tlr2

Pam2CSK4 TFA (PUL-042 TFA) is a potent dual agonist of TLR2 and TLR6, a peptide that mimics bacterial lipoproteins.Pam2CSK4 TFA promotes platelet aggregation, and can be used to study the effects of lipoproteins on the periodontium.

FSL-1 TFA, a toll-like receptor 2/6 (TLR2/6) agonist derived from bacteria, bolsters resistance against experimental HSV-2 infection[1] and stimulates MMP-9 production via the TLR2 and NF-κB/AP-1 signaling pathways in monocytic THP-1 cells[2].

Toll-like receptor 2/6 (TLR2/6) agonist. Induces TNF-α production in human mononuclear cells. Also induces proliferation and activation of mouse splenic B cells.

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

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.

PSMα3 TFA is a peptide used to direct dendritic cells (DCs) towards a tolerogenic state, critical for DC vaccination approaches. It modulates human monocyte-derived DCs by disrupting maturation induced by TLR2 or TLR4, suppressing pro-inflammatory and anti-inflammatory cytokine secretion, and reducing antigen assimilation. Notably, PSMα3 TFA is a significant toxin secreted by highly virulent methicillin-resistant Staphylococcus aureus (MRSA) strains [1] [2].

TLR2/6 agonist (also a putative TLR10 ligand). Activates NF-κB. Induces pro-inflammatory cytokines including IL-8, IL-1β, CCL20 and TNF-α in vitro. Synergizes with IFNγ to induce CXCL10 release from melanoma cells.