1. Measurement of Bioavailability:
Direct and indirect methods may be used to assess drug bioavailability. The in-vivo bioavailability of a drug product is demonstrated by the rate and extent of drug absorption, as determined by comparison of measured parameters, e.g., concentration of the active drug ingredient in the blood, cumulative urinary excretion rates, or pharmacological effects.
For drug products that are not intended to be absorbed into the bloodstream, bioavailability may be assessed by measurements intended to reflect the rate and extent to which the active ingredient or active moiety becomes available at the site of action.
The design of the bioavailability study depends on the objectives of the study, the ability to analyze the drug (and metabolites) in biological fluids, the pharmacodynamics of the drug substance, the route of drug administration, and the nature of the drug product.
Pharmacokinetic and/or pharmacodynamic parameters as well as clinical observations and in-vitro studies may be used to determine drug bioavailability from a drug product.
1.1. Pharmacokinetic methods:
These are very widely used and based upon the assumption that the pharmacokinetic profile reflects the therapeutic effectiveness of a drug. Thus these are indirect methods. The two major pharmacokinetic methods are:
The major pharmacokinetic methods are:
Plasma / blood level time profile.
o Time for peak plasma (blood) concentration (t max)
o Peak plasma drug concentration (Cmax)
o Area under the plasma drug concentration–time curve (AUC)
Urinary excretion studies.
o Cumulative amount of drug excreted in the urine (Du)
o Rate of drug excretion in the urine (dDu/dt)
o Time for maximum urinary excretion (t)
C. Other biological fluids
1.2. Pharmacodynamic methods:
IT involves direct measurement of drug effect on a (patho) physiological process as a function of time. Disadvantages of it may be high variability, difficult to measure, limited choices, less reliable, more subjective, drug response influenced by several physiological & environmental factors.
They involve determination of bioavailability from:
Acute pharmacological response.
Therapeutic response.
1.3. In-vitro dissolution studies
Closed compartment apparatus
Open compartment apparatus
Dialysis systems.
1.4. Clinical observations
Well-controlled clinical trials
1. Measurement of Bioavailability:
Direct and indirect methods may be used to assess drug bioavailability. The in-vivo bioavailability of a drug product is demonstrated by the rate and extent of drug absorption, as determined by comparison of measured parameters, e.g., concentration of the active drug ingredient in the blood, cumulative urinary excretion rates, or pharmacological effects.
For drug products that are not intended to be absorbed into the bloodstream, bioavailability may be assessed by measurements intended to reflect the rate and extent to which the active ingredient or active moiety becomes available at the site of action.
The design of the bioavailability study depends on the objectives of the study, the ability to analyze the drug (and metabolites) in biological fluids, the pharmacodynamics of the drug substance, the route of drug administration, and the nature of the drug product.
Pharmacokinetic and/or pharmacodynamic parameters as well as clinical observations and in-vitro studies may be used to determine drug bioavailability from a drug product.
1.1. Pharmacokinetic methods:
These are very widely used and based upon the assumption that the pharmacokinetic profile reflects the therapeutic effectiveness of a drug. Thus these are indirect methods. The two major pharmacokinetic methods are:
The major pharmacokinetic methods are:
Plasma / blood level time profile.
o Time for peak plasma (blood) concentration (t max)
o Peak plasma drug concentration (Cmax)
o Area under the plasma drug concentration–time curve (AUC)
Urinary excretion studies.
o Cumulative amount of drug excreted in the urine (Du)
o Rate of drug excretion in the urine (dDu/dt)
o Time for maximum urinary excretion (t)
C. Other biological fluids
1.2. Pharmacodynamic methods:
IT involves direct measurement of drug effect on a (patho) physiological process as a function of time. Disadvantages of it may be high variability, difficult to measure, limited choices, less reliable, more subjective, drug response influenced by several physiological & environmental factors.
They involve determination of bioavailability from:
Acute pharmacological response.
Therapeutic response.
1.3. In-vitro dissolution studies
Closed compartment apparatus
Open compartment apparatus
Dialysis systems.
1.4. Clinical observations
Well-controlled clinical trials
The study of absorption, distibution,metabolism,excretio of drug and their relationship to pharmacological response. In simple word ; what the body dose to the drug. Linear pharmacokinetics.In the pharmacokinetic parameter for drug would not change when difference dose or multiple dose of drug is given. Non linear pharmcokinetics-if any deviation cause linear pharmacokinetics called non linear, mixed, capacity – limited kinetics.
