等级
pharmaceutical primary standard
API类
cytarabine
制造商/商品名称
EDQM
应用
pharmaceutical (small molecule)
格式
neat
储存温度
2-8°C
SMILES字符串
NC1=NC(=O)N(C=C1)[C@@H]2O[C@H](CO)[C@@H](O)[C@@H]2O
InChI
1S/C9H13N3O5/c10-5-1-2-12(9(16)11-5)8-7(15)6(14)4(3-13)17-8/h1-2,4,6-8,13-15H,3H2,(H2,10,11,16)/t4-,6-,7+,8-/m1/s1
InChI key
UHDGCWIWMRVCDJ-CCXZUQQUSA-N
基因信息
human ... POLA1(5422) , POLA2(23649) , POLD1(5424) , POLD2(5425) , POLD3(10714) , POLD4(57804) , POLE(5426) , POLE2(5427) , POLE3(54107) , PRIM1(5557) , PRIM2(5558)
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Warning
危险声明
危险分类
Repr. 2 - Skin Sens. 1
WGK
WGK 3
Erinn S Gideons et al.
Proceedings of the National Academy of Sciences of the United States of America, 111(23), 8649-8654 (2014-06-10)
Ketamine is an NMDA receptor (NMDAR) antagonist that elicits rapid antidepressant responses in patients with treatment-resistant depression. However, ketamine can also produce psychotomimetic effects that limit its utility as an antidepressant, raising the question of whether the clinically tolerated NMDAR
M R Sapienza et al.
Leukemia, 28(8), 1606-1616 (2014-02-08)
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare disease of controversial origin recently recognized as a neoplasm deriving from plasmacytoid dendritic cells (pDCs). Nevertheless, it remains an orphan tumor with obscure biology and dismal prognosis. To better understand the
H Yang et al.
Leukemia, 28(6), 1280-1288 (2013-11-26)
Blockade of immune checkpoints is emerging as a new form of anticancer therapy. We studied the expression of programmed death ligand 1 (PD-L1), PD-L2, programmed death 1 (PD-1) and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) mRNA in CD34+ cells from
Fazila Asmar et al.
Oncotarget, 5(7), 1912-1925 (2014-04-12)
MiR34A, B and C have been implicated in lymphomagenesis, but information on their role in normal CD19+ B-cells (PBL-B) and de novo diffuse large B-cell lymphoma (DLBCL) is limited. We show that in normal and activated B-cells miR34A-5p plays a
Robert J Vanner et al.
Cancer cell, 26(1), 33-47 (2014-06-24)
Functional heterogeneity within tumors presents a significant therapeutic challenge. Here we show that quiescent, therapy-resistant Sox2(+) cells propagate sonic hedgehog subgroup medulloblastoma by a mechanism that mirrors a neurogenic program. Rare Sox2(+) cells produce rapidly cycling doublecortin(+) progenitors that, together
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