tlr 1

TLR7/8-IN-1, a crystalline TLR7/TLR8 inhibitor, is a valuable compound for autoimmune disease research[1].

TLR7 agonist 2 (TLR7-IN-1) is a specific and effective Toll-like Receptor 7 (TLR7) agonist (LEC=0.4 μM).

TLR1 is a cell-penetrating Toll/IL-1 receptor/resistance (TIR) domain/BB-Loop mimic and inhibits IL-1 receptor-mediated responses.

TLR4 agonist-1 (TEA, compound 17a) is a potent activator of Toll-like Receptor 4 (TLR4) and prompts the production of MIP-1β in RAW 264.7 and MM6 cells [1].

TLR4 agonist-1 (compound 17a) serves as a potent activator of Toll-like Receptor 4 (TLR4) and stimulates the production of MIP-1β in RAW 264.7 and MM6 cells [1].

TLR7/8/9-IN-1 is a potent inhibitor of Toll-like receptors 7/8/9 (TLR7/8/9) with an IC50 of 43 nM.

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

MD2-TLR4-IN-1 is a myeloid differentiation protein 2/toll-like receptor 4 (MD2-TLR4) complex inhibitor.

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.

Tri(TLR4-IN-C34-C2-amide-PEG1)-amide-C3-COOH is a chemical linker featuring the TLR4 inhibitor TLR4-IN-C34, known for inhibition of TLR4 in enterocytes and macrophages, thereby diminishing systemic inflammation in mouse models of endotoxemia and necrotizing enterocolitis [1].

TLR9-IN-1 is a selective and potent TLR9 inhibitor that acts on human TLR9 (IC50: 7 nM). TLR9-IN-1 can be used in the study of adverse immune response-related diseases.

Tri(TLR4-IN-C34-C2-amide-C3-amide-PEG1)-amide-C3-COOH, a chemical compound, serves as a linker incorporating TLR4 inhibitor TLR4-IN-C34. This compound effectively inhibits TLR4 in both enterocytes and macrophages, significantly reducing systemic inflammation in mouse models of endotoxemia and necrotizing enterocolitis [1].

Tri(TLR4-IN-C34-PEG2-amide-PEG1)-amide-C3-COOH is a chemical linker incorporating the TLR4 inhibitor, TLR4-IN-C34, which suppresses TLR4 activity in enterocytes and macrophages, consequently diminishing systemic inflammation observed in mouse models of endotoxemia and necrotizing enterocolitis [1].

TLR4/NF-κB/MAPK-IN-1 is a novel antineuroinflammatory agent that functions by inhibiting the TLR4/NF-κB/MAPK pathways.

Pam3CSK4 TFA (Pam3Cys-Ser-(Lys)4 TFA) is an agonist of toll-like receptor 1/2 (TLR1/2) (EC50 of 0.47 ng/mL for human TLR1/2).

Resiquimod (R848) is an imidazoquinoline amine and Toll-like receptor (TLR) agonist with potential immune response modifying activity. Resiquimod exerts its effect through the TLR signaling pathway by binding to and activating TLR7 and 8 mainly on dendritic cells, macrophages, and B-lymphocytes. This induces the nuclear translocation of the transcription activator NF-kB as well as activation of other transcription factors. This may lead to an increase in mRNA levels and subsequent production of cytokines, especially interferon-alpha (INF-a) and other cytokines, thereby enhancing T-helper 1 (Th1) immune responses. In addition, topical application of resiquimod appears to activate Langerhans' cells, leading to an enhanced activation of T-lymphocytes.

1V209 (TLR7 agonist T7) is a Toll-like receptor 7 (TLR7) agonist and has anti-tumor effects.

C29 is a novel inhibitor of TLR2/1 and TLR2/6 signaling induced by synthetic and bacterial TLR2 agonists in human HEK-TLR2 and THP-1 cells, but only TLR2/1 signaling in murine macrophages.

STAMBP-IN-1 is a novel selective antagonist of deubiquitinase STAM-binding protein (STAMBP), decreasing NALP7 protein levels and suppressing IL-1β release after TLR agonism.

CU-CPT9b (TLR8-specific antagonist 1) is an antagonist of toll-like receptor 8 (TLR8; Kd = 21 nM). It inhibits activation of NF- B induced by the TLR8 agonist R-848 in TLR8-overexpressing HEK-Blue cells with an IC50 value of 0.7 nM.

ODN 1668 is a class B CpG oligodeoxynucleotide (ODN) and serves as a TLR-9 agonist. It acts as an immunostimulatory sequence, making it effective as a vaccine adjuvant. Its sequence is 5'-tccatgacgttcctgatgct-3’ [1] [2].

ODN 1018 (1018 ISS), an oligodeoxynucleotide and a TLR-9 agonist, serves as a synthetic immunostimulatory sequence and vaccine adjuvant. The sequence is 5′-TGACTGTGAACGTTCGAGATGA-3′ [1] [2].

ODN 2007, a class B CpG ODN (oligodeoxynucleotide) and Toll-like receptor (TLR) ligand, serves as an immunomodulator and vaccine adjuvant, promoting enhanced immune responses across mammals, fish, and humans. Its sequence is 5'-TCGTCGTTGTCGTTTTGTCGTT-3' [1] [2] [3].

