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Chemical Compound Review

Semaxnib     (3Z)-3-[(3,5-dimethyl-1H- pyrrol-2...

Synonyms: Semoxind, Semaxanib, Semaxinib, Romiplostim, QCR-86, ...
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Disease relevance of Semaxinib


High impact information on Semaxinib


Chemical compound and disease context of Semaxinib


Biological context of Semaxinib

  • After 12 weeks of treatment with SU5416, the blast cell counts (blood and bone marrow) decreased to undetectable levels and the peripheral blood cell counts normalized with the exception of the platelet count (50-80 x 10(9)/L [50-80 x 10(3)/microL]) [6].
  • Both sFlk-1 and the Flk-1-specifc inhibitor SU5416 eliminated the resistance phenotype in GBM and melanoma microvasculature as determined by both the vascular window and Doppler blood flow methods [11].
  • The selective flk-1 inhibitor SU5416 partially rescued the flt-1-/- mutant phenotype, and this rescue was accompanied by a decrease in the relative amount of flk-1 tyrosine phosphorylation [12].
  • PURPOSE: To determine the biological modulatory dose of SU5416, we employed a novel trial design, where "dose de-escalation" was based on demonstrable biological changes observed at the maximum tolerated dose [13].
  • A significant increase in endothelial cell apoptosis was observed in one tumor exposed to SU5416 and was associated with an increase in vessel size, but these changes occurred without an increase in tumor cell death [14].

Anatomical context of Semaxinib


Associations of Semaxinib with other chemical compounds

  • These studies indicate that SU5416 and SU6668 inhibit biologic functions of c-kit in addition to exhibiting antiangiogenic properties and suggest that the combination of these activities may provide a novel therapeutic approach for the treatment of AML [7].
  • Moreover, ZD1839 almost completely blocked EGF-induced neovascularization of mice cornea, and SU5416 partially blocked neovascularization [17].
  • The inhibition of VEGFR-2 by epigallocatechin-3 gallate was similar to that induced by Semaxanib (SU5416), a specific VEGFR-2 inhibitor [18].
  • Finally, nephrin protein by immunofluorescence was decreased in the db/db mice but was significantly restored by SU5416 [19].
  • Design: SU11248, SU5416, and SU6668 were synthesized, and their inhibitory potencies were evaluated using an in vitro RET/PTC kinase assay [20].

