That the blood levels of Ida, with no detectable amounts after 8 h The formation of its major metabolite, Idarubicinol, and its effect was to the entire cycle of time is not included. SDC should be negatively charged Adrenergic Receptors under physiological conditions due to residual carboxyl groups on the PGA. This can hen the absorption by the components of the reticuloendothelial system to increased. Faster delivery can be examined by the metabolism of the polymer in the plasma, which caused the formation of the kinetics of the smaller units RECOMMENDED distribution of CSD vs. Ida in liver, kidney, heart, lung and spleen, the most vascularized organs of the K Rpers. The H Ufung of tumors at 4, 8 and 24 h after administration was significantly h Forth in CSD as Ida. This can utert by the passive accumulation as a result of a combination of longer plasma t1 / 2 and perhaps the EPR effect explained. For comparison, an increase of the tumor exposure for the PGA conjugates 6-fold compared to reported CPT CPT. In the clinical setting, the treatment with Ida Kardiotoxizit t, as the RESTRICTIONS LIMITATION, the dose, w While the gravity of doxorubicin is associated to the lowest in comparison. The only short-term Quivalentdosis pharmacokinetic study has shown that the accumulation of cardiac Ida significantly reduced with CSD. The maximum concentration detected in the heart of Ida was 4.8 times h Ago as the top level with the SDC. This can be found in a significant improvement in the doses that patients in the medical center can k Lead. However, the levels of the heart with CSD at a lower level because of the slower clearance remains with increasing concentrations of free Ida after 24 hours and beyond.
This is the reason that the predicted pharmacokinetic parameters of non-compartmental analysis showed comparable AUC values w Calculated during a mean residence time and increased Ht t1 / 2 for the CSD. It should be noted that the analysis by the trapezf Shaped process in AUC values of 9444.5 and 11591.7 SDC and Ida are in the heart tissue or out. A longitudinal study of multiple doses to ensure that those values under the sustained efficacy, the clinical toxicity of t k can cause To stay. The absorption of liver CSD was significantly h Forth as Ida with almost 15% of the injected dose in liver at 1 h found compared to 4% id Ida to 30 min after 5-alpha-reductase administration. Accumulation in the liver and spleen has for poly glutamine  Acid and D is m Was like that, the PGA Similar effects have been demonstrated. As mentioned above HNT, The charge and Molekülgr E on CSD subject to uptake by phagocytic cells in the circulation and in organs of the RES. The difference in the trailer Ufung of CDD and Ida in the spleen was not so great as observed in the liver. Ida significant accumulation in the kidney is a reflection of the rapid clearance from the plasma w During CSD in uniformly Sodium slow pace of the trailer Has been testing the kidney. 3.8. The antitumor efficacy of therapeutic index CDD, in relation to Ida, was 2 3 times h Ago when they found when tested in a 3-Q2d Ida 脳 regime and a dose-escalation study. Mice that were treated with 6 mg / kg showed a loss of 15 wt% of K Rpers after a second dose. The K Body weight was partly recovered by the end of the study to 30 days. The selection of the starting dose was based on our previously pub.