical high throughput confirmation assay for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS) | screening | Confirmation screen (MetRS inhibitors in triplicate) |
| 624413 | Counterscreen for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS): Luminescence-based cell-based high throughput assay to identify compounds that are cytotoxic to Jurkat human T lymphocyte cells | screening | Counterscreen (Jurkat human T lymphocyte cells in triplicate) |
| 651607 | Fluorescent Polarization-based biochemical high throughput orthogonal assay for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS) | screening | Counterscreen (MetRS orthogonal assay in triplicate) |
| 686967 | On Hold | ||
| 686968 | On Hold | ||
| 686969 | On Hold |
Description:
Source (MLPCN Center Name): The Scripps Research Institute Molecular Screening Center (SRIMSC)
Affiliation: University of Washington
Assay Provider: Wilhelmus Hol, University of Washington
Network: Molecular Library Probe Production Centers Network (MLPCN)
Grant Proposal Number: 1 R01 AI084004-01A1
Grant Proposal PI: Wilhelmus Hol, University of Washington
External Assay ID: JURKAT_INH_LUMI_1536_3XIC50 DCSRUN (MetRS)
Name: Counterscreen for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS): Luminescence-based cell-based high throughput dose response assay to identify compounds that are cytotoxic to Jurkat human T lymphocyte cells.
Description:
Human African trypanosomiasis (HAT; also called sleeping sickness) is a neglected tropical disease that is caused by the protozoan Trypanosoma brucei, which employs the tsetse fly as its insect vector. Related tropical diseases include Chagas disease (caused by Trypanosoma cruzi) and leishmaniasis (caused by Leishmania species). Each of these diseases has a major impact on human health around the world and they lack adequate chemotherapeutic treatment options (1), as current therapies suffer from poor efficacy, oral bioavailability (2), toxicity, and difficult treatment regimens (3). As a result there is a great need to develop novel, more selective, and effective treatments (4). The aminoacyl-tRNA synthetases (aaRS) play essential roles in protein synthesis and cell survival and thus are attractive targets for the design of novel chemotherapeutic agents for these diseases (3). aaRS enzymes are essential to translating nucleotide-encoded gene sequences into proteins. Thus, inhibitors that interfere with these enzymes will inhibit formation of properly charged tRNA, leading to accumulation of uncharged tRNA on the ribosome, and disruption of normal protein chain elongation during translation, which are detrimental to cell viability. In particular, genomic studies have revealed sequence differences between the T. brucei trypanosome and mammalian methionyl-tRNA synthetases (MetRSs: which are members of the aaRS family), suggesting that selective inhibition of this enzyme and protozoan death can be achieved using drug-like molecules (2). Using RNA interference, T. brucei MetRS has been shown to be essential for parasite survival (3). In addition, since the MetRS enzymes from Trypanosomatid organisms are highly homologous (particularly in the methionine-ATP binding pocket) it is possible that compounds active against T. brucei MetRS will exhibit activity against the MetRS enzymes from T. cruzi and Leishmania.
References:
1. Gonzalez, M. and H. Cerecetto, Novel compounds to combat trypanosomatid infections: a medicinal chemical perspective. Expert Opin Ther Pat, 2011. 21(5): p. 699-715
2. Finn, J., M. Stidham, M. Hilgers, and C.K. G, Identification of novel inhibitors of methionyl-tRNA synthetase (MetRS) by virtual screening. Bioorg Med Chem Lett, 2008. 18(14): p. 3932-7.
3. Shibata, S., J.R. Gillespie, A.M. Kelley, A.J. Napuli, Z. Zhang, K.V. Kovzun, R.M. Pefley, J. Lam, F.H. Zucker, W.C. Van Voorhis, E.A. Merritt, W.G. Hol, C.L. Verlinde, E. Fan, and F.S. Buckner, Selective inhibitors of methionyl-tRNA synthetase have potent activity against Trypanosoma brucei Infection in Mice. Antimicrob Agents Chemother, 2011. 55(5): p. 1982-9.
