3M-003| CAS 162397-26-4

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).

Cat. No.	Product name	Field of application
DC66456	TLR7/8 agonist 1	TLR7/8 agonist 1 is a toll-like receptor (TLR7)/TLR8 dual-agonistic imidazoquinoline.
DC66322	WAY-327512	activate TLR8-dependent NF-kB signaling
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.
DC31070	M1002	M1002 is a first-in-class HIF-2a agonists.
DC31025	TLR4-IN-C34	TLR4-IN-C34 is an orally active TLR4 inhibitor and reduces systemic inflammation in models of endotoxemia and necrotizing enterocolitis[1][2].
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.
DCC5384	Vb-201	Novel anticryptosporidial agent, acting as a toll-like receptor-2 (TLR2) antagonist
DCC4810	Smu-z1	Novel potent TLR1/2 Specific Agonist, Suppressing Leukemia Cancer Cell Growth by Stimulating Cytotoxic T Lymphocytes
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].