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  • 1
    Electronic Resource
    Electronic Resource
    Formation of Novel Hydrophobic Complexes between Cationic Lipids and Plasmid DNA (1995)
    s.l. : American Chemical Society
    Biochemistry 34 (1995), S. 12877-12883 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00039a050
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  • 2
    Electronic Resource
    Electronic Resource
    Comparison of methods for determination of ascorbic acid in animal tissues (1983)
    s.l. : American Chemical Society
    Analytical chemistry 55 (1983), S. 1229-1232 
    Details
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ac00259a008
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  • 3
    Electronic Resource
    Electronic Resource
    Poly(ethylene glycol)-Modified Phospholipids Prevent Aggregation during Covalent Conjugation of Proteins to Liposomes (1995)
    s.l. : American Chemical Society
    Bioconjugate chemistry 6 (1995), S. 187-194 
    Details
    ISSN: 1520-4812
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bc00032a006
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  • 4
    Electronic Resource
    Electronic Resource
    Identification of vesicle properties that enhance the antitumour activity of liposomal vincristine against murine L1210 leukemia (1993)
    Springer
    Cancer chemotherapy and pharmacology 33 (1993), S. 17-24 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of vesicle lipid composition, size and drug-to-lipid ratio on the antitumour activity of liposomal vincristine was assessed in the murine L1210 ascitic leukemia model. A pH gradient-dependent entrapment procedure was used to encapsulate vincristine and allowed such vesicle properties to be independently varied. Free vincristine delivered i.v. at the maximum tolerated dose (2.0 mg/kg) resulted in a 27.8% increase in the life span (ILS) of mice inoculated i.p. with L1210 cells. Encapsulation of the drug in egg phosphatidylcholine/cholesterol vesicles did not significantly increase the antitumour efficacy of vincristine (ILS, 38.9%). In contrast, administration of vincristine entrapped in vesicles composed of distearoylphosphatidylcholine (DSPC)/cholesterol resulted in ILS values as high as 133%. This enhanced antitumour activity of the DSPC/cholesterol formulations was sensitive to the size of the liposomes; increasing the vesicle size from 100 nm to 1 μm decreased the ILS from 133.3% to 55.6% at a drug dose of 2.0 mg/kg. Decreasing the drug-to-lipid ratio from 0.1∶1 to 0.05∶1 (w/w) had negligible effects on the activity of liposomal vincristine; however, a further decrease in the drug-to-lipid ratio to 0.01∶1 (w/w) decreased the antitumour potency at all drug doses studied. Pharmacology studies indicated that the antitumour activities of free and various liposomal forms of vincristine correlated well with the residence time of the drug in the circulation. These studies indicate that efforts to enhance the therapeutic activity of vincristine through liposome encapsulation must address not only the circulation life-time of the vesicle systems but also the capacity of the liposomes to retain entrapped drug in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686017
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  • 5
    Electronic Resource
    Electronic Resource
    Intratumor distribution of doxorubicin following i.v. administration of drug encapsulated in egg phosphatidylcholine/cholesterol liposomes (1997)
    Springer
    Cancer chemotherapy and pharmacology 40 (1997), S. 309-317 
    Details
    ISSN: 1432-0843
    Keywords: Key words Liposomes ; Doxorubicin ; Extravasation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Purpose: A pharmacological evaluation of an egg phosphatidylcholine/cholesterol (55:45 mole ratio, EPC/Chol) liposome doxorubicin formulation was carried out. The objective was to define liposomal lipid and drug distribution within sites of tumor growth following intravenous (i.v.) administration to female BDF1 mice bearing either Lewis lung carcinoma, B16/BL6 melanoma, or L1210 ascitic tumors. Methods: Mice were injected i.v. with EPC/Chol liposomal doxorubicin, and plasma and tumor levels of lipid and drug were determined 1, 4 and 24 h later with radiolabeled lipid and fluorimetry or fluorescence microscopy, respectively. In addition, single-cell suspensions of the Lewis lung and B16/BL6 tumors were prepared and the presence of macrophages was determined with an FITC-labeled rat antimouse CD11b (MAC-1) antibody. Results: For mice bearing the Lewis lung solid tumors, there