4. Ding, D., Q. Meng, G. Gao, Y. Zhao, Q. Wang, B. Nare, R. Jacobs, F. Rock, M.R. Alley, J.J. Plattner, G. Chen, D. Li, and H. Zhou, Design, synthesis, and structure-activity relationship of Trypanosoma brucei leucyl-tRNA synthetase inhibitors as antitrypanosomal agents. J Med Chem, 2011. 54(5): p. 1276-87.
Keywords:
DRUN, triplicate, dose, dose response, titration, counterscreen, DCSRUN, Jurkat, viability, cytotoxicity, proliferation, metabolism, CellTiter-Glo, enzyme, T. brucei, parasite, MetRS, methionyl tRNA synthetase, ligase, Aminoacyl-tRNA synthetase, aaRS, tRNA, methionine, methionyl, kinetic, biochemical, enzymatic, luciferase, luc, ATP depletion, luciferin, ATP, methionine, Luminescence, Lumi, RLU, inhibit, inhibitor, inhibition, Trypanosoma brucei, protozoa, HTS, high throughput screen, 1536, Scripps, Scripps Florida, MLSMR, The Scripps Research Institute Molecular Screening Center, SRIMSC, Molecular Libraries Probe Production Centers Network, MLPCN.
Affiliation: University of Washington
Assay Provider: Wilhelmus Hol, University of Washington
Network: Molecular Library Probe Production Centers Network (MLPCN)
Grant Proposal Number: 1 R01 AI084004-01A1
Grant Proposal PI: Wilhelmus Hol, University of Washington
External Assay ID: JURKAT_INH_LUMI_1536_3XIC50 DCSRUN (MetRS)
Name: Counterscreen for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS): Luminescence-based cell-based high throughput dose response assay to identify compounds that are cytotoxic to Jurkat human T lymphocyte cells.
Description:
Human African trypanosomiasis (HAT; also called sleeping sickness) is a neglected tropical disease that is caused by the protozoan Trypanosoma brucei, which employs the tsetse fly as its insect vector. Related tropical diseases include Chagas disease (caused by Trypanosoma cruzi) and leishmaniasis (caused by Leishmania species). Each of these diseases has a major impact on human health around the world and they lack adequate chemotherapeutic treatment options (1), as current therapies suffer from poor efficacy, oral bioavailability (2), toxicity, and difficult treatment regimens (3). As a result there is a great need to develop novel, more selective, and effective treatments (4). The aminoacyl-tRNA synthetases (aaRS) play essential roles in protein synthesis and cell survival and thus are attractive targets for the design of novel chemotherapeutic agents for these diseases (3). aaRS enzymes are essential to translating nucleotide-encoded gene sequences into proteins. Thus, inhibitors that interfere with these enzymes will inhibit formation of properly charged tRNA, leading to accumulation of uncharged tRNA on the ribosome, and disruption of normal protein chain elongation during translation, which are detrimental to cell viability. In particular, genomic studies have revealed sequence differences between the T. brucei trypanosome and mammalian methionyl-tRNA synthetases (MetRSs: which are members of the aaRS family), suggesting that selective inhibition of this enzyme and protozoan death can be achieved using drug-like molecules (2). Using RNA interference, T. brucei MetRS has been shown to be essential for parasite survival (3). In addition, since the MetRS enzymes from Trypanosomatid organisms are highly homologous (particularly in the methionine-ATP binding pocket) it is possible that compounds active against T. brucei MetRS will exhibit activity against the MetRS enzymes from T. cruzi and Leishmania.
References:
1. Gonzalez, M. and H. Cerecetto, Novel compounds to combat trypanosomatid infections: a medicinal chemical perspective. Expert Opin Ther Pat, 2011. 21(5): p. 699-715
2. Finn, J., M. Stidham, M. Hilgers, and C.K. G, Identification of novel inhibitors of methionyl-tRNA synthetase (MetRS) by virtual screening. Bioorg Med Chem Lett, 2008. 18(14): p. 3932-7.
