Name: Late stage results from the probe development effort to identify inhibitors of Wee1 degradation. ..more
Related BioAssays
Related BioAssays
Target
BioActive Compound: 1
Depositor Specified Assays
Show more |
| AID | Name | Type | Probe | Comment |
|---|---|---|---|---|
| 1321 | Primary Cell-based High Throughput Screening Assay for Inhibitors of Wee1 Degradation | screening | Primary screen. | |
| 1410 | Confirmation cell-based high throughput screening assay for inhibitors of Wee1 degradation | screening | Confirmation screen. | |
| 1412 | Dose Response Cell-based Assay for Inhibitors of Wee1 Degradation | confirmatory | Dose response (potency). | |
| 1413 | Cytotoxicity counterscreen assay for inhibitors of Wee1 degradation | confirmatory | Dose response (cytotoxicity). | |
| 1414 | Counterscreen assay for inhibitors of Wee1 degradation: dose response cell-based assay to identify inhibitors of cyclin B degradation | confirmatory | Dose response (cyclin B selectivity). | |
| 1807 | Summary of probe development efforts to identify inhibitors of Wee1 degradation | summary | 1 | Summary AID. |
| 463076 | Late stage assay provider results from the probe development effort to identify inhibitors of casein kinase 1 delta (CK1d): radioactivity-based in vitro biochemical kinase assay for inhibitors of fms-related tyrosine kinase 3 (FLT3) | confirmatory | ||
| 463186 | Late stage assay provider counterscreen results from the probe development effort to identify inhibitors of Wee1 degradation: luminescence-based cell-based assay to identify inhibitors of cyclin B degradation | other | ||
| 463169 | Late stage assay provider results from the probe development effort to identify inhibitors of Wee1 degradation: luminescence-based cell-based assay to identify inhibitors of Wee1 degradation | screening | ||
| 463171 | Late stage assay provider counterscreen results from the probe development effort to identify inhibitors of Wee1 degradation: luminescence-based cell-based assay to identify inhibitors of p27 (CDKN1B) degradation | other | ||
| 463177 | Late stage assay provider counterscreen results from the probe development effort to identify inhibitors of Wee1 degradation: fluorescence activated cell sorting (FACS)-based cell-based assay to identify inducers of Hela cell apoptosis | other | ||
| 434972 | Late stage results from the probe development effort to identify inhibitors of Wee1 degradation: luminescence-based cell-based assay to determine inhibition of Wee1 degradation by kinase inhibitors | other | ||
| 504930 | Late stage assay provider counterscreen results from the probe development effort to identify inhibitors of Wee1 degradation: radioactivity-based cell-based assay to identify inhibitors of granule cell progenitor (GCP) proliferation | confirmatory | 1 | |
| 463077 | Late stage assay provider results from the probe development effort to identify inhibitors of casein kinase 1 delta (CK1d): radioactivity-based in vitro biochemical kinase assay to identify CK1d inhibitors | confirmatory | ||
| 463080 | Late stage assay provider results from the probe development effort to identify inhibitors of WEE1 degradation: luminescence-based dose response assay to identify stabilizers of WEE1 | confirmatory | ||
| 463170 | Late stage assay provider counterscreen results from the probe development effort to identify inhibitors of Wee1 degradation: luminescence-based cell-based assay to identify inhibitors of p21 (CDKN1A) degradation | screening | ||
| 504935 | Late stage assay provider counterscreen results from the probe development effort to identify inhibitors of Wee1 degradation: luminescence-based cell-based dose response assay for cytotoxic compounds using neuroblastoma cell line | other | 1 | |
| 504929 | Late stage assay provider counterscreen results from the probe development effort to identify inhibitors of Wee1 degradation: Amplified proximity luminescence-based biochemical assay to identify inhibitors of residues 1-40 of amyloid beta | other | 1 |
Description:
Source (MLPCN Center Name): The Scripps Research Institute Molecular Screening Center
Center Affiliation: The Scripps Research Institute (TSRI)
Assay Provider: Nagi Ayad, TSRI
Network: Molecular Libraries Probe Production Centers Network (MLPCN)
Grant Proposal Number: 1R21NS056991-01
Grant Proposal PI: Nagi Ayad, TSRI
External Assay ID: WEE1DEG_INH_PROBES_LATE STAGE
Name: Late stage results from the probe development effort to identify inhibitors of Wee1 degradation.
