Bookmark and Share
BioAssay: AID 651969

Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify nonselective inhibitors of the Steroidogenic acute regulatory protein (StAR) promoter or luminescence assay artifacts

Name: Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify nonselective inhibitors of the Steroidogenic acute regulatory protein (StAR) promoter or luminescence assay artifacts. ..more
_
   
 Tested Compounds
 Tested Compounds
All(239)
 
 
Inactive(239)
 
 
 Tested Substances
 Tested Substances
All(239)
 
 
Inactive(239)
 
 
 Related BioAssays
 Related BioAssays
AID: 651969
Data Source: The Scripps Research Institute Molecular Screening Center (STAR_INH_LUMI_1536_3XIC50 DCSRUN for LRH1 IAG)
BioAssay Type: Confirmatory, Concentration-Response Relationship Observed
Depositor Category: NIH Molecular Libraries Probe Production Network
Deposit Date: 2013-01-08

Data Table ( Complete ):           View All Data
Tested Compounds:
Related Experiments
Show more
AIDNameTypeComment
602396Luminescence-based cell-based primary high throughput screening assay to identify inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2)Screeningdepositor-specified cross reference: Primary screen (LRH-1 inhibitors in singlicate)
602418Summary of the probe development efforts to identify inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2)Summarydepositor-specified cross reference: Summary (LRH-1 inverse agonists)
651611Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput assay to identify nonselective inhibitors of the Steroidogenic acute regulatory protein (StAR) promoter or luminescence assay artifactsScreeningdepositor-specified cross reference: Counterscreen (StAR promoter non-selective inhbitors or luminescence assay artifacts in quadruplicat
651613Luminescence-based cell-based high throughput confirmation assay for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2)Screeningdepositor-specified cross reference: Confirmation assay (LRH-1 inverse agonists in triplicate)
651614Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput assay to identify inverse agonists of the Steroidogenic Factor 1 Nuclear Receptor (SF1; NR5A1)Screeningdepositor-specified cross reference: Counterscreen (SF1 inverse agonists in triplicate)
651615Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput assay to identify inhibitors of the Herpes Virus Virion Protein 16 (VP16)Screeningdepositor-specified cross reference: Counterscreen (VP16 inhibitors in triplicate)
651974Late stage counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify inhibitors of the Herpes Virus Virion Protein 16 (VP16)Confirmatorydepositor-specified cross reference
651975Late stage counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify nonselective inhibitors of the Steroidogenic acute regulatory protein (StAR) promoter or luminescence assay artifactsConfirmatorydepositor-specified cross reference
651976Late stage luminescence-based cell-based high throughput dose response assay for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2)Confirmatorydepositor-specified cross reference
651977Late stage counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify inverse agonists of the Steroidogenic Factor 1 Nuclear Receptor (SF1; NR5A1)Confirmatorydepositor-specified cross reference
686941Late stage assay provider counterscreen for P450 inhibition. LC-MS/MS-based assay to determine inhibitory activity of compounds against purified recombinantly expressed CYP3A4 and CYP3A5Otherdepositor-specified cross reference
686944Late stage assay provider counterscreen for P450 inhibition based on the formation of Vincristine M1 formation in Genotyped HLMOtherdepositor-specified cross reference
651968Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify inverse agonists of the Steroidogenic Factor 1 Nuclear Receptor (SF1; NR5A1)Confirmatorysame project related to Summary assay
651970Luminescence-based cell-based high throughput dose response assay for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2)Confirmatorysame project related to Summary assay
651973Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify inhibitors of the Herpes Virus Virion Protein 16 (VP16)Confirmatorysame project related to Summary assay
Description:
Source (MLPCN Center Name): The Scripps Research Institute Molecular Screening Center (SRIMSC)
Affiliation: The Scripps Research Institute, TSRI
Assay Provider: Patrick Griffin, TSRI
Network: Molecular Library Probe Production Centers Network (MLPCN)
Grant Proposal Number: CA134873
Grant Proposal PI: Patrick Griffin, TSRI
External Assay ID: STAR_INH_LUMI_1536_3XIC50 DCSRUN for LRH1 IAG

Name: Counterscreen for inverse agonists of the liver receptor homolog-1 (LRH-1; NR5A2): Luminescence-based cell-based high throughput dose response assay to identify nonselective inhibitors of the Steroidogenic acute regulatory protein (StAR) promoter or luminescence assay artifacts.