MyD88-IN-1 is a potent MyD88 inhibitor MyD88-IN-1 has anti-inflammatory activity and inhibits downstream inflammatory signaling pathways, including the NF-κB pathway, of members of the Toll-like receptor (TLR) and interleukin-1 (IL-1) receptor family MyD88-IN-1 may be used for the study of cancer and the treatment of inflammation.

TLR3-IN-1 (CU CPT 4a) is a selective TLR3 inhibitor (IC50: 3.44 μM in RAW 264.7 cells). It can inhibit TLR3/dsRNA complex-mediated downstream signaling pathways and inhibit the production of TNF-α and IL-1β in whole cells.

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.

ODN 24991, a guanine-modified inhibitory oligonucleotide (INH-ODN) derivative of INH-ODN 2088, inhibits Toll-like receptors (TLR) 3, TLR7, and TLR9, thereby attenuating TLR3-, TLR7-, and TLR9-mediated immune responses. The sequence of ODN 24991 is 5'-C-C-T-G-G-C-c7rGm-G-G-G-3' [1].

ODN M362, a class C oligodeoxynucleotide and TLR-9 agonist, serves as a vaccine adjuvant and induces apoptosis in cancer cells [1] [2].

NecroX-7 (LC-280126) is a potent free radical scavenger and a HMGB1 (high-mobility group box 1) inhibitor. NecroX-7 can be used as an antidote to acetaminophen toxicity. NecroX-7 exerts a protective effect by preventing the release of HMGB1 in ischemia/reperfusion injury. Additionally, NecroX-7 inhibits the HMGB1-induced release of TNF and IL-6, as well as the expression of TLR-4 and receptor for advanced glycation end products. NecroX-7 may be use for treatment of graft-versus-host disease (GVHD) research [1].

MD2-IN-1 is a Myeloid differentiation protein 2 (MD2) inhibitor with a KD of 189  μM for the recombinant human MD2 (rhMD2).

Givinostat (ITF-2357) is a HDAC inhibitor with an IC50 of 198 and 157 nM for HDAC1 and HDAC3, respectively. Givinostat (ITF2357) suppresses total LPS-induced IL-1β production robustly compared with the reduction by ITF3056. At 25, 50, and 100 nM, Givinostat reduced IL-1β secretion more than 70%. Givinostat (ITF-2357) suppresses the production of IL-6 in PBMCs stimulated with TLR agonists as well as the combination of IL-12 plus IL-18. IL-6 secretion decreases to 50% at 50 nM Givinostat, but at 100 and 200 nM, there is no reduction[1]. As shown by the CCK-8 assay, Givinostat (ITF-2357) inhibits JS-1 cell proliferation in a concentration-dependent manner. Treatment with Givinostat ≥500 nM is associated with significant inhibition of JS-1 cell proliferation (P<0.01). Also, the cell inhibition rate significantly differs between the group cotreated with Givinostat ≥250 nM plus LPS and the group without LPS treatment (same Givinostat concentration) (P<0.05)[2]. Givinostat (ITF2357) at 10 mg/kg is used as a positive control and, as expected, reduced serum TNFα by 60%. Strikingly, pretreatment of ITF3056 starting at 0.1 mg/kg significantly reduces the circulating TNFα by nearly 90%. To achieve a significant increase in serum IL-1β production, a higher dose of LPS is injected (10 mg/kg), and blood is collected after 4 h. Similarly, when pretreated with lower doses of Givinostat (ITF-2357) (1 or 5 mg/kg), there is a 22% reduction for 1 mg/kg and 40% for 5 mg/kg[1]. [1]. Li S, et al. Specific inhibition of histone deacetylase 8 reduces gene expression and production of proinflammatory cytokines in vitro and in vivo. J Biol Chem. 2015 Jan 23;290(4):2368-78. [2]. Wang YG, et al. Givinostat inhibition of hepatic stellate cell proliferation and protein acetylation. World J Gastroenterol. 2015 Jul 21;21(27):8326-39. [3]. Leoni F, et al. The histone deacetylase inhibitor ITF2357 reduces production of pro-inflammatory cytokines in vitro and systemic inflammation in vivo. Mol Med. 2005 Jan-Dec;11(1-12):1-15.

1. Ginsenoside Rg5 could be a beneficial agent for the treatment of Alzheimer's disease. 2. Ginsenoside Rg5 suppresses LPS-induced nitric oxide (NO) production and proinflammatory TNF-α secretion. 3. Ginsenoside Rg5 can ameliorate lung inflammation possib

The Immuno-Oncology Screening Library consists of 2 plates and contains more than 90 cancer and immunology-associated compounds in a 96-well Matrix tube rack format as 10 mM stock solutions in DMSO. This library includes a variety of immuno-oncology target modulators, including but not limited to, adenosine, CCR, CXCR, and TLR agonists and antagonists, BTK, PI3K, VEGFR, and BRAF inhibitors, PD-1/PDL-1 interaction inhibitors, and HDAC inhibitors. Please review the product insert for a full list of targets. Stability data is not available for the compounds as supplied in the screening library.

TLR7 agonist 1 is a selective and oral TLR7 agonist (IC50: 90 nM).

Procyanidin B1, isolated from commonly eaten fruits, binds to the TLR4/MD-2 complex and has anti-inflammatory activity.

Pam3CSK4 is a synthetic triacylated lipopeptide (LP) that mimics the acylated amino terminus of bacterial LPs.