Direct compression is the most advanced technology. It involves only blending and compression. Thus offering advantage particularly in terms of speedy production. Because it requires fewer unit operations, less machinery, reduced number of personnel and considerably less processing time along with increased product stability.
What Is Disposition?
What Is Distribution?
Steps In Drug Distribution
Factors Affecting Distribution Of Drugs
Physiological Barriers To Distribution
Volume Of Distribution
Specific Tracers Or Markers
Methods For Studying Drug Distribution Pattern
D M Brahmankar and Sunil B.Jaiswal Biopharmaceutics and Pharmacokinetics A Treatise
ROLE OF PHARMACIST IN PREVENTION & MANAGEMENT OF DRUG INTERACTIONSKomal Haleem
This presentation describes the steps to be performed by a pharmacist to play a major role in prevention and management of drug interactions and includes a case study.
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
The study of absorption, distibution,metabolism,excretio of drug and their relationship to pharmacological response. In simple word ; what the body dose to the drug. Linear pharmacokinetics.In the pharmacokinetic parameter for drug would not change when difference dose or multiple dose of drug is given. Non linear pharmcokinetics-if any deviation cause linear pharmacokinetics called non linear, mixed, capacity – limited kinetics.
Direct compression is the most advanced technology. It involves only blending and compression. Thus offering advantage particularly in terms of speedy production. Because it requires fewer unit operations, less machinery, reduced number of personnel and considerably less processing time along with increased product stability.
What Is Disposition?
What Is Distribution?
Steps In Drug Distribution
Factors Affecting Distribution Of Drugs
Physiological Barriers To Distribution
Volume Of Distribution
Specific Tracers Or Markers
Methods For Studying Drug Distribution Pattern
D M Brahmankar and Sunil B.Jaiswal Biopharmaceutics and Pharmacokinetics A Treatise
ROLE OF PHARMACIST IN PREVENTION & MANAGEMENT OF DRUG INTERACTIONSKomal Haleem
This presentation describes the steps to be performed by a pharmacist to play a major role in prevention and management of drug interactions and includes a case study.
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
Pharmacokinetics - drug absorption, drug distribution, drug metabolism, drug ...http://neigrihms.gov.in/
A power point presentation on general aspects of Pharmacokinetics suitable for undergraduate medical students beginning to study Pharmacology. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
In vitro enzyme inhibition studies on new sulfonamide derivatives of 4-tosyl ...Jing Zang
Sulfonamides are considered to be pharmaceutically important class of compounds. In the present work, N-(2,4-dimethylphenyl)-4-toluenesulfonamide (3) was synthesized by the reaction of 2,4-dimethylaniline (1) and 4-tosyl chloride (2; 4-methylbenzenesulfonyl chloride) using 10% aqueous Na2CO3 solution as reaction medium. At the second step, the synthesized molecule 3 was made to react with different alkyl/aralkyl halides (4a-o) to yield the target compounds, 5a-o, using N,N-dimethylformamide (DMF) as reaction medium and lithium hydride as an activator. The synthesis of all the compounds was verified by spectral techniques using IR, 1H-NMR and EIMS; and further examined for their anti-enzymatic activities. The synthesized compound 5f represented a suitable inhibitory potential against α-glucosidase and lipoxygenase enzymes.
02.10.09(a): Self-Study: The Complement System in Human DiseaseOpen.Michigan
Slideshow is from the University of Michigan Medical
School's M1 Immunology sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M1Immunology
Part of our assignment in which we have to make a paperwork and presentation of a few sub-topics (hepatotoxicity, renal toxicity, neurotoxicity, skeletal-muscle-toxicity) under the topic of Drug-induced Toxicity.
Paperwork can be found in: http://www.slideshare.net/annisahayatunnufus/druginduced-toxicity-liver-kidney-nervous-system-muscle-54844837
Students of Bachelor of Pharmacy
Management & Science University
Predictive Models for Mechanism of Action Classification from Phenotypic Assa...Ellen Berg
Predictive Models for Mechanism of Action Classification from Phenotypic Assay Data – Application to Phenotypic Drug Discovery
Presentation at SLAS 2014 conference in San Diego, 21 January 2014
Answer four fundamental questions on how to develop the most innovative cancer immunotherapy treatments, starting with screening for lead molecules and ending with evaluation of combination therapies.
