等级
reagent grade
蒸汽密度
3.1 (vs air)
蒸汽压
<1 mmHg ( 20 °C)
产品线
Vetec™
检测方案
99%
形式
viscous liquid
自燃温度
698 °F
expl. lim.
2.6-11.3 % (lit.)
技术
electrophoresis: suitable
杂质
≤1.0% water
water
折射率
n20/D 1.474 (lit.)
pH值（酸碱度）
5 (20 °C, 100 g/L)
bp
182 °C/20 mmHg (lit.)
mp
20 °C (lit.)
密度
1.25 g/mL (lit.)
SMILES字符串
OCC(O)CO
InChI
1S/C3H8O3/c4-1-3(6)2-5/h3-6H,1-2H2
InChI key
PEDCQBHIVMGVHV-UHFFFAOYSA-N
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法律信息
Vetec is a trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 1
闪点(°F)
320.0 °F
闪点(°C)
160 °C
Shelley L Forrest et al.
The Journal of comparative neurology, 522(17), 3900-3927 (2014-07-22)
Artemin is a member of the glial cell line-derived neurotrophic factor (GDNF) family that has been strongly implicated in development and regeneration of autonomic nerves and modulation of nociception. Whereas other members of this family (GDNF and neurturin) primarily target
Nazish Ahmed et al.
Tissue engineering. Part A, 20(15-16), 2224-2233 (2014-03-13)
One of the factors preventing clinical application of regenerative medicine to degenerative cartilage diseases is a suitable source of cells. Chondrocytes, the only cell type of cartilage, grown in vitro under culture conditions to expand cell numbers lose their phenotype
T W Chew et al.
Oncogene, 33(21), 2717-2727 (2013-07-03)
RAS and Rho small GTPases are key molecular switches that control cell dynamics, cell growth and tissue development through their distinct signaling pathways. Although much has been learnt about their individual functions in both cell and animal models, the physiological
Benoît Ranchoux et al.
The American journal of pathology, 185(2), 356-371 (2014-12-17)
Pulmonary veno-occlusive disease (PVOD) is an uncommon form of pulmonary hypertension (PH) characterized by progressive obstruction of small pulmonary veins and a dismal prognosis. Limited case series have reported a possible association between different chemotherapeutic agents and PVOD. We evaluated
Daniel K C Chung et al.
Nature communications, 6, 7742-7742 (2015-07-25)
DNA double-strand breaks (DSBs) are often targeted to nuclear pore complexes (NPCs) for repair. How targeting is achieved and the DNA repair pathways involved in this process remain unclear. Here, we show that the kinesin-14 motor protein complex (Cik1-Kar3) cooperates
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