STRIPE: An interactive computer program for the analysis of drug pharmacokinetics

Johnston, Atholl; Woollard, R.

doi:10.1016/0160-5402(83)90038-4

Cited by 116 publications

(48 citation statements)

References 3 publications

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“…Pharmacokinetic parameters were calculated by standard techniques using the STRIPE computer program (Johnston & Woollard, 1983). The significance of differences between treatments was assessed by one-way analysis of variance.…”

Section: Analysis Ofdatamentioning

confidence: 99%

Pharmacokinetics and pharmacodynamics of verapamil in combination with atenolol, metoprolol and propranolol.

Warrington¹,

Holt²,

Johnston³

et al. 1984

Brit J Clinical Pharma

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Treatment of angina pectoris with beta‐adrenoceptor antagonists and verapamil in combination is effective and increasingly common. The study reported here was designed to show whether the pharmacokinetics of verapamil are influenced by concurrent treatment with three different beta‐adrenoceptor blockers, and whether there is any pharmacodynamic interaction between these drugs. Twelve healthy volunteers (eight men, four women) aged 21‐25 years and weighing 48‐82 kg consented to participate in the study. They received verapamil 50 mg three times daily for four 1‐week periods, each separated by a 1 week ‘washout’ period. During three of the four treatment periods, the subjects took either atenolol 100 mg once daily, metoprolol 100 mg twice daily or propranolol 80 mg twice daily; in the remaining period they took verapamil alone. The concentration/time curve and plasma elimination half‐life of verapamil and norverapamil, its major metabolite, were not influenced by 1 weeks co‐administration atenolol, metoprolol or propranolol. As expected, co‐administration of each of the beta‐adrenoceptor blockers significantly reduced exercise heart rate when compared with verapamil alone.

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Section: Analysis Ofdatamentioning

confidence: 99%

Pharmacokinetics and pharmacodynamics of verapamil in combination with atenolol, metoprolol and propranolol.

Warrington¹,

Holt²,

Johnston³

et al. 1984

Brit J Clinical Pharma

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“…Cross-reactivity with the antisera was 0.6%. The plasma concentrationtime profile of xamoterol was fitted by a triexponential function using the programme STRIPE (Johnston & Woollard, 1983) Only small differences between patients and volunteers were observed. The terminal plasma elimination half-life (t, ) was prolonged in patients when compared with the volunteers, but this difference was not significant (P = 0.08).…”

Section: Discussionmentioning

confidence: 99%

The pharmacokinetics of xamoterol in liver disease.

Nicholls

Taggart

McCann

et al. 1989

Brit J Clinical Pharma

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The pharmacokinetics of xamoterol, a beta 1‐adrenoceptor partial agonist, have been studied in patients with liver disease and a group of age‐ and sex‐matched normal controls. No significant differences were observed after the oral administration of xamoterol 200 mg. The low bioavailability of xamoterol was confirmed (6.1% in patients, 6.9% in controls). After i.v. xamoterol 0.2 mg kg‐1, no significant differences between the groups were observed. A small increase in the terminal plasma elimination half‐life (t1/2) was observed in patients when compared with controls (15.3 +/‐ 6.4 vs 8.4 +/‐ 2.8 h, mean +/‐ s.d., P = 0.08). Renal clearance accounted for about 50% of total clearance in patients and about 30% in controls. It is suggested that in patients with heart failure, hepatic dysfunction would probably not influence xamoterol disposition.

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“…Pharmacokinetic parameters were estimated using the interactive computer program, STRIPE (Johnstone & Woolard, 1983). The data were entered as the mean values for analysis.…”

Section: Methodsmentioning

confidence: 99%

Disposition of the prodrug 4-(bis (2-chloroethyl) amino) benzoyl-L-glutamic acid and its active parent drug in mice

Antoniw

Cj²,

Bagshawe³

et al. 1990

Br J Cancer

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Sunmary A novel therapy for improving selectivity in cancer chemotherapy aims to modify distribution of a cytotoxic drug by generating it selectively at tumour sites. In this approach an antibody-enzyme conjugate is allowed to localise at the tumour sites before injecting a prodrug which is converted to an active drug specifically by the targeted enzyme in the conjugate. We present here pharmacokinetic studies on the prodrug 4-(bis (2-chloroethyl) amino) benzoyl-L-glutamic acid and its activated derivative, benzoic acid mustard. The glutamic acid is cleaved from the prodrug to form the active drug by carboxypeptidase G2 (CPG2), an enzyme from Pseudomonas sp., which is not found in mammalian cells. The prodrug and its parent active drug were rapidly distributed in plasma and tissues after administration of prodrug or active drug (41 tsmol kg-' intraperitoneally) to mice bearing human choriocarcinoma xenografts. Prodrug and active drug both followed a two-compartment kinetic model. Prodrug was eliminated more rapidly (t,/2 = 0.12 h, t,/2P = 0.70 h) than active drug (t,/2a = 0.37 h, t,12P = 1.61 h). Conversion of the prodrug to the activated parent drug was detected within 5 min of administration to mice which had previously received a F(ab')2-anti-human chorionic gonadotrophin antibody (W14A) conjugated to the enzyme, CPG2 (1,000 U kg-'). Tumour was the only tissue that activated all the prodrug reaching the site. It contained the highest concentration of targeted enzyme conjugate capable of catalysing the reaction of prodrug to drug. Plasma and other tissues were also capable of activating the prodrug but active drug production was limited by the amount of enzyme present. The active drug measured in plasma and tissues other than tumour was attributable to residual antibody-enzyme conjugate at non-tumour sites. Low levels of conjugate in tissues and plasma militate against the advantage of tumour localised enzyme therefore necessitating removal of non-localised enzyme.

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STRIPE: An interactive computer program for the analysis of drug pharmacokinetics

Cited by 116 publications

References 3 publications

Pharmacokinetics and pharmacodynamics of verapamil in combination with atenolol, metoprolol and propranolol.

Pharmacokinetics and pharmacodynamics of verapamil in combination with atenolol, metoprolol and propranolol.

The pharmacokinetics of xamoterol in liver disease.

Disposition of the prodrug 4-(bis (2-chloroethyl) amino) benzoyl-L-glutamic acid and its active parent drug in mice

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