TLR

TLR

A group of proteins known as toll-like receptors (TLRs) are essential components of the innate immune system. They are single, membrane-spanning, non-catalytic receptors that recognize structurally conserved molecules derived from microbes and are typically expressed in sentinel cells like macrophages and dendritic cells. Once these microbes have gotten past physical barriers like the skin or mucosa of the gastrointestinal tract, TLRs recognize them and trigger immune cell responses.

TLR1 through TLR13 are among the TLRs, along with TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10, TLR11, TLR12, and TLR13. Toll-Like Receptors (TLRs) are involved in both the detection of endogenous danger signals and the early innate immune response to encroaching pathogens. TLRs are homologs of the Drosophila Toll protein, which was found to be crucial for defense against microbial infection. They are evolutionarily conserved receptors. TLRs identify pathogen-associated microbial patterns (PAMPs), which are only expressed by microbial pathogens and are highly conserved structural motifs.

TLR related products

Structure Cat No. Product Name CAS No. Product Description
V74351 Magnesium citrate (Trimagnesium dicitrate) 3344-18-1 Magnesium citrate is a form of magnesium salt that effectively penetrates into the brain and muscle tissue.
V4032 MD2-IN-1 111797-22-9 MD2-IN-1, a chalcone derivative, is a novel potent and specific inhibitor ofMyeloid differentiation protein 2(MD2) with potential anti-inflammatory activity.
V31431 MD2-TLR4-IN-1 2249801-12-3 MD2-TLR4-IN-1 (compound 22m) is an inhibitor of myeloid differentiation protein 2/toll-like receptor 4 (MD2-TLR4) complex, inhibiting lipopolysaccharides (LPS)-induced expression of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in macrophages with IC50 of 0.89 μM and 0.53 μM, respectively.
V51766 MHV-370 2205095-75-4 TLR7/8-IN-1 is an inhibitor of TLR7/TLR8, found in patent WO2019220390, compound 2b.
V76757 MMG-11 quarterhydrate MMG-11 quarterhydrate is a potent and specific human TLR2 antagonist.
V50923 Monophosphoryl lipid A (MPLA; Glucopyranosyl lipid A) 1246298-63-4 Monophosphoryl lipid A (glucopyranosyl lipid A) is a Toll-like receptor 4 agonist.
V1872 Motolimod (VTX-2337) 926927-61-9 Motolimod (also known as VTX-2337;VTX 378; VTX2337) is a novel, selective and potent small molecule agonist of the Toll-like receptor (TLR) 8 with immunostimulating/modulatory and anticancer effects.
V80853 MTvkPABC-P5 MTvkPABC-P5d, a potent TLR7 agonist/activator, is an immunostimulatory agent.
V80989 ODN 105870 sodium ODN 105870 sodium is a G-modified inhibitory oligonucleotide (INH-ODN), a selective TLR7 inhibitor.
V51779 ODN 105871 1965342-41-9 ODN 105871 is a G-modified inhibitory oligonucleotide (INH-ODN) and a TLR7 coupling agent.
V80990 ODN 105871 sodium ODN 105871 sodium is a G-modified inhibitory oligonucleotide (INH-ODN), a selective TLR7 inhibitor.
V80991 ODN 21158 sodium ODN 21158 sodium is a potent G-modified TLR3 and TLR9 inhibitor.
V80992 ODN 21595 sodium ODN 21595 sodium is a guanine-modified inhibitory oligonucleotide (INH-ODN).
V74359 ODN 4084-F 1934318-44-1 ODN 4084-F is a class B inhibitory oligonucleotide.
V80993 ODN 4084-F sodium ODN 4084-F sodium is a Class B inhibitory oligonucleotide.
V74358 ODN 5328 (ODN 2395 Control) 500239-51-0 ODN 5328 (ODN 2395 Control) could be utilized as a control for ODN 2395.
V80994 ODN 5328 sodium (ODN 2395 Control sodium) ODN 5328 (ODN 2395 Control) sodium could be utilized as a control for ODN 2395.
V74370 ODN INH 18 1934318-43-0 ODN INH-18 is a linear class B inhibitory oligonucleotide that randomly extends 12 nucleotides after the INH-ODN 4084-F sequence and lacks the ability to form important secondary structures.
V80996 ODN INH 18 sodium ODN INH-18 sodium is a linear class B inhibitory oligonucleotide that randomly extends 12 nucleotides after the INH-ODN 4084-F sequence and lacks the ability to form important secondary structures.
V74367 ODN INH-1 1934318-42-9 ODN INH-1 is a palindromic inhibitory oligonucleotide.
Contact Us Back to top