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Merck
CN

V001981

2-Butanone

puriss., ACS reagent, reag. Ph. Eur., 99.5%

Synonym(s):

Ethyl methyl ketone, MEK, Methyl ethyl ketone

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About This Item

Linear Formula:
C2H5COCH3
CAS Number:
78-93-3
Molecular Weight:
72.11
EC Number:
201-159-0
PubChem Substance ID:
329828321
MDL number:
MFCD00011648
Beilstein/REAXYS Number:
741880

Key Documents

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InChI

1S/C4H8O/c1-3-4(2)5/h3H2,1-2H3

InChI key

ZWEHNKRNPOVVGH-UHFFFAOYSA-N

SMILES string

CC(CC)=O

grade

ACS reagent, puriss.

agency

reag. Ph. Eur.

vapor density

2.49 (vs air)

vapor pressure

71 mmHg ( 20 °C)

assay

99.5%

autoignition temp.

960 °F

expl. lim.

10.1 %

refractive index

n20/D 1.379 (lit.)

bp

80 °C (lit.)

mp

−87 °C (lit.)

density

0.805 g/mL at 25 °C (lit.)

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pictograms

FlameExclamation mark
GHS02,GHS07

signalword

Danger

Hazard Classifications

Eye Irrit. 2 - Flam. Liq. 2 - STOT SE 3

target_organs

Central nervous system

supp_hazards

EUH066

Storage Class

3 - Flammable liquids

wgk

WGK 1

flash_point_f

30.2 °F - closed cup

flash_point_c

-1 °C - closed cup

Regulatory Information

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Jeong-Hwan Yoon et al.
Nature communications, 6, 7600-7600 (2015-07-22)
Transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) are the pivotal cytokines to induce IL-17-producing CD4(+) T helper cells (TH17); yet their signalling network remains largely unknown. Here we show that the highly homologous TGF-β receptor-regulated Smads (R-Smads): Smad2 and Smad3
Federico Mele et al.
Nature communications, 6, 6431-6431 (2015-03-17)
T helper (TH) cell polarization during priming is modulated by a number of signals, but whether polarization to a given phenotype also influences recall responses of memory TH cells is relatively unknown. Here we show that miR-181a is selectively induced
Sherille D Bradley et al.
Cancer immunology research, 3(6), 602-609 (2015-03-22)
Oncogene activation in tumor cells induces broad and complex cellular changes that contribute significantly to disease initiation and progression. In melanoma, oncogenic BRAF(V600E) has been shown to drive the transcription of a specific gene signature that can promote multiple mechanisms
L Schafranek et al.
Leukemia, 29(1), 76-85 (2014-05-13)
Kinase inhibitors block proliferative signals in BCR-ABL1+ leukemic cells, but their capacity to induce apoptosis is poorly understood. Initial studies suggested that very brief exposure to kinase inhibitors was sufficient to induce apoptosis in chronic myeloid leukemia (CML) cells. However
Brinda Alagesan et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 21(2), 396-404 (2014-10-29)
Improved therapeutic approaches are needed for the treatment of pancreatic ductal adenocarcinoma (PDAC). As dual MEK and PI3K inhibition is presently being used in clinical trials for patients with PDAC, we sought to test the efficacy of combined targeting of
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