2014 11-27 ODDP 2014 course, Amsterdam, Alain van GoolAlain van Gool
Presentation as part of a comprehensive oncology drug development course, to discuss a pharmaceutical approach to identify, validate and develop biomarkers for personalized medicine for melanoma.
Los días 11 y 12 de diciembre de 2014, la Fundación Ramón Areces celebró el Simposio Internacional 'Neuropatías periféricas hereditarias. Desde la biología a la terapéutica' en colaboración con CIBERER-ISCIII y el Centro de Investigación Príncipe Felipe. El tipo más común de estas patologías es la enfermedad de Charcot-Marie-Tooth, un trastorno neuromuscular hereditario con una prevalencia estimada de 17-40 afectados por 100.000 habitantes. Durante estos dos días, investigadores mostraron sus avances en la mejora del diagnóstico y el tratamiento y, por ende, de la aproximación clínica y la calidad de vida de las personas afectadas por estas patologías.
Target Validation Academy Of Medical Sciences 1 Dec 2006Mike Romanos
An overview of the issues and approaches in selecting the best targets for drug discovery and validating them. Given at the Drug Discovery Forum held at the Royal Society, London and organised by the Academy of Medical Sciences
Detection and quantification of mutant alleles in tumor tissue allow for research disease monitoring and the research of drug efficacy. Detection of emerging secondary mutations in the same tumor tissue causing resistance to potential treatment will help guide decisions on future treatment plans. Testing for the presence of mutations in cell free DNA (cfDNA) is a less invasive research method than using tumor tissue. We created a research tool for mutation detection at a sensitivity level of 1% and below. This allows researchers to find correlation between types of mutations and types of tumors and determination of potential secondary mutations.
The tool combines TaqMan® SNP Genotyping Assays with digital PCR. A set of assays was optimized for use
in digital PCR with the QuantStudio® 3D Digital PCR System. In digital PCR, partitioning the sample into many individual reaction wells facilitates detection and quantification of rare mutant alleles. TaqMan® SNP Genotyping Assays ensure reliable discrimination of mutant and wild-type allele. Our current set of 60 assays covers mutations commonly found in tumor tissues, such as: BRAF V600E, mutations in EGFR exons 19, 20 and 21, KRAS codons 12 and 13, PIK3CA exons 9 and 20, and the JAK2 V617F mutations. All assays were wet-lab tested at a 10% mutation rate and a 1% mutation rate using mutant plasmid spiked into wild-type genomic DNA. Additionally, selected assays were tested at the 0.1% mutation rate using mutant cell lines spiked into wild-type genomic DNA. Wet-lab results confirm that all assays showed superior performance discriminating mutant and wild-type alleles. Mutant alleles were successfully detected as low as 0.1%.
1. Sample & Assay Technologies
Welcome !
Drug Metabolism and Toxicity
Contact Technical Support
support@SABiosciences.com
1-888-503-3187
International customers:
SABio@Qiagen.com
Wei Cao, Ph.D.
Webinar related questions:
Qiawebinars@qiagen.com
Wei.Cao@Qiagen.com
The products described in this webinar are intended for molecular biology
applications. These products are not intended for the diagnosis, prevention or
treatment of disease.
1
2. Sample & Assay Technologies
Topics will be covered
Overview
Drug metabolism & metabolism-based
toxicity
Current approaches
Research solutions @ QIAGEN
Detect the drug metabolism abnormality
Identify the mechanism of toxicity
Monitor genotoxicity
Application examples
What’s next
2
3. Sample & Assay Technologies
10k compound
1 compound
Drug toxicity: why is it concerned ?
Cost of developing a drug is high: average $800m-1b
Toxicity is a major barrier for new drugs
Responsible for the failure of 1/3 drug candidates
A major contributor to the high cost of drug development
1/3 profitable
F. Peter Guengerich, Drug Metab. Pharmacokinet, 2011, 26(1): 3
F. Peter Guengerich, The AAPS Journal, 2006, 8(1), E101
3
4. Current hot spots in toxicity risk assessment
Sample & Assay Technologies
Sites for toxicology attrition - target organs or tissues
Hepato
Toxicity
Neuro
Toxicity
Pulmonary
Toxicity
Geno
Toxicity
Cardio
Toxicity
Renal
Toxicity
Immuno
Toxicity
Hepatotoxicity: a major
issue in both pre-clinical and
clinical development; Many
drugs withdrawn due to
hepatotoxicity.
