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Chemical Compound Review

Gleevac     methanesulfonic acid; 4-[(4...

Synonyms: Gleevec, Shantinib, Glivec, CHEMBL1642, PubChem18211, ...
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Disease relevance of benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-


Psychiatry related information on benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-

  • Understanding and using this tool should improve our ability to accurately follow response in GIST patients treated with imatinib mesylate, and permit this new therapeutic approach to be used optimally with accurate follow-up assessments and informed therapeutic decision-making [6].

High impact information on benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-

  • Sequencing of the BCR-ABL gene in patients who have relapsed after STI-571 chemotherapy has revealed a limited set of kinase domain mutations that mediate drug resistance [1].
  • Structural modeling implies that a novel class of variants acts allosterically to destabilize the autoinhibited conformation of the ABL kinase to which STI-571 preferentially binds [1].
  • To obtain a more comprehensive survey of the amino acid substitutions that confer STI-571 resistance, we performed an in vitro screen of randomly mutagenized BCR-ABL and recovered all of the major mutations previously identified in patients and numerous others that illuminate novel mechanisms of acquired drug resistance [1].
  • In agreement with these results, treatment of normal mice with the Kit tyrosine kinase inhibitor imatinib (Gleevec) leads to deficits in pro T and pro B cell development, similar to those seen in KitY567F/Y567F and KitW/W mice [7].
  • Here we show that Gleevec can act on host DCs to promote NK cell activation [4].

Chemical compound and disease context of benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-


Biological context of benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-


Anatomical context of benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-


Associations of benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]- with other chemical compounds


Gene context of benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-


Analytical, diagnostic and therapeutic context of benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-


