OG-L002

LSD1 inhibitor,potent and specific CAS# 1357302-64-7

OG-L002

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Catalog No. BCC4549----Order now to get a substantial discount!

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OG-L002

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Chemical Properties of OG-L002

Cas No. 1357302-64-7 SDF Download SDF
PubChem ID 56639570 Appearance Powder
Formula C15H15NO M.Wt 225.29
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : 250 mg/mL (1109.68 mM; Need ultrasonic)
Chemical Name 3-[4-[(1R,2S)-2-aminocyclopropyl]phenyl]phenol
SMILES C1C(C1N)C2=CC=C(C=C2)C3=CC(=CC=C3)O
Standard InChIKey DSOJSZXQRJGBCW-CABCVRRESA-N
Standard InChI InChI=1S/C15H15NO/c16-15-9-14(15)11-6-4-10(5-7-11)12-2-1-3-13(17)8-12/h1-8,14-15,17H,9,16H2/t14-,15+/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of OG-L002

DescriptionOG-L002 is a potent and specific inhibitor of LSD1 with IC50 value of 20 nM.
TargetsLSD1    
IC5020 nM     

OG-L002 Dilution Calculator

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OG-L002 Molarity Calculator

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Preparing Stock Solutions of OG-L002

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.4387 mL 22.1936 mL 44.3872 mL 88.7745 mL 110.9681 mL
5 mM 0.8877 mL 4.4387 mL 8.8774 mL 17.7549 mL 22.1936 mL
10 mM 0.4439 mL 2.2194 mL 4.4387 mL 8.8774 mL 11.0968 mL
50 mM 0.0888 mL 0.4439 mL 0.8877 mL 1.7755 mL 2.2194 mL
100 mM 0.0444 mL 0.2219 mL 0.4439 mL 0.8877 mL 1.1097 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on OG-L002

OG-L002 is a specific and potent inhibitor of lysine (K)-specific demethylase 1A (LSD1) with IC50 value of 20 nM [1].
LSD1 is a flavin-dependent monoamine oxidase, which can demethylate lysines. LSD1 plays critical roles in oocyte growth, embryogenesis and tissue-specific differentiation [2].
OG-L002 potently inhibited HSV IE gene expression in both HFF and HeLa cells with IC50 of ~3 μM and ~10 μM, respectively. OG-L002 treatment can potently reduce production of progeny virus (~100-fold) with no significant toxicity in HeLa or HFF cells. In chromatin immunoprecipitation assays, OG-L002 increased the levels of total histone H3K9-me2 and H3 (20- to 30-fold) associated with viral IE promoters, which resulted in decreased viral IE gene expression. In addition, OG-L002 also repressed the expression of adenovirus E1A gene and hCMV IE genes [1].
In a mouse model, OG-L002 repressed primary HSV infection in a dose-dependent manner. Moreover, OG-L002 plays an important role in the viral latency-reactivation cycle in a mouse ganglion explant model [1].
References:
[1]. Liang Y, Quenelle D, Kristie TM, et al. A Novel Selective LSD1/KDM1A Inhibitor epigenetically blocks herpes simplex virus lytic replication and reactivation from latency. mBio, 2013, 4(1), e00558-12.
[2]. Pedersen MT, Helin K. Histone demethylases in development and disease. Trends in Cell Biology, 2010, 20 (11): 662-71.

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References on OG-L002

Effect of a Histone Demethylase Inhibitor on Equine Herpesvirus-1 Activity In Vitro.[Pubmed:29594155]

Front Vet Sci. 2018 Mar 12;5:34.

Equine herpesvirus type 1 (EHV-1) is a ubiquitous and highly contagious pathogen that causes a range of disease severities with outbreaks of notable economic impact. Given the limitations in immune protection of current vaccines and the limited effectiveness of antiviral drugs on EHV-1 infections in vivo, improved treatment measures are needed to control disease. The use of drugs that alter the epigenetic state of herpes simplex virus genome has been shown to limit viral primary infection and reactivation both in vitro and in vivo. Therefore, we tested the hypothesis that maintaining a repressive epigenetic state on the EHV-1 genome in the host equine cell would decrease viral load during lytic infection. Equine fetal kidney cells (EFKCs) or isolated peripheral blood leukocytes were treated in vitro with (a) the nucleoside analog ganciclovir; (b) the histone demethylase inhibitor OG-L002; (c) both ganciclovir and OG-L002; or (d) dimethyl sulfoxide (DMSO, vehicle control); and then infected with a clinical EHV-1 isolate. Treatment of EFKCs with ganciclovir (mean 22.3 DNA copies per cell, p = 0.0005), OG-L002 (mean 25.6, p = 0.005) or both ganciclovir and OG-L002 (mean 7.1, p = 0.0001) resulted in decreased EHV-1 viral load at 24 h post-infection (hpi) in comparison with DMSO (mean 42.0), with greater impact using the combined treatment. Further, EHV-1 gene expression at 3 hpi decreased when EFKCs were infected in the presence of ganciclovir (p = 0.04) and combined treatment of ganciclovir and OG-L002 (p = 0.0003). In contrast, under similar conditions, neither ganciclovir nor OG-L002 suppressed EHV-1 infection in leukocytes. Differences between cell types, drug penetrance, or drug turnover, may have contributed to the distinct effects observed in this study.

Role of the DNA repair glycosylase OGG1 in the activation of murine splenocytes.[Pubmed:28843610]

DNA Repair (Amst). 2017 Oct;58:13-20.

OGG1 (8-oxoguanine-DNA glycosylase) is the major DNA repair glycosylase removing the premutagenic DNA base modification 8-oxo-7,8-dihydroguanine (8-oxoG) from the genome of mammalian cells. In addition, there is accumulating evidence that OGG1 and its substrate 8-oxoG might function in the regulation of certain genes, which could account for an attenuated immune response observed in Ogg1(-/-) mice in several settings. Indications for at least two different mechanisms have been obtained. Thus, OGG1 could either act as an ancillary transcription factor cooperating with the lysine-specific demethylase LSD1 or as an activator of small GTPases. Here, we analysed the activation by lipopolysaccaride (LPS) of primary splenocytes obtained from two different Ogg1(-/-) mouse strains. We found that the induction of TNF-alpha expression was reduced in splenocytes (in particular macrophages) of both Ogg1(-/-) strains. Notably, an inhibitor of LSD1, OG-L002, reduced the induction of TNF-alpha mRNA in splenocytes from wild-type mice to the level observed in splenocytes from Ogg1(-/-) mice and had no influence in the latter cells. In contrast, inhibitors of the MAP kinases p38 and JNK as well as the antioxidant N-acetylcysteine attenuated the LPS-stimulated TNF-alpha expression both in the absence and presence of OGG1. The free base 8-oxo-7,8-dihydroguanine had no influence on the TNF-alpha expression in the splenocytes. The data demonstrate that OGG1 plays a role in an LSD1-dependent pathway of LPS-induced macrophage activation in mice.

Description

OG-L002 is a potent and highly selective LSD1 inhibitor with an IC50 of 0.02 μM. OG-L002 is a potent monoamine oxidases (MAO) inhibitor with IC50s of 1.38 μM and 0.72 μM for MAO-A and MAO-B, respectively. OG-L002 potently inhibits the expression of HSV IE genes.

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