Genotoxicity: not limit to a
specific organ or tissue
type; Compounds causing
genotoxicity are the most
dangerous ones as
classified by FDA.
F. Peter Guengerich, Drug Metab. Pharmacokinet, 2011, 26(1): 3
F. Peter Guengerich, The AAPS Journal, 2006, 8(1), E101
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5. Sample & Assay Technologies
Drug metabolism induced toxicity
Drug metabolism phases:
Phase I: Oxidation/reduction/hydrolysis
Phase II: Conjugation
Outcome of drug metabolism
Toxicity
Nucleic acid
Toxic metabolite
Carcinogenicity
Genotoxicity
Enzyme
Altered activity
Transport
proteins
Active metabolite
Drug
Enhanced activity
Inactive metabolite
Loss of activity
Reversible
metabolite
Prolonged activity
Signaling
proteins
Necrosis
Apoptosis
Receptors
Autologous
proteins
Hypersensitivity
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6. Sample & Assay Technologies
Approach to evaluate metabolism-based toxicity
Prediction of human drug toxicity is difficult:
•
Lack of mechanistic understanding
•
Species differences
•
Other factors affecting drug metabolism, such as age, gender, genetic
polymorphism, disease state, and environmental factors
A systematic evaluation of the roles of drug metabolism in drug
toxicity in pre-clinical stage is needed
FAIL IT EARLIER, FAIL IT CHEAPER !
6
7. Sample & Assay Technologies
Drug metabolism induced toxicity
FDA guidance on metabolism-based drug-drug interaction
http://www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/ucm292362.pdf
7
8. Sample & Assay Technologies
Evaluation of drug induced toxicity
in vitro approaches
Specificity
IC50
EC50
Metabolic
Stability
Stability in Human (M,
D, R, Monkey) liver
microsome & Human
Hepatocyte
Inhibition
Induction
Inhibition of drug
metabolizing
enzymes in Human
Hepatocytes
Induction of drug
metabolizing
enzymes in
Human
Hepatocytes
Permeability
Substrate of Pg-P
Inhibitor of Pg-P
Inducer of Pg-P
Metabolite profile
Metabolite ID
Interspecies comparisons
Feed information to in vivo studies and the types
of clinical trials needed to assess potential DDIs
http://www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/ucm
292362.pdf
8
9. Sample & Assay Technologies
Research solutions @ QIAGEN
Research solutions @ QIAGEN
Detect the drug metabolism abnormality
Identify the mechanism of toxicity
Monitor genotoxicity
Application examples
What’s next
9
10. Sample & Assay Technologies
Gene expression regulates biology
All require molecular signaling for action
10
11. Sample & Assay Technologies
Gene expression and drug toxicity
Gene expression profiles should be able to
discriminate compounds that have different
mechanisms.
The toxicity of unknown compounds can be predicted
by comparing their molecular fingerprints with those
obtained with compounds of known toxicity.
Specific to drug metabolism:
Induction of drug metabolizing enzymes usually
results from overexpression of the respective
genes
The major mechanisms for enzyme inhibition is
due to the down-regulation of gene expression
11
12. Sample & Assay Technologies
Differential gene expression analysis for drug toxicity
Q: How to assess the expression of different
mRNAs in a sample involved in a process and
compare it across multiple conditions?
A:
- 12 -
12
13. Sample & Assay Technologies
Principles of qRT-PCR: overview
• Real-Time PCR
• Amplify and simultaneously quantify target DNA
• RT2 PCR (Reverse transcription teal-time PCR)
• Amplify and simultaneously quantify mRNA
• Ct Values: Threshold Cycle
13
14. Sample & Assay Technologies
96-well plate format
Pathway- or diseased- focused PCR Arrays
84 Pathway-Specific Genes
of Interest
5 Housekeeping Genes
Genomic DNA Contamination
Control
Reverse Transcription
Controls (RTC) n=3
Positive PCR Controls
(PPC) n=3
100-well rotor gene ring
384-well plate
96x96 chips
Customizable
14
15. Sample & Assay Technologies
How RT2 Profiler PCR Arrays work?
