#	Aladdin ID	Assay Type	Description	Organism	Compounds	Reference	BAO Format	Source
1.	ALA3784831	F	Anticlonogenic activity against 129sv mouse APL blast cells assessed as inhibition of colony formation of cells at 0.25 uM measured after 7 days relative to control	Mus musculus	9		cell-based format	Scientific Literature
2.	ALA3782870	B	Inhibition of KDM1A in human NB4 cells assessed as increase in GFI1B mRNA expression at biochemical IC50 measured after 24 hrs by RT-PCR analysis relative to control	Homo sapiens	9		cell-based format	Scientific Literature
3.	ALA3782872	B	Inhibition of human recombinant KDM1A/CoREST expressed in Escherichia coli using mono-methylated H3-K4 peptide as substrate assessed as H2O2 release preincubated for 15 mins followed by substrate addition measured for 12 mins by fluorescence-based microplate reader analysis	Homo sapiens	14		assay format	Scientific Literature
4.	ALA3782873	B	Inhibition of human recombinant MAOA expressed in Pichia pastoris preincubated for 15 mins measured after 30 mins by bioluminescent-coupled assay	Homo sapiens	14		assay format	Scientific Literature
5.	ALA3782874	B	Inhibition of human recombinant MAOB expressed in Pichia pastoris preincubated for 15 mins measured after 30 mins by bioluminescent-coupled assay	Homo sapiens	14		assay format	Scientific Literature
6.	ALA3782875	B	Inhibition of KDM1B (unknown origin)	Homo sapiens	14		single protein format	Scientific Literature
7.	ALA3782877	B	Inhibition of KDM1A in human NB4 cells assessed as increase in CD11b mRNA expression at biochemical IC50 measured after 24 hrs by RT-PCR analysis relative to control	Homo sapiens	9		cell-based format	Scientific Literature
8.	ALA3782878	F	Anticlonogenic activity against human THP1 cells assessed as inhibition of colony formation of cells at 0.5 uM measured after 13 days relative to control	Homo sapiens	9		cell-based format	Scientific Literature
9.	ALA3782879	F	Induction of differentiation of human THP1 cells assessed assessed as alteration in morphology of colonies after 13 days by May Grunwald-Giemsa staining based assay	Homo sapiens	5		cell-based format	Scientific Literature
10.	ALA3782890	F	Antitumor activity against 129SvEv mouse APL blast cells implanted in nonirradiated 129SvEv mouse assessed as increase in survival of leukemic mouse at 0.0125 mg/kg, ip administered for 5 days per week for 2 weeks by Kaplan-Meier plot analysis relative to vehicle control	Mus musculus	1		organism-based format	Scientific Literature
11.	ALA3782895	F	Induction of differentiation of human THP1 cells after 13 days by cytospin assay	Homo sapiens	5		cell-based format	Scientific Literature
12.	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
13.	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
14.	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
15.	ALA4008790	B	Inhibition of recombinant human KDM1A/CoREST complex expressed in Escherichia coli using [Lys(Me1)4]-Histone H3 (1 to 21 residues)-GGK(biotin) as substrate incubated for 20 mins measured after 1 hr by TR-FRET assay	Homo sapiens	53		assay format	Scientific Literature
16.	ALA4008794	B	Inhibition of recombinant human MAOA incubated for 15 mins measured after 30 mins by luminescence-Glo assay	Homo sapiens	4		single protein format	Scientific Literature
17.	ALA4008795	B	Inhibition of recombinant human MAOB incubated for 15 mins measured after 30 mins by luminescence-Glo assay	Homo sapiens	4		single protein format	Scientific Literature
18.	ALA4008796	B	Inhibition of KDM1B (unknown origin)	Homo sapiens	4		single protein format	Scientific Literature
19.	ALA4008798	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
20.	ALA4008800	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