tlr7/8 agonist 1

TLR7 8 agonist 1 is a toll-like receptor TLR7 TLR8 agonist with anticancer and antiviral activities and can be used to study immune-related diseases.

TLR7 8 agonist 1 dihydrochloride (TLR7 8 agonist-5d) is a TLR7 8 agonist which shows prominent immunostimulatory activities.

TLR7 8 agonist 12 (compound 9) is a human TLR7 8 agonist with EC50 values of 11 nM for hTLR7 and 150 nM for hTLR8, indicating its potential for immune modulation.

TLR7 8 agonist 11 (compound 30) serves as a powerful agonist for hTLR7 and hTLR8, exhibiting EC50 values of 31.1 nM and 13.1 nM, respectively. This compound is crucial in the functioning of both adaptive and innate immune responses.

D18 is an immune modulator that acts as a dual agonist for TLR7 8 (with EC50 values of 24 nM for hTLR7 and 10 nM for hTLR8, respectively). It enhances the expression of PD-L1 through epigenetic regulation, thereby increasing the sensitivity of tumors to PD-1 PD-L1 blockade. Additionally, D18 functions as a cytotoxin for ADC synthesis, specifically for the ADC HE-S2 [1].

Gardiquimod diTFA, an imidazoquinoline analog and TLR7 8 agonist, inhibits HIV-1 infection of macrophages and activated peripheral blood mononuclear cells (PBMCs), and specifically activates TLR7 at concentrations below 10 μM. As an immune system modifier and reverse transcriptase inhibitor, it serves as a novel therapeutic agent to block systemic and mucosal transmission of HIV-1.[1][2]

TLR7 8 agonist 4 (compound 41) is a potent TLR7 8 agonist with demonstrated anti-cancer activity [1].

TLR7 8 agonist 9 (Compound 25a), with EC50 values of 40 nM for hTLR7 and 23 nM for hTLR8, demonstrates anti-tumor properties and enhances the efficacy of PD-1 PD-L1 blockade treatments, making it valuable for cancer immunotherapy research [1].

Gardiquimod (hydrochloride) is an imidazoquinoline class TLR7 8 agonist. It can inhibit HIV-1 infection in macrophages and activated peripheral blood mononuclear cells (PBMCs). At concentrations below 10 μM, Gardiquimod (hydrochloride) specifically activates TLR7.

ORN 06 (Compound R-0006) is a U-rich single-stranded RNA containing 6 repeats of the UUG sequence motif, and it functions as a TLR7 8 agonist. This compound stimulates human TLR7 8-mediated or murine TLR7-mediated immunity [1].

TLR7 8 agonist 8 (compound 24m) is a potent dual agonist for toll-like receptors 7 and 8 (TLR7 8), exhibiting half-maximal effective concentrations (EC50s) of 27 nM for human TLR7 (hTLR7) and 12 nM for human TLR8 (hTLR8). This compound enhances the efficacy of PD-1 PD-L1 inhibitors in antitumor activity [1].

3M-011, a potent dual toll-like receptor TLR7 8 agonist and cytokine inducer, serves as a powerful adjuvant to radiotherapy, eliciting significant local and systemic immune responses. Additionally, it effectively inhibits H3N2 influenza viral replication in the nasal cavity and exhibits strong antitumor activity[1][2][3].

TLR7 8 antagonist 2 (Compound 15) is a highly potent and orally active agonist of TLR7 8 with IC50 values of 4.9 nM for TLR7 and 0.6 nM for TLR8, making it a promising candidate for treating and investigating autoimmune diseases like lupus erythematosus, which involves inappropriate activation of TLR7 and TLR8. Consequently, TLR7 8 antagonist 2 is a valuable tool for autoimmune disease research [1].

TLR7 8 Antagonist 1 (Compound 16c), an imidazoquinoline derivative, is a potent TLR7 8 agonist with IC50 values of 3.91 and 2.19 μM for TLR7 and TLR8, respectively. rel-O-2050 (TLR-2050) is a key target for drug development in infectious diseases, cancer, and autoimmune diseases.

NCI 126224, a toll-like receptor 4 (TLR4) antagonist, demonstrates selective inhibition of nitric oxide (NO) production in RAW 264.7 macrophages, triggered by the TLR4 agonist LPS (IC50 = 0.31 µM), as opposed to minimal effects on NO production induced by agonists for TLR7/8 (R-848), TLR1/2 (Pam3CSK4), and TLR3 (poly(I:C)). Nevertheless, it also effectively inhibits NO production initiated by the TLR2/6 agonist FSL-1 at an IC50 of 0.6 µM in the same cell line. Moreover, NCI 126224 suppresses LPS-induced NF-κB activity in BV-2 microglial cells and reduces LPS-triggered increases in IL-1β and TNF-α levels in RAW 264.7 macrophages with IC50 values of 5.92, 0.42, and 1.54 µM, respectively.

Gardiquimod is a TLR7 8 agonist. When used at concentrations below 10 μM, Gardiquimod specifically activates TLR7. Gardiquimod could inhibit HIV-1 infection of macrophages and activated peripheral blood mononuclear cells.

TLR7 8 agonist 4 hydroxy-PEG6-acid hydrochloride, a Drug-Linker Conjugate for ADC synthesis, is the hydrochloride variant of TLR7 8 agonist 4 hydroxy-PEG6-acid, with the TLR7 8 agonist 4 component attached to the hydroxy-PEG6-acid linker [1].

TLR7 8 agonist 4 hydroxy-PEG6-acid, a drug-linker conjugate for antibody-drug conjugates (ADCs), comprises the TLR7 8 agonist 4 and a hydroxy-PEG6-acid linker, suitable for ADC synthesis [1].