Detail of "159351-69-6"

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CAS Number:
159351-69-6
Name:
Rapamycin,42-O-(2-hydroxyethyl)-
Superlist Name:
Everolimus
Molecular Structure:
Formula:
C₅₃H₈₃NO₁₄
Molecular Weight:
958.22
Synonyms:
40-O-(2-Hydroxyethyl)rapamycin;42-O-(2-Hydroxy)ethylrapamycin;Certican;RAD;RAD 001;SDZ-RAD;XIENCE V;
Density:
1.18 g/cm³
Boiling Point:
998.7 °C at 760 mmHg
Flash Point:
557.8 °C
Appearance:
off white solid
Hazard Symbols:
T
Risk Codes:
48/25
Safety:
45 Details

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Reference

The rapamycin derivative RAD inhibits mesangial cell migration through the CDK-inhibitor p27KIP1: The rapamycin derivative RAD inhibits mesangial cell migration through the CDK-inhibitor p27KIP1. Daniel, Christoph; Pippin, Jeffrey; Shankland, Stuart J.; Hugo, Christian (Medizinische Klinik IV, Universitaet Erlangen-Nuernberg, Erlangen, Germany). Laboratory Investigation, 84(5), 588-596 (English) 2004 Nature Publishing Group. CODEN: LAINAW. ISSN: 0023-6837. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The link between mesangial cell (MC) proliferation and migration during glomerular repair in the exptl. mesangial proliferative glomerulonephritis suggests that cell cycle regulation and cell migration require similar pathways, such as cell cycle proteins. The immunosuppressant RAD inhibits mouse mesangial cell (MMC) proliferation via G1/S arrest. Moreover, RAD dramatically impairs glomerular healing in the anti-Thy1 model. We tested the hypothesis that RAD alters MC migration in vitro and that this effect was mediated by the CDK-inhibitors p21CIP1 and p27KIP1. 159351-69-6 and 53123-88-9 which are cas registry numbers are also used here. Using a modified Boyden chamber in vitro migration assay, our results showed that RAD dose dependently (1-50 nM) inhibited fibronectin-induced chemotaxis in wild-type (wt) MC. RAD treatment prevented the decrease in p27KIP1 induced by mitogenic growth factors, but had no effect on p21CIP1 by Western blot anal. The antimigratory effect of RAD in wt MC was substantially dependent on p27KIP1, but not p21CIP1, since the inhibitory effects of 1-10 nM RAD on MC migration were similar in p21CIP1 deficient and wild-type MC. The effect of RAD on MC migration was also examd. in the anti-Thy1 model by BrdU-labeling of proliferating MC on day 3 that typically repopulate the glomerulus from the hilus. A control biopsy on day 3 was taken to define the starting point prior to the initiation of RAD (3 mg/kg or placebo). MC migration was detd. on day 7 by measuring the distances of BrdU-labeled MC (OX-7+/BrdU+cells) from the glomerular hilus using computerized morphometry. RAD significantly reduced the migratory response of BrdU-labeled MC compared to controls. We conclude that the immunosuppressant RAD effectively inhibits MC migration in vivo and in vitro thereby limiting the normal glomerular repair process after severe injury. Moreover, RAD-induced inhibition of MC migration in vitro is partially mediated by the CDK-inhibitor p27KIP1, but not p21CIP1. .

Immunosuppressive TOR kinase inhibitor everolimus (RAD) suppresses growth of cells derived from posttransplant lymphoproliferative disorder at allograft-protecting doses: Immunosuppressive TOR kinase inhibitor everolimus (RAD) suppresses growth of cells derived from posttransplant lymphoproliferative disorder at allograft-protecting doses. Majewski, Miroslaw; Korecka, Magdalena; Joergensen, Joanne; Fields, Leona; Kossev, Plamen; Schuler, Walter; Shaw, Leslie; Wasik, Mariusz A. (Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA). Transplantation, 75(10), 1710-1717 (English) 2003 Lippincott Williams & Wilkins. CODEN: TRPLAU. ISSN: 0041-1337. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Posttransplant lymphoproliferative disorders (PTLDs) represent a life-threatening complication of std. immunosuppressive therapy. The impact of novel, rapamycin-related immunosuppressive drugs on the pathogenesis of PTLDs remains undefined. We tested the effect of everolimus (RAD, Novartis Pharma AG, Basel, Switzerland) on human PTLD-derived cells using in vitro assays and an in vivo severe combined immunodeficiency disease mouse xenotransplant model. Everolimus profoundly inhibited the proliferation, cell-cycle progression, and survival of the PTLD-1 cell line established from a pulmonary PTLD. Equally profound inhibition of PTLD-1 growth was achieved in vivo at well-tolerated everolimus doses of 0.5 to 5 mg/kg per day. Five mg/kg per day of everolimus, given once per day, inhibited PTLD-1 tumor vol. gain by more than 10-fold in treated mice compared with untreated mice. Because the subsequent pharmacokinetic anal. indicated rapid everolimus absorption, distribution, and clearance in mice (with a half-life of 3 to 6 h and max. drug blood concn. reached after 0.5 to 1 h), treatment was changed to a twice-daily regimen. Everolimus given twice daily at 0.There are some commonly used reagents with their cas registry numbers 159351-69-6 and 171715-28-9 in this article.5 mg/kg per dose inhibited tumor-vol. gain by more than 60-fold and at 0.25 mg/kg per dose by more than 10-fold. Similar everolimus doses were required to prevent graft rejection in a mouse heart allotransplantation model; the highest dose tested (1.5 mg/kg twice daily) resulted in long-term graft survival in all mice that underwent transplantation. Everolimus displays a potent inhibitory effect on PTLD-derived cells in vitro and in vivo in a dose range leading to prevention of allograft rejection and may prove effective in both the prevention and treatment of PTLDs in transplant patients. .

Detail of "159351-69-6"

Rapamycin,42-O-(2-hydroxyethyl)-

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Reference