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DNA is the repository of genetic information in all living cells. Genomic integrity and stability are amongst the key considerations for effective and coordinated biological function. However, DNA is not inert. Cells are continuously exposed to several endogenous and exogenous insults that often cause DNA damage. Despite its role in cellular signalling, ROS, a by-product of mitochondrial respiration, is known to cause severe oxidative DNA damage. Lesions in genomic DNA may also be caused by hydrolysis (deamination, depurination and depyrimidination) and alkylation (6-O-methylguanine) brought about other endogenous insults.Additionally, normal cellular processes, such as replication, are also prone to error. Such erroneous processes often result in the incorporation of incorrect nucleotides leading to formation of lesions in the genome. Exogenous sources of damage may be physical (UV light, ionizing radiations) or chemical (chemotherapeutic drugs, industrial chemicals, cigarette smoke). Overall, it is estimated that every cell experiences up to 105 spontaneous or induced DNA lesions per day.
To detect and correct spontaneous and induced DNA damage, and maintain the integrity and stability of the genome, cells have evolved complex and robust DNA repair mechanisms. The DDR network is a specialized network of proteins and enzymes that is actively engaged in the identification and rectification of lesions and breaks in DNA. Complex organisms have multiple DNA repair pathways, namely the direct repair pathway, excision repair pathways (BER, NER and mismatch repair), and the indirect pathway (HRR and NHEJ). In case one pathway is compromised or rendered dysfunctional, alternate repair pathways are activated to maintain genomic integrity.
Tumor cells that are deficient of a particular repair pathway make optimum use of alternate repair pathways. Such cells up-regulate the expression of certain repair proteins, thereby conferring resistance to therapies that involve DNA damage. Therefore, inhibitors of such compensatory repair pathways have the potential to sensitize cancer cells to DNA damaging agents and associated forms of therapy. The mechanism of action of these drugs relies on the principle of synthetic lethality. PARP inhibitors are an emerging class of drugs that inhibit the BER pathway and lead to the selective elimination of certain types of cancer cells. Normal cells with functional repair pathways remain unaffected by this class of chemotherapeutic drugs.
Currently, only one PARP inhibitor, LynparzaTM (olaparib), is commercially available. Four other PARP inhibitors are being tested in phase III of development for several oncological indications; in addition, molecules are also being developed for non-oncological indications such as smoke inhalation injury and stroke.
Scope of the Report
The ‘DNA Repair Drugs: Focus on PARP Inhibitors, 2016-2026’ report is an elaborate study of drugs targeting DNA damage and repair systems, particularly, the enzyme PARP. DNA, the repository of genetic information, is susceptible to damage caused by several environmental and synthetic agents. DNA damage leads to the incorporation of defects and aberrations in the genome that often result in functional mutations. When these mutations occur in genes coding for vital proteins and/or enzymes, it leads to the development of genetic diseases. However, our biological system is equipped with a robust repair mechanism capable of correcting damaged DNA sequences. PARP inhibitors and other similar therapeutics are designed to augment the body’s innate DNA repair mechanism and aid in the treatment of diseases associated with genetic aberrations. So far, this emerging class of drugs has only been evaluated across a niche population segment. This has led to increased efforts in the development of therapeutics targeting cells that harbor defects in their repair systems. There are several targets, other than PARP, that are also under clinical evaluation.
The PARP inhibitors market consists of a thin but promising pipeline of products targeting various indications. Since its serendipitous discovery, the developmental history of these candidate therapeutics has been full of ups and downs. The recalling of the late stage molecule, iniparib, and the termination of several other candidate therapeutics significantly impacted the growth of this segment of the industry. However, it has picked up pace after the commercialization of LynparzaTM (olaparib), the only marketed PARP inhibitor till date. It is important to highlight the role of companion diagnostics, which have significantly contributed to growth in this segment. These molecular tools enabled therapy developers to accurately identify eligible patient groups. Encouraging clinical results demonstrating prolonged PFS and overall survival rates have also accelerated the progress of this drug class.