Gene context of Semaxinib


Analytical, diagnostic and therapeutic context of Semaxinib


  1. Inhibition of VEGF receptors causes lung cell apoptosis and emphysema. Kasahara, Y., Tuder, R.M., Taraseviciene-Stewart, L., Le Cras, T.D., Abman, S., Hirth, P.K., Waltenberger, J., Voelkel, N.F. J. Clin. Invest. (2000) [Pubmed]
  2. SU5416, a small molecule tyrosine kinase receptor inhibitor, has biologic activity in patients with refractory acute myeloid leukemia or myelodysplastic syndromes. Giles, F.J., Stopeck, A.T., Silverman, L.R., Lancet, J.E., Cooper, M.A., Hannah, A.L., Cherrington, J.M., O'Farrell, A.M., Yuen, H.A., Louie, S.G., Hong, W., Cortes, J.E., Verstovsek, S., Albitar, M., O'Brien, S.M., Kantarjian, H.M., Karp, J.E. Blood (2003) [Pubmed]
  3. Paradoxical secondary polycythemia in von Hippel-Lindau patients treated with anti-vascular endothelial growth factor receptor therapy. Richard, S., Croisille, L., Yvart, J., Casadeval, N., Eschwège, P., Aghakhani, N., David, P., Gaudric, A., Scigalla, P., Hermine, O. Blood (2002) [Pubmed]
  4. A phase 2 clinical study of SU5416 in patients with refractory acute myeloid leukemia. Fiedler, W., Mesters, R., Tinnefeld, H., Loges, S., Staib, P., Duhrsen, U., Flasshove, M., Ottmann, O.G., Jung, W., Cavalli, F., Kuse, R., Thomalla, J., Serve, H., O'Farrell, A.M., Jacobs, M., Brega, N.M., Scigalla, P., Hossfeld, D.K., Berdel, W.E. Blood (2003) [Pubmed]
  5. Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors. Bergers, G., Song, S., Meyer-Morse, N., Bergsland, E., Hanahan, D. J. Clin. Invest. (2003) [Pubmed]
  6. Stable remission after administration of the receptor tyrosine kinase inhibitor SU5416 in a patient with refractory acute myeloid leukemia. Mesters, R.M., Padró, T., Bieker, R., Steins, M., Kreuter, M., Göner, M., Kelsey, S., Scigalla, P., Fiedler, W., Büchner, T., Berdel, W.E. Blood (2001) [Pubmed]
  7. The antiangiogenic protein kinase inhibitors SU5416 and SU6668 inhibit the SCF receptor (c-kit) in a human myeloid leukemia cell line and in acute myeloid leukemia blasts. Smolich, B.D., Yuen, H.A., West, K.A., Giles, F.J., Albitar, M., Cherrington, J.M. Blood (2001) [Pubmed]
  8. Arginine deiminase and other antiangiogenic agents inhibit unfavorable neuroblastoma growth: potentiation by irradiation. Gong, H., Pöttgen, C., Stüben, G., Havers, W., Stuschke, M., Schweigerer, L. Int. J. Cancer (2003) [Pubmed]
  9. Pharmacodynamic-mediated effects of the angiogenesis inhibitor SU5416 on the tumor disposition of temozolomide in subcutaneous and intracerebral glioma xenograft models. Ma, J., Li, S., Reed, K., Guo, P., Gallo, J.M. J. Pharmacol. Exp. Ther. (2003) [Pubmed]
  10. Triple combination of irradiation, chemotherapy (pemetrexed), and VEGFR inhibition (SU5416) in human endothelial and tumor cells. Bischof, M., Abdollahi, A., Gong, P., Stoffregen, C., Lipson, K.E., Debus, J.U., Weber, K.J., Huber, P.E. Int. J. Radiat. Oncol. Biol. Phys. (2004) [Pubmed]
  11. Inhibition of vascular endothelial growth factor receptor signaling leads to reversal of tumor resistance to radiotherapy. Geng, L., Donnelly, E., McMahon, G., Lin, P.C., Sierra-Rivera, E., Oshinka, H., Hallahan, D.E. Cancer Res. (2001) [Pubmed]
  12. The vascular endothelial growth factor (VEGF) receptor Flt-1 (VEGFR-1) modulates Flk-1 (VEGFR-2) signaling during blood vessel formation. Roberts, D.M., Kearney, J.B., Johnson, J.H., Rosenberg, M.P., Kumar, R., Bautch, V.L. Am. J. Pathol. (2004) [Pubmed]
  13. Novel Phase I dose de-escalation design trial to determine the biological modulatory dose of the antiangiogenic agent SU5416. Dowlati, A., Robertson, K., Radivoyevitch, T., Waas, J., Ziats, N.P., Hartman, P., Abdul-Karim, F.W., Wasman, J.K., Jesberger, J., Lewin, J., McCrae, K., Ivy, P., Remick, S.C. Clin. Cancer Res. (2005) [Pubmed]
