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Chemical Compound Review

FHPI     4-[4-(4-fluorophenyl)-5- pyridin-4-yl-1,3...

Synonyms: Oxindole 94, Lopac-S-7067, Tocris-1264, Kinome_3708, S1077_Selleck, ...
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Disease relevance of SB 202190

  • SB202190 treatment enhanced FGF-2-induced neovascularization in the CAM, but the vessels displayed abnormal features indicative of hyperplasia of endothelial cells [1].
  • In an effort to evaluate the impact of p38 signaling on colorectal cancer cell fate, we treated HT29, Caco2, Hct116, LS174T and SW480 cell lines with the inhibitor SB202190 specific for p38alpha/beta kinases [2].
  • Consistent with this, the transcriptional activity of endogenous PR in MCF-7 breast cancer cells was preferentially inhibited by small interfering RNA for PPM1D; SB202190 failed to reverse the inhibition [3].
  • Both 12(S)-HETE and AngII increased cellular hypertrophy with similar potency, and this was significantly blocked by SB202190 [4].
  • Here, we demonstrate a significant reduction in rat chondrosarcoma cell proliferation following treatment with pharmacological inhibitors (SB202190 and PD169316) of p38 mitogen-activated protein (MAP) kinases [5].

High impact information on SB 202190


Chemical compound and disease context of SB 202190


Biological context of SB 202190


Anatomical context of SB 202190

  • Inhibition of p38 kinase by SB202190 (10 microM) blocks the rapid initiation of this checkpoint both in an immortalized cell line (mIMCD3) and in second-passage IME cells from mouse renal inner medulla. p38 inhibition does not affect exit from G(2) arrest [9].
  • This last phenomenon was inhibited when hepatocytes were treated with SB 202190, which was described as a potent inhibitor of p38 and JNK activities [17].
  • In contrast, a specific inhibitor of p38/HOG (SB202190) blocked PDT-induced apoptosis in LY-R cells with a lesser effect in CHO cells [18].
  • SB202190 dramatically inhibited eosinophil differentiation by 71% [19].
  • Pretreatment of neutrophils with MEK1 inhibitor PD98059, but not p38 MAPK inhibitor SB202190, prevented Entamoeba-induced apoptosis [20].

Associations of SB 202190 with other chemical compounds


Gene context of SB 202190

  • The induction of COX-2 was blocked by the p38 MAP kinase inhibitor SB202190, even when added 12-16 h after stimulation with Ag when p38 MAP kinase activity had returned to near basal, but still minimally elevated, levels [25].
  • In contrast, SB202190, a specific inhibitor of p38(MAPK), enhanced IL-1beta-induced LDL receptor expression, with a concomitant increase in ERK-1/2 activity [26].
  • SB202190 or anti-PGE(2) monoclonal antibody compromised the stabilization of COX-2 mRNA by PGE(2) [27].
  • Hence, VEGF mRNA induction is inhibited by SB202190, an inhibitor of JNK and p38/HOG kinase [28].
  • EMSAs showed that SB 202190 inhibited GBS-induced AP-1 activation, but had no effect on NF-kappaB-DNA binding activity [29].

Analytical, diagnostic and therapeutic context of SB 202190

  • Expression of p38beta attenuated the apoptotic effect of SB202190 and the cell death induced by Fas ligation and UV irradiation [30].
  • Inhibition of p38 kinase with SB-202190 (10 micrometer) potentiated beta-AR-stimulated apoptosis as measured by flow cytometry and terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) staining [31].
  • Wortmannin, an inhibitor of PI3K, did not block the preconditioning induced stimulation of 2DG6P production, but perfusion with SB202190, an inhibitor of p38 MAP kinase, did attenuate 2DG6P accumulation (111% of initial ATP, p < 0. 05 compared with preconditioned hearts) [32].
  • Dissection of individual response elements on IL-4-regulated promoter showed that C/EBP beta-mediated transcription was insensitive to SB202190 treatment in B cells whereas STAT6-mediated transcription was regulated by p38 MAPK [33].
  • Interestingly, higher concentrations of SB, which drastically activated JNK, blocked megakaryocytic differentiation, and considerably increased cell death in the presence of PMA. c-DNA microarray membranes and PCR analysis allow us to identify a set of genes modulated during PMA-induced K562 cell differentiation [34].