3. Shibata, S., J.R. Gillespie, A.M. Kelley, A.J. Napuli, Z. Zhang, K.V. Kovzun, R.M. Pefley, J. Lam, F.H. Zucker, W.C. Van Voorhis, E.A. Merritt, W.G. Hol, C.L. Verlinde, E. Fan, and F.S. Buckner, Selective inhibitors of methionyl-tRNA synthetase have potent activity against Trypanosoma brucei Infection in Mice. Antimicrob Agents Chemother, 2011. 55(5): p. 1982-9.
4. Ding, D., Q. Meng, G. Gao, Y. Zhao, Q. Wang, B. Nare, R. Jacobs, F. Rock, M.R. Alley, J.J. Plattner, G. Chen, D. Li, and H. Zhou, Design, synthesis, and structure-activity relationship of Trypanosoma brucei leucyl-tRNA synthetase inhibitors as antitrypanosomal agents. J Med Chem, 2011. 54(5): p. 1276-87.
Keywords:
DRUN, triplicate, dose, dose response, titration, counterscreen, DCSRUN, Jurkat, viability, cytotoxicity, proliferation, metabolism, CellTiter-Glo, enzyme, T. brucei, parasite, MetRS, methionyl tRNA synthetase, ligase, Aminoacyl-tRNA synthetase, aaRS, tRNA, methionine, methionyl, kinetic, biochemical, enzymatic, luciferase, luc, ATP depletion, luciferin, ATP, methionine, Luminescence, Lumi, RLU, inhibit, inhibitor, inhibition, Trypanosoma brucei, protozoa, HTS, high throughput screen, 1536, Scripps, Scripps Florida, MLSMR, 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 whether compounds that confirmed MetRS inhibitor activity in a set of previous experiments entitled, "Luminescence-based biochemical high throughput confirmation assay for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS)" (AID 624412) are nonselective or cytotoxic. This assay determines dose response curves.
This assay employs Jurkat cells, a human T-cell line originally isolated from an adolescent male with T cell leukemia (2). The cells are grown in suspension. The end point assays presented here employed the CellTiter-Glo luminescent reagent (3), which contains luciferase enzyme to catalyze the oxidation of beetle luciferin to oxyluciferin and light in the presence of Jurkat cell ATP. Since metabolically active cells produce ATP, an increase in the number of dead or dying cells will correlate with a reduction in ATP levels. As designed, compounds that inhibit cell viability and reduce intracellular ATP will reduce the catalytic conversion of luciferin into oxyluciferin, resulting in decreased luciferase activity and well luminescence. This assay included as a positive control doxorubicin, an antibiotic used as an anti-cancer drug. Compounds are tested in triplicate using a 10-point 1:3 dilution series starting at a maximum nomimal test concentration of 83 uM.
Protocol Summary:
Jurkat cells (clone E6.1) were routinely cultured in suspension in T-175 standing flasks at 37 C in 95% relative humidity (RH) at 5% CO2 in growth media. Growth media consisted of RPMI-1640 containing 10% dialyzed fetal bovine serum, 0.1 mM NEAA, 1mM Sodium Pyruvate, 25mM HEPES, 5mM L Glutamine, and 1x antibiotic.
Prior to the start of the assay, cells were suspended to a concentration of 100,000 cells/ml in assay media consisting of RPMI-1640 containing 10% dialyzed fetal bovine serum, 0.1 mM NEAA, 1mM Sodium Pyruvate, 25 mM HEPES, 5 mM L Glutamine, and 1x antibiotic. To start the assay, 5 uL of assay media was dispensed into the first two columns of a 1536 well plate and 5 ul of cell suspension to the remaining wells (500 cells per well). The assay was started immediately by dispensing 42 nL of test compound in DMSO, Doxurubicin (8 uM final concentration) or DMSO alone (0.6% final concentration) to the appropriate wells. The plates were then incubated for 48 hours at 37 C, 5% CO2 and 95% RH).
