Re: PD model

From: Paul Hutson Date: January 14, 2010 technical Source: mail-archive.com
Title: Paul R Yuhong: Otilia makes useful recommendations, and I would just reinforce the caution of having a good baseline and an understanding of the individual's diurnal changes. There is increasingly recognized to be a very large natural variability in QTc that will need to be considered. Daily swings of 90msec are apparently not uncommon when 24 hr recordings are made in normal adults. Paul [email protected] wrote: Dear Otilia, Thank you very much for your suggestions. They are very helpful. Thanks, Yuhong
Quoted reply history
---------- Original Message ---------- From: "Lillin - de Vries, O. \(Otilia\)" < [email protected] > To: < [email protected] > , < [email protected] > Subject: RE: [NMusers] PD model Date: Thu, 14 Jan 2010 11:45:16 +0100 Dear Yuhong, Here you have my 5 cents (in top-down fashion): 1. You need a PK-PD model quantifying the QTc prolongation; since you don't know what causes the QTc prolongation, this breaks down to testing: 1a. DrugA - QTc model 1b. DrugB - QTc model 1c. DrugA+DrugB - QTc model 1d. DrugC - QTc model In order to be able to compare models 1a - 1d you need a good Baseline QTc model (i.e you need to describe well all non-drug related influences on QTc like gender, circadian rhythm, age, placebo effect, etc - see e.g. the paper of V. Piotrovsky, Pharmacokinetic-Pharmacodynamic Modeling in the Data Analysis and Interpretation of Drug-induced QT/QTc Prolongation, AAPS Journal 2005 ). If a combination of more than one of your three moieties can be responsible for the effect on QTc (I do not have experience with this case) I would simply add upp the concentrations (see the Nonmem code below for your convenience, without circadian rhythm for keeping it simple). On the other hand be aware that a PK-PD model can not tell you for sure which one of the moieties is responsible for the QTc prolongation; a model can only quantify the magnitude of the effect and give you a hint on which moiety is most probably causing it. You need to make assumptions on physiological bases as well, and: - check whether drugB alone causes QTc prolongation (model 1b? litterature? previous studies with limited ECG? ...) if yes, you need model 1c. - check the time point at which you have the largest QTc prolongation: does it occur at Tmax_drugA? then a direct effect model (1a or 1c) are most probable; does it occur at Tmax_drugC? since C is a metabolite, it takes some time to be formed and probably Tmax_C > Tmax_A, this hints you in the direction of the metabolite and you need a delayed effect model to describe the parent's effect on QTc (1a) and the concentrations in the hypothetical compartment should agree with the metabolite profile. In other words, you should be able to tell the effect from the parent(s) and metabolite from each other. Hope this helps. Cheers, Otilia $PRED OCC2=0 ; steady state IF (DAY.EQ.11) OCC2=1 QTC0 = THETA(1)+ETA(1 ) ;baseline QTc SHFT = THETA(2) ;shift factor placebo effect QTCB = QTC0+SHFT*OCC2+THETA(3)*GEN ;baseline with placebo and gender effect SL = THETA(4) ; slope of drug effect CP = CA + CB ; add upp concentrations causing the effect EFF = SL*CP ; linear direct effect QTC = QTCB+EFF Y = QTC+EPS(1) IPRE = QTC IRES = DV-IPRE Otilia Lillin-de Vries, MSc Modeling and Simulation Expert Pharmacokinetics, Pharmacodynamics & Pharmacometrics (P3) Department of Drug Metabolism and Pharmacokinetics T: +31 412 669321 M: + 31 6 22004827 F: +31 412 662506 [email protected] MSD Gasstraat Oost 10, 5349 AV, Oss P.O. Box 20, 5340 BH, Oss The Netherlands www.merck.com From: [email protected] [ mailto: [email protected] ] On Behalf Of [email protected] Sent: Thursday, 14 January, 2010 2:45 To: [email protected] Subject: [NMusers] PD model Dear All, I am looking for a help. Currently I am working on a population PD model to evaluate the effects of drugs on QT prolongation. Drug A and drug B are given to the study subjects (healthy volunteer) at the same time. Drug B is the inhibitor for the metabolism of drug A, also compound C is the metabolite of drug A. I am wondering how to evaluate the effects for drug A or B or the metabolite of drug A (compound C). These three moieties will be present together in the blood for most of the time. Is anyone has experience and would like to share with us. Any comment will be greatly appreciated. Best regards, Yuhong ____________________________________________________________ Diet Help Reach your goals of being healthier and happier. Click here for diet tips and solutions. This message and any attachments are solely for the intended recipient. If you are not the intended recipient, disclosure, copying, use or distribution of the information included in this message is prohibited --- Please immediately and permanently delete. ____________________________________________________________ Weight Loss Program Best Weight Loss Program - Click Here! -- Paul R. Hutson, Pharm.D. Associate Professor UW School of Pharmacy 777 Highland Avenue Madison WI 53705-2222 Tel 608.263.2496 Fax 608.265.5421 Pager 608.265.7000, p7856
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