was a time-dependent accumulation of liposomal lipid, with a plateau of approximately 500 μg lipid/g tumor at 48 h. In contrast, the apparent plateau (μg doxorubicin/g tumor) for doxorubicin was achieved at 1 h and remained constant over a 72-h time course. In comparison with free drug administered at the maximum tolerated dose (MTD, 20 mg/kg) doxorubicin levels in tumors were two- to threefold greater when the drug was administered in liposomal form. The increase in drug delivery was comparable for both solid tumors. With animals bearing the L1210 ascitic tumor, drug exposure was as much as ten times greater (in comparison with free drug) when doxorubicin was administered in liposomes. An evaluation of single-cell suspensions prepared from the two solid tumors suggested that more than 98% of the tumor-associated drug and liposomal lipid was not tumor cell-associated. Histological studies with the Lewis lung carcinoma, however, revealed that a proportion of the drug did colocalize with tumor-associated macrophages. Analysis of cells obtained from mice bearing ascitic tumors showed that more than 80% of the cell-associated drug could be removed by procedures designed to remove adherent cells. Conclusion: The results summarized here suggest drug concentrations within a solid tumor, such as the Lewis lung carcinoma, are constant over time when the drug is given in a “leaky” EPC/Chol formulation. The results also suggest that liposomal lipid within sites of tumor growth is primarily localized within the interstitial spaces or tumor-associated macrophages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050662
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  • 6
    Electronic Resource
    Electronic Resource
    Preclinical pharmacology, toxicology and efficacy of sphingomyelin/cholesterol liposomal vincristine for therapeutic treatment of cancer (1998)
    Springer
    Cancer chemotherapy and pharmacology 42 (1998), S. 461-470 
    Details
    ISSN: 1432-0843
    Keywords: Key words Vincristine ; Liposome ; Pharmacology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: To establish the pharmacodynamic relationships between drug biodistribution and drug toxicity/efficacy, a comprehensive preclinical evaluation of sphingomyelin/cholesterol (SM/chol) liposomal vincristine and unencapsulated vincristine in mice was undertaken. Methods: Pharmaceutically acceptable formulations of unencapsulated vincristine and liposomal vincristine at drug/lipid ratios of 0.05 or 0.10 (wt/wt) were evaluated for toxicity, antitumor activity and pharmacokinetics following intravenous administration. Results: Mice given liposomal vincristine at 2 mg/kg vincristine had concentrations of vincristine in blood and plasma at least two orders of magnitude greater then those achieved after an identical dose of unencapsulated drug. One day after administration of the liposomal vincristine, there were at least tenfold greater drug quantities, relative to unencapsulated vincristine, in the axillary lymph nodes, heart, inguinal lymph nodes, kidney, liver, skin, small intestines and spleen. Increased plasma and tissue exposure to vincristine as a result of encapsulation in SM/chol liposomes was not associated with increased drug toxicities. Treatment of the murine P388 ascitic tumor with a single intravenous dose of unencapsulated drug at 2, 3 and 4 mg/kg, initiated 1 day after tumor cell inoculation, resulted in a 33 to 38% increase in lifespan. In contrast, long-term survival rates of 50% or more were achieved in all groups treated with the SM/chol liposomal vincristine formulations at doses of 2, 3 and 4 mg/kg. At the 4 mg/kg dose, eight of ten and nine of ten animals survived past day 60 when treated with SM/chol liposomal vincristine prepared at the 0.05 and 0.1 drug/lipid ratios, respectively. Conclusions: Overall, increased and prolonged plasma concentrations of vincristine achieved by liposomal encapsulation were correlated with dramatically increased antitumor activity in comparison with the unencapsulated drug, but no correlations could be established between pharmacokinetic parameters and toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050846
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  • 7
    Electronic Resource
    Electronic Resource
    Studies on the myelosuppressive activity of doxorubicin entrapped in liposomes (1990)
    Springer
