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Chemical Compound Review

Tyrphostin B56     (E)-2-cyano-3-(3,4- dihydroxyphenyl)-N-(4...

Synonyms: Tocris-0616, CHEMBL440298, AG-556, SureCN2533402, ZINC02557954, ...
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Disease relevance of AG 556

  • These data are consistent with the conclusion that AG 556 prevented cytokine-induced multiorgan failure and death during septic shock by inhibiting cell-signaling pathways without impairing host defenses as determined by clearance of bacteria and endotoxin [1].
  • Tyrphostin AG 556 improves survival and reduces multiorgan failure in canine Escherichia coli peritonitis [1].
  • Moreover, treatment with AG 556 significantly increased the survival rate of rats after trauma-hemorrhage and induction of subsequent sepsis compared with vehicle-treated rats [2].
  • In the present study, tyrphostin AG556, which is more lipophilic than those of the AG126 family, was effective in preventing LPS-induced lethal toxicity when administered 2 h after LPS [3].
  • Suppression of experimental autoimmune encephalomyelitis by tyrphostin AG-556 [4].

High impact information on AG 556

  • During the first 48 h after infection, AG 556 also improved mean arterial pressure, left ventricular ejection fraction, cardiac output, oxygen delivery, and alveolar-arterial oxygen gradient compared to controls (all P < or = 0.05) [1].
  • Treatment with AG 556 had no effect on clearance of endotoxin or bacteria from the blood (both P = NS); however, AG 556 did significantly lower serum TNF levels (P = 0.03) [1].
  • RESULTS: AG 556 treatment restored the depressed cardiovascular and hepatocellular functions after trauma-hemorrhage and resuscitation, which was associated with reduced phosphorylation of mitogen-activated protein kinases p44/42 and p38 [2].
  • AG-556 does not block the activation of JNK/SAPK and of p38/HOG and therefore seems to act at a target down stream to these kinases which is activated in stress or at a target on an obligatory parallel pathway [4].
  • These findings together with previous results showing inhibition of sepsis in mice and dogs suggest that protein tyrosine kinase (PTK) blockers of the AG-556 family may be considered in the management of human autoimmune disorders such as multiple sclerosis (MS) [4].

Chemical compound and disease context of AG 556


Biological context of AG 556


Anatomical context of AG 556


Gene context of AG 556

  • The effects of EGF and IGF-1 were studied in combination with inhibiting receptor antibodies and an EGF-R-specific tyrosine kinase inhibitor, tyrphostin B56 [11].
  • TNF-alpha and IFN-gamma production by in vitro sensitized splenocytes from AG-556-treated rats was significantly diminished as compared with control cells from EAM animals [5].

Analytical, diagnostic and therapeutic context of AG 556


  1. 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]
  2. Inhibition of tyrosine kinase signaling after trauma-hemorrhage: a novel approach for improving organ function and decreasing susceptibility to subsequent sepsis. Jarrar, D., Wang, P., Song, G.Y., Cioffi, W.G., Bland, K.I., Chaudry, I.H. Ann. Surg. (2000) [Pubmed]
  3. Late administration of a lipophilic tyrosine kinase inhibitor prevents lipopolysaccharide and Escherichia coli-induced lethal toxicity. Vanichkin, A., Patya, M., Gazit, A., Levitzki, A., Novogrodsky, A. J. Infect. Dis. (1996) [Pubmed]
  4. 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]
  5. 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]
  6. Genistein and tyrphostin AG 556 block the action potential shortening in septic shock. Chiang, C.E., Luk, H.N., Wang, T.M., Sheu, J.R., Ding, P.Y. Zhonghua Yi Xue Za Zhi (Taipei) (2002) [Pubmed]
  7. Effects of the tyrosine kinase inhibitor tyrphostin AG 556 on acute necrotising pancreatitis in rats. Alhan, E., Cicek, R., Erçin, C., Orem, A., Vanizor, B., Cinel, A. The European journal of surgery = Acta chirurgica. (2002) [Pubmed]
  8. Protein from chromaffin granules promotes survival of mesencephalic dopaminergic neurons by an EGF-receptor ligand-mediated mechanism. Krieglstein, K., Unsicker, K. J. Neurosci. Res. (1997) [Pubmed]
  9. Transforming growth factor alpha (TGF-alpha) increases cell number in a human pancreatic cancer cell line but not in normal mouse pancreas. Kullenberg, B., Jansen, C., Fredäng, N., Ohlsson, B., Axelson, J. Int. J. Pancreatol. (2000) [Pubmed]
  10. The reduction of myocardial damage and leukocyte polymorphonuclear accumulation following coronary artery occlusion by the tyrosine kinase inhibitor tyrphostin AG 556. Altavilla, D., Squadrito, F., Campo, G.M., Saitta, A., Squadrito, G., Quartarone, C., Deodato, B., Arlotta, M., Ferlito, M., Minutoli, L., Tringali, M., Urna, G., Sardella, A., Caputi, A.P. Life Sci. (2000) [Pubmed]
  11. The inhibitory effect of an EGF receptor-specific tyrosine kinase inhibitor on pancreatic cancer cell lines was more potent than inhibitory antibodies against the receptors for EGF and IGF I. Kobari, M., Kullenberg, B., Björkman, A., Matsuno, S., Ihse, I., Axelson, J. Int. J. Pancreatol. (1998) [Pubmed]
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