公开(公告)号：EP3286164A1

公开(公告)日：2018-02-28

申请号：EP16783866

申请日：2016-04-21

申请人： GTX INC ,  UNIV OF TENNESSEE RESEARCH FOUNDATION

发明人： NARAYANAN RAMESH ,  MILLER DUANE D ,  PONNUSAMY THAMARAI ,  HWANG DONG-JIN ,  HE YALI ,  PAGADALA JAYAPRAKASH ,  DUKE CHARLES B ,  COSS CHRISTOPHER C ,  DALTON JAMES T

IPC分类号： C07C271/02 ,  A61K31/325 ,  A61K45/06

CPC分类号： A61K31/404 ,  A61K9/0014 ,  A61K31/403 ,  A61K31/405 ,  A61K31/416 ,  A61K31/4184 ,  A61K31/437 ,  A61K31/47 ,  A61K31/472 ,  A61K45/06 ,  C07C271/02 ,  C07D209/08 ,  C07D209/42 ,  C07D215/18 ,  C07D217/04 ,  C07D231/56 ,  C07D235/16 ,  C07D487/04

摘要： This invention provides novel indole, indazole, benzimidazole, indoline, quinolone, isoquinoline, and carbazole selective androgen receptor degrader (SARD) compounds, pharmaceutical compositions and uses thereof in treating prostate cancer, advanced prostate cancer, castration resistant prostate cancer, androgenic alopecia or other hyper androgenic dermal diseases, Kennedy's disease, amyotrophic lateral sclerosis (ALS), and uterine fibroids, and to methods for reducing the levels of androgen receptor-full length (AR-FL) including pathogenic and/or resistance mutations, AR-splice variants (AR-SV), and pathogenic polyglutamine (polyQ) polymorphisms of AR in a subject.

公开(公告)号：EP3285757A1

公开(公告)日：2018-02-28

申请号：EP16783846

申请日：2016-04-21

申请人： GTX INC ,  UNIV OF TENNESSEE RESEARCH FOUNDATION

发明人： NARAYANAN RAMESH ,  MILLER DUANE D ,  PONNUSAMY THAMARAI ,  HWANG DONG-JIN ,  DUKE CHARLES B ,  COSS CHRISTOPHER C ,  JONES AMANDA ,  DALTON JAMES T

IPC分类号： A61K31/277 ,  A61P35/00 ,  C07C13/47

CPC分类号： C07C255/58 ,  A61K9/0014 ,  A61K31/277 ,  C07B2200/07 ,  C07C255/60

摘要： This invention provides novel 3-amino propanamide selective androgen receptor degrader (SARD) compounds, pharmaceutical compositions and uses thereof in treating prostate cancer, advanced prostate cancer, castration resistant prostate cancer, androgenic alopecia or other hyperandrogenic dermal diseases, Kennedy's disease, amyotrophic lateral sclerosis (ALS), and uterine fibroids, and to methods for reducing the levels of androgen receptor-full length (AR-FL) including pathogenic or resistance mutations, AR-splice variants (AR-SV), and pathogenic polyglutamine (polyQ) polymorphisms of AR in a subject.