RNF5-IN-1

RNF5-IN-1 (compound FX12) (4 h) inhibits the retrotranslocation of misfolded NHK from the endoplasmic reticulum to the cytosol in HeLa NHK-drGFP cells, with an IC₅₀ of 2.7 μM^[1].
RNF5-IN-1 (10 μM) induces proteasome-dependent degradation of RNF5; BTZ blocks the reduction of RNF5, while CQ does not. The p97/VCP inhibitor NMS-873 also inhibits the reduction of RNF5, indicating that RNF5 degradation relies on p97/VCP-mediated ERAD^[1].
RNF5-IN-1 directly binds to the N-terminal cytoplasmic domain (aa1-117) of RNF5, with a K_D of 594 nM determined by SPR^[1].
RNF5-IN-1 enhances the thermal stability of RNF5 and can still stabilize RNF5 in Derlin1 KO cells, supporting the cellular target engagement of RNF5-IN-1 to RNF5^[1].
RNF5-IN-1 (24 h) dose-dependently reduces RNF5 and increases the ER core-glycosylated B form and mature complex-glycosylated C form of ΔF508 CFTR in BHK cells stably expressing ΔF508 CFTR; combined exposure of RNF5-IN-1 with VX809 or VX661 further increases the mature C form of wt-CFTR and ΔF508 CFTR ^[1].
RNF5-IN-1 (5-10 μM) reduces the ubiquitination of ΔF508 CFTR and inhibits its degradation, thereby enhancing the stability of ΔF508 CFTR^[1].
RNF5-IN-1 (5 μM; 24 h) produces only a small amount of mature ΔF508 CFTR in ΔF508/ΔF508 primary HBE cultures, does not significantly enhance the CFTR current response, and does not further augment the CFTR functional response under VX809 or VX809/VX770 conditions^[1].
RNF5-IN-1 (10-20 μM; 23 h) significantly attenuates its inhibitory effect on NHK retrotranslocation after RNF5 knockdown, and reduces its stabilization effect on ΔF508 CFTR, which further supports that RNF5 is the functional molecular target of RNF5-IN-1^[1].
RNF5-IN-1 (5-10 μM; 30 min) inhibits the auto-ubiquitination of RNF5, but does not affect the ubiquitin-related activities of Hrd1C, Praja1, E1 UBA1, or E2 UbcH5B^[1].
RNF5-IN-1 (24 h) exhibits an IC₅₀ of 32.2 μM against the growth of HepG2 cells; it barely inhibits IL-6-induced STAT3 phosphorylation at the maximum concentration of 20 μM, indicating that its STAT3 inhibitory activity is significantly weaker than that of Stattic^[1].
RNF5-IN-1 (1.25-20 μM; 16 h) reduces the RNF5 protein level in HeLa cells in a dose-dependent manner; at 10 μM, RNF5 protein is significantly decreased after 9 h of exposure, while RNF5 mRNA remains essentially unchanged^[1].
RNF5-IN-1 (10 μM; 24 h) increases the localization of paxillin to focal adhesions in HeLa cells, which is consistent with the inhibition of RNF5 function^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.