Following the two day incubation, plates were equilibrated to room temperature for 10 minutes and 5 ul of CellTiter-Glo reagent was added to each well. Plates were centrifuged and incubated at room temperature for 10 minutes. Well luminescence was measured on the ViewLux plate reader. The percent inhibition for each compound was calculated as follows:
%_Inhibition = ( ( Test_Compound - Median_Low_Control ) / ( Median_High_Control - Median_Low_Control ) ) * 100
Where:
Test_Compound is defined as wells containing test compound.
Low_Control is defined as wells containing 0.6% DMSO. (0% inhibition)
High_Control is defined as wells containing 8 uM doxorubicin in 0.6% DMSO (100% inhibition).
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. 83 uM) did not result in greater than 50% activation, the IC50 was determined manually as greater than 83 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 100-92, and for inactive compounds 84-0.
List of Reagents:
Jurkat cells (clone E6.1; ATCC Cat# TIB-152, Invitrogen Cat# K1045)
Cell Titer Glo (Promega, part G7573)
Doxorubicin (Fisher, part BP251610)
RPMI (Invitrogen, part 11875)
Fetal Bovine Serum (Fisher, part SH3008803)
NEAA (Invitrogen, part 11140-050)
Hepes (Invitrogen, part 15630-080)
Anti-Anti (Invitrogen, part 15240)
L-Glutamine (Invitrogen, part 25030-081)
Sodium Pyruvate (Invitrogen, part 11360-070)
T-175 culture flasks (Thermo Scientific Nunc, part 12562000)
1536-well plates (Corning, part 7254)
The purpose of this assay is to determine whether compounds that confirmed MetRS inhibitor activity in a set of previous experiments entitled, "Luminescence-based biochemical high throughput confirmation assay for inhibitors of Trypanosoma brucei methionyl tRNA synthetase (MetRS)" (AID 624412) are nonselective or cytotoxic. This assay determines dose response curves.
This assay employs Jurkat cells, a human T-cell line originally isolated from an adolescent male with T cell leukemia (2). The cells are grown in suspension. The end point assays presented here employed the CellTiter-Glo luminescent reagent (3), which contains luciferase enzyme to catalyze the oxidation of beetle luciferin to oxyluciferin and light in the presence of Jurkat cell ATP. Since metabolically active cells produce ATP, an increase in the number of dead or dying cells will correlate with a reduction in ATP levels. As designed, compounds that inhibit cell viability and reduce intracellular ATP will reduce the catalytic conversion of luciferin into oxyluciferin, resulting in decreased luciferase activity and well luminescence. This assay included as a positive control doxorubicin, an antibiotic used as an anti-cancer drug. Compounds are tested in triplicate using a 10-point 1:3 dilution series starting at a maximum nomimal test concentration of 83 uM.
Protocol Summary:
Jurkat cells (clone E6.1) were routinely cultured in suspension in T-175 standing flasks at 37 C in 95% relative humidity (RH) at 5% CO2 in growth media. Growth media consisted of RPMI-1640 containing 10% dialyzed fetal bovine serum, 0.1 mM NEAA, 1mM Sodium Pyruvate, 25mM HEPES, 5mM L Glutamine, and 1x antibiotic.
Prior to the start of the assay, cells were suspended to a concentration of 100,000 cells/ml in assay media consisting of RPMI-1640 containing 10% dialyzed fetal bovine serum, 0.1 mM NEAA, 1mM Sodium Pyruvate, 25 mM HEPES, 5 mM L Glutamine, and 1x antibiotic. To start the assay, 5 uL of assay media was dispensed into the first two columns of a 1536 well plate and 5 ul of cell suspension to the remaining wells (500 cells per well). The assay was started immediately by dispensing 42 nL of test compound in DMSO, Doxurubicin (8 uM final concentration) or DMSO alone (0.6% final concentration) to the appropriate wells. The plates were then incubated for 48 hours at 37 C, 5% CO2 and 95% RH).
Following the two day incubation, plates were equilibrated to room temperature for 10 minutes and 5 ul of CellTiter-Glo reagent was added to each well. Plates were centrifuged and incubated at room temperature for 10 minutes. Well luminescence was measured on the ViewLux plate reader. The percent inhibition for each compound was calculated as follows:
%_Inhibition = ( ( Test_Compound - Median_Low_Control ) / ( Median_High_Control - Median_Low_Control ) ) * 100
Where:
Test_Compound is defined as wells containing test compound.
