Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (10)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sacks, S. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sacks, S. H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (1999) 14: 2087-2089
© 1999 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

Rapamycin on trial

Steven H. Sacks

Guy's, King's College and St Thomas' Hospitals' Medical School, Renal Medicine and Transplantation, Guy's Hospital, London, UK

Correspondence and offprint requests to: Steven H. Sacks, Guy's, King's College and St Thomas' Hospitals' Medical School, Renal Medicine and Transplantation, 5th Floor, Thomas Guy House, Guy's Hospital, London SE1 9RT, UK. E-mail: steven.sacks@kcl.ac.uk.

The need for additional immunosuppressive agents

Do we need another T-cell suppressive agent, when calcineurin inhibitors (cyclosporin and tacrolimus) seem to work so well? The arrival of rapamycin, structurally similar to tacrolimus and binding the same intracellular protein, but with a more downstream mode of action in the T-cell activation cascade, is likely to challenge this view. The Seventeenth World Congress of the Transplant Society heard the results of early phase III trials [1,2].

At present, cyclosporin and tacrolimus are the drugs of choice in clinical transplantation. However, both are toxic to kidneys and other organs. . . . [Full Text of this Article]

Discovery and mode of action of rapamycin

The ongoing trials

Rapamycin in addition to cyclosporin
Rapamycin instead of cyclosporine
Rapamycin and chronic graft nephropathy

Side-effects of rapamycin

Conclusion

References


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
HypertensionHome page
C. M. McNicholas and K. H. Berecek
Mammalian Target of Rapamycin: MasTOR Mediator of Cellular Changes in Pathological States?
Hypertension, December 1, 2009; 54(6): 1221 - 1222.
[Full Text] [PDF]


Home page
BloodHome page
A. M. Woltman, J. W. de Fijter, S. W. A. Kamerling, S. W. van der Kooij, L. C. Paul, M. R. Daha, and C. van Kooten
Rapamycin induces apoptosis in monocyte- and CD34-derived dendritic cells but not in monocytes and macrophages
Blood, July 1, 2001; 98(1): 174 - 180.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
J. M. Slavik, D.-G. Lim, S. J. Burakoff, and D. A. Hafler
Uncoupling p70s6 Kinase Activation and Proliferation: Rapamycin-Resistant Proliferation of Human CD8+ T Lymphocytes
J. Immunol., March 1, 2001; 166(5): 3201 - 3209.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
B. Geoerger, K. Kerr, C.-B. Tang, K.-M. Fung, B. Powell, L. N. Sutton, P. C. Phillips, and A. J. Janss
Antitumor Activity of the Rapamycin Analog CCI-779 in Human Primitive Neuroectodermal Tumor/Medulloblastoma Models as Single Agent and in Combination Chemotherapy
Cancer Res., February 1, 2001; 61(4): 1527 - 1532.
[Abstract] [Full Text]