  1. Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. Azam, M., Latek, R.R., Daley, G.Q. Cell (2003) [Pubmed]
  2. Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia. Hu, Y., Liu, Y., Pelletier, S., Buchdunger, E., Warmuth, M., Fabbro, D., Hallek, M., Van Etten, R.A., Li, S. Nat. Genet. (2004) [Pubmed]
  3. Gleevec casts a pox on poxviruses. McFadden, G. Nat. Med. (2005) [Pubmed]
  4. Novel mode of action of c-kit tyrosine kinase inhibitors leading to NK cell-dependent antitumor effects. Borg, C., Terme, M., Taïeb, J., Ménard, C., Flament, C., Robert, C., Maruyama, K., Wakasugi, H., Angevin, E., Thielemans, K., Le Cesne, A., Chung-Scott, V., Lazar, V., Tchou, I., Crépineau, F., Lemoine, F., Bernard, J., Fletcher, J.A., Turhan, A., Blay, J.Y., Spatz, A., Emile, J.F., Heinrich, M.C., Mécheri, S., Tursz, T., Zitvogel, L. J. Clin. Invest. (2004) [Pubmed]
  5. Potential use of imatinib in Ewing's Sarcoma: evidence for in vitro and in vivo activity. Merchant, M.S., Woo, C.W., Mackall, C.L., Thiele, C.J. J. Natl. Cancer Inst. (2002) [Pubmed]
  6. Use of positron emission tomography in oncology and its potential role to assess response to imatinib mesylate therapy in gastrointestinal stromal tumors (GISTs). Van den Abbeele, A.D., Badawi, R.D. Eur. J. Cancer (2002) [Pubmed]
  7. Critical role for Kit-mediated Src kinase but not PI 3-kinase signaling in pro T and pro B cell development. Agosti, V., Corbacioglu, S., Ehlers, I., Waskow, C., Sommer, G., Berrozpe, G., Kissel, H., Tucker, C.M., Manova, K., Moore, M.A., Rodewald, H.R., Besmer, P. J. Exp. Med. (2004) [Pubmed]
  8. Disabling poxvirus pathogenesis by inhibition of Abl-family tyrosine kinases. Reeves, P.M., Bommarius, B., Lebeis, S., McNulty, S., Christensen, J., Swimm, A., Chahroudi, A., Chavan, R., Feinberg, M.B., Veach, D., Bornmann, W., Sherman, M., Kalman, D. Nat. Med. (2005) [Pubmed]
  9. Protein kinase inhibitors as a therapeutic modality. Levitzki, A. Acc. Chem. Res. (2003) [Pubmed]
  10. Imatinib mesylate (STI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukemia in blast phase. Kantarjian, H.M., Cortes, J., O'Brien, S., Giles, F.J., Albitar, M., Rios, M.B., Shan, J., Faderl, S., Garcia-Manero, G., Thomas, D.A., Resta, D., Talpaz, M. Blood (2002) [Pubmed]
  11. Coordination of intrinsic, extrinsic, and endoplasmic reticulum-mediated apoptosis by imatinib mesylate combined with arsenic trioxide in chronic myeloid leukemia. Du, Y., Wang, K., Fang, H., Li, J., Xiao, D., Zheng, P., Chen, Y., Fan, H., Pan, X., Zhao, C., Zhang, Q., Imbeaud, S., Graudens, E., Eveno, E., Auffray, C., Chen, S., Chen, Z., Zhang, J. Blood (2006) [Pubmed]
  12. Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3. George, P., Bali, P., Annavarapu, S., Scuto, A., Fiskus, W., Guo, F., Sigua, C., Sondarva, G., Moscinski, L., Atadja, P., Bhalla, K. Blood (2005) [Pubmed]
  13. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Schindler, T., Bornmann, W., Pellicena, P., Miller, W.T., Clarkson, B., Kuriyan, J. Science (2000) [Pubmed]
  14. AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec. Wang, Y.Y., Zhou, G.B., Yin, T., Chen, B., Shi, J.Y., Liang, W.X., Jin, X.L., You, J.H., Yang, G., Shen, Z.X., Chen, J., Xiong, S.M., Chen, G.Q., Xu, F., Liu, Y.W., Chen, Z., Chen, S.J. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  15. Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop. Roumiantsev, S., Shah, N.P., Gorre, M.E., Nicoll, J., Brasher, B.B., Sawyers, C.L., Van Etten, R.A. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  16. Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations. Wong, S., McLaughlin, J., Cheng, D., Zhang, C., Shokat, K.M., Witte, O.N. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  17. Loss of p53 impedes the antileukemic response to BCR-ABL inhibition. Wendel, H.G., de Stanchina, E., Cepero, E., Ray, S., Emig, M., Fridman, J.S., Veach, D.R., Bornmann, W.G., Clarkson, B., McCombie, W.R., Kogan, S.C., Hochhaus, A., Lowe, S.W. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  18. Gleevec inhibits beta-amyloid production but not Notch cleavage. Netzer, W.J., Dou, F., Cai, D., Veach, D., Jean, S., Li, Y., Bornmann, W.G., Clarkson, B., Xu, H., Greengard, P. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  19. The third-generation bisphosphonate zoledronate synergistically augments the anti-Ph+ leukemia activity of imatinib mesylate. Kuroda, J., Kimura, S., Segawa, H., Kobayashi, Y., Yoshikawa, T., Urasaki, Y., Ueda, T., Enjo, F., Tokuda, H., Ottmann, O.G., Maekawa, T. Blood (2003) [Pubmed]