Low_Control is defined as wells containing 0.6% DMSO. (0% inhibition)
High_Control is defined as wells containing 8 uM doxorubicin in 0.6% DMSO (100% inhibition).
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. 83 uM) did not result in greater than 50% activation, the IC50 was determined manually as greater than 83 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 100-92, and for inactive compounds 84-0.
List of Reagents:
Jurkat cells (clone E6.1; ATCC Cat# TIB-152, Invitrogen Cat# K1045)
Cell Titer Glo (Promega, part G7573)
Doxorubicin (Fisher, part BP251610)
RPMI (Invitrogen, part 11875)
Fetal Bovine Serum (Fisher, part SH3008803)
NEAA (Invitrogen, part 11140-050)
Hepes (Invitrogen, part 15630-080)
Anti-Anti (Invitrogen, part 15240)
L-Glutamine (Invitrogen, part 25030-081)
Sodium Pyruvate (Invitrogen, part 11360-070)
T-175 culture flasks (Thermo Scientific Nunc, part 12562000)
1536-well plates (Corning, part 7254)
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 luminescence. 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. The MLSMR was not able to provide all compounds selected for testing in this assay.
Categorized Comment
Assay: Dictionary: Version: 0.1
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: CurveFit [1]: Equation: =( ( [Maximal Response] * [Concentration]^[Hill Slope] ) / ( [Inflection Point Concentration]^[Hill Slope] + [Concentration]^[Hill Slope] ) ) + [Baseline Response]
Assay: CurveFit [1]: Mask: Excluded Points
Result Definitions
Show more |
| TID | Name | Description | Histogram | Type | Unit | |
|---|---|---|---|---|---|---|
| Outcome | The BioAssay activity outcome | Outcome | ||||
| Score | The BioAssay activity ranking score |  | Integer | |||
| 1 | Qualifier | Activity 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 | |||
| 2 | IC50* | The concentration at which 50 percent of the activity in the inhibitor assay is observed; (IC50) shown in micromolar. | | Float | μM | |
| 3 | LogIC50 | Log10 of the qualified IC50 (IC50) from the inhibitor assay in M concentration | | Float | ||
| 4 | Maximal Response | The maximal or asymptotic response above the baseline as concentration increases without bound. | | Float | ||
| 5 | Baseline Response | Adjustable baseline of the curve fit, minimal response value. | | Float | ||
| 6 | Inflection Point Concentration | The concentration value for the inflection point of the curve. | | Float | μM | |
| 7 | Hill Slope | The 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 | ||
| 8 | Response Range | The range of Y. | | Float | ||
| 9 | Chi Square | A 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 | ||
| 10 | Rsquare | This 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 | ||
| 11 | Number of DataPoints | Overall 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 | ||
| 12 | Excluded Points | Flags 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 | |||
| 13 | Inhibition at 0.004 uM [1] (0.004μM**) | Value of % inhibition at 0.004 uM compound concentration; replicate [1] | | Float | % | |
| 14 | Inhibition at 0.004 uM [2] (0.004μM**) | Value of % inhibition at 0.004 uM compound concentration; replicate [2] | | Float | % | |
| 15 | Inhibition at 0.004 uM [3] (0.004μM**) | Value of % inhibition at 0.004 uM compound concentration; replicate [3] | | Float | % | |
| 16 | Inhibition at 0.013 uM [1] (0.013μM**) | Value of % inhibition at 0.013 uM compound concentration; replicate [1] | | Float | % | |
| 17 | Inhibition at 0.013 uM [2] (0.013μM**) | Value of % inhibition at 0.013 uM compound concentration; replicate [2] | | Float | % | |
