Enasidenib mesylate (AG-221 mesylate) 1650550-25-6 GlpBio

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Product Data Sheet

Product Name:Cat. No.:

Enasidenib mesylate (AG-221 mesylate)GC32904

Chemical Properties

Cas No.ChemicalNameCanonicalSMILESFormulaSolubilityGeneral tipsShippingCondition

1650550-25-6N/A

CS(=O)(O)=O.CC(O)(C)CNC1=NC(C2=NC(C(F)(F)F)=CC=C2)=NC(NC3=CC(C(F)(F)F)=NC=C3)=N1C20H21F6N7O4S

DMSO : ≥ 100 mg/mL (175.60 mM)

M.WtStorage

569.48Store at -20°C

For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bathfor a while.Stock solution can be stored below -20℃ for several months.

Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice uponrequest.

Structure

Background

Enasidenib mesylate is a first-in-class, oral, potent, reversible, selective inhibitor of the IDH2 mutant enzymes.

Caution: Producthasnot been fully validated for medical applications. For research use only.

Tel: (626) 353-8530 Fax: (626) 353-8530 E-mail: tech@glpbio.com

Address: 10292 Central Ave. #205, Montclair, CA, USA

1www.glpbio.com

Peptides, Inhibitors, Agonists

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Product Data Sheet

Enasidenib (AG-221) reverses the effects of mutant IDH2 on DNA methylation in mutant stem/progenitor cells.Enasidenib induces differentiation and impairs self-renewal of IDH2-mutant leukemia cells, effects that are furtherenhanced by simultaneous inhibition of Flt3ITD. Enasidenib (AG-221) therapy induces differentiation of leukemic

cells, with an increase in the CD11b+ population and a decrease in the c-Kit+ population in the peripheral blood at 2wks[2].

Treatment with enasidenib (AG-221) significantly improves survival in an IDH2-mutant acute myeloid leukemia (AML)primary xenograft mouse model[1]. Enasidenib (AG-221), a mutant IDH2 inhibitor, remodels the epigenetic state ofIDH2-mutant cells and induces alterations in self-renewal/differentiation in IDH2-mutant AML model in vivo.

Enasidenib treatment (10 mg/kg or 100 mg/kg bid) leads to a reduction in 2-HG in vivo (96.7% below pre-treatmentlevels). Moreover, Enasidenib treatment restores megakaryocyte-erythroid progenitor (MEP) differentiation that issuppressed by mutant IDH2 expression (mean MEP% mean, 39% Veh vs 50% AG-221). Enasidenib therapy reversesthe effects of mutant IDH2; a significant reduction is observed in DNA methylation, including 180 genes that have 20or more hypomethylated differentially methylated cytosines (DMCs) following treatment. Enasidenib (100 mg/kg bid)treatment of mice engrafted with Mx1-Cre IDH2R140QFlt3ITD AML cells markedly reduces 2-hydroxyglutarate (2-HG)levels consistent with on target inhibition. Enasidenib inhibits mutant IDH2-mediated 2-HG production[2].

[1]. Exploring the Pathway: IDH Mutations and Metabolic Dysregulation in Cancer Cells: A Novel Therapeutic Target.MAY 29, 2015 [2]. Alan H. Shih, et al. AG-221, a Small Molecule Mutant IDH2 Inhibitor, Remodels the Epigenetic Stateof IDH2-Mutant Cells and Induces Alterations in Self-Renewal/Differentiation in IDH2-Mutant AML Model in Vivo. Blood2014 124:437.

Caution: Producthasnot been fully validated for medical applications. For research use only.

Tel: (626) 353-8530 Fax: (626) 353-8530 E-mail: tech@glpbio.com

Address: 10292 Central Ave. #205, Montclair, CA, USA

2www.glpbio.com