One of the key objectives of this study was to review and quantify the opportunities laid by the academia/industry players involved in this space. Considering the success of olaparib and clinical data from other active late stage development programs, we have presented an opinion on the anticipated success of PARP inhibitors. Amongst other elements, the report elaborates upon the following key areas:
The analysis in the report is backed by a deep understanding of key drivers behind the market’s growth. With an intent to add comprehensiveness to the market projections, we have provided three market forecast scenarios; the base, optimistic and conservative scenarios represent the likely trends of the future evolution of the market. All actual figures have been sourced and analyzed from publicly available information. The financial figures mentioned in this report are in USD, unless otherwise specified.
Chapter 2 presents an executive summary of the report. It offers a high level view on where the PARP inhibitors market is headed in the coming few years.
Chapter 3 provides a general introduction to DNA damage and repair. In this section, we have comprehensively discussed DNA damage, providing information on the various types of damages that occur and their causative agents. The chapter also provides information on DNA repair systems and associated biological pathways that are activated during DNA repair. Additionally, it includes a summary of the key clinical findings related to DNA damage and repair that culminated in the development of PARP inhibitors and other similar therapies.
Chapter 4 provides an introduction to PARP inhibitors. It includes information on the classification, anatomical layout and therapeutic potential of PARP inhibitors. The chapter provides a detailed account on the mechanism supporting PARP inhibitors as chemo- and radiosensitizers and their evaluation as combination therapies for oncological indications.
Chapter 5 outlines the evolutionary journey of PARP inhibitors in the current pharmaceutical space. The chapter features a case study on iniparib, the recalled PARP inhibitor; it provides details related to its clinical trial design, key clinical endpoints, key clinical findings, associated side effects and structural features. Additionally, the chapter also talks about other PARP inhibitor programs that were terminated/suspended during clinical development due to various technical reasons.
Chapter 6 provides an overview of the market landscape of PARP inhibitors. This chapter includes information on all the PARP inhibitors that we identified during our research, providing details such as target indications, type of study (combination/monotherapy/maintenance), sub-segment of patients targeted (frontline/pre-treated), phase of development and the active developers engaged in this space.
Chapter 7 contains detailed drug profiles of late stage (phase III) candidate molecules in the PARP inhibitor market. Each drug profile covers information such as mechanism of action, history of development, clinical trial status and assessment of clinical trial endpoints, clinical trial results, manufacturing and a brief overview of the developer company.
Chapter 8 provides a comprehensive view on the market forecast measuring the opportunity over the coming ten years (2016-2026). We have provided the key assumptions, forecast methodology and patient population of the target indications. In addition, we have separately highlighted the contribution of the approved and phase III PARP inhibitors.
Chapter 9 presents a detailed publication analysis of all peer-reviewed, published literature available on the clinical development of late stage PARP inhibitors in the past few years. The chapter presents a robust analysis showcasing the active drugs, evolving trend of publications, focused clinical endpoints and therapeutic areas across the published data.
Chapter 10 provides an insight on the competitive landscape of PARP inhibitors. In this chapter, we have provided a glimpse of the various drug classes that are likely to compete with this emerging class of therapeutics. The chapter outlines the specific mechanisms of competing drugs/therapies, along with a summary of their clinical pipeline. These include drug classes such as APE1 inhibitors, NER inhibitors, MGMT inhibitors, DNA-PK inhibitors, HDAC inhibitors, CDK inhibitors and CHK1 inhibitors.
Chapter 11 summarizes the overall report. In this chapter, we have provided a list of key takeaways and have expressed our independent opinion based on the research and analysis described in previous chapters.
Chapter 12 is an appendix, which provides tabulated data and numbers for all the figures provided in the report.
Chapter 13 is an appendix, which provides the list of companies and organizations mentioned in the report.