Description:

The goal of this project is to identify modulators (inverse agonists) of the orphan nuclear receptor LRH-1, which has been implicated in cancer by enhancing proliferation and cell cycle progression and metabolic disorders through its regulation of genes involved cholesterol and bile acid homeostasis.

NR5A2 or Liver receptor homologue-1 (LRH-1) is a member of the NR5A, or Ftz-F1, subfamily V nuclear receptors for which there are four members (1). Murine LRH-1 was originally identified due to its sequence homology to the Drosophila Fushi tarazu factor-1 but orthologs have been subsequently identified in several other species including rat, chicken, horse, zebrafish and human (2-7). LRH-1, and its closest family member steroidogenic factor-1 (SF-1, NR5A1), bind to identical DNA consensus sequences (response elements or REs) and both have the ability to bind phospholipids in their ligand binding domains (LBDs) (8-10). However, LRH-1 and SF-1 are expressed in different tissues and thus are considered likely to have non-overlapping, non-redundant functions. SF-1 expression is confined to steroidogenic tissues and adrenals where it regulates development, differentiation, steroidogenesis and sexual determination (5, 7, 11). LRH-1 is highly expressed in tissues of endodermal origin and its expression is essential for normal liver, intestine, and pancreas function. LRH-1 has also been shown to be expressed in the ovary and adipose tissue.

In a recent report, Chand and colleagues investigated the mechanism of action of LRH-1 in invasive breast cancer cells. They found that LRH-1 promotes motility and cell invasiveness in both ER-positive (MCF-7) and ER-negative (MDA-MB-231) breast cancer cells and similar effects were observed in non-tumorigenic mammary epithelial cells. Interestingly, both remodeling of the actin cytoskeleton and E-cadherin processing were observed when LRH-1 was over-expressed. These findings implicate LRH-1 in promotion of migration and invasion in breast cancer independent of estrogen sensitivity. Together these findings provided strong evidence that LRH-1 plays a significant role in tumor formation both in vitro and in vivo. Therefore, the identification of potent and selective LRH-1 inverse agonists may provide new approaches for the treatment of cancer.

References:

1. Fayard, E., J. Auwerx, and K. Schoonjans, LRH-1: an orphan nuclear receptor involved in development, metabolism and steroidogenesis. Trends Cell Biol, 2004. 14(5): p. 250-60.
2. Galarneau, L., J.F. Pare, D. Allard, D. Hamel, L. Levesque, J.D. Tugwood, S. Green, and L. Belanger, The alpha1-fetoprotein locus is activated by a nuclear receptor of the Drosophila FTZ-F1 family. Mol Cell Biol, 1996. 16(7): p. 3853-65.
3. Kudo, T. and S. Sutou, Molecular cloning of chicken FTZ-F1-related orphan receptors. Gene, 1997. 197(1-2): p. 261-8.
4. Boerboom, D., N. Pilon, R. Behdjani, D.W. Silversides, and J. Sirois, Expression and regulation of transcripts encoding two members of the NR5A nuclear receptor subfamily of orphan nuclear receptors, steroidogenic factor-1 and NR5A2, in equine ovarian cells during the ovulatory process. Endocrinology, 2000. 141(12): p. 4647-56.
5. Broadus, J., J.R. McCabe, B. Endrizzi, C.S. Thummel, and C.T. Woodard, The Drosophila beta FTZ-F1 orphan nuclear receptor provides competence for stage-specific responses to the steroid hormone ecdysone. Mol Cell, 1999. 3(2): p. 143-9.
6. Ellinger-Ziegelbauer, H., A.K. Hihi, V. Laudet, H. Keller, W. Wahli, and C. Dreyer, FTZ-F1-related orphan receptors in Xenopus laevis: transcriptional regulators differentially expressed during early embryogenesis. Mol Cell Biol, 1994. 14(4): p. 2786-97.
7. Lavorgna, G., H. Ueda, J. Clos, and C. Wu, FTZ-F1, a steroid hormone receptor-like protein implicated in the activation of fushi tarazu. Science, 1991. 252(5007): p. 848-51.
8. Li, Y., M. Choi, G. Cavey, J. Daugherty, K. Suino, A. Kovach, N.C. Bingham, S.A. Kliewer, and H.E. Xu, Crystallographic identification and functional characterization of phospholipids as ligands for the orphan nuclear receptor steroidogenic factor-1. Mol Cell, 2005. 17(4): p. 491-502.
9. Solomon, I.H., J.M. Hager, R. Safi, D.P. McDonnell, M.R. Redinbo, and E.A. Ortlund, Crystal structure of the human LRH-1 DBD-DNA complex reveals Ftz-F1 domain positioning is required for receptor activity. J Mol Biol, 2005. 354(5): p. 1091-102.
10. Krylova, I.N., E.P. Sablin, J. Moore, R.X. Xu, G.M. Waitt, J.A. MacKay, D. Juzumiene, J.M. Bynum, K. Madauss, V. Montana, L. Lebedeva, M. Suzawa, J.D. Williams, S.P. Williams, R.K. Guy, J.W. Thornton, R.J. Fletterick, T.M. Willson, and H.A. Ingraham, Structural Analyses Reveal Phosphatidyl Inositols as Ligands for the NR5 Orphan Receptors SF-1 and LRH-1. Cell, 2005. 120(3): p. 343-355.
11. Luo, X., Y. Ikeda, and K.L. Parker, A cell-specific nuclear receptor isa essential for adrenal and gonadal development and sexual differentiation. Cell, 1994. 77(4): p. 481-90.

