C25-140 是一种首创的，具有口服活性和一定选择性的 TRAF6-Ubc13 相互作用的抑制剂，直接与 TRAF6 结合，阻断 TRAF6 和 Ubc13 的相互作用，从而降低 TRAF6 活性，降低 NF-κB 的活性，并对抗自身免疫。

C25-140, a first-in-class, orally active, and fairly selective TRAF6-Ubc13 inhibitor, directly binds to TRAF6, and blocks the interaction of TRAF6 with Ubc13. C25-140 lowers TRAF6 activity, reduces NF-κB activation, and combats autoimmunity.

Solid

TRAF6-Ubc13

C25-140 dose-dependently impedes TRAF6-Ubc13 interaction.
C25-140 (10-30 μM; 2 hours) effectively reduces TRAF6-mediated ubiquitin chain formation.
C25-140 affects TNFα-induced phosphorylation of IκBα as well as NF-κB-induced target gene expression.
C25-140 efficiently inhibits IL-1β- and TNFα-mediated receptor signaling in the context of cytokine activation. has not independently confirmed the accuracy of these methods. They are for reference only.

C25-140 (~1.5 mg/kg; topically to the shaved back and the right ear; twice daily for 6 days) ameliorates symptoms of autoimmune psoriasis in R 837-induced psoriasis mouse model.
C25-140 (6-14 mg/kg; given i.p.; twice daily for 14 days) shows a dose-dependent improvement of RA disease outcome in Collagen-induced arthritis (CIA) model.
C25-140 (10 mg/kg; i.v.) treatment shows that the C max , AUC, t 1/2 and V d are 9.7 μg/mL, 274083 ng min/mL, 80.62 min, and 4.13 L/kg, respectively.
. C25-140 (10 mg/kg; p.o.) treatment shows that the C max , AUC, t 1/2 and V d are 3.4 μg/mL, 124034 ng min/mL, 127.33 min and 13.3 L/kg, respectively.
C25-140 (10 mg/kg; i.p.) treatment shows that the C max , AUC, t 1/2 and V d are 4.2μg/mL, 100000 ng min/mL, 184 min, 25.6 L/kg, respectively.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Brenke JK, et al. Targeting TRAF6 E3 ligase activity with a small-molecule inhibitor combats autoimmunity. J Biol Chem. 2018 Aug 24;293(34):13191-13203.

In Vitro: DMSO : 41.67 mg/mL (91.07 mM; Need ultrasonic)配制储备液