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Pharmacology cyclosporine

D. W. (2004) Rosuvastatin pharmacokinetics in heart transplant recipients administered an antirejection regimen including cyclosporine. Clinical Pharmacology and Therapeutics, 76, 167-177. [Pg.358]

Borel JF. (2002) History of the discovery of cyclosporin and of its early pharmacological development. Wien Klin Wochenschr 114 433 37. [Pg.186]

Tacrolimus, a macrolide, derives from a streptomyces species pharmacologically it resembles cyclosporin A, but is more potent and efficacious. [Pg.300]

Simonson, S.G., Raza, A., Martin, P.D., Mitchell, P.D., Jarcho, J.A., Brown, C.D.A., Windass, A.S. and Schneck, D.W. (2004) Rosuvastatin pharmacokinetics in heart transplant recipients administered an antirejection regimen including cyclosporine. Clinical Pharmacology and Therapeutics (St. Louis), 76, 167-177. [Pg.68]

Simon, N., DaiDy, E., Combes, O., Malaurie, E., Lemaire, M., Tdlement, J.P. and Urien, S. (1998) Role oflipoproteins in the plasma binding of SDZ PSC 833 a novel multidrug resistance-reversing cyclosporin. British Journal of Clinical Pharmacology, 45, 173-175. [Pg.217]

Two molecular mechanisms for the interactions have been established. First, both hypericin and hy-perforin, two of the pharmacologically active constituents of the herb, cause induction of the enzyme CYP3A4 which is responsible for much of the metabolism of many commonly used drugs. Giving SJW to patients also taking the immunosuppressant, cyclosporine, which is metabolized primarily by CYP3A4, has led to near-rejection of transplanted organs as cyclosporine plasma concentrations fell due to increased metabolism. The same mechanism has led to reduced efficacy of indinavir in patients... [Pg.153]

The available case reports in the FDA AERS support the published literature that there are pharmacokinetic interactions between St. John s wort and CYP3A4 and/or p-glycoprotein substrates, such as cyclosporine, levonorgestrel/estradiol and sildenafil, and pharmacodynamic interactions with the SSRIs or MAOI. Subsequent clinical studies including those conducted via a CDER clinical pharmacology research cooperative agreement (14—16) provided mechanistic basis of many of these interactions (refer to Chapter 4). [Pg.291]

DiPavoda FE. 1990. Pharmacology of cyclosporine (Sandimmune). V. Pharmacological effects on immune function in vitro studies. Pharmacol Rev. 41 373 105. [Pg.103]

As indicated earlier, most cases of type 1 diabetes are caused by an autoimmune response that selectively attacks and destroys pancreatic beta cells in susceptible individuals. Therefore, drugs that suppress this autoimmune response may be helpful in limiting beta cell destruction, thereby decreasing the severity of this disease.4,41 Several immunosuppressants have been investigated as a way to potentially minimize beta cell loss from the autoimmune reactions underlying type 1 diabetes some immunosuppressants that have been considered for this situation include cyclosporine, azathioprine, cyclophosphamide, methotrexate, and glucocorticoids.11 The pharmacology of these immunosuppressants is discussed in more detail in Chapter 37. [Pg.489]

Bowers WF, Fulton, Thompson J (1984) Ultrafiltration vs equilibrium dialysis for determination of free fraction. Clin Pharmacokinetic 9(Suppl l) 49-60 Brprs O, Jacobsen S (1985) pH lability in serum during equilibrium dialysis. Br J Clin Pharmacokinetic 20 85-88 Henricsson S (1987) Equilibrium Dialysis in a Stainless Steel Chamber Measurement of the Free Plasma Fraction of Cyclosporin. Pharmacy and Pharmacology Communications 6(10) 447-450... [Pg.483]


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See also in sourсe #XX -- [ Pg.236 , Pg.237 , Pg.237 , Pg.238 , Pg.238 , Pg.239 ]

See also in sourсe #XX -- [ Pg.5 , Pg.492 , Pg.493 ]




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