  1. p38 MAP kinase negatively regulates endothelial cell survival, proliferation, and differentiation in FGF-2-stimulated angiogenesis. Matsumoto, T., Turesson, I., Book, M., Gerwins, P., Claesson-Welsh, L. J. Cell Biol. (2002) [Pubmed]
  2. A novel cell type-specific role of p38alpha in the control of autophagy and cell death in colorectal cancer cells. Comes, F., Matrone, A., Lastella, P., Nico, B., Susca, F.C., Bagnulo, R., Ingravallo, G., Modica, S., Lo Sasso, G., Moschetta, A., Guanti, G., Simone, C. Cell Death Differ. (2007) [Pubmed]
  3. Dual roles for the phosphatase PPM1D in regulating progesterone receptor function. Proia, D.A., Nannenga, B.W., Donehower, L.A., Weigel, N.L. J. Biol. Chem. (2006) [Pubmed]
  4. The oxidized lipid and lipoxygenase product 12(S)-hydroxyeicosatetraenoic acid induces hypertrophy and fibronectin transcription in vascular smooth muscle cells via p38 MAPK and cAMP response element-binding protein activation. Mediation of angiotensin II effects. Reddy, M.A., Thimmalapura, P.R., Lanting, L., Nadler, J.L., Fatima, S., Natarajan, R. J. Biol. Chem. (2002) [Pubmed]
  5. p38 MAP kinase signaling is necessary for rat chondrosarcoma cell proliferation. Halawani, D., Mondeh, R., Stanton, L.A., Beier, F. Oncogene (2004) [Pubmed]
  6. Interleukin-22, a member of the IL-10 subfamily, induces inflammatory responses in colonic subepithelial myofibroblasts. Andoh, A., Zhang, Z., Inatomi, O., Fujino, S., Deguchi, Y., Araki, Y., Tsujikawa, T., Kitoh, K., Kim-Mitsuyama, S., Takayanagi, A., Shimizu, N., Fujiyama, Y. Gastroenterology (2005) [Pubmed]
  7. 14-3-3 proteins block apoptosis and differentially regulate MAPK cascades. Xing, H., Zhang, S., Weinheimer, C., Kovacs, A., Muslin, A.J. EMBO J. (2000) [Pubmed]
  8. MNK1, a new MAP kinase-activated protein kinase, isolated by a novel expression screening method for identifying protein kinase substrates. Fukunaga, R., Hunter, T. EMBO J. (1997) [Pubmed]
  9. Rapid activation of G2/M checkpoint after hypertonic stress in renal inner medullary epithelial (IME) cells is protective and requires p38 kinase. Dmitrieva, N.I., Bulavin, D.V., Fornace, A.J., Burg, M.B. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  10. Rho inhibition decreases TNF-induced endothelial MAPK activation and monolayer permeability. Nwariaku, F.E., Rothenbach, P., Liu, Z., Zhu, X., Turnage, R.H., Terada, L.S. J. Appl. Physiol. (2003) [Pubmed]
  11. Interfering with TGFbeta-induced Smad3 nuclear accumulation differentially affects TGFbeta-dependent gene expression. Lindemann, R.K., Nordheim, A., Dittmer, J. Mol. Cancer (2003) [Pubmed]
  12. Fibronectin upregulates gelatinase B (MMP-9) and induces coordinated expression of gelatinase A (MMP-2) and its activator MT1-MMP (MMP-14) by human T lymphocyte cell lines. A process repressed through RAS/MAP kinase signaling pathways. Esparza, J., Vilardell, C., Calvo, J., Juan, M., Vives, J., Urbano-Márquez, A., Yagüe, J., Cid, M.C. Blood (1999) [Pubmed]
  13. ZBP-89-induced apoptosis is p53-independent and requires JNK. Bai, L., Yoon, S.O., King, P.D., Merchant, J.L. Cell Death Differ. (2004) [Pubmed]
  14. Retinoblastoma protein and CCAAT/enhancer-binding protein beta are required for 1,25-dihydroxyvitamin D3-induced monocytic differentiation of HL60 cells. Ji, Y., Studzinski, G.P. Cancer Res. (2004) [Pubmed]
  15. The activation of c-Jun NH2-terminal kinase (JNK) by DNA-damaging agents serves to promote drug resistance via activating transcription factor 2 (ATF2)-dependent enhanced DNA repair. Hayakawa, J., Depatie, C., Ohmichi, M., Mercola, D. J. Biol. Chem. (2003) [Pubmed]
  16. Activation of Rac1 and the p38 mitogen-activated protein kinase pathway in response to all-trans-retinoic acid. Alsayed, Y., Uddin, S., Mahmud, N., Lekmine, F., Kalvakolanu, D.V., Minucci, S., Bokoch, G., Platanias, L.C. J. Biol. Chem. (2001) [Pubmed]
  17. Protein kinase activation by warm and cold hypoxia- reoxygenation in primary-cultured rat hepatocytes-JNK(1)/SAPK(1) involvement in apoptosis. Crenesse, D., Gugenheim, J., Hornoy, J., Tornieri, K., Laurens, M., Cambien, B., Lenegrate, G., Cursio, R., De Souza, G., Auberger, P., Heurteaux, C., Rossi, B., Schmid-Alliana, A. Hepatology (2000) [Pubmed]
