Assessing the role of hepatic uptake in drug clearance - Pharmacokinetic and experimental considerations

Similar documents
Building innovative drug discovery alliances. Hepatic uptake and drug disposition o in vitro and in silico approaches

RSC, February Interplay between enzymes and. clearance and intracellular concentration of drugs. Centre for Applied Pharmacokinetic Research

Drug disposition classification systems: A comparative review of BDDCS, ECCS and ECCCS

Under prediction of hepatic clearance from in vitro studies: prospects for resolution. J Brian Houston

The extended clearance model and its use for the interpretation of hepatobiliary elimination data

DMPK. APRIL 27 TH 2017 Jan Neelissen Scientific Adviser Science & Technology

Stimulate your kinetic understanding Permeability Binding Metabolism Transporters

Quantifying and Communicating Uncertainty in Human PK and Dose Prediction Douglas Ferguson

Pursuing the holy grail of predicting and verifying tissue drug concentrations: A proteomics and PET imaging approach

Pharmacokinetic Modeling & Simulation in Discovery and non-clinical Development

Regulation of the cell surface expression and transport capacity of BSEP by small chemical molecules

HTPK: Conducting PK modeling and

Mechanistic Modeling of in vitro Assays to Improve in vitro/in vivo Extrapolation

DRUG METABOLISM AND PHARMACOKINETICS (DMPK) Lena Gustavsson, H. Lundbeck A/S, November 2015

Culture Hepatocytes in Human Plasma to Count the free Concentration of Drug in Evaluation of Drug-drug Interaction. Chuang Lu

PHA First Exam Fall 2003

Absolute bioavailability and pharmacokinetic studies in early clinical development using microdose and microtracer approaches.

Simultaneous Assessment of Uptake and Metabolism in Rat Hepatocytes: A. Comprehensive Mechanistic Model

Basic Pharmacokinetics and Pharmacodynamics: An Integrated Textbook with Computer Simulations

Modeling of Ac-ve Transport and Metabolism for in vitro Suspended and Sandwich Hepatocyte Assays U-lizing MembranePlus

Renal Function. 1. Glomerular filtration 2. Active tubular secretion 3. Passive tubular reabsorption 4. Excretion

Complexities of Hepatic Drug Transport: How Do We Sort It All Out?

Comparison Between the US FDA, Japan PMDA and EMA In Vitro DDI Guidance: Are we Close to Harmonization?

Physiologically-Based Simulation of Daclatasvir Pharmacokinetics With Antiretroviral Inducers and Inhibitors of Cytochrome P450 and Drug Transporters

Exploiting BDDCS and the Role of Transporters

Click to edit Master title style

PHA Second Exam. Fall On my honor, I have neither given nor received unauthorized aid in doing this assignment.

Supplemental Information

Effects of Liver Disease on Pharmacokinetics Juan J.L. Lertora, M.D., Ph.D. Director Clinical Pharmacology Program October 29, 2015 National

WHY... 8/21/2013 LEARNING OUTCOMES PHARMACOKINETICS I. A Absorption. D Distribution DEFINITION ADME AND THERAPEUIC ACTION

Effects of Liver Disease on Pharmacokinetics Juan J.L. Lertora, M.D., Ph.D. Director Clinical Pharmacology Program November 4, 2010 National

Prediction of in vivo hepatic clearance and DDI of OATP substrates: Comparison of different in vitro approaches. Yuichi Sugiyama

Effects of Liver Disease on Pharmacokinetics

PHA5128 Dose Optimization II Case Study I Spring 2013

Basic Concepts in Pharmacokinetics. Leon Aarons Manchester Pharmacy School University of Manchester

Leslie Z. Benet, PhD. Professor of Bioengineering and Therapeutic Sciences Schools of Pharmacy and Medicine University of California San Francisco

PREDICTING PHARMACOKINETICS FOLLOWING TOPICAL APPLICATION USING NON-ANIMAL METHODS IAN SORRELL, MI-YOUNG LEE, RICHARD CUBBERLEY

Bridging In Vitro and In Vivo Metabolism and Transport of Faldaprevir in Human Using a Novel Cocultured Human Hepatocyte System, HepatoPac

Simultaneous Assessment of Uptake and Metabolism in Rat Hepatocytes: A Comprehensive Mechanistic Model S

Kinetic characterization of rat hepatic uptake of 16 actively transported drugs. Yoshiyuki Yabe, Aleksandra Galetin and J Brian Houston

The Future of In Vitro Systems for the Assessment of Induction and Suppression of Enzymes and Transporters

Deuteration of Drugs for Pharmacokintic Enhancement: Considerations Essential for Success

PHA First Exam. Fall 2004

PHA Second Exam Fall On my honor, I have neither given nor received unauthorized aid in doing this assignment.