Isolate Total RNA
Control
Hot Sauce
cDNA Synthesis
–
–
Genomic DNA Removal Step (5
min.)
Reverse Transcription Step (20
min.)
Load Plates
1 Sample per PCR Array
2 minutes with multi-channel pipet
Run 40 cycle qPCR Program
Standard cycling conditions for all
Real Time PCR Instruments
2 hours
Upload and Analyze Data (FREE)
15 minutes from Raw Ct to
Fold Change Data
15
16. Sample & Assay Technologies
Gene expression profiling applications in drug toxicity
Application 1
Profile gene expression of 84 drugmetabolizing enzymes in primary human
hepatocytes
Webinar 1: Meeting the Challenges of miRNA Research
16
18. Sample & Assay Technologies
Application 1 – Induction & inhibition
3 compounds: 20uM Rifampicin, 50uM Omeprazole, 8uM 3-MC (3-methylcholanthrene)
Experimental workflow
Control
Sample
Incubate with primary human
hepatocytes, 3 male donors
Reverse
transcription
Isolate total RNA using
RNeasy system
Data Analysis
Upload raw data (Ct) and analyze data
cDNA synthesis
RT2 PCR Array
18
19. Sample & Assay Technologies
Application 1- Interpretation of Ct Values
Fold Change Calculations: PCR Array Results / Data
Raw Ct Value:
Relative expression level of that gene in the sample
Data normalization ∆Ct
per Gene = Ct Gene X - Ct HKGs (Avg)
Up or Down-Regulation
= ∆∆Ct per Gene = ∆Ct Sample - ∆Ct Control
Fold change result per gene = 2-∆∆Ct
The gene is present 4x more in the treated sample
than in control sample.
FREE Complete & easy data analysis with web-based software
19
23. Sample & Assay Technologies
Gene expression profiling applications in drug toxicity
Application 2
Identify the mechanism of toxicity
Webinar 1: Meeting the Challenges of miRNA Research
23
25. Sample & Assay Technologies
Application 2 - Hepatotoxicity
Drug metabolism RT2 PCR Array
Background:
Acetaminophen (APAP) is an endoplasmic reticulum (ER) inducer
APAP overdose causes acute liver failure
APAP hepatotoxicity is mainly mediated by its metabolite, NAPQI (N-acetyl-pbenzoquinone imine) generated by APAP oxidation by CYP450 enzymes
NAPQI is detoxified primarily by glutathione (GSH) conjugation
Excessive amount of NAPQI depletes GSH and covalently binds to
macromolecules, resulting in cytotoxicity
The mechanism of APAP caused hepatotoxicity?
25
26. Sample & Assay Technologies
Application 2 – Experimental overview & results
In vivo application
Mice model
XBP1 is deleted
High dose
APAP treatment
CYP1A2 and CYP2E1, crucial for APAP oxidation to toxic
RNA isolation
NAPQI were significantly decreased in XBP1∆ mice
Gene involved in GSH synthesis were not affected
qRT-PCR
Genetic ablation of XBP1 activates IRE1a in liver, leads to the
degradation of CYP1A2 and CYP2E1 mRNAs, and protect
mice from APAP-induced hepatotoxicity;
Data analysis
APAP metabolism in liver: upon ER stress, APAP activate
IRE1a suppressed expression of CYP1A2 and CYP2E1, which
drive the conversion of APAP to hepatotoxic metabolites.
26
31. Sample & Assay Technologies
In vitro: HepG2
Application 3 -Stress & Toxicity PathwayFinder PCR Array
3 anti-diabetic drugs:
Rezulin (Troglitazone): withdrawn due to idiosyncratic liver toxicity
Actos (Pioglitazone) and Avandia (Rosiglitazone): safe
Treat cells with
3 diabetes
drugs
RNA isolation
qRT-PCR
Data analysis
Uncovered distinct gene expression profiles associated with liver toxicity
caused by 3 PPARγ agonists (Actos, Avandia, and Rezulin).
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31
32. Sample & Assay Technologies
Gene expression profiling applications in drug toxicity
Application 4
Monitor genotoxicity via gene
expression profiling
Webinar 1: Meeting the Challenges of miRNA Research
32
33. Sample & Assay Technologies
Standard Battery for Genotoxicity Testing
Genotoxicity tests are defined as in vitro and in vivo
tests designed to detect compounds that induce
genetic damage directly or indirectly by various
mechanisms.