Description:
Cell cycle progression and entry into mitosis are regulated by a highly conserved cellular process known as checkpoint signaling (1-4). The Wee1 nuclear tyrosine kinase functions in this process by regulating the cdc2/cyclin B protein complex. Specifically, Wee1 mediates inhibitory phosphorylation of cdc2, leading to delayed mitosis and cell cycle arrest in cells with DNA damage so that DNA repair and replication can occur (1-4). Wee1 activity is inhibited during mitosis by its phosphorylation and ubiquitination by E3 ligases, and its subsequent degradation by the proteasome (5, 6). Studies showing that Wee1 expression is reduced in colon carcinoma cells (7) and that Wee1 overexpression can block cell division (8), suggest that Wee1 may act as a tumor suppressor. Thus, the identification of probes that selectively increase levels of Wee1 may provide useful insights into the roles of Wee1 in cell cycle control and tumor pathogenesis.
Summary of Probe Development Effort:
Following primary HTS in singlicate to identify Wee1 degradation inhibitors (AID 1321), confirmation of hit activity in triplicate (AID 1410), titration assays to determine compound potency (AID 1412), cytotoxicity (AID 1413), and selectivity against cyclin B (AID 1414), several compounds belonging to different chemical scaffolds were identified as possible candidates for probe development. Representative compounds from three scaffolds (SID 4243143, SID3713089, and SID4256064) and their analogs were ordered as powders (SIDs 87235992, 87235990, 87235991, respectively) for testing to determine potency and selectivity. The best probe candidates were subsequently tested in G2/M arrest assays in the laboratory of the assay provider. One probe was identified (SID 87235992 powder/ SID4243143 liquid). This probe was found to induce a noticeable increase in the G2/M population, without increasing the sub-G1 population after treatment, suggesting that compound treatment was not toxic. While this compound acts as an inhibitor of cell cycle progression, it is not a general proteasome inhibitor like the positive control compound MG132, since it does not affect turnover of another proteasome substrate, N-cyclin B-luciferase. As a result this compound was selected as a probe.
The above probe development effort resulted in the identification of one probe. A probe report has been published (http://mlpcn.florida.scripps.edu/index.php/probes/probe-reports.html). Details of protocols, compound structures, and results from the original assays can be found in PubChem at the respective AIDs below.
References:
1. Lee MH, Yang HY. Negative regulators of cyclin-dependent kinases and their roles in cancers. Cell Mol Life Sci 2001; 58: 1907-1922.
2. Heald R, McLoughlin M, McKeon F. Human Wee1 maintains mitotic timing by protecting the nucleus from cytoplasmically activated Cdc2 kinase. Cell 1993; 74: 463-474.
3. Coleman, TR & Dunphy, WG. Cdc2 regulatory factors. Curr Opin Cell Biol. 1994 Dec;6(6):877-82.
4. Kellogg, DR. Wee1-dependent mechanisms required for coordination of cell growth and cell division. J Cell Sci. 2003 Dec 15;116(Pt 24):4883-90.
5. Smith A, Simanski S, Fallahi M, Ayad NG. Redundant ubiquitin ligase activities regulate wee1 degradation and mitotic entry. Cell Cycle. 2007 Aug;6(22):2795-9.
6. Watanabe N, Arai H, Nishihara Y, Taniguchi M, Watanabe N, Hunter T, and Osada H. M-phase kinases induce phospho-dependent ubiquitination of somatic Wee1 by SCFbeta-TrCP. PNAS 2004 101: 4419-4424.
7. Backert S, Gelos M, Kobalz U, Hanski ML, Bohm C, Mann B, Lovin N, Gratchev A, Mansmann U, Moyer MP, Riecken EO, Hanski C. Differential gene expression in colon carcinoma cells and tissues detected with a cDNA array. Int J Cancer. 1999 Sep 9;82(6):868-74.