1. PREFACE
1.1. Scope of the Report
1.2. Research Methodology
1.3. Chapter Outlines
2. EXECUTIVE SUMMARY
3. DNA DAMAGE AND REPAIR SYSTEMS
3.1. Chapter Overview
3.2. DNA Damage
3.3. DNA Damaging Agents
3.3.1. Endogenous DNA Damaging Agents
3.3.2. Exogenous DNA Damaging Agents
3.3.3. Other DNA Damaging Agents
3.4. DNA Damage Response System
3.4.1. Key Components of the DNA Repair System
3.5. Types of DNA Repair Systems
3.5.1. Direct Repair
3.5.1.1. Photo Reactivation
3.5.1.2. Alkyl Transferase Mediated Direct DNA Repair
3.5.1.3. AlkB Mediated Direct DNA Repair
3.5.1.4. DNA Ligase Mediated Direct DNA Repair
3.5.2. Excision Repair
3.5.2.1. Base Excision Repair (BER)
3.5.2.1.1. BER Pathway: Key Enzymes
3.5.2.1.1.1. DNA glycosylases: Initiators of the Repair Process
3.5.2.1.1.2. AP Endonucleases
3.5.2.1.1.3. Other Enzymes
3.5.2.1.2. Short-Patch Base Excision Repair
3.5.2.1.3. Long Base Excision Repair
3.5.2.2. Nucleotide Excision Repair (NER)
3.5.2.3. Mismatch Repair (MMR)
3.5.3. Indirect Repair
3.5.3.1. Homologous Recombination Repair (HRR)
3.5.3.2. Non-Homologous End-Joining Repair (NHEJ)
3.6. Defects in DNA Repair: Onset of Disease
4. POLY ADP-RIBOSE POLYMERASE INHIBITORS
4.1. Chapter Overview
4.2. PARP Proteins
4.3. Classification of PARP Proteins
4.4. Anatomical Layout of PARP Proteins
4.5. Applications of PARP Proteins
4.6. Therapeutic Potential of PARP Inhibition
4.6.1. Mechanism of Action: Synthetic Lethality
4.6.2. Mechanism of Action: PARP Trapping
4.7. Genetic Mutations and Susceptibility to PARP Inhibition
4.8. BRCAness and PARP Inhibitor Sensitivity
4.9. Key Clinical Findings
4.10. PARP Inhibitors as Chemosynthesizers and Radiosensitizers
5. HISTORY OF DEVELOPMENT
5.1. Chapter Overview
5.2. Discovery of PARP Inhibitors
5.3. Pioneering Research on PARP Inhibitors
5.4. Early Failure of PARP Inhibitors
5.5. Case Study: Iniparib
5.5.1. Iniparib: Clinical Development Plan
5.5.2. Iniparib: Clinical Trial Endpoints
5.5.3. Iniparib: Key Clinical Findings
5.5.4. Iniparib: Reasons for Failure
6. MARKET LANDSCAPE
6.1. Chapter Overview
6.2. PARP Inhibitors: Current Market Landscape
6.3. PARP Inhibitors: Development Pipeline
6.4. PARP Inhibitors: Oncological Indications Emerge as the Most Targeted Therapeutics Area
6.5. PARP Inhibitors: An Evolving Market
6.6. PARP Inhibitors Pipeline: Ovarian and Breast Cancer are the Primary Target Indications
6.7. PARP Inhibitors Pipeline: Catering to a Unique and Niche Patient Segment
6.8. PARP Inhibitors Pipeline: Significant Results Driving PARP Inhibitors as Combination Therapy
6.9. PARP Inhibitors Pipeline: Oral Administration Continues to be the Preferred Choice
7. DRUG PROFILES
7.1. Chapter Overview
7.2. Olaparib (AstraZeneca)
7.2.1. Introduction
7.2.2. History of Development
7.2.3. Dosage Regimen and Pricing
7.2.4. Companion Diagnostic
7.2.5. Historical Sales
7.2.6. Current Development Status
7.2.7. Clinical Trials
7.2.8. Clinical Trial Endpoints
7.2.9. Key Clinical Trial Results
7.2.9.1. Ovarian Cancer
7.2.9.2. Breast Cancer
7.2.9.3. Gastric Cancer
7.2.9.4. Pancreatic Cancer
7.2.9.5. Prostate Cancer
7.2.9.6. Solid Tumors
7.2.10. Key Preclinical Findings
7.2.11. Developer Overview