| 18 | Inhibition at 0.013 uM [3] (0.013μM**) | Value of % inhibition at 0.013 uM compound concentration; replicate [3] | | Float | % | |
| 19 | Inhibition at 0.038 uM [1] (0.038μM**) | Value of % inhibition at 0.038 uM compound concentration; replicate [1] | | Float | % | |
| 20 | Inhibition at 0.038 uM [2] (0.038μM**) | Value of % inhibition at 0.038 uM compound concentration; replicate [2] | | Float | % | |
| 21 | Inhibition at 0.038 uM [3] (0.038μM**) | Value of % inhibition at 0.038 uM compound concentration; replicate [3] | | Float | % | |
| 22 | Inhibition at 0.114 uM [1] (0.114μM**) | Value of % inhibition at 0.114 uM compound concentration; replicate [1] | | Float | % | |
| 23 | Inhibition at 0.114 uM [2] (0.114μM**) | Value of % inhibition at 0.114 uM compound concentration; replicate [2] | | Float | % | |
| 24 | Inhibition at 0.114 uM [3] (0.114μM**) | Value of % inhibition at 0.114 uM compound concentration; replicate [3] | | Float | % | |
| 25 | Inhibition at 0.343 uM [1] (0.343μM**) | Value of % inhibition at 0.343 uM compound concentration; replicate [1] | | Float | % | |
| 26 | Inhibition at 0.343 uM [2] (0.343μM**) | Value of % inhibition at 0.343 uM compound concentration; replicate [2] | | Float | % | |
| 27 | Inhibition at 0.343 uM [3] (0.343μM**) | Value of % inhibition at 0.343 uM compound concentration; replicate [3] | | Float | % | |
| 28 | Inhibition at 1.0 uM [1] (1μM**) | Value of % inhibition at 1.0 uM compound concentration; replicate [1] | | Float | % | |
| 29 | Inhibition at 1.0 uM [2] (1μM**) | Value of % inhibition at 1.0 uM compound concentration; replicate [2] | | Float | % | |
| 30 | Inhibition at 1.0 uM [3] (1μM**) | Value of % inhibition at 1.0 uM compound concentration; replicate [3] | | Float | % | |
| 31 | Inhibition at 3.1 uM [1] (3.1μM**) | Value of % inhibition at 3.1 uM compound concentration; replicate [1] | | Float | % | |
| 32 | Inhibition at 3.1 uM [2] (3.1μM**) | Value of % inhibition at 3.1 uM compound concentration; replicate [2] | | Float | % | |
| 33 | Inhibition at 3.1 uM [3] (3.1μM**) | Value of % inhibition at 3.1 uM compound concentration; replicate [3] | | Float | % | |
| 34 | Inhibition at 9.3 uM [1] (9.3μM**) | Value of % inhibition at 9.3 uM compound concentration; replicate [1] | | Float | % | |
| 35 | Inhibition at 9.3 uM [2] (9.3μM**) | Value of % inhibition at 9.3 uM compound concentration; replicate [2] | | Float | % | |
| 36 | Inhibition at 9.3 uM [3] (9.3μM**) | Value of % inhibition at 9.3 uM compound concentration; replicate [3] | | Float | % | |
| 37 | Inhibition at 27.8 uM [1] (27.8μM**) | Value of % inhibition at 27.8 uM compound concentration; replicate [1] | | Float | % | |
| 38 | Inhibition at 27.8 uM [2] (27.8μM**) | Value of % inhibition at 27.8 uM compound concentration; replicate [2] | | Float | % | |
| 39 | Inhibition at 27.8 uM [3] (27.8μM**) | Value of % inhibition at 27.8 uM compound concentration; replicate [3] | | Float | % | |
| 40 | Inhibition at 83.5 uM [1] (83.5μM**) | Value of % inhibition at 83.5 uM compound concentration; replicate [1] | | Float | % | |
| 41 | Inhibition at 83.5 uM [2] (83.5μM**) | Value of % inhibition at 83.5 uM compound concentration; replicate [2] | | Float | % | |
| 42 | Inhibition at 83.5 uM [3] (83.5μM**) | Value of % inhibition at 83.5 uM compound concentration; replicate [3] | | Float | % |
* Activity Concentration. ** Test Concentration.
Additional Information
Grant Number: 1 R01 AI084004-01A1
Data Table (Concise)
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