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Pharmacokinetics model for

Chen HS, Gross JF. Physiologically based pharmacokinetic models for anticancer drngs. Cancer Chemother Pharmacol 1979 2(2) 85-94. Review. [Pg.553]

Lntz RJ, Dedrick RL, Matthews FEB, Fling TE, Anderson MW. A preliminary pharmacokinetic model for several chlorinated biphenyls in the rat. Drug Metab Dispos 1977 5 386-396... [Pg.553]

D Shen, M Gibaldi. Critical evaluation of use of effective protein fractions in developing pharmacokinetic models for drug distribution. J Pharm Sci 63 1698-1702, 1974. [Pg.100]

CN Chen, JD Andrade. Pharmacokinetic model for simultaneous determination of drug levels in organs and tissues. J Pharm Sci 65 717-724, 1976. [Pg.102]

Mirfazaelian A, Kim K, Anand SS, Kim HJ, Tomero-Velez R, Bruckner JV, Fisher JW (2006) Development of a physiologically based pharmacokinetic model for deltamethrin in the adult male Sprague-Dawley rat. Toxicol Sci 93(2) 432-442... [Pg.136]

Pharmacokinetic Model for Simulation of Concentration-Time Profiles for Orally Administered Extended-Release Dosage Forms... [Pg.311]

McCarley K, Bunge AL (1998) Physiologically relevant one-compartment pharmacokinetic models for skin. 1. Development of models. J Pharm Sci 87 470-481. [Pg.484]

Absorption, Distribution, Metabolism, and Excretion. Levels of cresols in blood were obtained from a single case report of a dermally exposed human (Green 1975). Data on the toxicokinetics of cresols in animals were contained in two acute oral studies that provided only limited quantitative information on the absorption, metabolism, and excretion of cresols (Bray et al. 1950 Williams 1938). A more complete oral toxicokinetics study, in addition to studies using dermal and inhalation exposure, would provide data that could be used to develop predictive pharmacokinetic models for cresols. Inclusion of several dose levels and exposure durations in these studies would provide a more complete picture of the toxicokinetics of cresols and allow a more accurate route by route comparison, because it would allow detection of saturation effects. Studies of the tissue distribution of cresols in the body might help identify possible target organs. [Pg.70]

Peters, S.A. (2008) Evaluation of a generic physiologically based pharmacokinetic model for lineshape analysis. Clinical... [Pg.239]

Leung HW. 1991. Development and utilization of physiologically based pharmacokinetic models for toxicological applications. J Toxicol Environ Health 32 247-267. [Pg.171]

Paustenbach DJ, Clewell HJ, Gargas ML, et al. 1988. A physiologically based pharmacokinetic model for inhaled carbon tetrachloride. Toxicol AppI Pharmacol 96 191-211. [Pg.178]

Hughes MA, Glass PS, Jacobs JR. Context-sensitive half-time in multicompartment pharmacokinetic models for intravenous anesthetic drugs. Anesthesiology 1992 76 334—41. [Pg.49]

Mathews HB, Tuey DB, Anderson MW. 1977b. Pharmacokinetic models for lipiphilic compounds. Environ Health Perspect 20 257-262. [Pg.440]

Johanson. G. Filser, J.G. (1993) A physiologically based pharmacokinetic model for butadiene and its metabolite butadiene monoxide in rat and mouse and its significance for risk extrapolation. Arch. Toxicol., 61, 151-163... [Pg.211]

A physiologically based pharmacokinetic model for predicting ethylene dibromide kinetics and consequent toxicity, based on in-vitro metabolic parameters of rodents and humans and on the use of scaling factors, has been presented (Ploemen et al., 1997). Its most important prediction is that the GST pathway is significantly active even at low ethylene dibromide concentrations, which has important implications for risk assessment. [Pg.648]

In attempting to correlate the human and animal data, Nolan et al. (1984) validated a physiologically based pharmacokinetic model for 1,1,1-trichloroethane. The model predicted greater absorption, blood levels and metabolism of 1,1,1-trichloroethane in rodents than in humans. On the basis of toxicokinetic data, rats were suggested to be a better model than mice to evaluate potential health effects in humans. [Pg.889]

