Motolimod (VTX-2337) analog and a toll-like receptor 8 (TLR8)-selective agonist with stronger activity than resiquimod (R848) and CL075 (3M002).
TL8-506 is a motolimod (VTX-2337) analog and a benzoazepine class toll-like receptor 8 (TLR8)-selective agonist. TL8-506 is commonly employed in the concentration range from 0.1 μg/mL to 1 μg/mL for stimulating cell surface TLR8 in cultures and is reported to be a stronger TLR8 ligand than the imidazoquinoline (IMDQ) derivatives (IQDs) resiquimod (R848) and CL075 (3M002).
Messenger RNA (mRNA) represents an attractive therapeutic modality for potentially a wide range of clinical indications but requires uridine chemistry modification and/or tuning of the production process to prevent activation of cellular innate immune sensors and a concomitant reduction in
Human trichinellosis is acquired by eating raw or undercooked meats carrying muscle larvae of Trichinella spp. Toll-like receptors (TLRs) are essential components of the innate immune system. However, little is known about the potential application of TLR agonists for immunotherapy
Inborn errors of immunity (IEI) are a genetically heterogeneous group of disorders with a broad clinical spectrum. Identification of molecular and functional bases of these disorders is important for diagnosis, treatment, and an understanding of the human immune response. We
Human toll-like receptor 8 (TLR8) activation induces a potent T helper-1 (Th1) cell response critical for defense against intracellular pathogens, including protozoa. The receptor harbors two distinct binding sites, uridine and di- and/or trinucleotides, but the RNases upstream of TLR8
Human Vγ9Vδ2 γδ T cells can kill a variety of cancer cells and have attracted substantial interest for cancer immunotherapy. Toll-like receptor (TLR) ligands are promising adjuvants for cancer immunotherapy, but TLR7/8 ligand Resiquimod has been shown to inhibit CD4
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