  14. Pharmacodynamic analysis of target inhibition and endothelial cell death in tumors treated with the vascular endothelial growth factor receptor antagonists SU5416 or SU6668. Davis, D.W., Takamori, R., Raut, C.P., Xiong, H.Q., Herbst, R.S., Stadler, W.M., Heymach, J.V., Demetri, G.D., Rashid, A., Shen, Y., Wen, S., Abbruzzese, J.L., McConkey, D.J. Clin. Cancer Res. (2005) [Pubmed]
  15. SU5416 and SU5614 inhibit kinase activity of wild-type and mutant FLT3 receptor tyrosine kinase. Yee, K.W., O'Farrell, A.M., Smolich, B.D., Cherrington, J.M., McMahon, G., Wait, C.L., McGreevey, L.S., Griffith, D.J., Heinrich, M.C. Blood (2002) [Pubmed]
  16. Combined therapy with direct and indirect angiogenesis inhibition results in enhanced antiangiogenic and antitumor effects. Abdollahi, A., Lipson, K.E., Sckell, A., Zieher, H., Klenke, F., Poerschke, D., Roth, A., Han, X., Krix, M., Bischof, M., Hahnfeldt, P., Grone, H.J., Debus, J., Hlatky, L., Huber, P.E. Cancer Res. (2003) [Pubmed]
  17. ZD1839 (Iressa) induces antiangiogenic effects through inhibition of epidermal growth factor receptor tyrosine kinase. Hirata, A., Ogawa, S., Kometani, T., Kuwano, T., Naito, S., Kuwano, M., Ono, M. Cancer Res. (2002) [Pubmed]
  18. Green tea catechins inhibit vascular endothelial growth factor receptor phosphorylation. Lamy, S., Gingras, D., Béliveau, R. Cancer Res. (2002) [Pubmed]
  19. Blockade of vascular endothelial growth factor signaling ameliorates diabetic albuminuria in mice. Sung, S.H., Ziyadeh, F.N., Wang, A., Pyagay, P.E., Kanwar, Y.S., Chen, S. J. Am. Soc. Nephrol. (2006) [Pubmed]
  20. An Orally Administered Multitarget Tyrosine Kinase Inhibitor, SU11248, Is a Novel Potent Inhibitor of Thyroid Oncogenic RET/Papillary Thyroid Cancer Kinases. Kim, D.W., Jo, Y.S., Jung, H.S., Chung, H.K., Song, J.H., Park, K.C., Park, S.H., Hwang, J.H., Rha, S.Y., Kweon, G.R., Lee, S.J., Jo, K.W., Shong, M. J. Clin. Endocrinol. Metab. (2006) [Pubmed]
  21. The antiangiogenic agent SU5416 down-regulates phorbol ester-mediated induction of cyclooxygenase 2 expression by inhibiting nicotinamide adenine dinucleotide phosphate oxidase activity. Saha, D., Sekhar, K.R., Cao, C., Morrow, J.D., Choy, H., Freeman, M.L. Cancer Res. (2003) [Pubmed]
  22. Matrix metalloproteinases (MMP9 and MMP2) induce the release of vascular endothelial growth factor (VEGF) by ovarian carcinoma cells: implications for ascites formation. Belotti, D., Paganoni, P., Manenti, L., Garofalo, A., Marchini, S., Taraboletti, G., Giavazzi, R. Cancer Res. (2003) [Pubmed]
  23. CEACAM1/VEGF cross-talk during neuroblastic tumour differentiation. Poliani, P., Mitola, S., Ravanini, M., Ferrari-Toninelli, G., D'Ippolito, C., Notarangelo, L., Bercich, L., Wagener, C., Memo, M., Presta, M., Facchetti, F. J. Pathol. (2007) [Pubmed]
  24. Apoptosis of pulmonary microvascular endothelial cells stimulates vascular smooth muscle cell growth. Sakao, S., Taraseviciene-Stewart, L., Wood, K., Cool, C.D., Voelkel, N.F. Am. J. Physiol. Lung Cell Mol. Physiol. (2006) [Pubmed]
  25. Vascular endothelial growth factor and hepatocyte regeneration in acetaminophen toxicity. Donahower, B., McCullough, S.S., Kurten, R., Lamps, L.W., Simpson, P., Hinson, J.A., James, L.P. Am. J. Physiol. Gastrointest. Liver Physiol. (2006) [Pubmed]
  26. Inhibition of angiogenesis by blocking activation of the vascular endothelial growth factor receptor 2 leads to decreased growth of neurogenic sarcomas. Angelov, L., Salhia, B., Roncari, L., McMahon, G., Guha, A. Cancer Res. (1999) [Pubmed]
  27. Inhibition of the VEGF receptor 2 combined with chronic hypoxia causes cell death-dependent pulmonary endothelial cell proliferation and severe pulmonary hypertension. Taraseviciene-Stewart, L., Kasahara, Y., Alger, L., Hirth, P., Mc Mahon , G., Waltenberger, J., Voelkel, N.F., Tuder, R.M. FASEB J. (2001) [Pubmed]
  28. Protein tyrosine kinase inhibitors as novel therapeutic agents. Levitzki, A. Pharmacol. Ther. (1999) [Pubmed]
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