7.2.12. Collaborations
7.3. Veliparib (AbbVie)
7.3.1. Introduction
7.3.2. Current Status of Development
7.3.3. Clinical Trials
7.3.4. Clinical Trial Endpoints
7.3.5. Key Clinical Trial Results
7.3.5.1. Lung Cancer
7.3.5.2. Brain Cancer
7.3.5.3. Liver Cancer
7.3.5.4. Pancreatic Cancer
7.3.5.5. Breast Cancer
7.3.5.6. Ovarian Cancer
7.3.5.7. Prostate Cancer
7.3.5.8. Solid Tumors
7.3.6. Key Preclinical Findings
7.3.7. Developer Overview
7.3.8. Collaborations
7.4. Niraparib (Tesaro)
7.4.1. Introduction
7.4.2. Dosage Regimen
7.4.3. Companion Diagnostic
7.4.4. Patents
7.4.5. Current Development Status
7.4.6. Clinical Trials
7.4.7. Clinical Trial Endpoints
7.4.8. Key Clinical Trial Results
7.4.8.1. Solid Tumors
7.4.9. Key Preclinical Findings
7.4.10. Developer Overview
7.4.11. Collaborations
7.5. Talazoparib (Medivation)
7.5.1. Introduction
7.5.2. History of Development
7.5.3. Dosage Regimen
7.5.4. Current Status of Development
7.5.5. Clinical Trials
7.5.6. Planned Studies
7.5.7. Clinical Trial Endpoints
7.5.8. Key Clinical Trial Results
7.5.8.1. Metastatic Breast Cancer
7.5.8.2. Solid Tumors
7.5.9. Key Preclinical Findings
7.5.10. Developer Overview
7.5.11. Collaborations
7.6. Rucaparib (Clovis Oncology)
7.6.1. Introduction
7.6.2. History of Development
7.6.3. Dosage Regimen
7.6.4. Companion Diagnostics
7.6.5. Patents
7.6.6. Current Status of Development
7.6.7. Clinical Trials
7.6.8. Clinical Trial Endpoints
7.6.9. Key Clinical Trial Results
7.6.9.1. Ovarian Cancer
7.6.9.2. Solid Tumors
7.6.9.3. Pancreatic Cancer
7.6.10. Key Preclinical Findings
7.6.11. Developer Overview
7.6.12. Collaborations
8. MARKET FORECAST
8.1. Chapter Overview
8.2. Forecast Methodology
8.3. Overall PARP Inhibitors Market, 2016-2026
8.3.1. Olaparib (Lynparza) (AstraZeneca)
8.3.1.1. Target Patient Population
8.3.1.2. Sales Forecast
8.3.2. Veliparib (AbbVie)
8.3.2.1. Target Patient Population
8.3.2.2. Sales Forecast
8.3.3. Niraparib (Tesaro)
8.3.3.1. Target Patient Population
8.3.3.2. Sales Forecast
8.3.4. Talazoparib (Medivation)
8.3.4.1. Target Patient Population
8.3.4.2. Sales Forecast
8.3.5. Rucaparib (Clovis Oncology)
8.3.5.1. Target Patient Population
8.3.5.2. Sales Forecast
9. PUBLICATION ANALYSIS
9.1. Chapter Overview
9.2. PARP Inhibitors: Overview of Research
9.3. Olaparib Leads the PARP Inhibitors Research Space; Veliparib to Follow
9.4. 2015 Suggests Renewed Interest in This Drug Class
9.5. Combination Therapy Leads the Research Space of PARP Inhibitors
9.6. Phase I Clinical Trial Data is The Most Documented Literature
9.7. Industry and Academia have Both Contributed to the Development of PARP Inhibitors
9.8. Safety: One of the Most Evaluated Clinical Endpoint
9.9. Ovarian Cancer is The Major Focus Area
10. COMPETING CLASSES
10.1. Chapter Overview
10.2. Direct Approach
10.2.1. APE Inhibitors (BER)
10.2.2. NER Pathway Inhibitors (NER)
10.2.3. MGMT Inhibitors (Direct Repair Pathway)
10.2.4. DNA Protein Kinase Inhibitors (NHEJ; HRR)
10.3. Indirect Mechanism
10.3.1. Histone Deacetylase (HDAC) Inhibitors
10.3.2. Cyclin Dependent Kinase (CDK) Inhibitors
10.3.3. CHK1Inhibitors
10.4. Other Novel DNA Repair Inhibitors
10.4.1. SINE XPO1 Antagonist
