| Bioactivity | JTE-607, a highly selective inflammatory cytokine synthesis inhibitor, protects from endotoxin shock in mice. JTE-607 inhibits inflammatory cytokine production, including TNF-α, IL-1β, IL-6, IL-8 and IL-10, from LPS-stimulated human PBMCs, with IC50s of 11, 5.9, 8.8, 7.3 and 9.1 nM, respectively[1]. Cleavage and Polyadenylation Specificity Factor 3 (CPSF3) is the target of JTE-607[2]. |
| Invitro | JTE-607 inhibits inflammatory cytokine production, including TNF-α, IL-1β, IL-6, IL-8 and IL-10, from LPS-stimulated human PBMCs, with IC50s of 11, 5.9, 8.8, 7.3 and 9.1 nM, respectively. The inhibitory effects of JTE-607 are also seen in mRNA expression of those cytokines[1].JTE-607 inhibits inflammatory cytokine production from LPS-stimulated human PBMCs with an IC50 of approximately 10 nM[1]. JTE607 inhibits LPS-stimulated IL-8 production from monkey and rabbit PBMCs, and TNF-α production from mouse and rat PBMCs with IC50s of 59, 780, 1600 and 19000 nM, respectively[1].JTE607 also suppresses other cytokines, granulocyte-macrophage colony stimulating factor and IL-1RA with IC50s of 2.4±0.8 and 5.4±0.4 nM, respectively[1].JTE-607 inhibits cytokine production in monkey, rabbit, mouse and rat with IC50s of 59±26, 780±120, 1600±650 and 19000±3200 nM, respectively[1]. RT-PCR[1] Cell Line: |
| In Vivo | JTE-607 (0.3-10 mg/kg, i.v.) shows dose dependent inhibition of mortality after LPS challenge in C. parvum sensitized mice in accordance with a decrease of plasma TNF-α[1]. Animal Model: |
| Name | JTE-607 |
| CAS | 188791-09-5 |
| Formula | C25H33Cl4N3O5 |
| Molar Mass | 597.36 |
| Appearance | Solid |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | 4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture) |
| Reference | [1]. M Kakutani, et al. JTE-607, a novel inflammatory cytokine synthesis inhibitor without immunosuppression, protects from endotoxin shock in mice. Inflamm Res. 1999 Aug;48(8):461-8. [2]. Nathan T Ross, et al. CPSF3-dependent pre-mRNA processing as a druggable node in AML and Ewing's sarcoma. Nat Chem Biol. 2020 Jan;16(1):50-59. |