Biopharmaceutics Drug Disposition Classification System (BDDCS) --- Its Impact and Application

Pharmacokinetic and absolute bioavailability studies in early clinical development using microdose and microtracer approaches.

EVALUATION OF DRUG-DRUG INTERACTION POTENTIAL BETWEEN SACUBITRIL/VALSARTAN (LCZ696) AND STATINS USING A PHYSIOLOGICALLY- BASED PHARMACOKINETIC MODEL

Biopharmaceutics Drug Disposition Classification System (BDDCS) and Its Application in Drug Discovery and Development

T Eley, Y-H Han, S-P Huang, B He, W Li, W Bedford, M Stonier, D Gardiner, K Sims, P Balimane, D Rodrigues, RJ Bertz

Pharmacokinetics and pharmacodynamics of peptide and protein drugs

Clearance Concepts: Fundamentals and Application to Pharmacokinetic Behavior of Drugs

CLINICAL PHARMACOKINETICS INDEPENDENT LEARNING MODULE

Monica Edholm Medica Medic l a Pr oducts Agency

When does the rate-determining step in the hepatic clearance of a drug switch from

Viera Lukacova Director, Simulation Sciences

Membrane transport. Small molecules. pumps. Large molecules

Use of PBPK in simulating drug concentrations in pediatric populations: Case studies of Midazolam and Gabapentin

BASIC PHARMACOKINETICS

TDM. Generally, hepatic clearance is determined by three main factors: These three factors can be employed in the following equation:

Inhibition of Human Hepatic Bile Acid Transporters as Contributing Factors to Drug-Induced Liver Injury

Mechanistic Modeling of Pitavastatin Disposition in Sandwich-Cultured Human Hepatocytes: A Proteomics-Informed Bottom-Up Approach s

Take-Home Exam Distributed: October 16, 2013, at 1:30 p.m. Due: October 21, 2013, at 10:00 a.m.

Manthena V. Varma, PhD 1 and Ayman F. El-Kattan, PhD 2

Practical Application of PBPK in Neonates and Infants, Including Case Studies

We will begin momentarily at 2pm ET. Slides available now! Recordings will be available to ACS members after one week.

Hepatic Efflux Transporters: Relevance to Drug-Drug Interactions and Drug Toxicity

PHA Second Exam. Fall On my honor, I have neither given nor received unauthorized aid in doing this assignment.

Chapter-V Drug use in renal and hepatic disorders. BY Prof. C.Ramasamy, Head, Dept of Pharmacy Practice SRM College of Pharmacy, SRM University

UNIVERSITY OF THE WEST INDIES, ST AUGUSTINE

Introduction to Pharmacokinetics (PK) Anson K. Abraham, Ph.D. Associate Principal Scientist, PPDM- QP2 Merck & Co. Inc., West Point, PA 5- June- 2017

DEPARTMENT OF PHARMACOLOGY AND THERAPEUTIC UNIVERSITAS SUMATERA UTARA

Minireview. Low-Turnover Drug Molecules: A Current Challenge for Drug Metabolism Scientists

BIOPHARMACEUTICS and CLINICAL PHARMACY

Cryo Characterization Report (CCR)

Understand the physiological determinants of extent and rate of absorption

Using Accelerator Mass Spectrometry to Explain the Pharmacokinetics of Vismodegib Cornelis E.C.A. Hop

Caveat: Validation and Limitations of Phenotyping Methods for Drug Metabolizing Enzymes and Transporters

General Principles of Pharmacology and Toxicology

Pharmacokinetics of Drugs. Assistant Prof. Dr. Najlaa Saadi PhD Pharmacology Faculty of Pharmacy University of Philadelphia

Quantitative Evaluation of the Effect of P-Glycoprotein on Oral Drug Absorption

Drug Distribution. Joseph K. Ritter, Ph.D., Assoc. Prof. Medical Sciences Building, Room

Biopharmaceutics. Tips Worth Tweeting. Contributor: Sandra Earle

Current Approaches and Applications of Phenotyping Methods for Drug Metabolizing Enzymes and Transporters

It the process by which a drug reversibly leaves blood and enter interstitium (extracellular fluid) and/ or cells of tissues.