10.4.2. Pyrrolobenzodiazepine Dimers (PBDs)
10.4.3. RAD51 Inhibitors
10.4.4. DNA Binding Antibody Platform
11. CONCLUSION
11.1. A Robust DNA Damage Response Network Helps Maintain the Integrity and Stability of DNA
11.2. Targeting DNA Repair has Demonstrated Tremendous Anti-Cancer Potential
11.3. PARP Inhibitors: A Leading Class of DNA Repair Inhibitors
11.4. A Thin Therapeutic Pipeline Targeting a Niche Population Across Various Cancer Indications
11.5. Companion Diagnostics Aid in the Identification of the Correct Target Population
11.6. Significant Opportunity Amongst Targeted Inhibitors Highlights A Promising Market Ahead
12. APPENDIX I: TABULATED DATA
13. APPENDIX II: LIST OF COMPANIES AND ORGANIZATIONS
Figure 3.1 Types of DNA Damage
Figure 3.2 DNA Damage: Types of Causative Agents
Figure 3.3 Types of DNA Damage and Repair
Figure 3.4 DNA Damage Response System
Figure 3.5 Types of DNA Repair Systems
Figure 3.6 Base Excision Repair Pathway
Figure 3.7 Nucleotide Excision Repair Pathway
Figure 3.8 Mismatch Repair Pathway
Figure 3.9 Homologous Recombination Repair Pathway
Figure 3.10 Non-Homologous End-Joining Repair
Figure 3.11 Genetic Disorders Caused due to Defects in DNA Repair Pathways
Figure 4.1 PARP Proteins: Mechanism of Action
Figure 4.2 Family Tree of PARP Proteins
Figure 4.3 Structure of PARP-1 and PARP-2
Figure 4.4 Functions of PARP Proteins
Figure 4.5 Mutated Tumors Cells and PARP Inhibition
Figure 4.6 Mechanism of Action: PARP Trapping
Figure 4.7 Systematic Natural DNA Repair vs PARP Inhibition
Figure 6.1 PARP Inhibitors Pipeline: Distribution by Phase of Development (PI/II/III/Preclinical)
Figure 6.2 PARP Inhibitors Pipeline: Distribution by Target Therapeutic Area
Figure 6.3 PARP Inhibitors Pipeline: Distribution by Patient Segment
Figure 6.4 PARP Inhibitors Pipeline: Distribution by Type of Study
Figure 6.5 PARP Inhibitors Pipeline: Distribution by Route of Administration
Figure 7.1 BRACAnalysisCDx Diagnostic Kit: Historical Timeline
Figure 7.2 BRACAnalysisCDx Diagnostic Kit: Working Process
Figure 7.3 AstraZeneca: Revenues, 2009-2015 (USD Billion)
Figure 7.4 AbbVie: Revenues, 2010-2015 (USD Billion)
Figure 7.5 Talazoparib: Unique Features
Figure 7.6 Talazoparib: Planned Studies
Figure 7.7 Rucaparib: Development Timeline
Figure 8.1 Overall PARP Inhibitors Market (USD Million), 2016-2026
Figure 8.2 Olaparib Sales Forecast: Base Scenario (USD Million)
Figure 8.3 Veliparib Sales Forecast: Base Scenario (USD Million)
Figure 8.4 Niraparib Sales Forecast: Base Scenario (USD Million)
Figure 8.5 Talazoparib Sales Forecast: Base Scenario (USD Million)
Figure 8.6 Rucaparib Sales Forecast: Base Scenario (USD Million)
Figure 9.1 PARP Inhibitors Publications: Distribution by Focus Drug
Figure 9.2 PARP Inhibitors Publications: Distribution by Year of Publication
Figure 9.3 PARP Inhibitors Publications: Distribution by Study Type
Figure 9.4 PARP Inhibitors Publications: Distribution by Focus Drug and Study Type
Figure 9.5 PARP Inhibitors Publications: Distribution by Phase of Development
Figure 9.6 PARP Inhibitors Publications: Distribution by Focus Drug and Phase of Development
Figure 9.7 PARP Inhibitors Publications: Distribution by Type of Sponsor
