MS2734
MS2734 is a dual-substrate NNMT inhibitor that acts as a SAM (HY-B0617) competitor and a non-competitor of Nicotinamide (HY-B0150), with an IC50 of 14 μM and a Kd of 2.7 μM against hNNMT. MS2734 inhibits the methyltransferase activities of DOT1L (IC50 1.3 μM), PRMT7 (IC50 20 μM), BCDIN3D (IC50 40 μM) and SMYD2 (IC50 62 μM). MS2734 is applicable to research related to diabetes, obesity and various cancers.
For research use only. We do not sell to patients.
- CAS No.: 2587612-25-5
- Formula: C24H32N8O6
- Molecular Weight:528.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Histone Methyltransferase Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
NNMT 14 μM (IC50) |
DOT1L 1.3 μM (IC50) |
PRMT7 20 μM (IC50) |
SMYD2 62 μM (IC50) |
BCDIN3D 40 μM (IC50) |
In Vitro
MS2734 (250 nM-250 μM) inhibits the methyltransferase activity of purified hNNMT in the SAHH-coupled fluorescence assay, with an IC50 of 14 μM[1].
MS2734 binds directly to purified hNNMT, with a Kd value of 2.7 μM measured by ITC[1].
MS2734 exhibits better selectivity for hNNMT than most tested methyltransferases and acetyltransferases, and shows significant inhibitory effects on DOT1L (IC50 = 1.3 μM), PRMT7 (IC50 = 20 μM), BCDIN3D (IC50 = 40 μM) and SMYD2 (IC50 = 62 μM)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2587612-25-5
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Molecular Weight 528.56
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Formula C24H32N8O6
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SMILES
O[C@@H]1[C@H](O)[C@@H](CN(CCC[C@H](N)C(O)=O)CCC2=CC(C(N)=O)=CC=C2)O[C@H]1N3C=NC4=C(N)N=CN=C43
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
[1]. Babault N, et al. Discovery of Bisubstrate Inhibitors of Nicotinamide N-Methyltransferase (NNMT). J Med Chem. 2018 Feb 22;61(4):1541-1551. doi: 10.1021/acs.jmedchem.7b01422. Epub 2018 Jan 31. Erratum in: J Med Chem. 2018 Jul 12;61(13):5771-5772. [Content Brief]
[2]. Policarpo RL, et al. High-Affinity Alkynyl Bisubstrate Inhibitors of Nicotinamide -Methyltransferase (NNMT). Journal of medicinal chemistry. 2019 Nov 14;62(21):9837-9873. [Content Brief]
[3]. Li XY, et al. Nicotinamide N-Methyltransferase: A Promising Biomarker and Target for Human Cancer Therapy. Frontiers in oncology. 2022;12:894744. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)