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Therapeutics, experimental

Courtesy of the A.merican Society forPharmacolog and Experimental Therapeutics (52). See Table 4. [Pg.277]

Markus Grube, Heyo K. Kroemer Department of Pharmacology, Center of Pharmacology and Experimental Therapeutics, Ernst-Moritz-Arndt University Greifswald, Greifswald, Germany... [Pg.4]

Numerous experimental therapeutics have shown potency in vitro however, when they are tested in vivo, they often lack significant efficacy. This is often attributed to unfavorable pharmacokinetic properties and systemic toxicity, which limit the maximum tolerated dose. These limitations can be overcome by use of drug carriers. Two general types of carrier systems have been designed drug conjugation to macromolecular carriers, such as polymers and proteins and drug encapsulation in nanocarriers, such as liposomes, polymersomes and micelles. [Pg.84]

Figure 4. Effects of dihydro-brevetoxin B (H2BVTX-B) on Na currents in crayfish axon under voltage-clamp. (A) A family of Na currents in control solution each trace shows the current kinetics responding to a step depolarization (ranging from -90 to -I-100 mV in 10 mV increments). Incomplete inactivation at large depolarizations is normal in this preparation. (B) Na currents after internal perfusion with H2BVTX-B (1.2 a M). inactivation is slower and less complete than in the control, and the current amplitudes are reduced. (C) A plot of current amplitudes at their peak value (Ip o, o) and at steady-state (I A, A for long depolarizations) shows that toxin-mOdified channels (filled symbols) activate at more negative membrane potentials and correspond to a reduced peak Na conductance of the axon (Reproduced with permission from Ref. 31. Copyright 1984 American Society for Pharmacology and Experimental Therapeutics). Figure 4. Effects of dihydro-brevetoxin B (H2BVTX-B) on Na currents in crayfish axon under voltage-clamp. (A) A family of Na currents in control solution each trace shows the current kinetics responding to a step depolarization (ranging from -90 to -I-100 mV in 10 mV increments). Incomplete inactivation at large depolarizations is normal in this preparation. (B) Na currents after internal perfusion with H2BVTX-B (1.2 a M). inactivation is slower and less complete than in the control, and the current amplitudes are reduced. (C) A plot of current amplitudes at their peak value (Ip o, o) and at steady-state (I A, A for long depolarizations) shows that toxin-mOdified channels (filled symbols) activate at more negative membrane potentials and correspond to a reduced peak Na conductance of the axon (Reproduced with permission from Ref. 31. Copyright 1984 American Society for Pharmacology and Experimental Therapeutics).
Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, MD 21201 Department of Chemistry, University of California, Berkeley, CA 94720 Department of Pharmacology and Toxicology, Medical College of Georgia,... [Pg.107]

Current address Department of Pharmacology and Experimental Therapeutics, School of Pharmacy, The Hebrew University, P.O. Box 1172,91010 Jerusalem, Israel... [Pg.347]

Departments of Neuroscience, Pharmacology and Experimental Therapeutics, Psychiatry and Behavioral Sciences The Johns Hopkins University School of Medicine 725 North Wolfe Street Bal timore, MD 21205... [Pg.26]

Patri ci a C. Contreras Experimental Therapeutics Branch National Institute of Neurological... [Pg.49]

Zhang, Y. and Wells, J., The effects of chronic caffeine administration on peripheral adenosine receptors, Journal of Pharmacology and Experimental Therapeutics, 254, 757, 1990. [Pg.252]

Rush, C., Sullivan, J. and Griffiths, R., Intravenous caffeine in stimulant drug abusers Subjective reports and physiological effects. Journal of Pharmacology and Experimental Therapeutics 273(1), 351-358, 1995. [Pg.295]

Jacobson KA, van Rhee AM. Development of selective purinoceptor agonists and antagonists. In Jacobson KA, Jarvis MF, eds. Purinergic Approaches in Experimental Therapeutics. New York Wiley-Liss, 1997 101-128. [Pg.247]

Lauver DA, Lockwood SF, and Lucchesi BR. 2005. Disodium disuccinate astaxanthin (Cardax) attenuates complement activation and reduces myocardial injury following ischemia/reperfusion. Journal of Pharmacology and Experimental Therapeutics 314(2) 686-692. [Pg.56]

S. R. PANDI-PERUMAL is affiliated with the Division of Clinical Pharmacology and Experimental Therapeutics, Department of Medicine,... [Pg.486]

Case Study 1 Safety Pharmacology Studies for an IND for Beta Thalassemia Susan Perrine, M.D., Professor of Pediatrics, Medicine, Pharmacology, and Experimental Therapeutics, Boston University School of Medicine... [Pg.366]

A variety of experimental therapeutic strategies have been tested in mutant SOD1 mice 737... [Pg.731]

A variety of experimental therapeutic strategies have been tested in mutant SOD1 mice. Lines of mutant SOD1 mice have been used for pharmacological and genetic therapeutic trials [10,21,22,25,137-139]. Selected examples of these approaches are briefly described below. [Pg.737]

Transgenic mouse models are being used to test a variety of novel therapies, including ways of reducing secretase activities and decreasing Ap burden by Ap immunotherapy. Many experimental therapeutic efforts... [Pg.786]

Zeng, H., Lozinskaya, I.M., Lin, Z., Willette, R.N., Brooks, D.P. and Xu, X. (2006) Mallotoxin is a novel human ether-a-go-go-related gene (hERG) potassium channel activator. The Journal of Pharmacology and Experimental Therapeutics, 319, 957-962. [Pg.78]

Conti, M. (2004) Targeting K+ channels for cancer therapy. Journal of Experimental Therapeutics and Oncology, 4, 161-166. [Pg.78]


See other pages where Therapeutics, experimental is mentioned: [Pg.340]    [Pg.135]    [Pg.20]    [Pg.201]    [Pg.1048]    [Pg.1517]    [Pg.1520]    [Pg.348]    [Pg.49]    [Pg.295]    [Pg.194]    [Pg.283]    [Pg.363]    [Pg.368]    [Pg.735]    [Pg.786]    [Pg.635]   
See also in sourсe #XX -- [ Pg.140 , Pg.485 , Pg.505 ]




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