    Cancer chemotherapy and pharmacology 27 (1990), S. 13-19 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The myelosuppressive activity of doxorubicin encapsulated in liposomes of differing lipid composition and size was quantified in mice by measurement of changes in spleen weight, peripheral white blood cells (WBC), and bone marrow nucleated cells. Following i. v. administration of free doxorubicin at a dose of 20 mg/kg, a 90% reduction in marrow cellularity was observed on day 3. The marrow nucleated cell count was similar to control values by day 7. Administration of an equivalent dose of doxorubicin that was encapsulated in large (diameter, ∼1.0 μm) egg phosphatidylcholine/cholesterol (EPC/Chol)(molar ratio, 55∶45) liposomes induced an 80% reduction in bone marrow cellularity that lasted for periods of 〉7 days. Similar results were obtained following administration of large (1.0 μm) liposomal doxorubicin systems formulated with distearoylphosphatidylcholine/cholesterol (DSPC/Chol) (molar ratio 55∶45). In contrast, liposomal doxorubicin prepared using small (diameter, ∼0.1 μm) DSPC/Chol liposomes induced only a 40% reduction (day 3) in bone marrow cellularity, which returned to control values by day 7. Other indicators of doxorubicin-mediated myelosuppressive activity (spleen weight loss and peripheral leukopenia) correlated well with changes observed in marrow cellularity. An exception to this, however, was observed in animals treated with small (0.1-μm) DSPC/Chol liposomal doxorubicin, which displayed peripheral leukopenia for periods of 〉14 days. This extended leukopenia was not observed following administration of small (0.1-μm) EPC/Chol liposomal doxorubicin. Marrow-associated liposomal lipid and doxorubicin were quantified to determine if the extent of doxorubicin-mediated myeloid toxicity could be correlated to changes in biodistribution of the entrapped drug. It was demonstrated that 10–20 times more doxorubicin is delivered to the bone marrow when the drug is given encapsulated in largeliposomes than when it is associated with small liposomes. These data are useful in defining characteristics of liposomal preparations that modulate the myelosupressive behaviour of entrapped antineoplastic agents.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689270
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  • 8
    Electronic Resource
    Electronic Resource
    Transfer of liposomal drug carriers from the blood to the peritoneal cavity of normal and ascitic tumor-bearing mice (1994)
    Springer
    Cancer chemotherapy and pharmacology 34 (1994), S. 137-146 
    Details
    ISSN: 1432-0843
    Keywords: Liposomes ; doxorubucin ; extravasation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previously we have demonstrated that the L1210 antitumor activity of liposomal doxorubicin increased significantly as the size of the liposomal carrier was reduced from 1.0 to 0.1 μm. It is demonstrated herein that empty and drug-loaded small (0.1-μm diameter) liposomes accumulate efficiently into the peritoneal cavity of normal and ascitic L1210 tumor-bearing animals following i.v. administration. In normal mice injected with 100 nm DSPC/chol liposomal doxorubicin (drug-to-lipid ratio of 0.2; wt/wt) approximately 2.8 μg drug could be recovered from the peritoneal cavity following peritoneal lavage at 24 h. Although this represents only 0.7% of the injected doxorubicin dose, this level of drug is 2 orders of magnitude greater than that achieved following administration of an equivalent dose of free drug (20 mg/kg). The drug levels achieved within the peritoneal cavity are dependent on the physical characteristics (size, drug-to-lipid ratio and lipid composition) of the liposomes employed. Optimal delivery is obtained employing 100 nm DSPC/chol liposomal doxorubicin, a vesicle system that is known to retain entrapped drug following i.v. administration and exhibits extended circulation lifetimes. Analysis of drug and liposome distribution within the peritoneal cavity of normal mice indicates that as much as 50% of the measured doxorubicin and liposomal lipid is cell-associated. Flow cytometric analysis of the peritoneal cells demonstrated that cell-associated doxorubicin resides almost exclusively within resident peritoneal macrophages. The increased delivery of doxorubicin to the peritoneal cavity of normal mice following i.v. administration of small (0.1-μm) liposomal doxorubicin is correlated with a pronounced (〉90%) and prolonged (〉14-day) suppression of resident peritoneal cells. Liposomal drug accumulation increased dramatically in animals with an established L1210 ascitic tumor. More than 5% of the injected dose was found in the peritoneal cavity of these animals 24 h after treatment with DSPC/chol liposomal doxorubicin as compared with a value of 0.03% of the injected dose achieved with free drug. It is proposed that accumulation of liposomes into the peritoneal cavity of normal and tumor-bearing mice may serve as a useful model for characterizing factors mediating the transfer of liposomes from the vascular compartment to extravascular sites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685931