8. McGowan, C. H.; Russell, P. Human Wee1 kinase inhibits cell division by phosphorylating p34cdc2 exclusively on Tyr15. EMBO J. 1993. 12: 75-85.
Keywords:
Late stage, probes, probe, Wee1, WEE1hu, FLJ16446, DKFZp686I18166, cell cycle, cancer, HeLa, degradation, inhibitor, inhibition, luminescence, luciferase, dose response, counterscreen, 1536, HTS, assay, Scripps, Scripps Florida, Scripps Research Institute Molecular Screening Center, SRIMSC, Molecular Libraries Probe Production Centers Network, MLPCN.
Center Affiliation: The Scripps Research Institute (TSRI)
Assay Provider: Nagi Ayad, TSRI
Network: Molecular Libraries Probe Production Centers Network (MLPCN)
Grant Proposal Number: 1R21NS056991-01
Grant Proposal PI: Nagi Ayad, TSRI
External Assay ID: WEE1DEG_INH_PROBES_LATE STAGE
Name: Late stage results from the probe development effort to identify inhibitors of Wee1 degradation.
Description:
Cell cycle progression and entry into mitosis are regulated by a highly conserved cellular process known as checkpoint signaling (1-4). The Wee1 nuclear tyrosine kinase functions in this process by regulating the cdc2/cyclin B protein complex. Specifically, Wee1 mediates inhibitory phosphorylation of cdc2, leading to delayed mitosis and cell cycle arrest in cells with DNA damage so that DNA repair and replication can occur (1-4). Wee1 activity is inhibited during mitosis by its phosphorylation and ubiquitination by E3 ligases, and its subsequent degradation by the proteasome (5, 6). Studies showing that Wee1 expression is reduced in colon carcinoma cells (7) and that Wee1 overexpression can block cell division (8), suggest that Wee1 may act as a tumor suppressor. Thus, the identification of probes that selectively increase levels of Wee1 may provide useful insights into the roles of Wee1 in cell cycle control and tumor pathogenesis.
Summary of Probe Development Effort:
Following primary HTS in singlicate to identify Wee1 degradation inhibitors (AID 1321), confirmation of hit activity in triplicate (AID 1410), titration assays to determine compound potency (AID 1412), cytotoxicity (AID 1413), and selectivity against cyclin B (AID 1414), several compounds belonging to different chemical scaffolds were identified as possible candidates for probe development. Representative compounds from three scaffolds (SID 4243143, SID3713089, and SID4256064) and their analogs were ordered as powders (SIDs 87235992, 87235990, 87235991, respectively) for testing to determine potency and selectivity. The best probe candidates were subsequently tested in G2/M arrest assays in the laboratory of the assay provider. One probe was identified (SID 87235992 powder/ SID4243143 liquid). This probe was found to induce a noticeable increase in the G2/M population, without increasing the sub-G1 population after treatment, suggesting that compound treatment was not toxic. While this compound acts as an inhibitor of cell cycle progression, it is not a general proteasome inhibitor like the positive control compound MG132, since it does not affect turnover of another proteasome substrate, N-cyclin B-luciferase. As a result this compound was selected as a probe.
The above probe development effort resulted in the identification of one probe. A probe report has been published (http://mlpcn.florida.scripps.edu/index.php/probes/probe-reports.html). Details of protocols, compound structures, and results from the original assays can be found in PubChem at the respective AIDs below.
References:
1. Lee MH, Yang HY. Negative regulators of cyclin-dependent kinases and their roles in cancers. Cell Mol Life Sci 2001; 58: 1907-1922.
2. Heald R, McLoughlin M, McKeon F. Human Wee1 maintains mitotic timing by protecting the nucleus from cytoplasmically activated Cdc2 kinase. Cell 1993; 74: 463-474.
3. Coleman, TR & Dunphy, WG. Cdc2 regulatory factors. Curr Opin Cell Biol. 1994 Dec;6(6):877-82.
4. Kellogg, DR. Wee1-dependent mechanisms required for coordination of cell growth and cell division. J Cell Sci. 2003 Dec 15;116(Pt 24):4883-90.