Rational Dose Prediction. Pharmacology. φαρμακον. What does this mean? pharmakon. Medicine Poison Magic Spell

Decision-Making with Predictive ADME Data in Context of Experimental Variability

Development & Characterization of Pooled and Plated Hepatocytes to Support the Evolving DMPK Landscape

Excretion of Drugs. Prof. Hanan Hagar Pharmacology Unit Medical College

Investigating Transporter-Mediated Drug-Drug Interactions Using a Physiologically Based Pharmacokinetic Model of Rosuvastatin

Pharmacokinetics in Drug Development. Edward P. Acosta, PharmD Professor & Director Division of Clinical Pharmacology Director, CCC PK/PD Core

Yuichi Sugiyama Sugiyama Laboratory, RIKEN Innovation Center, RIKEN, Research Cluster for Innovation,

Importance of Multi-P450 Inhibition in Drug Drug Interactions: Evaluation of Incidence, Inhibition Magnitude, and Prediction from in Vitro Data

Lippincott Questions Pharmacology

PK-UK Challenges and benefits of using PBPK to evaluate an IVIVC for drugs with nonideal solubility and/or permeability. Bath, November 2014

The ADME properties of most drugs strongly depends on the ability of the drug to pass through membranes via simple diffusion.

Case studies of in vitro/in vivo and in vivo/in vivo predictions of pharmacokinetic parameters and clinical doses

Section 5.2: Pharmacokinetic properties

Chapter 7 Cell Structure and Function. Chapter 7, Section 3 Cell Boundaries and Transport

Automation of TRANSIL assays outperforms. terms of speed, cost-effectiveness and reproducibility. Dr. Hinnerk Boriss

Pharmacokinetics of strong opioids. Susan Addie Specialist palliative care pharmacist

Transcription:

Assessing the role of hepatic uptake in drug clearance - Pharmacokinetic and experimental considerations Peter Webborn ISSX Short course Toronto 2013 1

Defining the why, when and how of Transporter studies is rapidly maturing Methods Brouwer et al (2013) In vitro methods to support transporter evaluation in drug discovery and development Regulatory Drug Transporter White Paper. Nature Reviews Drug Discovery 9, 215 236, (2010) Modelling Chu et al (2013) Intracellular drug concentrations and transporters: Measurement, modelling and implications for the liver 2 Key challenge: Predicting human kinetics Plasma clearance Free intracellular concentrations Fraction of clearance though biliary secretion

This talk addresses two Key issues using hepatocytes for clearance predictions You need to know precisely what you are trying to measure and predict. Understand the PK models that underpin the test system Making measurements of key compounds is often at the limits, - it s really important to have a good understanding of the test system and the variability in measurements Characterise the biological system you are using Simultaneously model as much data as possible In this talk there is no discussion of specific transporters or compounds, the focus is on underlying principles and scenarios 3

Hepatic uptake adds a layer of complexity / risk to candidate drugs CYP DDI Transporter DDI Target organ toxicity Predicting Human kinetics Higher clearance / lower bioavailability 4 Unless the drug target is within hepatocytes - Uptake needs to be managed /reduced/avoided

How would you know a chemical series is susceptible to active uptake? Charged molecules (Acid /zwitterions) Higher Vss than expected Screened for it Clearance could not be predicted by standard methods Transporters will only affect the kinetics of a minority of compounds 5

Hepatocyte based experimental systems Binary systems = media + cells Used for metabolism and/or uptake studies eg suspended cells Tertiary systems = media + cells + canaliculi eg sandwich / 3D cultured hepatocytes Used for metabolism and/or uptake studies Key Issue Expression levels/activity System must be appropriate for compounds

What is happening in a hepatocyte assay used to estimate rate of metabolism (int) of a permeable compound? Total Conc Cell Cell and Medium Time Medium int 0.693V T 1 2 Binding dominates early phase, followed by elimination int is corrected for binding in the system to obtain int,u int,u = int / fu inc This correction is really for defining to the true medium concentration (on the assumption that this equals the free intra-cellular concentration)