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  • 9
    Electronic Resource
    Electronic Resource
    A two-step targeting approach for delivery of doxorubicin-loaded liposomes to tumour cells in vivo (1995)
    Springer
    Cancer chemotherapy and pharmacology 36 (1995), S. 91-101 
    Details
    ISSN: 1432-0843
    Keywords: Liposomes ; Targeting ; Doxorubicin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A two-step targeting approach was used to deliver doxorubicin-loaded liposomes to a murine tumour cell (P388 leukaemia) grown in culture and, more importantly, in vivo. Targeting was mediated through the use of an antibody specific for the Thy 1.2 antigen that is highly expressed on P388 cells. Briefly, the approach consists of prelabeling target cells with biotinylated anti-Thy 1.2 antibody prior to administration of drug-loaded liposomes that have streptavidin covalently attached to their surface. Results from in vitro studies demonstrate that a 30-fold increase in cell-associated lipid and a 20-fold increase in cell-associated doxorubicin can be achieved over control liposomes using this two-step procedure. Flow-cytometry and fluorescent-microscopy data were used to confirm that P388 cells can be stably labeled with the biotinylated anti-Thy 1.2 antibody in vivo. Subsequently, liposome-targeting studies were initiated in vivo, where target cell binding was assessed following i.p. or i.v. injection of doxorubicinloaded liposomes into animals bearing P388 tumours prelabeled with biotinylated antibody. A streptavidin-mediated 3.7-fold increase in cell-associated lipid and drug was achieved when the liposomes were given i.p. When doxorubicin-loaded streptavidin liposomes were injected i.v., P388 cells located in the peritoneal cavity were specifically labeled, although the efficiency of this targeting reaction was low. Less than a 2-fold increase in cell-associated lipid was achieved through the use of target-specific (streptavidin-coated) liposomes. These studies demonstrate that the presence of a well-labeled target cell population within the peritoneal cavity will not promote accumulation of an i.v. injected, targeted liposomal drug. Furthermore, the importance of separating target-cell-specific binding from non-specific uptake by tumour-associated macrophages is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689191
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  • 10
    Electronic Resource
    Electronic Resource
    Vincristine-induced dermal toxicity is significantly reduced when the drug is given in liposomes (1996)
    Springer
    Cancer chemotherapy and pharmacology 37 (1996), S. 351-355 
    Details
    ISSN: 1432-0843
    Keywords: Key words Vincristine ; Liposomes ; Dermal toxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A problem associated with the intravenous delivery of vincristine concerns drug extravasation at the site of injection or infusion. This can result in extensive local soft-tissue damage. A new formulation of vincristine has recently been developed based on encapsulation of the drug in liposomes. The liposomal drug is somewhat less toxic and substantially more efficacious than free drug. The studies described here assessed, using a murine model of drug extravasation, whether vincristine encapsulation in liposomes influences drug-induced dermal toxicity. It was shown that subcutaneous injection of vincristine in liposomes does not result in the gross skin necrosis and ulceration observed following injection of free drug. Histological analysis of the dermal tissue surrounding the injection site suggests that free drug induces a pronounced inflammatory reaction as judged by the presence of infiltrating leukocytes. In contrast, the liposomal formulation of vincristine engenders a mild prolonged inflammatory condition. These toxicological studies were correlated with an evaluation of drug retention at the site of administration. It was shown using radiolabelled vincristine as a drug marker, that free vincristine is rapidly eliminated from the injection site. In contrast, the level of drug at the site of injection was far greater when the drug was given in liposomal form.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050396
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