5. Smith A, Simanski S, Fallahi M, Ayad NG. Redundant ubiquitin ligase activities regulate wee1 degradation and mitotic entry. Cell Cycle. 2007 Aug;6(22):2795-9.
6. Watanabe N, Arai H, Nishihara Y, Taniguchi M, Watanabe N, Hunter T, and Osada H. M-phase kinases induce phospho-dependent ubiquitination of somatic Wee1 by SCFbeta-TrCP. PNAS 2004 101: 4419-4424.
7. Backert S, Gelos M, Kobalz U, Hanski ML, Bohm C, Mann B, Lovin N, Gratchev A, Mansmann U, Moyer MP, Riecken EO, Hanski C. Differential gene expression in colon carcinoma cells and tissues detected with a cDNA array. Int J Cancer. 1999 Sep 9;82(6):868-74.
8. McGowan, C. H.; Russell, P. Human Wee1 kinase inhibits cell division by phosphorylating p34cdc2 exclusively on Tyr15. EMBO J. 1993. 12: 75-85.
Keywords:
Late stage, probes, probe, Wee1, WEE1hu, FLJ16446, DKFZp686I18166, cell cycle, cancer, HeLa, degradation, inhibitor, inhibition, luminescence, luciferase, dose response, counterscreen, 1536, HTS, assay, Scripps, Scripps Florida, Scripps Research Institute Molecular Screening Center, SRIMSC, Molecular Libraries Probe Production Centers Network, MLPCN.
Panel Information
Assays
§ Panel component ID.
| PID§ | Name | Substance | Panel Targets | Description | Additional Information | ||
|---|---|---|---|---|---|---|---|
| Active | Inactive | ||||||
| 1 | Wee1 Degradation | 10 | 29 | WEE1 homolog (S. pombe) [Homo sapiens] [gi:47123300] | Taxonomy id: 9606 Gene id: 7465 | ||
| 2 | Cyclin B Degradation | 39 | cyclin B1 [Homo sapiens] [gi:119571691] | Taxonomy id: 9606 Gene id: 891 | |||
| 3 | G2/M Arrest Assay | Taxonomy id: 9606 | |||||
§ Panel component ID.
Protocol
Please see AIDs 1321, 1410, 1412, 1413, 1414, 1807 and below for protocols performed in this probe development effort.
Wee1 Degradation Inhibition Assay (Assay 1):
The purpose of this assay is to identify compounds that act as inhibitors of Wee1 degradation. The assay uses HeLa cells transfected with a kinase negative mutant of Wee1 (Wee1K328M) fused to a luciferase reporter gene. As designed, compounds that increase Wee1K328M-luciferase stability and/or prevent its degradation will lead to increased well luminescence compared to untreated wells. Specifically, compounds that increase luminescence are considered Wee1 degradation inhibitors. Compounds were tested in triplicate using a 10-point, 1:3 dilution series, starting at a nominal concentration of 50 micromolar.
Cyclin B Degradation Inhibition Assay (Assay 2):
The purpose of this assay is to determine whether compounds identified as active in a previous set of experiments entitled, "Primary cell-based high throughput screening assay for inhibitors of Wee1 degradation" (PubChem AID 1321), and that confirmed activity in a set of experiments entitled, "Confirmation cell-based high throughput screening assay for inhibitors of Wee1 degradation" (PubChem AID 1410), were non-selective inhibitors of protein degradation, as measured by inhibition of cyclin B degradation. The assay uses HeLa cells transfected with a plasmid that encodes a cyclin B-luciferase fusion protein to monitor cyclin B levels. The cyclin B-luciferase complex is rapidly turned over in these cells. As designed, compounds that inhibit cyclin B degradation will increase cyclin B-luciferase stability, leading to increased well luminescence. Compounds were tested in triplicate using a 10-point, 1:3 dilution series, starting at a nominal concentration of 50 micromolar.
