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Cancer Vaccines: From First-in-Class to Best-in-Class?
Date:4/9/2013

rgets 154
6.2.32 Receptor Signaling Protein Tyrosine Phosphatase Activity Targets 155
6.2.33 RNA-directed DNA Polymerase Activity Targets 156
6.2.34 Serine-type Peptidase Activity Targets 158
6.2.35 T Cell Receptor Activity Targets 161
6.2.36 Transcription Factor Activity Targets 164
6.2.37 Transcription Regulator Activity Targets 169
6.2.38 Translation Regulator Activity Targets 170
6.2.39 Transmembrane Receptor Activity Targets 171
6.2.40 Transmembrane Receptor Protein Tyrosine Kinase Activity Targets 173
6.2.41 Transporter Activity Targets 186
6.2.42 Other Targets 191
6.3 Mutation Profiles of Cancer Vaccine Drug Targets 201
6.3.1 Targets of Cancer Vaccine Drugs Present in the Cancer Gene Census and in the Catalogue of Somatic Mutations in Cancer 201
6.4 Target-Target Interactions among Identified Targets of Cancer Vaccine Drugs 205
6.5 Protein Expression Levels of Identified Targets of Cancer Vaccine Drugs 208
6.6 The Drug-Target Competitive Landscape 210
6.7 Pathway Assessment of Cancer Vaccine Drugs 214
6.7.1 Tools for Analysis of Cancer Pathways 215
6.7.2 Pathway Assessment 216
7 First-in-Class and Me-too Analysis of Cancer Vaccine Drugs 246
7.1 First-in-Class and Me-too in Marketed Drugs 249
7.2 First-in-Class and Me-too in Phase III Clinical Development 250
7.3 First-in-Class and Me-too in Phase II Clinical Development 252
7.4 First-in-Class and Me-too in Phase I Clinical Development 255
7.5 First-in-Class and Me-too in Preclinical Development 258
7.6 Drug Target Strategies of Suspended or Terminated Cancer Vaccine Drugs 261
8 Is First-in-Class the Best-in-Class? 263
8.1.1 Marketed 266
8.1.2 Phase III 269
8.1.3 Phase II 293
8.1.4 Phase I 325
8.1.5 Preclinical 339
8.1.6 Suspended 358
8.1.7 Ceased 359
9 Compound Strategies at Work: Competitive Benchmarking of Cancer Vaccine Drugs by Compound Strategy 387
9.1 Small Mole
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SOURCE Reportlinker
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