Figure 9.8 PARP Inhibitors Publications: Distribution by Focus Drug and Type of Sponsor
Figure 9.9 PARP Inhibitors Publications: Distribution by Evaluable Clinical Endpoints
Figure 9.10 PARP Inhibitors Publications: Distribution by Focus Drug and Evaluable Clinical Endpoints
Figure 9.11 PARP Inhibitors Publications: Distribution by Therapeutic Area
Figure 9.12 PARP Inhibitors Publications: Distribution by Drug and Focus Therapeutic Area
Figure 10.1 Classification of HDACs
Figure 10.2 Cell Cycle Regulation
Figure 11.1 PARP Inhibitors And Companion Diagnostics: Collaborations
Figure 11.2 Overall PARP Inhibitors Market Summary (USD Million): 2016, 2021, 2026
Table 3.1 Components of DNA Repair System
Table 3.2 Difference between the HR and NHEJ Pathway
Table 4.1 DNA Damaging Agents Used in Cancer Therapy
Table 5.1 List of Terminated/Withdrawn PARP Inhibitors
Table 5.2 Iniparib: Clinical Trials
Table 5.3 Iniparib: Phase III Clinical Trial Endpoints
Table 5.4 Iniparib: Phase II Clinical Trial Endpoints-1
Table 5.5 Iniparib: Phase II Clinical Trial Endpoints-2
Table 6.1 PARP Inhibitors: Clinical/Preclinical Pipeline
Table 6.2 PARP Inhibitors: Clinical Development Scenario
Table 7.1 Olaparib: Current Status of Development
Table 7.2 Olaparib: Industry Sponsored Clinical Trials
Table 7.3 Olaparib: Non-Industry Sponsored Clinical Trials
Table 7.4 Olaparib: Phase III Clinical Trial Endpoints-1
Table 7.5 Olaparib: Phase III Clinical Trial Endpoints-2
Table 7.6 Company Overview: AstraZeneca
Table 7.7 Veliparib: Current Status of Development
Table 7.8 Veliparib: Industry Sponsored Clinical Trials
Table 7.9 Veliparib: Non-Industry Sponsored Clinical Trials
Table 7.10 Veliparib: Phase III Clinical Trial Endpoints
Table 7.11 Company Overview: AbbVie
Table 7.12 Niraparib: Patent Portfolio
Table7.13 Niraparib: Current Status of Development
Table7.14 Niraparib: Clinical Trials
Table 7.15 Niraparib: Phase III Clinical Trial Endpoints
Table 7.16 Niraparib: Phase II Clinical Trial Endpoints
Table 7.17 Niraparib: Phase I Clinical Endpoints
Table 7.18 Company Overview: Tesaro
Table7.19 Talazoparib: Current Status of Development
Table 7.20 Talazoparib: Industry Sponsored Clinical Trials
Table 7.21 Talazoparib: Non-Industry Clinical Trials
Table 7.22 Talazoparib: Phase II Clinical Trial Endpoints
Table 7.23 Talazoparib: Phase I Clinical Trial Endpoints
Table 7.24 Company Overview: Medivation
Table 7.25 Rucaparib: Current Status of Development
Table 7.26 Rucaparib: Clinical Trials
Table 7.27 Rucaparib: Phase II Clinical Trial Endpoints
Table 7.28 Rucaparib: Phase I Clinical Trial Endpoints
Table 7.29 Company Overview: Clovis Oncology
Table 8.1 PARP Inhibitors: Market Potential for Candidates
Table 8.2 Olaparib: Target Patient Population
Table 8.3 Rucaparib: Target Patient Population
Table 8.4 Niraparib: Target Patient Population
Table 8.5 Veliparib: Target Patient Population
Table 8.6 Talazoparib: Target Patient Population
Table 9.1 PARP Inhibitors Publications
Table 10.1 APE1 Inhibitors Pipeline
Table 10.2 NER Inhibitors Pipeline
Table 10.3 DNA PK Inhibitors Pipeline
Table 10.4 DNA Repair: Effect of Histone Modifications