G2/M Arrest Assay (Assay 3):
In order to determine whether the identified probe candidate could inhibit cell cycle progression, cell cycle analyses were made by performing FACS analysis. This assay was performed by the assay provider. Compound-treated HeLa cells were resuspended in 70% ethanol, incubated at -20C overnight, and washed with 10ml cold PBS. The supernatant was removed and the cell pellet was resuspended in 38 mM sodium citrate containing 69 mM of propidium iodide and 19 mg/mL of RNase A. FACS analysis was performed on a BD Bioscience LSR II system and analyzed using Flowjo 8.7.3 software. The compound was tested in triplicate using a 3-point, 1:10 dilution series, starting at a nominal concentration of 5 micromolar.
PubChem Activity Score:
A PubChem Activity Score of 100 was assigned to active compounds, 0 to inactives.
Wee1 Degradation Inhibition Assay (Assay 1):
The purpose of this assay is to identify compounds that act as inhibitors of Wee1 degradation. The assay uses HeLa cells transfected with a kinase negative mutant of Wee1 (Wee1K328M) fused to a luciferase reporter gene. As designed, compounds that increase Wee1K328M-luciferase stability and/or prevent its degradation will lead to increased well luminescence compared to untreated wells. Specifically, compounds that increase luminescence are considered Wee1 degradation inhibitors. Compounds were tested in triplicate using a 10-point, 1:3 dilution series, starting at a nominal concentration of 50 micromolar.
Cyclin B Degradation Inhibition Assay (Assay 2):
The purpose of this assay is to determine whether compounds identified as active in a previous set of experiments entitled, "Primary cell-based high throughput screening assay for inhibitors of Wee1 degradation" (PubChem AID 1321), and that confirmed activity in a set of experiments entitled, "Confirmation cell-based high throughput screening assay for inhibitors of Wee1 degradation" (PubChem AID 1410), were non-selective inhibitors of protein degradation, as measured by inhibition of cyclin B degradation. The assay uses HeLa cells transfected with a plasmid that encodes a cyclin B-luciferase fusion protein to monitor cyclin B levels. The cyclin B-luciferase complex is rapidly turned over in these cells. As designed, compounds that inhibit cyclin B degradation will increase cyclin B-luciferase stability, leading to increased well luminescence. Compounds were tested in triplicate using a 10-point, 1:3 dilution series, starting at a nominal concentration of 50 micromolar.
G2/M Arrest Assay (Assay 3):
In order to determine whether the identified probe candidate could inhibit cell cycle progression, cell cycle analyses were made by performing FACS analysis. This assay was performed by the assay provider. Compound-treated HeLa cells were resuspended in 70% ethanol, incubated at -20C overnight, and washed with 10ml cold PBS. The supernatant was removed and the cell pellet was resuspended in 38 mM sodium citrate containing 69 mM of propidium iodide and 19 mg/mL of RNase A. FACS analysis was performed on a BD Bioscience LSR II system and analyzed using Flowjo 8.7.3 software. The compound was tested in triplicate using a 3-point, 1:10 dilution series, starting at a nominal concentration of 5 micromolar.
PubChem Activity Score:
A PubChem Activity Score of 100 was assigned to active compounds, 0 to inactives.
Comment
A probe was identified. The nonselective positive control/prior art compound MG132 had an EC50 value of 4.5 uM in AID 1412 (Wee1 dose response assay) and an EC50 of 4.7 uM in AID 1414 (cyclin B dose response counterscreen).