Keywords:

DCSRUN, counterscreen, StAR, dose response, dose, titration, crc, triplicate, HTS, high throughput, 1536, Nuclear receptor, NR, CYP7A promoter-binding factor; alpha-1-fetoprotein transcription factor; b1-binding factor, hepatocyte transcription factor which activates enhancer II of hepatitis B virus; fetoprotein-alpha 1 (AFP) transcription factor; hepatocytic transcription factor; liver receptor homolog 1; liver receptor homolog-1; nuclear receptor NR5A2; nuclear receptor subfamily 5 group A member 2, LRH1, liver, activator, inverse agonist, transcriptional assay, luciferase, luminescence, 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 of compounds deemed promising after beeing evaluated in single-dose, triplicate experiments in the LRH-1, SF-1, VP16 and StAR promoter assays (AIDs 651613, 651614, 651615 and 651611, respectively).

This assay is specifically designed to determine whether or not previously selected compounds are luminescence artifacts.

This assay determines dose response inhibition curves for compounds against the StAR promoter. This cell-based counterscreen employs HEK293 cells transfected only with a luciferase reporter driven by the Steroidogenic acute regulatory protein (StAR) promoter. As designed, compounds that inhibit general transcription, are luminescence artifacts, will prevent activation of the 5xSFREStAR-luciferase reporter, leading to a decrease in well luminescence. Compounds are tested in triplicate using a 10-point 1:3 dilution series starting at a maximum nomimal test concentration of 36 uM.

Protocol Summary:

Seven million HEK293 cells were seeded in T-175 flasks 23 mL of DMEM media supplemented with 10% v/v fetal bovine serum and 1% v/v Anti-Anti. Flasks were then incubated for 48 hours at 37 C, 5% CO2 and 95% relative humidity (RH). The day prior to run the assay, cells were harvested using TrypLE, resuspended in fresh media at a density of 1 million cells per mL and seeded into new T-175 flasks (23 mL per flask). After being allowed to attach for one hour at 37 C, 5% CO2 and 95% RH, cells were transfected with 1 mL of preincubated mix of serum-free OptiMEM containing 23 ug of the pGL4.31 reporter plasmid, 100 ng of the Gal4-VP16 expression vector and 80 uL of transfection reagents. Twenty four hours post transfection, cells were harvested using 5 mL of TrypLE and resuspended at a concentration of 750,000 cells per mL in phenol-red free DMEM media supplemented as described above.