  18. Promotion of photodynamic therapy-induced apoptosis by stress kinases. Xue, L., He, J., Oleinick, N.L. Cell Death Differ. (1999) [Pubmed]
  19. The differential role of extracellular signal-regulated kinases and p38 mitogen-activated protein kinase in eosinophil functions. Adachi, T., Choudhury, B.K., Stafford, S., Sur, S., Alam, R. J. Immunol. (2000) [Pubmed]
  20. NADPH oxidase-derived reactive oxygen species-mediated activation of ERK1/2 is required for apoptosis of human neutrophils induced by Entamoeba histolytica. Sim, S., Yong, T.S., Park, S.J., Im, K.I., Kong, Y., Ryu, J.S., Min, D.Y., Shin, M.H. J. Immunol. (2005) [Pubmed]
  21. Deletion of the loop region of Bcl-2 completely blocks paclitaxel-induced apoptosis. Srivastava, R.K., Mi, Q.S., Hardwick, J.M., Longo, D.L. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  22. The transcription factor GATA4 is activated by extracellular signal-regulated kinase 1- and 2-mediated phosphorylation of serine 105 in cardiomyocytes. Liang, Q., Wiese, R.J., Bueno, O.F., Dai, Y.S., Markham, B.E., Molkentin, J.D. Mol. Cell. Biol. (2001) [Pubmed]
  23. Angiotensin II and epidermal growth factor induce cyclooxygenase-2 expression in intestinal epithelial cells through small GTPases using distinct signaling pathways. Slice, L.W., Chiu, T., Rozengurt, E. J. Biol. Chem. (2005) [Pubmed]
  24. Characterization of the structure and function of the fourth member of p38 group mitogen-activated protein kinases, p38delta. Jiang, Y., Gram, H., Zhao, M., New, L., Gu, J., Feng, L., Di Padova, F., Ulevitch, R.J., Han, J. J. Biol. Chem. (1997) [Pubmed]
  25. Elevated levels of cyclooxygenase-2 in antigen-stimulated mast cells is associated with minimal activation of p38 mitogen-activated protein kinase. Hundley, T.R., Prasad, A.R., Beaven, M.A. J. Immunol. (2001) [Pubmed]
  26. Differential roles of extracellular signal-regulated kinase-1/2 and p38(MAPK) in interleukin-1beta- and tumor necrosis factor-alpha-induced low density lipoprotein receptor expression in HepG2 cells. Kumar, A., Middleton, A., Chambers, T.C., Mehta, K.D. J. Biol. Chem. (1998) [Pubmed]
  27. Prostaglandin E(2) regulates the level and stability of cyclooxygenase-2 mRNA through activation of p38 mitogen-activated protein kinase in interleukin-1 beta-treated human synovial fibroblasts. Faour, W.H., He, Y., He, Q.W., de Ladurantaye, M., Quintero, M., Mancini, A., Di Battista, J.A. J. Biol. Chem. (2001) [Pubmed]
  28. Stress-activated protein kinases (JNK and p38/HOG) are essential for vascular endothelial growth factor mRNA stability. Pagès, G., Berra, E., Milanini, J., Levy, A.P., Pouysségur, J. J. Biol. Chem. (2000) [Pubmed]
  29. Group B Streptococcus induces TNF-alpha gene expression and activation of the transcription factors NF-kappa B and activator protein-1 in human cord blood monocytes. Vallejo, J.G., Knuefermann, P., Mann, D.L., Sivasubramanian, N. J. Immunol. (2000) [Pubmed]
  30. Induction of apoptosis by SB202190 through inhibition of p38beta mitogen-activated protein kinase. Nemoto, S., Xiang, J., Huang, S., Lin, A. J. Biol. Chem. (1998) [Pubmed]
  31. p38 mitogen-activated protein kinase pathway protects adult rat ventricular myocytes against beta -adrenergic receptor-stimulated apoptosis. Evidence for Gi-dependent activation. Communal, C., Colucci, W.S., Singh, K. J. Biol. Chem. (2000) [Pubmed]
  32. Preconditioning enhanced glucose uptake is mediated by p38 MAP kinase not by phosphatidylinositol 3-kinase. Tong, H., Chen, W., London, R.E., Murphy, E., Steenbergen, C. J. Biol. Chem. (2000) [Pubmed]
  33. p38 Mitogen-activated protein kinase regulates interleukin-4-induced gene expression by stimulating STAT6-mediated transcription. Pesu, M., Aittomäki, S., Takaluoma, K., Lagerstedt, A., Silvennoinen, O. J. Biol. Chem. (2002) [Pubmed]
  34. A survey of the signaling pathways involved in megakaryocytic differentiation of the human K562 leukemia cell line by molecular and c-DNA array analysis. Jacquel, A., Herrant, M., Defamie, V., Belhacene, N., Colosetti, P., Marchetti, S., Legros, L., Deckert, M., Mari, B., Cassuto, J.P., Hofman, P., Auberger, P. Oncogene (2006) [Pubmed]
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