JTE 607 dihydrochloride
Chemical Name: N-[3,5-Dichloro-2-hydroxy-4-[2-(4-methyl-1-piperazinyl)ethoxy]benzoyl]-L-phenylalanine ethyl ester dihydrochloride
Purity: ≥98%
Biological Activity
JTE 607 is a pro-drug that is cleaved by carboxylesterase 1 (CES1) to its active metabolite, which then binds to cleavage and polyadenylation specificity factor 3 (CPSF3; Kd = 370 nM at human CPSF3). Treatment of A-673 cells with JTE 607 results in inhibition of mRNA cleavage and accumulation of nuclear R-loops. JTE 607 induces apoptosis in leukemia cells in vitro and prolongs survival in a mouse leukemia model.JTE 607 also inhibits cytokine release; it inhibits production of IL-1β, IL-8, IL-6, IL-10 and TNFα (IC50 values are 5.9, 7.3, 8.8, 9.1 and 11.0 nM, respectively) from LPS-stimulated PBMCs. In a rat model of lung injury, JTE 607 reduces proinflammatory cytokine-release and attenuates lung permeability.
Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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JTE-607, a multiple cytokine production inhibitor, induces apoptosis accompanied by an increase in p21waf1/cip1 in acute myelogenous leukemia cells.
Tajima et al.
Cancer Sci., 2010;101:774 -
JTE-607, a novel inflammatory cytokine synthesis inhibitor without immunosuppression, protects from endotoxin shock in mice.
Kakutani et al.
Inflamm.Res., 1999;48:461 -
JTE-607, a cytokine release blocker, attenuates acid aspiration-induced lung injury in rats.
Jian
Eur.J.Pharmacol., 2004;488:231 -
CPSF3-dependent pre-mRNA processing as a druggable node in AML and Ewing's sarcoma.
Ross et al.
Nat.Chem.Biol., 2020;16:50
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