#	Aladdin ID	Assay Type	Description	Organism	Compounds	Reference	BAO Format	Source
1.	ALA3887027	B	Fluorescence-Based (Inhibitor)-Screening Assay: In order to monitor MAO enzymatic activities and/or their inhibition rate by inhibitor(s) of interest, a fluorescence-based (inhibitor)-screening assay was set up. 3-(2-Aminophenyl)-3-oxopropanamine (kynuramine dihydrobromide, Sigma Aldrich), a non fluorescent compound was chosen as a substrate. Kynuramine is a non-specific substrate for both MAO-A and MAO-B activities. While undergoing oxidative deamination by MAO activities, kynuramine is converted into 4-hydroxyquinoline (4-HQ), a resulting fluorescent product.The monoamine oxidase activity was estimated by measuring the conversion of kynuramine into 4-hydroxyquinoline. Assays were conducted in 96-well black plates with clear bottom (Corning) in a final volume of 100 uL. The assay buffer was 100 mM HEPES, pH 7.5. Each experiment was performed in duplicate within the same experiment.Briefly, a fixed amount of MAO (0.25 ug for MAO-A and 0.5 ug for MAO-B) was incubated on ice for 15 minutes in the reaction buffer, in the absence and/or in the presence of at least eight 3-fold serial dilutions each. Clorgyline and Deprenyl (Sigma Aldrich) was used as a control for specific inhibition of MAO-A and MAO-B respectively. After leaving the enzyme(s) interacting with the inhibitor, KM of kynuramine was added to each reaction for MAO-B and MAO-A assay respectively, and the reaction was left for 1 hour at 37° C. in the dark. The oxidative deamination of the substrate was stopped by adding 50 uL of NaOH 2N. The conversion of kynuramine to 4-hydroxyquinoline, was monitored by fluorescence (excitation at 320 nm, emission at 360 nm) using a microplate reader (Infinite 200, Tecan). Arbitrary units were used to measure levels of fluorescence produced in the absence and/or in the presence of inhibitor. The maximum of oxidative deamination activity was obtained by measuring the amount of 4-hydroxyquinoline formed from kynuramine deamination in the absence of inhibitor and corrected for background fluorescence in the absence of MAO enzymes. The IC50 values of each inhibitor were calculated with GraphPad Prism Software.	Homo sapiens	57		single protein format	BindingDB Database
2.	ALA3887028	B	Fluorescence-Based (Inhibitor)-Screening Assay: In order to monitor MAO enzymatic activities and/or their inhibition rate by inhibitor(s) of interest, a fluorescence-based (inhibitor)-screening assay was set up. 3-(2-Aminophenyl)-3-oxopropanamine (kynuramine dihydrobromide, Sigma Aldrich), a non fluorescent compound was chosen as a substrate. Kynuramine is a non-specific substrate for both MAO-A and MAO-B activities. While undergoing oxidative deamination by MAO activities, kynuramine is converted into 4-hydroxyquinoline (4-HQ), a resulting fluorescent product.The monoamine oxidase activity was estimated by measuring the conversion of kynuramine into 4-hydroxyquinoline. Assays were conducted in 96-well black plates with clear bottom (Corning) in a final volume of 100 uL. The assay buffer was 100 mM HEPES, pH 7.5. Each experiment was performed in duplicate within the same experiment.Briefly, a fixed amount of MAO (0.25 ug for MAO-A and 0.5 ug for MAO-B) was incubated on ice for 15 minutes in the reaction buffer, in the absence and/or in the presence of at least eight 3-fold serial dilutions each. Clorgyline and Deprenyl (Sigma Aldrich) was used as a control for specific inhibition of MAO-A and MAO-B respectively. After leaving the enzyme(s) interacting with the inhibitor, KM of kynuramine was added to each reaction for MAO-B and MAO-A assay respectively, and the reaction was left for 1 hour at 37° C. in the dark. The oxidative deamination of the substrate was stopped by adding 50 uL of NaOH 2N. The conversion of kynuramine to 4-hydroxyquinoline, was monitored by fluorescence (excitation at 320 nm, emission at 360 nm) using a microplate reader (Infinite 200, Tecan). Arbitrary units were used to measure levels of fluorescence produced in the absence and/or in the presence of inhibitor. The maximum of oxidative deamination activity was obtained by measuring the amount of 4-hydroxyquinoline formed from kynuramine deamination in the absence of inhibitor and corrected for background fluorescence in the absence of MAO enzymes. The IC50 values of each inhibitor were calculated with GraphPad Prism Software.	Homo sapiens	57		single protein format	BindingDB Database
