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Chemical Compound Review

UPCMLD-DP015     2-[(3-hydroxy-4-nitro- phenyl)methylidene]p...

Synonyms: Lopac-T-9177, CHEMBL77387, AG-126, AG-127, AG-J-10399, ...
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Disease relevance of AG-127

  • Protein tyrosine kinase inhibitors of the tyrphostin AG 126 family protect mice against LPS-induced lethal toxicity [1].
  • Animals were infected intraperitoneally with Escherichia coli 0111: B4, and then, in a randomized, blinded fashion, were treated immediately with one of two tyrphostins, AG 556 (n = 40) or AG 126 (n = 10), or with control (n = 50), and followed for 28 d or until death [2].
  • These results demonstrate that inhibition of AG 126-sensitive tyrosine kinase pathways may provide new approaches for preventing excessive inflammation and reducing the increases in blood flow and intracranial pressure in the acute phase of bacterial meningitis [3].
  • Tyrphostin AG 126 inhibits development of postoperative ileus induced by surgical manipulation of murine colon [4].
  • The tyrosine kinase inhibitor tyrphostin AG 126 reduced the development of colitis in the rat [5].

High impact information on AG-127

  • Furthermore, this inhibitory effect correlated with the potency of AG 126 to block LPS-induced tyrosine phosphorylation of a p42MAPK protein substrate in the murine macrophage [1].
  • Of 10 substances tested, only the protein tyrosine kinase inhibitor tyrphostin AG 126 discriminated significantly between PG and LPS: TNF-alpha release induced by PG, but not by LPS, was dose-dependently suppressed [6].
  • These data indicate that increased K(+) efflux via P2X(7) nucleotide receptor stimulation activates AG-126- and bromoenol lactone-sensitive signaling pathways in murine macrophages that result in stably maintained signals for caspase-1 regulation in cell-free assays [7].
  • Inhibition of extracellular signal-regulated kinase (ERK)-1/2 (with PD-98059 or AG-126) also reduced VEGF-induced hyperpermeability but did not block VEGF-induced vasodilation [8].
  • Furthermore, tyrphostin AG 126 pretreatment significantly inhibited activation of multifactorial transcription factor NF-kappaB, which could form the basis for reduction in proinflammatory mediator expression [4].

Anatomical context of AG-127


Associations of AG-127 with other chemical compounds

  • Furthermore, treatment of rats with tyrphostin AG 126 significantly reduced the production of peroxynitrite and of pro-inflammatory cytokines TNF-alpha and IL-1beta [10].

Gene context of AG-127

  • The degree of staining for nitrotyrosine, PAR, iNOS, and COX-2 were markedly reduced in tissue sections obtained from zymosan-treated rats which had received tyrphostin AG 126 [10].
  • Tyrphostins AG-126 and AG-556 were previously shown to reduce TNF-alpha production and its end-organ cytotoxicity, thus proving beneficial in animal models of septic shock and experimental autoimmune encephalomyelitis [11].
  • Using a rodent model of colonic postoperative ileus, we demonstrate that a single bolus injection of the PTK inhibitor tyrphostin AG 126 (15 mg/kg sc) before surgery significantly attenuates the surgically induced impairment of colonic contractility both in vivo and in vitro [4].
  • Similarly, AG-556 administered for an additional 10 days after myosin immunization (when signs of inflammation are already present) attenuated the progression of myocarditis, though AG-126 did not [11].


  1. Prevention of lipopolysaccharide-induced lethal toxicity by tyrosine kinase inhibitors. Novogrodsky, A., Vanichkin, A., Patya, M., Gazit, A., Osherov, N., Levitzki, A. Science (1994) [Pubmed]
  2. Tyrphostin AG 556 improves survival and reduces multiorgan failure in canine Escherichia coli peritonitis. Sevransky, J.E., Shaked, G., Novogrodsky, A., Levitzki, A., Gazit, A., Hoffman, A., Elin, R.J., Quezado, Z.M., Freeman, B.D., Eichacker, P.Q., Danner, R.L., Banks, S.M., Bacher, J., Thomas, M.L., Natanson, C. J. Clin. Invest. (1997) [Pubmed]
  3. Tyrosine kinase inhibition reduces inflammation in the acute stage of experimental pneumococcal meningitis. Angstwurm, K., Hanisch, U.K., Gassemi, T., Bille, M.B., Prinz, M., Dirnagl, U., Kettenmann, H., Weber, J.R. Infect. Immun. (2004) [Pubmed]
  4. Tyrphostin AG 126 inhibits development of postoperative ileus induced by surgical manipulation of murine colon. Moore, B.A., Türler, A., Pezzone, M.A., Dyer, K., Grandis, J., Bauer, A.J. Am. J. Physiol. Gastrointest. Liver Physiol. (2004) [Pubmed]
  5. The tyrosine kinase inhibitor tyrphostin AG 126 reduced the development of colitis in the rat. Cuzzocrea, S., McDonald, M.C., Mazzon, E., Mota-Filipe, H., Lepore, V., Ciccolo, A., Terranova, M.L., Britti, D., Caputi, A.P., Thiemermann, C. Lab. Invest. (2000) [Pubmed]
  6. Intracellular pathways involved in tumor necrosis factor-alpha release by human monocytes on stimulation with lipopolysaccharide or staphylococcal peptidoglycan are partly similar. Mattsson, E., Van Dijk, H., Van Kessel, K., Verhoef, J., Fleer, A., Rollof, J. J. Infect. Dis. (1996) [Pubmed]
  7. Mechanisms of caspase-1 activation by P2X7 receptor-mediated K+ release. Kahlenberg, J.M., Dubyak, G.R. Am. J. Physiol., Cell Physiol. (2004) [Pubmed]
  8. Vascular endothelial growth factor stimulates differential signaling pathways in in vivo microcirculation. Aramoto, H., Breslin, J.W., Pappas, P.J., Hobson, R.W., Durán, W.N. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  9. Suppression of experimental autoimmune encephalomyelitis by tyrphostin AG-556. Brenner, T., Poradosu, E., Soffer, D., Sicsic, C., Gazit, A., Levitzki, A. Exp. Neurol. (1998) [Pubmed]
  10. The tyrosine kinase inhibitor tyrphostin AG 126 reduces the multiple organ failure induced by zymosan in the rat. Dugo, L., Chatterjee, P.K., Mazzon, E., McDonald, M.C., Paola, R.D., Fulia, F., Caputi, A.P., Thiemermann, C., Cuzzocrea, S. Intensive care medicine. (2002) [Pubmed]
  11. The effect of early and late treatment with the tyrphostin AG-556 on the progression of experimental autoimmune myocarditis. George, J., Barshack, I., Goldberg, I., Keren, P., Gazit, A., Levitzki, A., Keren, G., Roth, A. Exp. Mol. Pathol. (2004) [Pubmed]
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