  20. Imatinib mesylate affects the development and function of dendritic cells generated from CD34+ peripheral blood progenitor cells. Appel, S., Boehmler, A.M., Grünebach, F., Müller, M.R., Rupf, A., Weck, M.M., Hartmann, U., Reichardt, V.L., Kanz, L., Brümmendorf, T.H., Brossart, P. Blood (2004) [Pubmed]
  21. Hematopathologic and cytogenetic findings in imatinib mesylate-treated chronic myelogenous leukemia patients: 14 months' experience. Braziel, R.M., Launder, T.M., Druker, B.J., Olson, S.B., Magenis, R.E., Mauro, M.J., Sawyers, C.L., Paquette, R.L., O'Dwyer, M.E. Blood (2002) [Pubmed]
  22. Imatinib mesylate inhibits T-cell proliferation in vitro and delayed-type hypersensitivity in vivo. Dietz, A.B., Souan, L., Knutson, G.J., Bulur, P.A., Litzow, M.R., Vuk-Pavlovic, S. Blood (2004) [Pubmed]
  23. Gain-of-function mutations of platelet-derived growth factor receptor alpha gene in gastrointestinal stromal tumors. Hirota, S., Ohashi, A., Nishida, T., Isozaki, K., Kinoshita, K., Shinomura, Y., Kitamura, Y. Gastroenterology (2003) [Pubmed]
  24. Combined effects of novel tyrosine kinase inhibitor AMN107 and histone deacetylase inhibitor LBH589 against Bcr-Abl-expressing human leukemia cells. Fiskus, W., Pranpat, M., Bali, P., Balasis, M., Kumaraswamy, S., Boyapalle, S., Rocha, K., Wu, J., Giles, F., Manley, P.W., Atadja, P., Bhalla, K. Blood (2006) [Pubmed]
  25. A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL-positive human leukemic cells: caspase-independent, necrosis-like programmed cell death mediated by serine protease activity. Okada, M., Adachi, S., Imai, T., Watanabe, K., Toyokuni, S.Y., Ueno, M., Zervos, A.S., Kroemer, G., Nakahata, T. Blood (2004) [Pubmed]
  26. Comparison of imatinib mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl-N-nitrosourea (ENU)-based mutagenesis screen: high efficacy of drug combinations. Bradeen, H.A., Eide, C.A., O'hare, T., Johnson, K.J., Willis, S.G., Lee, F.Y., Druker, B.J., Deininger, M.W. Blood (2006) [Pubmed]
  27. PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia. Wolff, N.C., Veach, D.R., Tong, W.P., Bornmann, W.G., Clarkson, B., Ilaria, R.L. Blood (2005) [Pubmed]
  28. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Kerkelä, R., Grazette, L., Yacobi, R., Iliescu, C., Patten, R., Beahm, C., Walters, B., Shevtsov, S., Pesant, S., Clubb, F.J., Rosenzweig, A., Salomon, R.N., Van Etten, R.A., Alroy, J., Durand, J.B., Force, T. Nat. Med. (2006) [Pubmed]
  29. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Gorre, M.E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P.N., Sawyers, C.L. Science (2001) [Pubmed]
  30. The kinase inhibitor imatinib mesylate inhibits TNF-{alpha} production in vitro and prevents TNF-dependent acute hepatic inflammation. Wolf, A.M., Wolf, D., Rumpold, H., Ludwiczek, S., Enrich, B., Gastl, G., Weiss, G., Tilg, H. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  31. CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy. Pardanani, A., Ketterling, R.P., Brockman, S.R., Flynn, H.C., Paternoster, S.F., Shearer, B.M., Reeder, T.L., Li, C.Y., Cross, N.C., Cools, J., Gilliland, D.G., Dewald, G.W., Tefferi, A. Blood (2003) [Pubmed]
  32. Imatinib mesylate therapy for relapse after allogeneic stem cell transplantation for chronic myelogenous leukemia. Kantarjian, H.M., O'Brien, S., Cortes, J.E., Giralt, S.A., Rios, M.B., Shan, J., Giles, F.J., Thomas, D.A., Faderl, S., De Lima, M., Garcia-Manero, G., Champlin, R., Arlinghaus, R., Talpaz, M. Blood (2002) [Pubmed]
  33. BCR-ABL mRNA levels at and after the time of a complete cytogenetic response (CCR) predict the duration of CCR in imatinib mesylate-treated patients with CML. Press, R.D., Love, Z., Tronnes, A.A., Yang, R., Tran, T., Mongoue-Tchokote, S., Mori, M., Mauro, M.J., Deininger, M.W., Druker, B.J. Blood (2006) [Pubmed]
  34. Imatinib mesylate (STI571) in the treatment of relapse of chronic myeloid leukemia after allogeneic stem cell transplantation. Olavarria, E., Craddock, C., Dazzi, F., Marin, D., Marktel, S., Apperley, J.F., Goldman, J.M. Blood (2002) [Pubmed]
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