The assay was started by dispensing 5 uL of cell suspension into each well of a white, solid-bottom 1536-well plate using a flying reagent dispenser (i.e. 3,750 cells per well). The first two columns received non-transfected cells only as a control for background luminescence (no StAR promoter activity). Cells were then treated with 18 nL/well of test compoundsor DMSO as a negative control (final concentration 0.36%) using a PinTool transfer unit (GNF). Plates were then placed in the incubator at 37 C, 5% CO2 and 95%RH. Twenty four hours later, plates were removed from the incubator and equilibrated to room temperature for 10 minutes. Luciferase was detected by adding 5 uL per well of ONE-Glo luciferase detection reagent. After a 15 minutes incubation time, light emission was measured with the ViewLux reader (PerkinElmer).

The percent inhibition for each compound was calculated as follows:

%_Inhibition = ( 1 - ( Median_Positive_Control - Test_Compound ) / ( Median_Positive_Control - Median_Negative_Control ) * 100

Where:

Test_Compound is defined as wells containing test compound.
Low_Control is defined as wells containing DMSO.
High_Control is defined as wells containing untransfected cells.

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. 36 uM) did not result in greater than 50% activation, the IC50 was determined manually as greater than 36 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 inactive compounds is 100-0. There are no active compounds.

List of Reagents:

