Metabolite Kinetics II

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Presentation transcript:

Metabolite Kinetics II Arthur G. Roberts

Question Is there a drug that you need to reduce the dosage after subsequent dosing? Answer: Yes, if the drug exhibits product inhibition.

Outline In vitro cell systems In vitro plasma binding In vitro methods Separation and metabolite quantification

In vitro Systems Purified Recombinant proteins Baculovirus insect cell expressed proteins Liver microsomes Liver cytosol Liver S9 Liver Cancer Cell Lines Transfected Cancer Cell Lines Hepatocytes Liver slices Isolated perfused liver (in situ)

Purified Recombinant Proteins Clone Gene Insert Gene into Cells E. coli Grow Cells E. coli, Yeast, Sf9 insect cells Crack Cells Isolate by Centrifugation Microsomes/Supernant Column Chromatography e.g. Ni2+ affinity resin

Baculovirus insect cell expressed proteins

Liver Cancer Cell Lines Hep G2 Hepatocellular carcinoma C3A Hepatoblastoma PLC/PRF/5 Hepatoma

Transfected Cell Lines Overexpression of Phase I and Phase II enzymes into Cells Cell Lines V79 Chinese hamster Hep G2 MLC-5 human lymphoblast

Hepatocytes trypan blue dye exclusion method http://en.wikipedia.org/wiki/Trypan_blue They often use the tryptan blue method to assess viability. selectively colour dead tissues and cells blue. trypan blue dye exclusion method

Liver Slices

Isolated Perfused Liver

In vitro Methods Practical aspects Plasma protein binding Metabolite Formation Kinetics Inhibition Enzyme Mapping/Reaction Phenotyping Metabolic Stability Metabolite Profiling Computational Methods Cross species ADME http://www.moldiscovery.com/soft_metasite.php

Practical Aspects Incubation vessel Assay buffer Cofactor sources Initiating incubations Maintaining incubations Stopping incubations Storage Other Considerations http://hstalks.com/dl/handouts/HST9/1089.pdf

Other Considerations Many enzymes are inhibited or stimulated by organic solvent. Flavin-containing monooxygenase (FMO) nortorious sensitive freezing. UGT enzymes in tissue fractions demonstrate “latency” detergents or pore forming agents alamethicin Industry institutes automation.

In vitro plasma binding Drug Drug

Metabolite Formation Kinetics Purpose: Determine kinetic parameters Km, Vmax, estimate Clint=Vmax/Km Metabolite formation linear with [E] low [E], below Km Beware of substrate depletion because velocities are measured from initial slopes

Metabolite Formation Kinetics phenacetin (CYP1A2) tolbutamide (CYP2C9) Hyperbolic alprazolam (CYP3A4) midazolam (CYP3A4) http://dmd.aspetjournals.org/content/38/9/1449.long Atypical Sigmoidal Product Inhibition (Donato, 2010)

Inhibition Inhibition major cause of drug-drug interactions (DDIs) CYPs Reversible Inhibition Competitive, noncompetitive, uncompetitive, mixed-type Suicide/Mechanism-based (Reactive Intermediate) Covalently binds to enzyme (kills enzyme) Idiosyncratic reactions toxic/fatal immunogenic response Potency increases with time Auto-inhibition (non-linear PK) Rational Drug Design Specific Few side effects.

Enzyme Mapping/Reaction Phenotyping Estimation of the relative contributions of specific enzymes to the metabolism of a test compound Approaches Recombinant Proteins (Specific) Selective Inhibition (Microsomes, Pooled Specimens) Beware of inhibitor depletion (partial inhibition) Correlation (Multiple Specimens) (Chapter 15 of Drug Metabolism in Drug Design and Development)

Example #1: Selective Inhibition with Dextromethorphan in microsomes

Uninhibited ketoconazole (CYP3A4) quinidine (CYP3A4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2751464/ shorthand: P = CH3-O-R-N-CH3 M1= CH3-O-R-NH M2= HO-R-N-CH3 M3= HO-R-NH M4= GluO-R-N-CH3 M5= GluO-R-NH hexamethoxyflavone (HMF) (UGT1A1)