Log(Qh* b )/(Qh- b ) Even in the simplest case (highly permeable compounds, eliminated by metabolism) hepatocytes do not directly predict hepatic clearance Raw int In vitro scaling factors, fu P, R b, fu inc Scaled int Lab specific correction Predicted In vivo int Well stirred model (WSM) Predicted in vivo clearance A regression approach adjusts for systematic underpredictions observed when scaling in vitro int directly using the well stirred model, unbound fractions in blood and the in vitro matrix, and physiological scaling factors. Riley, McGinnity and Austin (2005) Log(int*SF*fu b /fu inc ) All evidence suggests transporter assays underestimate in vivo parameters - Correction factors will need to be established and applied

Uptake is the rate-limiting step in the overall hepatic elimination of pravastatin at steady-state in rats Yamazaki, M., Akiyama, S., Nishigaki, R., Sugiyama, Y. 1996 Pharmaceutical Research 13 (10), 1559 What is this really saying? Consider this example: in a 3 step reaction: For the formation of D (excretion into bile) - The rate determining step is always the slowest step in the process. For loss of A, the rate determining step is always k1 (plasma clearance) In this scenario: The rate of conversion of A to B depends on K1, K2 and K4. For poorly permeable compounds uptake is the rate determining step in the plasma clearance of active uptake substrates (because the back-rate is insignificant) 9

Modelling Uptake substrates: The well-stirred model applied to uptake substrates Standard WSM - metabolism + highly permeable compounds Q Q h h. f ub f. ub. int, met int, met WSM - uptake and metabolism (intracellular free extracellular free) Q Q h h. f ub f. ub. int, app int, app int, app int, met [ Cu ] [ C ] u liver plasma [ C [ C u u ] ] liver plasma int, uptake int, met int, pass int, pass int, app int, met int, uptake int, met int, pass int, pass Webborn et al 2007

Low permeability uptake substrates Clint,uptake >>Clint,pass Clint,met >>Clint,pass int, app int, met int, uptake int, met int, pass int, pass int, app Cl int, uptake Plasma clearance determined by uptake rate ( Uptake is the rate limiting step in the hepatic elimination of pravastatin in the rat )

Simulation of the effect of changes in passive diffusion and uptake on hepatic extraction. Cl int,met fixed to give a hepatic extraction of 0.5 (if no transporters involved + permeable) int,uptake was varied from 1 to 1000 ml/min 1.2 int,app int,met int,uptake int,met int,pass int,pass E h 1.0 0.8 0.6 0.4 0.2 0.0 1 3 10 32 100 316 1000 1 10 100 1000 10000 Estimate parameters Apply Model Assess predictivity Good example Umehara and Camenish (2012) (radiolabelled drugs) Cl int,pass

Experimental / Data handling challenges 1. Uptake into suspended hepatocytes 2. Biliary clearance estimates using sandwich cultured hepatocytes 13

The Core Issues Uptake For permeable compounds active uptake gets difficult to measure Because acidic/zwitterionic compounds have low volumes, clearance must be low for half-life to be reasonable: Small contributions from transporters can be critical. Efflux Estimation of biliary Clearance using Sandwich culture systems requires a subtraction step Drug in cells + Bile minus Drug in cells = Drug in bile IVIVE is challenging in complex systems In vivo measurements are difficult (and rare) in man When measurements are at the limits, it s really important to have a real understanding of the errors in the system 14

pmol/million cells Uptake assays - Data Measuring int,uptake int = V/S (S<<<Km) or int = Vmax / Km 140 Compound + inhibitor Measure rate (V in pmol /min) not rate constant (k min -1 ) Requires [S] to be constant. Is it? What about the Intercept? Concentration dependence can yield Vmax, Km and int,pass (Pdiff) V = (Vmax*S)/(Km+S) + Pdiff*S 120 100 80 60 40 20 0 0.0 0.2 0.4 0.6 0.8 Time (min) Model whole data set a in one step - Include all replicates 15

pmol /10^6 cells Uptake assays - Data Measuring int,up int = V/S (S<<<Km) or int = Vmax / Km 500 450 Measure rate (V in pmol /min) not rate constant (k min -1 ) Requires [S] to beconstant. Is it? What about the Intercept? Concentration dependence can yield Vmax, Km and int,pass (Pdiff) V = (Vmax*S)/(Km+S) + Pdiff*S 400 350 300 250 200 150 100 50 0 0 0.25 0.5 0.75 1 1.25 Time (min) 1 um 5 um 10 um 25 um 50 um 100 um 150 um Model whole data set a in one step - Include all replicates 16

