EM982

EM982 (2-64 mg/mL; 24 h) shows very low antibacterial activity against S. aureus NILS6^[1].
EM982 inhibits LPS-induced TNF-α at 10 mg/mL in THP-1 macrophages and inhibits IL-6, IL-8, and IL-10 at ≥3 mg/mL; and inhibits TLR4-induced NF-κB and/or AP-1 activation at ≥3 mg/mL in HEK-Blue hTLR4 cells^[1].
EM982 (10 mg/mL; 9 h) does not significantly alter the transcription of TLR signaling molecules in THP-1 macrophages, and all detected fold changes range from 0.72 to 1.42^[1].
EM982 (10 mg/mL; 10-60 min) inhibits the NF-κB pathway by reducing the phosphorylation of IKKβ and IκBα in LPS-stimulated THP-1 macrophages^[1].
EM982 inhibits NF-κB-dependent SEAP activity in PMA-untreated THP-1-Blue cells; it inhibits PMA-untreated THP-1 cells to reduce IL-6 and IL-8 production, but does not reduce TNF-α production^[1].
EM982 (1‑5 μg/mL; 2 h) inhibits TLR2/1- and TLR2/6-triggered NF‑κB reporter gene activation in THP‑1‑Blue NF‑κB cells, and inhibits TLR2 ligand- and bacterial cell-induced NF‑κB/AP‑1 SEAP reporter gene activation in HEK‑Blue hTLR2 cells^[2].

EM982 (1-5 μg/mL; 2 h) modulates TLR2 ligand-induced cytokine production in THP-1 cells, downregulating the pro-inflammatory factors IL-6, TNF-α, and IL-8, and upregulating the anti-inflammatory factor IL-10^[2].
EM982 (1-5 μg/mL; 2 h) does not reduce the viability of THP-1 or HEK-Blue hTLR2 cells under the tested TLR2 ligand conditions, nor does it induce cytotoxicity^[2].

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