推荐产品
化驗
≥98.0% (TLC)
形狀
powder
脂質類型
sphingolipids
儲存溫度
−20°C
SMILES 字串
OC[C@@](N)([H])[C@]([H])(O)/C=C/CCCCCCCCCCCCC
InChI
1S/C18H37NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-18(21)17(19)16-20/h14-15,17-18,20-21H,2-13,16,19H2,1H3/b15-14+/t17-,18+/m0/s1
InChI 密鑰
WWUZIQQURGPMPG-KRWOKUGFSA-N
正在寻找类似产品? 访问 产品对比指南
生化／生理作用
细胞膜的一种组成部分。神经酰胺的前体。蛋白激酶 C 的选择性抑制剂，但不抑制蛋白激酶 A 或肌球蛋白轻链激酶。钙调蛋白依赖性酶的抑制剂。
包裝
无底玻璃瓶。内含物在插入的融合锥体内。
危險聲明
防範說明
危險分類
Aquatic Chronic 4
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
Meret E Ricklin et al.
Neurology, 81(2), 174-181 (2013-05-24)
To study the immune response against varicella-zoster virus (VZV) in patients with multiple sclerosis before and during fingolimod therapy. The VZV-specific immune response was studied using interferon (IFN)-γ enzyme-linked immunosorbent spot assay, proliferation assays, and upregulation of T-cell activation markers
Tim Ting Chiu et al.
The Journal of biological chemistry, 288(24), 17520-17531 (2013-05-04)
Insulin activates a cascade of signaling molecules, including Rac-1, Akt, and AS160, to promote the net gain of glucose transporter 4 (GLUT4) at the plasma membrane of muscle cells. Interestingly, constitutively active Rac-1 expression results in a hormone-independent increase in
David Henault et al.
Neurology, 81(20), 1768-1772 (2013-10-18)
To determine the range of fluctuation in total lymphocyte counts (TLCs) in peripheral blood over a 4- to 7-year period in patients with MS receiving fingolimod (FTY720) and the relation between TLCs and T-cell subsets (CD4+, CD8+, CCR7+/-) that are
Vilija G Jokubaitis et al.
Neurology, 82(14), 1204-1211 (2014-03-13)
To determine early risk of relapse after switch from natalizumab to fingolimod; to compare the switch experience to that in patients switching from interferon-β/glatiramer acetate (IFN-β/GA) and those previously treatment naive; and to determine predictors of time to first relapse
Paolo Neviani et al.
The Journal of clinical investigation, 123(10), 4144-4157 (2013-09-04)
The success of tyrosine kinase inhibitors (TKIs) in treating chronic myeloid leukemia (CML) depends on the requirement for BCR-ABL1 kinase activity in CML progenitors. However, CML quiescent HSCs are TKI resistant and represent a BCR-ABL1 kinase-independent disease reservoir. Here we
我们的科学家团队拥有各种研究领域经验，包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系技术服务部门