poly(i:c)

Polyinosinic-polycytidylic acid (Poly(I:C)) is a double-stranded RNA (dsRNA) and a TLR3 agonist. Polyinosinic-polycytidylic acid induces natural immunity in mammals.

Polyinosinic-polycytidylic acid sodium (Poly(I:C) sodium) is a synthetic analog of double-stranded RNA and an agonist of toll-like receptor 3 (TLR3) and retinoic acid inducible gene I (RIG-I)-like receptors (RIG-I and MDA5).

Poly(I:C):Kanamycin (1:1) is a compound comprising an equal mixture of synthetic double-stranded RNA (dsRNA), specifically Poly(I:C), a Toll-like receptor 3 (TLR3) agonist, and kanamycin, a positively charged (poly-NH3) antibiotic. The positive charge of kanamycin interacts with the negatively charged Poly(I:C), stabilizing the molecule.

Poly(I:C):Kanamycin (1:1) sodium is a symmetric complex combining Poly(I:C) sodium, a synthetic double-stranded RNA analog acting as a TLR3 and RIG-I/MDA5 agonist, with Kanamycin, an antibacterial agent effective against both Gram-negative and positive bacteria by inhibiting translocation and causing miscoding on the 70S ribosomal subunit. Poly(I:C) sodium serves as a potent vaccine adjuvant, bolstering innate and adaptive immunity and prompting apoptosis in cancer cells [1] [2]. Meanwhile, Kanamycin exhibits significant efficacy against Mycobacterium tuberculosis, including drug-resistant strains, and Klebsiella pneumoniae, offering valuable insights for tuberculosis and pneumonia research [3] [4] [5] [6].

Polyinosinic-polycytidylic acid potassium (Poly(I:C) potassium), a synthetic double-stranded RNA analog, serves as an agonist for toll-like receptor 3 (TLR3) and retinoic acid-inducible gene I (RIG-I)-like receptors (RIG-I and MDA5), offering applications in immunotherapy. Its sodium variant enhances both innate and adaptive immune responses when used as a vaccine adjuvant and is instrumental in modifying the tumor microenvironment. Additionally, Poly(I:C) potassium can directly induce apoptosis in cancer cells [1] [2] [3].

Lonchocarpic acid shows an anti-inflammatory mechanism of lonchocarpine in LPS- or poly(I:C)-induced neuroinflammation.

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.