X X X Method #1 Dextromethorphan (Cough Suppressant) 20% M3 M1 M4 M2 http://www.sciencedirect.com/science/article/pii/S1570023208002523 Specific CYP3A4 inhibitor ketoconazole X M2 M5 Lutz, 2008

Example #2: Correlation with midazolam, CYP3A4 and CYP3A5 in microsomes

Midazolam 1’-OH Hydroxylation 0.02 mg/mL 0.01 mg/mL 1.2 nmol/mg*min [CYP3A4] [CYP3A5] Midazolam 1’-OH Hydroxylation 0.02 mg/mL 0.01 mg/mL 1.2 nmol/mg*min 1.0 nmol/mg*min etc. Rate [CYP3A5]/[CYP3A4] O http://dmd.aspetjournals.org/content/34/7/1198.full.pdf+html CYP3A4 rate Which one has the higher activity (CYP3A4 or CYP3A5)? How to determine the activity of CYP3A5?

Reaction Phenotyping: Drug Development Discovery High Throughput/Major CYPs Early Development Metabolites and Polymorphic CYPs Full Development Detailed kinetics HLM and recombinant protein

Metabolic Stability Required for Lead Compounds Must be stable in blood  target Drug metabolism major clearance pathway Desirable pharmacokinetic properties http://www.ncbi.nlm.nih.gov/pubmed/12793837 (Masimirembwa, 2003)

Metabolic Stability Which one has the higher metabolic stability?

Estimating Clint from Metabolic Stability Low [Enzyme] Low [S] << Km Measure parent at different times (Substrate Depletion) Estimate the elimination rate constant (K) or the t1/2 Calculate the Clint, in vitro and Clint, in vivo http://dmd.aspetjournals.org/content/27/11/1350.full.pdf+html http://dmd.aspetjournals.org/content/32/9/973.full.pdf+html http://www.ncbi.nlm.nih.gov/pubmed/12065442

Metabolite Profile identify possible active, toxic and inactive metabolites recombinant protein to liver hepatocytes assists in the interpretation of in vivo animal experiments.

Computational: Identification of Hot and Soft Spots Hot spots Reactive metabolic site on a drug. Soft spots Reactive metabolic site on a drug that leads to rapid metabolism (i.e. metabolic instability) http://www.nature.com/nrd/journal/v8/n3/pdf/nrd2836.pdf http://www.ncbi.nlm.nih.gov/pubmed/19108654 http://dmd.aspetjournals.org/content/34/6/976.abstract http://www.sciencedirect.com/science/article/pii/S1359644608004352 (Cross, 2010 Drug Discovery Today)

Computational: Metabolism Prediction Software Proprietary Metasite ADMET Predictor Free SMARTCyp (http://www.farma.ku.dk/smartcyp/) MetaPrint2D (http://www-metaprint2d.ch.cam.ac.uk/metaprint2d/)

Cross Species ADME Appropriate animal selection animals with “human livers” (Strom, 2010) In-vivo metabolic profile pharmacological and biological activity monitoring (bioanalytical method) human toxicity Reaction Phenotyping (Animal vs. Human) http://www.ncbi.nlm.nih.gov/pubmed/20645070 (p. 212, Drug Metabolism in Drug Design and Development)

Separation and Identification Liquid Chromatography Metabolite Identification Radio flow detection/scintillation counting Mass Spectrometry NMR Fluorescence spectroscopy UV-visible spectroscopy detects radiolavels

Example 0.05 mg/L of Ro15-4513 0.001 mg/mL liver microsomes Ro15-4513 was depleted at a rate of 0.02 hr-1 In vitro plasma binding, 90% In vivo human Clh = 56 to 70 L/hr Clh in vitroin vivo, in vitroExtraction Ratio, in vitro in vivo correlation?