NR-7h

NR-7h (0.01-10 μM; 1-24 h) specifically degrades p38-MAPK in PMA-differentiated human THP-1 macrophages in a concentration- and time-dependent manner via the ubiquitin-proteasome pathway, with a DC₅₀ of 162.9 nM^[1].
NR-7h specifically degrades p38-MAPK in human primary erythrocytes via the ubiquitin-proteasome pathway, and exerts no effect on ERK1/2 levels at a concentration of 1 μM^[1].
NR-7h (0.05-1 μM; 2-24 h) rapidly and potently induces the degradation of p38α and p38β isoforms in primary human dermal fibroblasts, with only extremely low cytotoxicity^[2].
NR-7h (0.1-1 μM; 6 h pre-treatment, followed by 12-60 h infection) reduces Leishmania donovani load in PMA-differentiated human THP-1 macrophages in a dose- and time-dependent manner via degradation of host p38-MAPK; this compound does not directly affect the viability of promastigotes^[1].
NR-7h (0.5-1 μM; 6 h pre-treatment, followed by 24 h co-treatment) acts synergistically with Amphotericin B (HY-B0221) to enhance the clearance of intracellular Leishmania donovani in PMA-differentiated human THP-1 macrophages^[1].
NR-7h (156 nM-20 μM; 72 h) inhibits the growth of Plasmodium falciparum strain 3D7 in primary human red blood cells, with an IC₅₀ of 1.047 μM; it also reduces the invasion rate of malaria parasites in a dose-dependent manner^[1].
NR-7h (1 μM; 6 h pre-treatment, followed by 10 min-24 h infection) mediates the degradation of p38-MAPK in PMA (HY-18739)-differentiated human THP-1 macrophages, thereby reshaping the host immune response to Leishmania donovani infection: it upregulates pro-inflammatory cytokines and oxidative stress mediators (ROS, NO, NOS2), while downregulating the anti-inflammatory factor IL-10^[1].
NR-7h (0.05-1 μM; 3 h pre-incubation, 24 h post-infection) reduces Mayaro virus replication levels in primary human dermal fibroblasts in a dose-dependent manner, and significantly decreases viral titers and the number of antigen-positive cells^[2].
NR-7h (0.05-1 μM; 3 h pre-incubation, 16-24 h post-infection) triggers the degradation of p38α/p38β, which downregulates the expression of Mayaro virus E1 structural protein in primary human dermal fibroblasts^[2].
NR-7h (24 h) induces the degradation of p38α and p38β proteins in human breast cancer T47D and MB-MDA-231 cells; the DC₅₀ values of p38α in the two cell lines are 24 nM and 27.2 nM, respectively, while the corresponding DC₅₀ values of p38β are 48.47 nM and 48.90 nM^[3].
NR-7h (1 µM; 16 h) selectively downregulates p38α in human breast cancer cell line MB-MDA-231 without affecting other cellular proteins^[3].
NR-7h not only inhibits UV-induced activation of the p38α pathway in human breast cancer MB-MDA-231 cells for at least two days after administration, but also blocks p38α pathway activation in LPS/IFN-γ-stimulated primary BMDMs^[3].

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