Test for gene mutation in bacteria (60% sensitivity)
In vitro test with cytogenetic evaluation of
chromosomal damage with mammalian cells
In vitro mouse lymphoma tk assay
In vivo test for chromosomal damage using rodent
hematopoietic cells
http://www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInf
ormation/Guidances/ucm074931.pdf
33
34. Sample & Assay Technologies
Application 4- Monitor Genotoxicity via gene expression
Selected 20 compounds for genotoxicity testing
34
35. Sample & Assay Technologies
Application 4- Genotoxicity Experiment Design
Cells:
HepG2 cells: 2 X 105 cells/ml at seeding.
96-well plate for cytotoxicity assays --- 3 to 5 biological
replicates.
6-well plate for RNA isolation --- 4 biological replicates.
Dose:
IC20 - low dose but substantial to trigger gene expression
changes.
Time:
24 hr – to avoid generic stress responses often observed
at shorter incubation time (e.g. 3 hr or 6 hr).
RNA Isolation and PCR Array Analysis:
RT2 PCR Array protocols.
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38. Sample & Assay Technologies
Application 4- Genotoxicity Testing Results
Expression profiles from different modes of action
We identified 11 genes in DNA damage repair and p53
pathways as a classifier for genotoxic and non-genotoxic
compounds.
Genotoxic compounds with different modes of action elicit
distinct gene expression profiles.
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39. Sample & Assay Technologies
Toxicology and drug metabolism @ QIAGEN
Many pathways important for drug discovery process
Drug Transporters
Cancer Drug Resistance
DNA Damage Signaling Pathway PCR array
Heat Shock Proteins PCR array
Unfolded Protein Response PCR array
Oxidative stress PCR Array
Cardiotoxicity PCR Array
Hepatotoxicity PCR Array
Custom PCR Arrays
39
40. Sample & Assay Technologies
Toxicology and drug metabolism @ QIAGEN
QIAGEN offers many methods to analyze the toxicology and
ADME profiles of drug candidates
Gene Expression
RT2 Profiler PCR Arrays & Assays
Mutational analysis
qBiomarker Somatic Mutation PCR Arrays & Assays
qBiomarker Copy Number PCR Arrays & Assays
Epigenetics
miScript miRNA PCR Arrays & Assays
EpiTect Methyl qPCR Arrays & Assays
Functional Studies
Cignal Reporter Assays
siRNA and plasmid-based shRNA
40
41. Sample & Assay Technologies
We provide service – send samples to us & receive results!
.
Whole Genome
Illumina Gene Expression Profiling
Illumina Genotyping
.
Pathway / Focused Panel
Mutation Profiling
Methylation
PCR Array
miRNA PCR Array
.
Individual Gene / Locus
Mutation Detection
Methylation
qPCR
.
Sample Preparation – DNA, RNA
Extraction and Purification
Cells, Tissue or Biofluids
Fixed Tissue
Small Sample
.
http://www.sabiosciences.com/servicecore.php
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42. Sample & Assay Technologies
New Products for toxicology
RT2 Profiler PCR Array Plus
Gene expression profiling
Gene expression profiling
+ SCORE
Upgrade from current RT2 Profile PCR Array
Same workflow as current RT2 Profile PCR array
Content
Signature genes (16)
Pathway relevant genes (68)
HK gene (5), GDC (1), RTC (3), PPC (3)
Data analysis
Profiling
Pathway activity readout
RT2 Predictor PCR Array
New product of RT2 PCR Array
Signature gene only plate
Process 4 samples per plate
Same workflow as current RT2 PCR array
Content
Signature gene (16)
HK gene (5), GDC (1), RTC (1), PPC (1)
Data analysis
Pathway activity readout
http://www.sabiosciences.com/biomarker_signature_genes.php
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43. Sample & Assay Technologies
Thank you for attending!
PCR Array Starter Pack- Promotion Code FDK-PAFAS12
PCR Arrays of any Pathway (FREE)
2 96-well/100-well (2 samples) OR 1 384-well (4 samples)
Required Reagents (w/ Purchase)
RT2 First-Strand cDNA Synthesis Kit
RT2 SYBR Green Mastermix (2-Pack)
Email: Support@SABiosciences.com OR
QIAWEBINARS@QIAGEN.COM
Call 1-888-503-3187 to order
(US and Canada only)
43