3.	ALA3887191	B	Biological Assay: The compounds of the invention can be tested for their ability to inhibit LSD1. The ability of the compounds of the invention to inhibit LSD1 can be tested as follows. Human recombinant LSD1 protein was purchased from BPS Bioscience Inc (catalog reference number 50100: human recombinant LSD1, GenBank accession no. NM_015013, amino acids 158-end with N-terminal GST tag, MW: 103 kDa). In order to monitor LSD1 enzymatic activity and/or its inhibition rate by our inhibitor(s) of interest, di-methylated H3-K4 peptide (Anaspec) was chosen as a substrate. The demethylase activity was estimated, under aerobic conditions, by measuring the release of H2O2 produced during the catalytic process, using the Amplex Red hydrogen peroxide/peroxidase assay kit (Invitrogen).Briefly, a fixed amount of LSD1 was incubated on ice for 15 minutes, in the absence and/or in the presence of at least eight 3-fold serial dilutions of the respective inhibitor (e.g., from 0 to 75 uM, depending on the inhibitor strength). Tranylcypromine (Biomol International) was used as a control for inhibition. Within the experiment, each concentration of inhibitor was tested in duplicate. After leaving the enzyme interacting with the inhibitor, KM of di-methylated H3-K4 peptide was added to each reaction and the experiment was left for 30 minutes at 37° C. in the dark. The enzymatic reactions were set up in a 50 mM sodium phosphate, pH 7.4 buffer. At the end of the incubation, Amplex Red reagent and horseradish peroxidase (HPR) solution were added to the reaction according to the recommendations provided by the supplier (Invitrogen), and left to incubate for 5 extra minutes at room temperature in the dark. A 1 uM H2O2 solution was used as a control of the kit efficiency. The conversion of the Amplex Red reagent to resorufin due to the presence of H2O2 in the assay, was monitored by fluorescence (excitation at 540 nm, emission at 590 nm) using a microplate reader (Infinite 200, Tecan). Arbitrary units were used to measure level of H2O2 produced in the absence and/or in the presence of inhibitor. The maximum demethylase activity of LSD1 was obtained in the absence of inhibitor and corrected for background fluorescence in the absence of LSD1. The IC50 value of each inhibitor was calculated with GraphPad Prism Software.		57		single protein format	BindingDB Database
4.	ALA4008766	B	Inhibition of recombinant human KDM1A/CoREST complex expressed in Escherichia coli using biotinylated H3K4me1 peptide as substrate preincubated for 20 mins measured after 1 hr by TR-FRET assay	Homo sapiens	59		assay format	Scientific Literature
5.	ALA4008772	B	Inhibition of KDM1B (unknown origin)	Homo sapiens	6		single protein format	Scientific Literature
6.	ALA4008773	B	Inhibition of recombinant human MAOA incubated for 15 mins measured after 30 mins by luminescence-Glo assay	Homo sapiens	6		single protein format	Scientific Literature
7.	ALA4008774	B	Inhibition of recombinant human MAOB incubated for 15 mins measured after 30 mins by luminescence-Glo assay	Homo sapiens	6		single protein format	Scientific Literature
8.	ALA4008779	B	Inhibition of KDM1A in human THP1 cells assessed as increase in CD14 mRNA expression level at 0.5 uM after 24 hrs by qRT-PCR analysis relative to control	Homo sapiens	1		cell-based format	Scientific Literature
9.	ALA4008781	B	Inhibition of KDM1A in human THP1 cells assessed as increase in CD11b mRNA expression level at 0.5 uM after 24 hrs by qRT-PCR analysis relative to control	Homo sapiens	1		cell-based format	Scientific Literature
10.	ALA4008783	F	Induction of apoptosis in human THP1 cells at 0.5 uM after 72 hrs by Annexin V-propidium iodide staining based flow cytometry	Homo sapiens	1		cell-based format	Scientific Literature
11.	ALA4008785	F	Induction of cell death in human THP1 cells at 0.5 uM after 72 hrs by propidium iodide staining based flow cytometry	Homo sapiens	1		cell-based format	Scientific Literature
12.	ALA4008787	F	Anticlonogenic activity against human THP1 cells assessed as inhibition of colony formation at 0.5 uM after 13 days relative to control	Homo sapiens	1		cell-based format	Scientific Literature
13.	ALA4008789	B	Inhibition of KDM1A in human THP1 cells assessed as increase in CD86 mRNA expression level at 0.5 uM after 24 hrs by qRT-PCR analysis relative to control	Homo sapiens	1		cell-based format	Scientific Literature
14.	ALA4135160	B	Inhibition of human recombinant MAO-A expressed in baculovirus infected insect cells by luminescence assay	Homo sapiens	22		cell-based format	Scientific Literature
15.	ALA4135161	B	Inhibition of human recombinant N-terminal His/GST-tagged LSD1 (172 to 852 residues) expressed in baculovirus infected insect cells using biotin-labeled H3K4me2 (1 to 24 residues) as substrate after 1 hr by TR-FRET assay	Homo sapiens	22		cell-based format	Scientific Literature
16.	ALA4135162	B	Inhibition of human recombinant MAO-B expressed in baculovirus infected insect cells by luminescence assay	Homo sapiens	22		cell-based format	Scientific Literature
17.	ALA4135163	B	Inhibition of human full length LSD2 using biotin-labeled H3K4me2 (1 to 24 residues) as substrate after 1 hr by TR-FRET assay	Homo sapiens	18		single protein format	Scientific Literature
18.	ALA4135164	B	Inhibition of LSD1 in human MV-4-11 cells assessed as increase in CD86 mRNA expression after 3 days by SYBR Green dye-bsed RT-qPCR analysis	Homo sapiens	3		cell-based format	Scientific Literature
19.	ALA4135165	B	Inhibition of LSD1 in human MV-4-11 cells assessed as increase in CD86 mRNA expression after 10 days by SYBR Green dye-bsed RT-qPCR analysis	Homo sapiens	3		cell-based format	Scientific Literature
20.	ALA4135166	F	Antiproliferative activity against human MV4-11 cells after 3 days by MTS assay	Homo sapiens	3		cell-based format	Scientific Literature