Table 10.5 HDAC Inhibitors Pipeline
Table 10.6 CDKs: Functions and Emerging Areas of Research
Table 10.7 CDK Inhibitors Pipeline
Table 10.8 CHK1 Inhibitors: Clinical Pipeline
Table 10.9 Other Novel DNA Repair Inhibitors
Table 10.10 Selinexor: Clinical Pipeline
Table 12.1 PARP Inhibitors Pipeline: Distribution by Phase of Development (PI/II/III/Preclinical)
Table 12.2 PARP Inhibitors Pipeline: Distribution by Target Therapeutic Area
Table 12.3 PARP Inhibitors Pipeline: Distribution by Patient Segment
Table 12.4 PARP Inhibitors Pipeline: Distribution by Type of Study
Table 12.5 PARP Inhibitors Pipeline: Distribution by Route of Administration
Table 12.6 AstraZeneca: Revenues, 2009-2015 (USD Billion)
Table 12.7 AbbVie: Revenues, 2010-2015 (USD Billion)
Table 12.8 Overall PARP Market: Conservative Scenario (USD Million), 2016 – 2026
Table 12.9 Overall PARP Market: Base Scenario (USD Million), 2016 – 2026
Table 12.10 Overall PARP Market: Optimistic Scenario (USD Million), 2016 – 2026
Table 12.11 Olaparib Sales Forecast: Conservative Scenario (USD Million)
Table 12.12 Olaparib Sales Forecast: Base Scenario (USD Million)
Table 12.13 Olaparib Sales Forecast: Optimistic Scenario (USD Million)
Table 12.14 Veliparib Sales Forecast: Conservative Scenario (USD Million)
Table 12.15 Veliparib Sales Forecast: Base Scenario (USD Million)
Table 12.16 Veliparib Sales Forecast: Optimistic Scenario (USD Million)
Table 12.17 Niraparib Sales Forecast: Conservative Scenario (USD Million)
Table 12.18 Niraparib Sales Forecast: Base Scenario (USD Million)
Table 12.19 Niraparib Sales Forecast: Optimistic Scenario (USD Million)
Table 12.20 Talazoparib Sales Forecast: Conservative Scenario (USD Million)
Table 12.21 Talazoparib Sales Forecast: Base Scenario (USD Million)
Table 12.22 Talazoparib Sales Forecast: Optimistic Scenario (USD Million)
Table 12.23 Rucaparib Sales Forecast: Conservative Scenario (USD Million)
Table 12.24 Rucaparib Sales Forecast: Base Scenario (USD Million)
Table 12.25 Rucaparib Sales Forecast: Optimistic Scenario (USD Million)
Table 12.26 PARP Inhibitors Publications: Distribution by Focus Drug
Table 12.27 PARP Inhibitors Publications: Distribution by Year of Publication
Table 12.28 PARP Inhibitors Publications: Distribution by Study Type
Table 12.29 PARP Inhibitors Publications: Distribution by Focus Drug and Study Type
Table 12.30 PARP Inhibitors Publications: Distribution by Phase of Development
Table 12.31 PARP Inhibitors Publications: Distribution by Focus Drug and Phase of Development
Table 12.32 PARP Inhibitors Publications: Distribution by Type of Sponsor
Table 12.33 PARP Inhibitors Publications: Distribution by Focus Drug and Type of Sponsor
Table 12.34 PARP Inhibitors Publications: Distribution by Evaluable Clinical Endpoints
Table 12.35 PARP Inhibitors Publications: Distribution by Focus Drug and Evaluable Clinical Endpoints
Table 12.36 PARP Inhibitors Publications: Distribution by Therapeutic Area
Table 12.37 PARP Inhibitors Publications: Distribution by Focus Drug and Focus Therapeutics Area
Table 12.38 Overall PARP Inhibitors Market Summary (USD Million): 2016, 2021, 2026
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