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Broad plati- percent of free guanosine as a function of time Fig. Whilst the —NH3 groups is sometimes observed around 4 ppm in freshly the sterically protected complex 11 has a reaction half-life of prepared samples, before it disappears from solvent exchange.
Both the unprotected and pro- tected platinum complexes show a single resonance in the region Glutathione. Glutathione was num complexes that contain two trans-ammine ligands and an incubated with the metal complexes in a 10 : 1 ratio to mimic the Dalton Trans.
As glutathione has no aromatic resonances, the degradation of the metal com- plexes can easily be followed through the appearance of Table 2 The in vitro cytotoxicity of the protected and unprotected dinuclear platinum complexes in the human ovarian carcinoma cell line additional resonances in the aromatic 1H NMR region.
As expected, the unprotected complex 8 reacted quick- 7 No 2 0.
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The sterically protected complex 10 Yes 2 1. As well as binding to intracellular a n. Human serum albumin HSA is the most abundant protein in human blood serum and has been shown to readily bind to platinum drugs. The unprotected platinum complex 8 has a HSA see if any protection against HSA binding was afforded to the reaction half-life of 24 h, whereas the protected complex 11 protected complex.
At intervals, aliquots were taken from the reaction mixture and immediately centrifuged on Viva-spin columns.
All The cytotoxicity of the six dinuclear platinum complexes was HSA and HSA-bound platinum remained in the top of the determined using in vitro growth inhibition assays with the column, with all unbound platinum complex washed to the human ovarian carcinoma cell line A and its cisplatin resis- bottom.
Such trinuclear complexes would better mimic the means it is closer to the preferred end-to-end distance, and structure of BBR while still having steric protection to the hence, results in more cytotoxic metal complexes.
We hope to make a family of these tri- Secondly, the protected complexes are less active than the nuclear complexes in the future.
This result is not unexpected given the short incubation periods used in in vitro assays and the reduced rate of reaction that the protected complexes will have in com- Experimental parison to the unprotected derivatives; their slower reaction rates Materials mean the onset of apoptosis is later and hence the cells reproduce more before the effects of the complexes are felt.
This reduced All reagents were purchased from Sigma Aldrich with the excep- cytotoxicity is also observed for picoplatin when compared with tion of 1-propylphosphonic acid cyclic anhydride T3P and cisplatin, and has been demonstrated in a panel of 11 different anhydrous dimethylformamide which were purchased from Alfa cell lines, where picoplatin displayed IC50 values that were Aesar.
Viva-spin columns with a molecular mass cut off of 3. This reduced cyto- toxicity of picoplatin was not a concern as the reduced reactivity Elemental analyses were performed on a Perkin Elmer also led to much reduced toxicity. Two versions of each ligand were Diaminoalkane 1.
The reduced rate of reaction with HSA by the pro- temperature and stirred for 2 days. Found: C, Next, the solution was Water was then removed in vacuo. The remaining solid was dissolved in the minimum amount of hot water and acetone was added until Synthesis of 2-methylpyridyl-based linkers the solution became cloudy.
The process was repeated until the product, a pale 4 mL. Found C, ESI-MS: 8. The solution was 4H, t , 1. Slow evaporation of a saturated aqueous solution yielded single crystals suitable for X-ray diffraction. The remaining solid was dis- isotropically. The solid was removed WinGX. Selected crystallo- rotary evaporation. The sample was 7. Upon Samples were taken periodically metric analysis analyses.
These were centrifuged at rpm for 25 min before unit. While hydrogen atoms were complex peaks compared to the new peaks which arise between mostly observed in the difference maps, they were placed in 8 and 9 ppm. Mangrum and N.
Farrell, Chem. In vitro growth assays using the human ovarian cancer cell line 11 F. Arnesano and G. Natile, Coord. Hay, Curr. Drugs, , 1, A were conducted using published methods. Treat, J. Schiller, E. Quoix, A. Mauer, M. Edelman, M. The P. Bonomi, R. Ramlau and E. Lemarie, Eur. Cancer, , 38, cells were trypsinised, counted and adjusted to — cells S13—S Chen, Z. Guo, S. Parsons and P. Sadler, Chem.
Cisplatin or metal complex stock solutions were diluted — Holford, F. Raynaud, B.
Murrer, K. Grimaldi, J. Hartley, num concentration 0. Abrams and L. Kelland, Anti-Cancer Drug Des. Munk, C. Diakos, L. Ellis, R. Fenton, B. Messerle and T. Hambley, Inorg. The plates were further incubated for 24 h 17 N. Wheate and J. Collins, Coord. Collins, Curr. Plates were then fed , 5, — Hegmans, S.
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Berners-Price, M. Davies, D. Humphreys and N. Farrell, J. The medium and MTT were removed — These 20 M. Kloster, J. Hannis, D.
Muddiman and N. Jodrell, T. Evans, W. Steward, D. Cameron, J. Plates were then read by their absor- C. Aschele, C. Noberasco, M. Lind, J. Carmichael, N.
Dobbs, G. Camboni, bance at nm with the resulting dose—response curve display- B. Gatti and F. De Braud, Eur. Cancer, , 40, — Hensing, N. Hanna, H. Gillenwater, M. Camboni, C. Allievi and M. Socinski, Anti-Cancer Drugs, , 17, — Oehlsen, Y. Qu and N. Farrell, Inorg. Summa, J. Maigut, R. Puchta and R. Abbreviations 25 M. Sarkar and K. Biradha, Cryst.
Growth Des. Ruhayel, J. Moniodis, X. Yang, J. Kasparkova, V.
Berners-Price and N. DSC differential scanning calorimetry 27 Y. Qu, M. Tran and N. Komeda, T. Moulaei, K.
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Woods, M. Chikuma, N. Farrell and TGA thermogravimetric analysis L. Williams, J. Wheate, C. Cullinane, L. Webster and J. Collins, Anti-Cancer Drug Des. Still, P. The features and the stability of your pdf program have convinced me so much that I switched to the Pro version About chip. Most of all, the clear user interface convinced me. And with your split and merge software, I'm also sure my files will stay on my Windows 10 system.
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