LUF7996

LUF7996 (compound 10) (10 μM) displaces [³H]CCR2-RA-[R] with pKi = 6.9 nM and displays < 50 % inhibiton in U2OS-CCR2 cells^[1].
LUF7996 (0.1-31.6 μM, 2 h) not display any substantial degradative capacity when tested at concentrations below 1 μM, has a rapid and concentration-dependent degradation of CCR2 with DC₅₀= 5.6 μM without indication of a hook effect at concentrations higher than 1 μM, D_max = 85% at 31.6 μM and D_max = 79% at 10 μM in HEK293-LgBiT cells^[1].
LUF7996 binds CCR2 with IC₅₀ = 7.858 μM, exhibits the strongest CRBN engagement with IC₅₀ = 143 μM^[1].
LUF7996 (10 μM, 12 or 24 h) mediated CCR2 degradation is rescued upon cotreatment with either a CRBN inhibitor (competing for the binding pocket) or a CRBN degrader^[1].
LUF7996 (10 μM, 3 h) result a significant increase in CCR2 ubiquitination, degrades CCR2 least partially through CRBN and ubiquitin-dependent mechanisms^[1].
LUF7996 (10 μM, 0-25 h) did not block CCR2 degradation but enhances CCR2 degradation after 16h when cotreat with proteasome inhibitors Bortezomib (HY-10227) or MG-132 (HY-13259) (10 μM) or the neddylation inhibitor MLN-4924 (HY-70062) (250 nM), suggesting a proteasome-and neddylation-independent mechanism of action^[1].
LUF7996 (10 μM, 0-25 h) has CCR2 degradative effect but prevented by inhibition of the lysosomal pathway, as evidenced by the full restoration of CCR2 levels with Baf-A1 (HY-100558) and the decreased degradation observed with Chloroquine (HY-17589A)^[1].
LUF7996 (10 μM, 24 h) results a significant reduction in [ 3 H]CCR2-RA- [R] binding in THP-1 cells, indicating a reduction of CCR2 levels^[1].
LUF7996 (10 μM) demonstrates 84% potent inhibition of CCL2-induced monocyte migration in THP-1 cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.