발생일자 |
2025.06.27 |
사건번호 |
1:25-cv-00800 |
법원국가 |
UNITED STATES OF AMERICA |
관할법원명 |
D.C.Delaware(지방법원) |
침해권리 |
특허 |
원고명 |
Novartis Pharmaceuticals Corporation / Novartis AG
(
스위스 /
외국기업
)
|
피고명 |
Eugia Pharma Specialities Ltd / Eugia US LLC / Aurobindo Pharma Ltd / Aurobindo Pharma USA Inc
(
인도 /
외국기업
)
|
소송유형 |
침해금지 |
분쟁내용 |
[Novartis Pharmaceuticals Corporation et al v. Eugia Pharma Specialities Ltd et al] 사건번호 1:25-cv-00800에 따르면 원고 Novartis Pharmaceuticals Corporation / Novartis AG은(는) 피고 Eugia Pharma Specialities Ltd / Eugia US LLC / Aurobindo Pharma Ltd / Aurobindo Pharma USA Inc을(를) 상대로 특허 US8163904|US8293756|US8389537|US8415363|US8501760|US9061029을(를) 침해했다는 이유로 미국 델라웨어 지방법원에 소를 제기하였다. |
분쟁경과 |
진행중
|
산업분류 |
화학∙바이오
> 유기화학기술
|
계쟁제품 |
[generic versions of Novartis's TasignaⓇ capsules, 50 mg, 150 mg, and 200 mg]
|
분류정보 |
C07D 40114, A61K 31506, A61P 3500|A61K 31506|A61K 31506, A61P 3500, C07D 40114|A01N 4354, A61K 31505, C07D 23902|A61K 31506|A61K 31506, C07D 23969, A61K 900
|
국내패밀리 정보 |
국내출원번호 : KR101755137B1, KR20080027855A, KR20140047737A, KR20150100946A| KR101598747B1, KR20090076931A, KR20140121903A| KR101755137B1, KR20080027855A, KR20140047737A, KR20150100946A| KR101651288B1, KR20080027853A, KR20130077915A, KR20130085444A| KR101598747B1, KR20090076931A, KR20140121903A| KR101743315B1, KR20120102635A
|
지재권번호/명칭 |
US8163904
|
원문 :
Salts of 4-methyl-N-[3-(4-methyl-imidazol-1-yl)-5-trifluoromethyl-phenyl]-3-(4-pyridin-3-yl-pyrimidin-2-ylamino)-Benzamide
|
|
US8293756
|
원문 :
Pharmaceutical compositions comprising nilotinib hydrochloride monohydrate
|
|
US8389537
|
원문 :
Salts of 4-methyl N-[3-(4-methyl-imidazol-1-yl)-5-trifluoromethyl-phenyl]-3-(4-pyridin-3-yl-pyrimidin-2-ylamino)-benzamide
|
|
US8415363
|
원문 :
Crystalline forms of 4-methyl-N-[3-(4-methyl-imidazol-1-yl)-5-trifluoromethyl-phenyl]-3-(4-pyridin-3-yl-pyrimidin-2-ylamino)-benzamide
|
|
US8501760
|
원문 :
Pharmaceutical compositions comprising nilotinib or its salt
|
|
US9061029
|
원문 :
Method of treating proliferative disorders and other pathological conditions mediated by Bcr-Abl, c-Kit, DDR1, DDR2 or PDGF-R kinase activity
|