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Home > RNA Delivery > Adjuvant Molecules > TLR agonist small molecule

3M-003

  Cat. No.:  DC22922   Featured
Chemical Structure
162397-26-4
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More than 5000 active chemicals with high quality for research!
Field of application
A potent TLR7/8 agonist that induces robust production of the Th1-polarizing cytokines TNF-alpha and IL-12 from neonatal antigen-presenting cells (APCs)..
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 162397-26-4
Chemical Name: 4-Amino-2-(ethoxymethyl)-6,7,8,9-tetrahydro-α,α-dimethyl-1H-imidazo[4,5-c]quinoline-1-ethanol
Synonyms: 3M003
Formula: C17H26N4O2
M.Wt: 318.421
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: A potent TLR7/8 agonist that induces robust production of the Th1-polarizing cytokines TNF-alpha and IL-12 from neonatal antigen-presenting cells (APCs).
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
Cat. No. Product name Field of application
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DC60236 Imiquimod hydrochloride Imiquimod hydrochloride (R 837 hydrochloride), an immune response modifier, is a selective toll like receptor 7 (TLR7) agonist. Imiquimod hydrochloride exhibits antiviral and antitumor effects in vivo. Imiquimod hydrochloride can be used for the research of external genital, perianal warts, cancer and COVID-19.
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DC73563 E6742 E6742 (E6742) is a potent, selective, dual TLR7/8 inhibitor with binding Kd of 1.7 uM/37 nM in ITC assays, respectively, inhibits TLR7/8 agonist CL097 induced reporter activation with IC50 values of 22, 68, and 3.0 nM for hTLR7, mTLR7, and hTLR8, respecti
DC73561 E104 E014 is a potent, selective TLR7 agonist with EC50 of 69 nM in Ramos Blue reporter assays, >500-fold selective for TLR7 over TLR8.
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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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