Initial rate (pmol/min/million cells) Uptake assays - Data Measuring int,up int = V/S (S<<<Km) or int = Vmax / Km Measure rate (V in pmol /min) not rate constant (k min -1 ) Requires [S] to beconstant. Is it? 8000 7000 6000 5000 37 C Exp87 37 C Exp86 4 C Exp87 4 C Exp86 Active Passive Total AZ12441665 What about the Intercept? 4000 Concentration dependence can yield Vmax, Km and int,pass (Pdiff) V = (Vmax*S)/(Km+S) + Pdiff*S 3000 2000 1000 0 0 50 100 150 200 250 300 Conc. µm Model whole data set a in one step - Include all replicates 17

Model the data 18 Menochet et al (2012) Drug Met Disp 40:1744-1756

Model the data 19 Menochet et al (2012) Drug Met Disp 40:1744-1756, see also Poirier et al (2009)

Predictions of human kinetics based on uptake data - scaling factors Menochet et al (2012) Large and variable scaling factors 20

Predicting biliary Clearance Some basics int,app What do we mean by biliary clearance? What do we mean by biliary intrinsic clearance? int,biliary int, biliary = V/S, int, biliary = rate of efflux/ Free intracellular conc Not that useful, in itself for predicting Plasma clearance? What you really want to know is the contribution of canalicular efflux to plasma clearance int, biliary app = V/S, concentration int, biliary app = rate of efflux/ media Note: For highly impermeable compounds, int,app =int,up For mixed canalicular efflux/ metabolism /uptake substrates - Use the int,app concept int,app ( int,biliary int,met ) int,biliary int,uptake int,met int,pass int,pass 21 Are transporter / metabolism systems active at physiological levels? - That s the real challenge. How good are your sandwich /3D cultures?

Sandwich Cultured hepatocytes Abe et al (2008) JPET 326,3 983-990 BEI = (Drug in cells + Bile) minus (Drug in cells) / (Drug in cells) Technical Challenge Estimation of int,biliary also requires the subtraction step Errors in BEI often less than expected from non-paired data What could drive this? 22

Sandwich Cultured hepatocytes IVIVE the real test Abe at al (2009) Use of Sandwich-Cultured Human Hepatocytes to Predict Biliary Clearance of Angiotensin II Receptor Blockers and HMG- CoA Reductase Inhibitors Nakakariya et al (2012) Predictions 7-300 fold out How to apply regression based corrections in multiparameter systems? 23

Two expressions for biliary clearance int,app Nakakariya et al (2012) int,biliary int,biliary from SCRH a better predictor of int,biliary in vivo Than int,app from SCRH predicts int,app in vivo Implies Uptake transporters are deficient in SCRH Not a useful approach for human predictions? Not an issue in SCHH? 24

Prediction of plasma clearance of compounds eliminated in bile Clint Clint,app Passive Uptake Biliary* Metabolic Apparent KPuu % in bile Biliary ** 200 0 0 10 10 1.0 0 0 200 0 10 10 18 0.9 50 9 1 50 10 10 49 2.4 50 24 1 50 20 10 49 1.6 67 33 1 50 30 10 50 1.2 75 37 1 50 40 10 50 1.0 80 40 1 30 40 10 30 0.6 80 24 1 10 40 10 11 0.2 80 9 int,app ( int,biliary * Biliary Clint based on free intracellular concentration ** Biliary Clint,app based on media concentration KPuu int,biliary int,uptake Both approaches should get to the correct answer, if activities conserved int,met ) int,met int,pass int,pass 25

Prediction of plasma clearance of compounds eliminated in bile and also metabolised Clint Clint,app Passive Uptake Biliary* Metabolic Apparent KPuu % in bile Biliary ** 1 50 10 10 49 2.4 50 24 1 50 10 0 46 4.6 100 46 1 50 30 0 49 1.6 100 49 int,app int,biliary x int,met int,biliary int,uptake int,met int,pass int,pass * Biliary Clint based on free intracellular concentration ** Biliary Clint,app based on media concentration Care needed if metabolic component estimated separately, eg from microsomes 26

Final Word Characterise your cells thoroughly, make extensive use of reference compounds In vitro transporter data should be relative to measured media concentrations If IVIVE not yet robust, performance of project compound relative to compound X can be useful. eg If the human kinetics was similar to valsartan, would our compound be credible Hepatic uptake can be the key process that determines the plasma clearance of compounds eliminated in bile this should direct your IVIVE experiments Emerging transporter expression level data may aid IVIVE issues 27 Set area descriptor Sub level 1