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Chemical Compound Review

SANGLIFEHRIN A     (3S,6S,9R,10R,11R,12R,13E,15E, 18S,21S)-18...

Synonyms: AC1NTUQB, CHEMBL410807, CHEBI:45527, 1ynd, SFA
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Disease relevance of SANGLIFEHRIN A


High impact information on SANGLIFEHRIN A


Biological context of SANGLIFEHRIN A


Anatomical context of SANGLIFEHRIN A


Associations of SANGLIFEHRIN A with other chemical compounds

  • METHODS: Isolated perfused rat hearts were subjected to 35 min ischaemia/120 min reperfusion, and were treated with (1) SFA (1.0 microM) or (2) DMSO vehicle for the first 15 min of reperfusion or (3) SFA (1.0 microM) after the first 15 min of reperfusion [2].
  • This may be mediated either by a direct interaction with the MPTP [e.g., by Cyclosporin A (CsA) and Sanglifehrin A (SfA)], or indirectly by decreasing calcium loading and reactive oxygen species (ROS; key inducers of pore opening) or lowering intracellular pH [10].

Gene context of SANGLIFEHRIN A

  • The CypA inhibitor cyclosporin A and non-immunosuppressive PPIase inhibitors such as NIM811 and sanglifehrin A block expression of Vpr without affecting pre- or post-translational events such as transcription, intracellular transport, or virus incorporation of Vpr [11].
  • Further analysis of different elements in the p53 promoter showed that sanglifehrin A activates p53 transcription primarily through the activation of the transcription factor NFkappaB by activating IkappaB kinase in a manner that is similar to several genotoxic agents [6].
  • In the early steps of M-CSF signaling, SfA inhibits the phosphorylation of Raf-1 and the external regulated kinases (ERK)1/2 and mitogen-activated protein kinase phosphatase-1, which are required for proliferation [8].
  • Sanglifehrin A, a novel cyclophilin-binding immunosuppressant, inhibits IL-2-dependent T cell proliferation at the G1 phase of the cell cycle [12].

Analytical, diagnostic and therapeutic context of SANGLIFEHRIN A


  1. Structure of human cyclophilin A in complex with the novel immunosuppressant sanglifehrin A at 1.6 A resolution. Kallen, J., Sedrani, R., Zenke, G., Wagner, J. J. Biol. Chem. (2005) [Pubmed]
  2. Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury. Hausenloy, D.J., Duchen, M.R., Yellon, D.M. Cardiovasc. Res. (2003) [Pubmed]
  3. The novel cyclophilin binding compound, sanglifehrin A, disassociates G1 cell cycle arrest from tolerance induction. Allen, A., Zheng, Y., Gardner, L., Safford, M., Horton, M.R., Powell, J.D. J. Immunol. (2004) [Pubmed]
  4. The novel cyclophilin-binding drug sanglifehrin A specifically affects antigen uptake receptor expression and endocytic capacity of human dendritic cells. Woltman, A.M., Schlagwein, N., van der Kooij, S.W., van Kooten, C. J. Immunol. (2004) [Pubmed]
  5. Sanglifehrin A acts as a potent inhibitor of the mitochondrial permeability transition and reperfusion injury of the heart by binding to cyclophilin-D at a different site from cyclosporin A. Clarke, S.J., McStay, G.P., Halestrap, A.P. J. Biol. Chem. (2002) [Pubmed]
  6. Inhibition of cell cycle progression by the novel cyclophilin ligand sanglifehrin A is mediated through the NFkappa B-dependent activation of p53. Zhang, L.H., Youn, H.D., Liu, J.O. J. Biol. Chem. (2001) [Pubmed]
  7. Sanglifehrin-cyclophilin interaction: degradation work, synthetic macrocyclic analogues, X-ray crystal structure, and binding data. Sedrani, R., Kallen, J., Martin Cabrejas, L.M., Papageorgiou, C.D., Senia, F., Rohrbach, S., Wagner, D., Thai, B., Jutzi Eme, A.M., France, J., Oberer, L., Rihs, G., Zenke, G., Wagner, J. J. Am. Chem. Soc. (2003) [Pubmed]
  8. Cyclophilin A is required for M-CSF-dependent macrophage proliferation. Sànchez-Tilló, E., Wojciechowska, M., Comalada, M., Farrera, C., Lloberas, J., Celada, A. Eur. J. Immunol. (2006) [Pubmed]
  9. Immunosuppressive activity of the immunophilin-binding drug Sanglifehrin A in human whole blood: potent inhibition of interleukin-6 produced by lymphocytes and monocytes. Härtel, C., Iblher, P., Puzik, A., Wortmeier, K., Ebel, B., Schultz, C., Müller-Steinhardt, M. Scand. J. Immunol. (2006) [Pubmed]
  10. Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection. Halestrap, A.P., Clarke, S.J., Javadov, S.A. Cardiovasc. Res. (2004) [Pubmed]
  11. Cyclophilin A interacts with HIV-1 Vpr and is required for its functional expression. Zander, K., Sherman, M.P., Tessmer, U., Bruns, K., Wray, V., Prechtel, A.T., Schubert, E., Henklein, P., Luban, J., Neidleman, J., Greene, W.C., Schubert, U. J. Biol. Chem. (2003) [Pubmed]
  12. Sanglifehrin A, a novel cyclophilin-binding immunosuppressant, inhibits IL-2-dependent T cell proliferation at the G1 phase of the cell cycle. Zhang, L.H., Liu, J.O. J. Immunol. (2001) [Pubmed]
  13. Synthesis of derivatives of the novel cyclophilin-binding immunosuppressant sanglifehrin A with reduced numbers of polar functions. Bänteli, R., Wagner, J., Zenke, G. Bioorg. Med. Chem. Lett. (2001) [Pubmed]
  14. Sanglifehrin A Blocks Key Dendritic Cell Functions In Vivo and Promotes Long-Term Allograft Survival Together with Low-Dose CsA. Hackstein, H., Steinschulte, C., Fiedel, S., Eisele, A., Rathke, V., Stadlbauer, T., Taner, T., Thomson, A.W., Tillmanns, H., Bein, G., Hölschermann, H. Am. J. Transplant. (2007) [Pubmed]
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