Result Definitions
| Show more |
| TID | Name | Description | PID§ | Panel Targets | Histogram | Type | Unit | |
|---|---|---|---|---|---|---|---|---|
| Outcome | The BioAssay activity outcome | Outcome | ||||||
| Score | The BioAssay activity ranking score |  | Integer | |||||
| 1 | Wee1 Degradation (Qualifier) | Activity Qualifier identifies if the resultant data EC50 came from a fitted curve or was determined manually to be less than or greater than its listed EC50 concentration. | 1 | WEE1 homolog (S. pombe) [Homo sapiens] | String | |||
| 2 | Wee1 Degradation (EC50)* | The concentration at which 50 percent of the activity in the assay is observed; (EC50) shown in micromolar. | 1 | | Float | μM | ||
| 3 | Wee1 Degradation (Outcome) | The Assay outcome, one of Active, Inactive or Not Tested. | 1 | | Outcome | |||
| 4 | Wee1 Degradation (Activation at 2.8 nM) (0.0028μM**) | Value of % activation at 2.8 nanomolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 5 | Wee1 Degradation (Activation at 8.5 nM) (0.0085μM**) | Value of % activation at 8.5 nanomolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 6 | Wee1 Degradation (Activation at 25.5 nM) (0.0255μM**) | Value of % activation at 25.5 nanomolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 7 | Wee1 Degradation (Activation at 76.4 nM) (0.0764μM**) | Value of % activation at 76.4 nanomolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 8 | Wee1 Degradation (Activation at 229.2 nM) (0.2292μM**) | Value of % activation at 229.2 nanomolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 9 | Wee1 Degradation (Activation at 687.5 nM) (0.6875μM**) | Value of % activation at 687.5 nanomolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 10 | Wee1 Degradation (Activation at 2.1 uM) (2.1μM**) | Value of % activation at 2.1 micromolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 11 | Wee1 Degradation (Activation at 6.2 uM) (6.2μM**) | Value of % activation at 6.2 micromolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 12 | Wee1 Degradation (Activation at 18.6 uM) (18.6μM**) | Value of % activation at 18.6 micromolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 13 | Wee1 Degradation (Activation at 55.7 uM) (55.7μM**) | Value of % activation at 55.7 micromolar activator concentration; average of triplicate measurement. | 1 | | Float | % | ||
| 14 | Cyclin B Degradation (Qualifier) | Activity Qualifier identifies if the resultant data EC50 came from a fitted curve or was determined manually to be less than or greater than its listed EC50 concentration. | 2 | cyclin B1 [Homo sapiens] | String | |||
| 15 | Cyclin B Degradation (EC50)* | The concentration at which 50 percent of the activity in the assay is observed; (EC50) shown in micromolar. | 2 | | Float | μM | ||
| 16 | Cyclin B Degradation (Outcome) | The Assay outcome, one of Active, Inactive or Not Tested. | 2 | | Outcome | |||
| 17 | Cyclin B Degradation (Activation at 2.8 nM) (0.0028μM**) | Value of % activation at 2.8 nanomolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 18 | Cyclin B Degradation (Activation at 8.5 nM) (0.0085μM**) | Value of % activation at 8.5 nanomolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 19 | Cyclin B Degradation (Activation at 25.5 nM) (0.0255μM**) | Value of % activation at 25.5 nanomolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 20 | Cyclin B Degradation (Activation at 76.4 nM) (0.0764μM**) | Value of % activation at 76.4 nanomolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 21 | Cyclin B Degradation (Activation at 229.2 nM) (0.2292μM**) | Value of % activation at 229.2 nanomolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 22 | Cyclin B Degradation (Activation at 687.5 nM) (0.6875μM**) | Value of % activation at 687.5 nanomolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 23 | Cyclin B Degradation (Activation at 2.1 uM) (2.1μM**) | Value of % activation at 2.1 micromolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 24 | Cyclin B Degradation (Activation at 6.2 uM) (6.2μM**) | Value of % activation at 6.2 micromolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 25 | Cyclin B Degradation (Activation at 18.6 uM) (18.6μM**) | Value of % activation at 18.6 micromolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 26 | Cyclin B Degradation (Activation at 55.7 uM) (55.7μM**) | Value of % activation at 55.7 micromolar activator concentration; average of triplicate measurement. | 2 | | Float | % | ||
| 27 | G2/M Arrest Assay (% compound treated cells) | Percent of compound treated HeLa cells in the G2/M phase as determined by FACS analysis after overnight incubation. | 3 | | Float | % | ||
| 28 | G2/M Arrest Assay (% DMSO treated cells) | Percent of DMSO treated HeLa cells in the G2/M phase as determined by FACS analysis after overnight incubation. | 3 | | Float | % | ||
| 29 | Probe Molecule Outcome | Indicates if this compound is a probe or not. One of Probe, Active or Inactive. | String |
* Activity Concentration. ** Test Concentration. § Panel component ID.
Additional Information
Grant Number: 1R21NS056991-01
Classification
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