Poly (I:C):Kanamycin (1:1) sodium is an isometric complex of Poly (I:C) and Kanamycin. Poly(I:C) sodium, a synthetic analog of double-stranded RNA, is a TLR3 and retinoic acid-inducible gene I receptor ( RIG-I and MDA5 ) agonist. Poly(I:C) sodium can be used as a vaccine adjuvant to enhance innate and adaptive immune responses and induce apoptosis in cancer cells [1] [2]. Kanamycin is an orally active antibacterial agent (Gram-negative/positive bacteria) that inhibits translocation and causes miscoding by binding to the 70S ribosomal subunit. Kanamycin shows good inhibitory activity against Mycobacterium tuberculosis (susceptible and drug-resistant) and Klebsiella pneumoniae, and can be used in the research of tuberculosis and pneumonia [3] [4] [5] [6].
In Vivo, Poly (I:C) sodium treatment inhibits tumor growth in NOD/SCID immunodeficient mice injected with 1205Lu cells. The level of human DNA is 50% lower in mice treated with Poly (I:C) sodium[1]. Kanamycin (2, 4 mg/kg; s.c.; once daily, 6 times a week for 3 weeks) inhibits growth of bovine tubercle bacilli in lung and spleen of mice[3]. Kanamycin (1.25, 5 mg/kg; s.c.; single (at 3 h after infection)) inhibits the multiplication of K. pneumonia DT-S in lung, trachea, and blood of mice and in proportion to the dose administration, and also increases the survival rate of mice[4].
In Vitro, Poly (I:C) sodium (20 ng/mL; 24 hours; WM793, WM278, WM239A, WM9 and 1205Lu cells) treatment strongly reduces viability from 100% in controls to 20%–50% within 24 hours[1]. Poly (I:C) sodium (200 ng/mL; 24 hours; 1205Lu cells) treatment induces apoptosis in 1205Lu cells[1]. Poly (I:C) sodium (3 ng/mL; 24 hours; 1205Lu cells) treatment induces IFN-β expression in melanoma cells. Silencing of RIG-I and MDA-5 confirmed that induction of IFN-β by Poly (I:C) sodium required RIG-I and MDA-5, respectively, and that required IPS-1[1]. Poly (I:C) sodiumd (5 ng/mL; 24 hours; 1205Lu cells) treatment reveals active subunits of caspase-9 and caspase-8 in melanoma cells[1]. Kanamycin (0.1-100 μg/mL; 2 weeks) exhibits good antibacterial activity (MIC=1-5 μg/mL) to various strains of mycobacteria in vitro[3].
References:
[1]. Robert Field, et al. Systemic challenge with the TLR3 agonist poly I:C induces amplified IFNalpha/beta and IL-1beta responses in the diseased brain and exacerbates chronic neurodegeneration. Brain Behav Immun. 2010 Aug;24(6):996-1007.
[2]. Besch R, et al. Proapoptotic signaling induced by RIG-I and MDA-5 results in type I interferon-independent apoptosis in human melanoma cells. J Clin Invest. 2009 Aug;119(8):2399-411.
[3]. Cheng YS, et al. Anticancer function of polyinosinic-polycytidylic acid. Cancer Biol Ther. 2010 Dec 15;10(12):1219-23.
In Vivo, Poly (I:C) sodium treatment inhibits tumor growth in NOD/SCID immunodeficient mice injected with 1205Lu cells. The level of human DNA is 50% lower in mice treated with Poly (I:C) sodium[1]. Kanamycin (2, 4 mg/kg; s.c.; once daily, 6 times a week for 3 weeks) inhibits growth of bovine tubercle bacilli in lung and spleen of mice[3]. Kanamycin (1.25, 5 mg/kg; s.c.; single (at 3 h after infection)) inhibits the multiplication of K. pneumonia DT-S in lung, trachea, and blood of mice and in proportion to the dose administration, and also increases the survival rate of mice[4].
In Vitro, Poly (I:C) sodium (20 ng/mL; 24 hours; WM793, WM278, WM239A, WM9 and 1205Lu cells) treatment strongly reduces viability from 100% in controls to 20%–50% within 24 hours[1]. Poly (I:C) sodium (200 ng/mL; 24 hours; 1205Lu cells) treatment induces apoptosis in 1205Lu cells[1]. Poly (I:C) sodium (3 ng/mL; 24 hours; 1205Lu cells) treatment induces IFN-β expression in melanoma cells. Silencing of RIG-I and MDA-5 confirmed that induction of IFN-β by Poly (I:C) sodium required RIG-I and MDA-5, respectively, and that required IPS-1[1]. Poly (I:C) sodiumd (5 ng/mL; 24 hours; 1205Lu cells) treatment reveals active subunits of caspase-9 and caspase-8 in melanoma cells[1]. Kanamycin (0.1-100 μg/mL; 2 weeks) exhibits good antibacterial activity (MIC=1-5 μg/mL) to various strains of mycobacteria in vitro[3].
References:
[1]. Robert Field, et al. Systemic challenge with the TLR3 agonist poly I:C induces amplified IFNalpha/beta and IL-1beta responses in the diseased brain and exacerbates chronic neurodegeneration. Brain Behav Immun. 2010 Aug;24(6):996-1007.
[2]. Besch R, et al. Proapoptotic signaling induced by RIG-I and MDA-5 results in type I interferon-independent apoptosis in human melanoma cells. J Clin Invest. 2009 Aug;119(8):2399-411.
[3]. Cheng YS, et al. Anticancer function of polyinosinic-polycytidylic acid. Cancer Biol Ther. 2010 Dec 15;10(12):1219-23.