추천 제품
Quality Level
분석
≥98% (HPLC)
형태
powder
색상
white to beige
solubility
DMSO: 20 mg/mL, clear
저장 온도
2-8°C
SMILES string
O=C1NN=C(CC2=CC=C(F)C(C(N3CCC(OC)CC3)=O)=C2)C4=CC=CC=C41
InChI
1S/C22H22FN3O3/c1-29-15-8-10-26(11-9-15)22(28)18-12-14(6-7-19(18)23)13-20-16-4-2-3-5-17(16)21(27)25-24-20/h2-7,12,15H,8-11,13H2,1H3,(H,25,27)
InChI key
HYNBNUYQTQIHJK-UHFFFAOYSA-N
생화학적/생리학적 작용
AZD2461, an olaparib analog, is an orally available, potent and selective PARP1 and PARP2 inhibitor that is a poor substrate for drug transporters. AZD2461 exhibits a high efficacy in olaparib-resistant tumors that overexpress P-glycoprotein.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
이미 열람한 고객
Proceedings of the National Academy of Sciences of the United States of America, 112(27), 8409-8414 (2015-06-24)
Metaplastic breast carcinoma (MBC) is a rare histological breast cancer subtype characterized by mesenchymal elements and poor clinical outcome. A large fraction of MBCs harbor defects in breast cancer 1 (BRCA1). As BRCA1 deficiency sensitizes tumors to DNA cross-linking agents
Cancer research, 76(20), 6084-6094 (2016-08-24)
The PARP inhibitor AZD2461 was developed as a next-generation agent following olaparib, the first PARP inhibitor approved for cancer therapy. In BRCA1-deficient mouse models, olaparib resistance predominantly involves overexpression of P-glycoprotein, so AZD2461 was developed as a poor substrate for
Journal of cancer prevention, 19(2), 125-136 (2014-10-23)
Cells harboring BRCA1/BRCA2 mutations are hypersensitive to inhibition of poly(ADP-ribose) polymerase-1 (PARP-1). We recently showed that interference with PARP-1 activity by NU1025 is strongly cytotoxic for BRCA1-positive BT-20 cells but not BRCA1-deficient SKBr-3 cells. These unexpected observations prompted speculation that
eLife, 10 (2021-08-04)
Poly(ADP-ribose) polymerase (PARP) enzymes initiate (mt)DNA repair mechanisms and use nicotinamide adenine dinucleotide (NAD+) as energy source. Prolonged PARP activity can drain cellular NAD+ reserves, leading to de-regulation of important molecular processes. Here, we provide evidence of a pathophysiological mechanism
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