Enpatoran

  Cat. No.:  DC44159   Featured
Chemical Structure
2101938-42-3
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More than 5000 active chemicals with high quality for research!
Field of application
Enpatoran (M5049) is an orally active and dual TLR7/8 inhibitor with IC50s of 11.1 nM and 24.1 nM in HEK293 cells, respectively. Enpatoran can block both innate and adaptive autoimmunity. Enpatoran is inactive against TLR3, TLR4 and TLR9. Enpatoran (M5049) can block molecule synthetic ligands and natural endogenous RNA ligands. Enpatoran (M5049) inhibits cytokine release, causing great potency in pharmacokinetic/pharmacodynamic properties.
Cas No.: 2101938-42-3
Chemical Name: Enpatoran free base
SMILES: N#CC(C=C1)=C(N=CC=C2)C2=C1N3C[C@@H](C(F)(F)F)C[C@@H](N)C3
Formula: C16H15F3N4
M.Wt: 320.319
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: Enpatoran (M5049) is an orally active and dual TLR7/8 inhibitor with IC50s of 11.1 nM and 24.1 nM in HEK293 cells, respectively. Enpatoran can block both innate and adaptive autoimmunity. Enpatoran is inactive against TLR3, TLR4 and TLR9. Enpatoran (M5049) can block molecule synthetic ligands and natural endogenous RNA ligands. Enpatoran (M5049) inhibits cytokine release, causing great potency in pharmacokinetic/pharmacodynamic properties.
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
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DC50032 CU-CPT17e CU-CPT17e shows strong NF-κB activation in TLR3, TLR8 and TLR9 HEK293 cells with EC50 values of 4.80±0.73, 13.5±0.58 and 5.66±0.17 μM, respectively. CU-CPT17e significantly improves the activity with 13.9±0.9 fold of NF-κB activation and an EC50 value of 4.8±0.7 μM. CU-CPT17e inhibits the proliferation of HeLa cancer cells by triggering apoptosis and arresting the cell cycle at the S phase. The induction of apoptosis by CU-CPT17e in HeLa cells is investigated. HeLa cells are cultured with increasing concentrations of CU-CPT17e or poly I:C or blank control (DMSO) for 24 h. Treatment with CU-CPT17e for 24 h at different concentrations (10 to 40 μM) results in an elevation of apoptotic cell population ranging from 10% to 17%, which is more effective than poly I:C at 5 μg/mL. These results suggest that the antiproliferative activity of CU-CPT17e against HeLa cells might result from its ability to directly induce apoptosis[1].
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