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

Imiquimod hydrochloride

  Cat. No.:  DC60236   Featured
Chemical Structure
99011-78-6
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More than 5000 active chemicals with high quality for research!
Field of application
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.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 99011-78-6
Chemical Name: Imiquimod hydrochloride
Synonyms: Imiquimod (hydrochloride);R 837 hydrochloride;Imiquimod hydrochloride;1-Isobutyl-1H-imidazo[4,5-c]quinolin-4-amine hydrochloride;Imiquimod HCl;1-(2-methylpropyl)-1H-imidazo[4,5-c]quinolin-4-amine hydrochloride;1-(2-methylpropyl)imidazo[4,5-c]quinolin-4-amine;hydrochloride
SMILES: Cl[H].N1(C([H])=NC2C(N([H])[H])=NC3=C([H])C([H])=C([H])C([H])=C3C1=2)C([H])([H])C([H])(C([H])([H])[H])C([H])([H])[H]
Formula: C14H17ClN4
M.Wt: 276.7646
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
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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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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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