Tardif et al. (1997) developed a physiologically based pharmacokinetic model for zneio-xylene in rats and humans. They also simulated interactions between weto-xylene, toluene and ethylbenzene, and showed that for exposures at air concentrations remaining within the permissible range for a mixture, biologically significant interactions at the pharmacokinetic level would not occur. [Pg.1194]

Lee, E. (1999) A physiologically based pharmacokinetic model for the ingestion of arsenic in humans, Dissertation in Environmental Toxicology, University of California, Irvine. [Pg.7]

Figure 19.1 Physiological pharmacokinetic model for evaluating in vivo disposition of a macromolecular drug. (A) A multi-compartment model in which every tissue compartment is connected with the plasma pool by blood flow. (B) Tissue uptake of a drug from vascular space to tissue parenchyma. Figure 19.1 Physiological pharmacokinetic model for evaluating in vivo disposition of a macromolecular drug. (A) A multi-compartment model in which every tissue compartment is connected with the plasma pool by blood flow. (B) Tissue uptake of a drug from vascular space to tissue parenchyma.
Figure 19.5 Physiological pharmacokinetic model for hepatic uptake of drug constantly infused in the isolated rat liver perfusion system. Q, flow rate (mL/min) Cb, inflow concentration (pg/mL) Cs, sinusoidal concentration (pg/mL) Vs, sinusoidal volume (mL) X, binding constant (pg) Xm, maximum binding amount (pg) K, binding constant (mL/pg) kmt, internalization rate constant (min-1). Figure 19.5 Physiological pharmacokinetic model for hepatic uptake of drug constantly infused in the isolated rat liver perfusion system. Q, flow rate (mL/min) Cb, inflow concentration (pg/mL) Cs, sinusoidal concentration (pg/mL) Vs, sinusoidal volume (mL) X, binding constant (pg) Xm, maximum binding amount (pg) K, binding constant (mL/pg) kmt, internalization rate constant (min-1).
Figure 19.7 Pharmacokinetic model for analyzing drug disposition following direct intratumoral injection. ku rate constant of transfer from poorly perfused region to well perfused region k2, venous appearance rate constant k2, rate constant of leakage from the surface A, and X2, drug amounts in well perfused and poorly perfused regions, respectively. Figure 19.7 Pharmacokinetic model for analyzing drug disposition following direct intratumoral injection. ku rate constant of transfer from poorly perfused region to well perfused region k2, venous appearance rate constant k2, rate constant of leakage from the surface A, and X2, drug amounts in well perfused and poorly perfused regions, respectively.
Physiological pharmacokinetic model for evaluating in vivo disposition of a 376... [Pg.496]

Physiological pharmacokinetic model for hepatic uptake of drag constantly infused in the 387... [Pg.496]

Pharmacokinetic model for analyzing drag disposition following direct intratumoral 391 injection... [Pg.496]

FIGURE 17-1 Pharmacokinetic model for PCA using opioid drugs. Conventional intramuscular injection is indicated by the long solid lines, PCA is indicated by the short dashed lines, and the therapeutic window for analgesia is indicated by the shaded area. CFrom Ferrante, et at Anesth Analg. 1988 67 457-461 with permission.)... [Pg.238]

Maximum value for total absorbed dose for each individual calculated by three methods based on the pharmacokinetic model for clearance after dermal exposure to 2,1+,5-T (l6). [Pg.143]

Emond, C, J.E. Michalek, L.S. Birnbaum, and M.J. DeVito. 2005b. Comparison of the use of a physiologically based pharmacokinetic model and a classical pharmacokinetic model for dioxin exposure assessment. Environ. Health Perspect. 113(12) 1666-1668. [Pg.220]

Stern, A.H. 1997. Estimation of the interindividual variability in the one-compartment pharmacokinetic model for methylmercury Implications for the derivation of a reference dose. Regul. Toxicol. Pharmacol. 25(3) 277-288. [Pg.224]

Fisher, J.W., D. Mahle, and R. Abbas. 1998. A human physiologically based pharmacokinetic model for trichloroethylene and its metabolites, trichloroacetic acid and free trichloro-ethanol. Toxicol Appl Pharmacol. 152(2) 339-359. [Pg.300]


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