NR-7h

The DC₅₀ values of NR-7h for degrading p38α in T47D and MDA-MB-231 cells are 24 nM and 27.2 nM, respectively, while its DC₅₀ values for degrading p38β in these two cell lines are 48.47 nM and 48.90 nM, respectively^[1].
NR-7h (1 μM; 24 h) selectively induces the degradation of p38α and p38β, but not that of p38γ, p38δ, ERK1/2 or JNK, in human cancer cell lines MCF7, HeLa and HT29^[1].
NR-7h (1 μM; 24 h, 48 h) inhibits UV-induced activation of the p38α pathway (detected by the phosphorylation level of MK2) in human breast cancer MB-MDA-231 cells for at least 48 h^[1].
NR-7h (1 μM; 24 h) inhibits LPS/IFNγ-induced activation of the p38α pathway (detected by the phosphorylation level of MK2) in mouse bone marrow-derived macrophages^[1].
NR-7h potently and selectively degrades human p38-MAPK in phorbol ester (PMA)-differentiated THP-1 macrophages in a concentration- and time-dependent manner via the ubiquitin-proteasome pathway, with a DC₅₀ of 162.9 nM^[2].
NR-7h (1-5 μM) efficiently and selectively degrades p38-MAPK in human red blood cells via the ubiquitin-proteasome pathway, with no effect on the closely related kinases ERK1/2^[2].
NR-7h (0.1-10 μM; 72 h) does not reduce the viability of PMA-differentiated human THP-1 macrophages even at concentrations up to 10 μM following 72 h of treatment^[2].
NR-7h (0.05-1 μM; 2-24 h) rapidly and completely degrades the p38α/p38β isoforms in primary human dermal fibroblasts at concentrations ≥0.05 μM^[3].
Treatment of human lung A549 cells with NR-7h (10 μM; 24 h) induces 74% degradation of p38 protein without causing cytotoxicity^[4].
NR-7h (10 μM; 24 h) induces 50% degradation of p38 protein in human lung fibroblast MRC-5 cells, and no cytotoxicity is observed after treatment with 10 μM for 24 h^[4].
NR-7h (0-25 μM; 72 h) does not directly inhibit the survival or proliferation of *Leishmania donovani* promastigotes in vitro^[2].
NR-7h (0.5-1 μM; 6 h pre-treatment, followed by 24 h infection) acts synergistically with amphotericin B to enhance the clearance of intracellular *Leishmania donovani* in PMA-differentiated THP-1 macrophages without increasing cytotoxicity^[2].
NR-7h (1 μM; 6 h pre-treatment, followed by 30 min-24 h infection) induces the degradation of p38-MAPK in PMA-differentiated THP-1 macrophages infected with *Leishmania donovani*, thereby shifting the immune response toward a pro-inflammatory phenotype, which is specifically characterized by increased expression of pro-inflammatory cytokines, ROS production and NO production, along with decreased expression of the anti-inflammatory cytokine IL-10^[2].
NR-7h (0.05-1 μM; 3 h pre-treatment + 24 h post-infection) reduces MAYV replication levels in primary human dermal fibroblasts in a dose-dependent manner, decreases the number of viral antigen-positive cells, viral titer and viral E1 protein levels, and shows no significant cytotoxicity at concentrations up to 1 μM^[3].
NR-7h (10 μM; 72 h post-infection) potently inhibits the infection of human lung A549 cells by human coronavirus OC43, reducing viral titer by 2.8 log₁₀ and decreasing viral RNA levels after 72 h of treatment at 10 μM, with no cytotoxicity^[4].
NR-7h (1.0 nM-10 μM; 72 h post-infection) inhibits human coronavirus OC43 infection in human lung A549 cells, with an IC₅₀ of 1.0 nM, and no cytotoxicity is observed even at concentrations as high as 10 μM^[4].
NR-7h (10 μM; 14 h total incubation post-infection) does not inhibit human coronavirus OC43 infection in BHK-21 cells when added at 0, 1, 3, or 6 h post-infection, as longer exposure is required to achieve sufficient p38 depletion for antiviral activity^[4].
NR-7h (10 μM; 72 h post-infection) potently inhibits human coronavirus 229E infection in human lung fibroblast MRC-5 cells, reducing viral titer by 3.1 log₁₀ and decreasing viral RNA levels after 72 h of treatment at 10 μM, with no cytotoxicity^[4].
NR-7h (10 μM; 72 h post-infection) depletes p38 protein in HeLa-ACE2 cells treated with 10 μM for 72 h without inducing cytotoxicity, but fails to inhibit spike protein-mediated entry of SARS-CoV-1 or SARS-CoV-2 pseudoviruses^[4].
The p38 degradation mediated by NR-7h (10 μM) and its antiviral activity against human coronavirus OC43 in human lung A549 cells are dependent on proteasome function, as co-treatment with 5 μM MG132 abolishes both effects^[4].

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