HEK-293 cells (ATCC, part CRL-1573)
DMEM media (Invitrogen, part 11965)
Fetal Bovine Serum (Hyclone, part SH30088.03)
Anti-Anti (Gibco, part 15240)
TrypLE (Invitrogen, part 12604)
T-175 flasks (Falcon, part 353112)
StAR-LUC plasmid (Assay Provider)
TransIT 293 transfection reagent (Mirus Corporation, part MIR-2700)
ONE-Glo luciferase reagent (Promega, part E6130)
White, solid-bottom 1536-well plates (Greiner, part 789173)
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 supply all compounds 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
From PubChem:
Assay Format: Cell-based
Assay Cell Type: MDA-MB-231
From ChEMBL:
Assay Format: Cell-based
Assay Type: Functional
Result Definitions
Show more
TIDNameDescriptionHistogramTypeUnit
OutcomeThe BioAssay activity outcomeOutcome
ScoreThe BioAssay activity ranking scoreInteger
1QualifierActivity 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 activity 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
7Hill 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
8Response RangeThe range of Y.Float
9Chi 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
10RsquareThis 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
11Number 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
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 0.002 uM [1] (0.002μM**)Value of % inhibition at 0.002 uM compound concentration; replicate [1]Float%
14Inhibition at 0.002 uM [2] (0.002μM**)Value of % inhibition at 0.002 uM compound concentration; replicate [2]Float%
15Inhibition at 0.002 uM [3] (0.002μM**)Value of % inhibition at 0.002 uM compound concentration; replicate [3]Float%
16Inhibition at 0.002 uM [4] (0.002μM**)Value of % inhibition at 0.002 uM compound concentration; replicate [4]Float%
17Inhibition at 0.005 uM [1] (0.005μM**)Value of % inhibition at 0.005 uM compound concentration; replicate [1]Float%
18Inhibition at 0.005 uM [2] (0.005μM**)Value of % inhibition at 0.005 uM compound concentration; replicate [2]Float%
19Inhibition at 0.005 uM [3] (0.005μM**)Value of % inhibition at 0.005 uM compound concentration; replicate [3]Float%
20Inhibition at 0.005 uM [4] (0.005μM**)Value of % inhibition at 0.005 uM compound concentration; replicate [4]Float%
21Inhibition at 0.016 uM [1] (0.016μM**)Value of % inhibition at 0.016 uM compound concentration; replicate [1]Float%
22Inhibition at 0.016 uM [2] (0.016μM**)Value of % inhibition at 0.016 uM compound concentration; replicate [2]Float%
23Inhibition at 0.016 uM [3] (0.016μM**)Value of % inhibition at 0.016 uM compound concentration; replicate [3]Float%
24Inhibition at 0.016 uM [4] (0.016μM**)Value of % inhibition at 0.016 uM compound concentration; replicate [4]Float%
25Inhibition at 0.049 uM [1] (0.049μM**)Value of % inhibition at 0.049 uM compound concentration; replicate [1]Float%
26Inhibition at 0.049 uM [2] (0.049μM**)Value of % inhibition at 0.049 uM compound concentration; replicate [2]Float%
27Inhibition at 0.049 uM [3] (0.049μM**)Value of % inhibition at 0.049 uM compound concentration; replicate [3]Float%
28Inhibition at 0.049 uM [4] (0.049μM**)Value of % inhibition at 0.049 uM compound concentration; replicate [4]Float%
29Inhibition at 0.148 uM [1] (0.148μM**)Value of % inhibition at 0.148 uM compound concentration; replicate [1]Float%
30Inhibition at 0.148 uM [2] (0.148μM**)Value of % inhibition at 0.148 uM compound concentration; replicate [2]Float%
31Inhibition at 0.148 uM [3] (0.148μM**)Value of % inhibition at 0.148 uM compound concentration; replicate [3]Float%
32Inhibition at 0.148 uM [4] (0.148μM**)Value of % inhibition at 0.148 uM compound concentration; replicate [4]Float%
33Inhibition at 0.442 uM [1] (0.442μM**)Value of % inhibition at 0.442 uM compound concentration; replicate [1]Float%
34Inhibition at 0.442 uM [2] (0.442μM**)Value of % inhibition at 0.442 uM compound concentration; replicate [2]Float%
35Inhibition at 0.442 uM [3] (0.442μM**)Value of % inhibition at 0.442 uM compound concentration; replicate [3]Float%
36Inhibition at 0.442 uM [4] (0.442μM**)Value of % inhibition at 0.442 uM compound concentration; replicate [4]Float%
37Inhibition at 1.3 uM [1] (1.3μM**)Value of % inhibition at 1.3 uM compound concentration; replicate [1]Float%
38Inhibition at 1.3 uM [2] (1.3μM**)Value of % inhibition at 1.3 uM compound concentration; replicate [2]Float%
39Inhibition at 1.3 uM [3] (1.3μM**)Value of % inhibition at 1.3 uM compound concentration; replicate [3]Float%
40Inhibition at 1.3 uM [4] (1.3μM**)Value of % inhibition at 1.3 uM compound concentration; replicate [4]Float%
41Inhibition at 4.0 uM [1] (4μM**)Value of % inhibition at 4.0 uM compound concentration; replicate [1]Float%
42Inhibition at 4.0 uM [2] (4μM**)Value of % inhibition at 4.0 uM compound concentration; replicate [2]Float%
43Inhibition at 4.0 uM [3] (4μM**)Value of % inhibition at 4.0 uM compound concentration; replicate [3]Float%
44Inhibition at 4.0 uM [4] (4μM**)Value of % inhibition at 4.0 uM compound concentration; replicate [4]Float%
45Inhibition at 12.0 uM [1] (12μM**)Value of % inhibition at 12.0 uM compound concentration; replicate [1]Float%
46Inhibition at 12.0 uM [2] (12μM**)Value of % inhibition at 12.0 uM compound concentration; replicate [2]Float%
47Inhibition at 12.0 uM [3] (12μM**)Value of % inhibition at 12.0 uM compound concentration; replicate [3]Float%
48Inhibition at 12.0 uM [4] (12μM**)Value of % inhibition at 12.0 uM compound concentration; replicate [4]Float%
49Inhibition at 35.9 uM [1] (35.9μM**)Value of % inhibition at 35.9 uM compound concentration; replicate [1]Float%
50Inhibition at 35.9 uM [2] (35.9μM**)Value of % inhibition at 35.9 uM compound concentration; replicate [2]Float%
51Inhibition at 35.9 uM [3] (35.9μM**)Value of % inhibition at 35.9 uM compound concentration; replicate [3]Float%
52Inhibition at 35.9 uM [4] (35.9μM**)Value of % inhibition at 35.9 uM compound concentration; replicate [4]Float%

* Activity Concentration. ** Test Concentration.
Additional Information
Grant Number: CA134873

Data Table (Concise)
Data Table ( Complete ):     View All Data
PageFrom: