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市場調查報告書

阿茲海默症的Tau及乙型澱粉樣蛋白的療法

Competitor Analysis: Tau and Amyloid Beta Targeted Therapy of Alzheimer's Disease

出版商 La Merie Publishing
出版日期 2010年08月 商品編碼 127639
內容資訊 英文 105 Pages
價格
US $ 890 PDF by E-mail ( Single User License)
US $ 1780 PDF by E-mail ( Site License)
US $ 2670 PDF by E-mail (Global Site License)


阿茲海默症的Tau及乙型澱粉樣蛋白的療法 是由出版商La Merie Publishing在2010年08月所出版的。 這份英文市場調查報告書包含105 Pages 價格從美金890起跳。

簡介

本報告書內容包括:阿茲海默症的Tau・乙型澱粉樣蛋白為標的的治療疫苗、抗體、小分子領域的總體分析、各公司的研究開發趨勢的彙整、內容綱要摘記如下:

第1章 Tau標的療法

  • Tau凝集抑制劑
  • Tau磷酸化抑制劑
  • 微小管安定劑
  • Tau免疫療法
  • Tau・乙型澱粉樣蛋白二重療法或其他Tau標的療法

第2章 乙型澱粉樣蛋白画像

第3章 乙型澱粉樣蛋白免疫療法

  • IV免疫球蛋白
  • 被動乙型澱粉樣蛋白免疫療法
  • 主動乙型澱粉樣蛋白免疫療法

第4章 乙型澱粉樣蛋白生産的防止

  • β分泌脢抑制劑及調整劑
  • Gamma分泌脢抑制劑
  • Gamma分泌脢修飾剤
  • 二重分泌脢抑制劑或其他乙型澱粉樣蛋白生産抑制劑

第5章 α分泌脢活性化

  • α7尼古丁乙醯膽鹼受體促效劑
  • GAGA-受體修飾、5-HT4受體促效劑及其他α分泌脢活性劑

第6章 乙型澱粉樣蛋白凝集低減和去除

各公司的抗感染抗體檔案和研究開發生產線

目錄

Abstract

The present Competitive Intelligence Report about Tau and Amyloid Beta Targeted Therapy of Alzheimer' s Disease provides a competitor evaluation in the field of therapeutic vaccines, antibodies and small molecules targeting Tau and/or Amyloid Beta for treatment of Alzheimer' s disease as of August 2010. Purchase of the downloadable pdf report includes a 6-month online access to the data of the report and any updates since the publication date. Credentials to access the database will be sent by e-mail and allow online work with the project data to print or export an individual report.

One of the main pillars of current drug discovery and development activities in the pharmaceutical industry for Alzheimer' s disease is prevention of the accumulation of misfolded proteins, i.e. amyloid beta and tau. At present, the majority of approaches are directed to the amyloidogenic pathway. Amyloid beta peptides derive from amyloid precursor protein (APP) by proteolytic cleavage by beta secretase and gamma secretase.

Thus, inhibitors of beta secretase (or beta-site APP-cleaving enzyme, BACE-1) are a main area of drug discovery complicated by the substate diversity of BACE-1 and the need to pass the blood-brain barrier (BBB) which explains that only very few inhibitors entered clinical development with no compound in phase III, but many ongoing discovery programs. The first representative of the class of inhibitors and modulators of gamma secretase has entered phase III but the studies recently failed to meet the efficacy endpoint and even worsened the clinical outcomes in the studies. It remains to be seen whether follower programs in clinical phases I and II will suffer the same fate or can be differentiated from Lilly' s semagacestat. Most of the gamma secretase inhibitors in development are Notch-sparing molecules, thereby avoiding typical side effects of the Notch signaling pathway, e-g. gastrointestinal and hematological toxicities.

Increasing the activy of alpha secretase is another means to reduce the activity of beta secretase. A number of compounds with different primary mechanisms of action are in clinical and preclinical development.Strong efforts are made by the industry in immunotherapy against amyloid beta to inhibit generation of toxic amyloid beta aggregates and remove soluble and aggregated amuyloid beta. At least eight therapeutic vaccines against amyloid beta are under clinical investigation and more candidates are in preclinical R&D stages. Passive immunotherapy with therapeutic antibodies against amyloid beta has already reached phase III testing in clinical studies. Ten antibody projects are in clinical or IND enabling study phases and more than ten candidates in preclinical stages. Intravenous infusion of human-plasma derived immunoglobulin preparations which contain naturally occurring plyclonal anti-amyloid beta antibodies are also in advanced clinical testing.

Another approach is the development of CNS-bioavailable compounds that inhibit amyloid beta aggregation or disintegrate amyloid beta oligomeric species without being toxic or immunogenic. The second generation of such molecules has at least ten representatives in clinical studies up to phase II.

The cytoplasmic protein Tau has recently gained much interest as a target for new therapies of Alzheimer' s disease where it is abnormally phosphorylated resulting in the generation of neurofibrillary tangles (aggregates) toxic to neurons. The main tau-targeted approaches include molecules inhibiting hyperphosphorylation and molecules that inhibit tau aggregation or promote aggregate disassembly. Only a few molecules have reached clinical stages, but strong research efforts are undertaken to come up with more clinical candidates.

The report includes a compilation of currently active projects in research and development of vaccines, antibodies, small molecules, proteins and peptides targeting Tau and/or the amyloid beta pathway. In addition, the report lists company-specific R&D pipelines of Tau and Amyloid Beta Targeted Therapeutics for Alzheimer' s disease. Competitor projects are listed in a tabular format providing information on:

  • Drug Codes,
  • Target / Mechanism of Action,
  • Class of Compound,
  • Company
  • Product Category
  • Indication,
  • R&D Stage and
  • additional comments with a hyperlink leading to the source of information.

Report Statistics

  • Pages: 105
  • Release Date: August of 2010
  • Format: PDF

Table of Contents

1. Tau Targeted Therapy

  • Tau Aggregation Inhibitors
  • Tau Phosphorylation Inhibitors
  • Microtubule Stabilizers
  • Tau Immunotherapy
  • Dual Tau & Amyloid Beta or Other Tau Targeted Therapy

2. Amyloid Beta Imaging

3. Amyloid Beta Immunotherapy (Amyloid Beta Clearance)

  • IV Immune Globulins (IVIG)
  • Passive Amyloid Beta Immunotherapy
  • Active Amyloid Beta Immunotherapy

4. Prevention of Amyloid Beta Production

  • Beta Secretase Inhibitors & Modulators
  • Gamma Secretase Inhibitors
  • Gamma Secretase Modulators
  • Dual α & γ Secretase Inhibitors & Other Amyloid Production Inhibitors

5. Alpha Secretase Activation (Non-Amyloidogenic Pathway of APP Processing)

  • Alpha7 Nicotinic Acetylcholine Receptor (NAChR) Agonists
  • GABA-A Receptor Modulation, 5-HT4 Receptor Agonism and Other α Secretase Activators

6. Amyloid Beta Aggregation Reduction and Aggregate Removal

Corporate Anti-Infective Antibody Portfolios and R&D Pipelines

  • Abbott
  • Abiogen Pharma
  • Ablynx
  • AC Immune
  • Actelion
  • Acumen Therapeutics
  • Affitech
  • Affiris
  • Alzprotect
  • Amgen
  • Archer Pharmaceuticals
  • ArmaGen Technologies
  • Astellas Pharma
  • Astex Therapeutics
  • AstraZeneca
  • Avid Radiopharmaceuticals
  • Axon Neuroscience
  • Baxter
  • Bayer Schering Pharma
  • Bellus Health
  • BioArctic Neuroscience
  • Biogen Idec
  • Boehringer Ingelheim
  • Bristol-Myers Squibb
  • Bruin Pharma
  • Cellzome
  • Chiesi Farmaceutici
  • CoMentis
  • Critical Outcome Technologies
  • Cytos Biotechnology
  • D-Pharm
  • Delenex
  • Diamedica
  • DNAVEC
  • Eisai
  • Elan
  • Eli Lilly
  • EnVivo Pharmaceuticals
  • Evotec
  • ExonHit Therapeutics
  • Galantos
  • Galapagos
  • GE Healthcare
  • GlaxoSmithKline
  • Grifols
  • Humanetics Pharmaceuticals
  • Immuno-Biological Laboratories
  • Intellect Neurosciences
  • Johnson & Johnson (Cilag-Janssen, Ortho-McNeil)
  • Kinexis
  • Lay Line Genomics
  • Ligand Pharmaceuticals
  • Link Medicine Corp.
  • Lundbeck
  • Medivir
  • Memory Pharmaceuticals
  • Merck & Co
  • Merz Pharmaceuticals
  • Mindset Pharmaceuticals
  • Mitsubishi Tanabe Pharmaceutical
  • NasVax
  • Neurimmune Therapeutics
  • NeuroGenetic Pharmaceuticals
  • Noscira
  • Novartis
  • Octapharma
  • Pfizer
  • Prana Biotechnology
  • Proteotech
  • QR Pharma
  • Roche (Genentech)
  • Samaritan Pharmaceuticals
  • Sanofi-Aventis
  • Senexis
  • Siena Biotech
  • Takeda Pharmaceutical Co.
  • TauRx Pharmaceuticals
  • Transition Therapeutics
  • TransTech Pharma
  • United Biomedical
  • Virionics
  • Vitae Pharmaceuticals
  • Xytis
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