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270695

2-Butanon

Name: 2-Butanon
Brand: ALDRICH

HPLC grade, suitable for HPLC, ≥99.5%

Synonym(e):

Ethyl-methylketon, MEK, Methyl-ethylketon

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About This Item

Lineare Formel:

C₂H₅COCH₃

CAS-Nummer:

78-93-3

Molekulargewicht:

72.11

Beilstein:

741880

EG-Nummer:

201-159-0

MDL-Nummer:

MFCD00011648

UNSPSC-Code:

12190000

PubChem Substanz-ID:

329752964

Qualität

HPLC grade

Dampfdichte

2.49 (vs air)

Dampfdruck

71 mmHg ( 20 °C)

Assay

≥99.5%

Selbstzündungstemp.

960 °F

Aufgereinigt durch

glass distillation

Expl.-Gr.

10.1 %

Methode(n)

HPLC: suitable

Verunreinigungen

<0.050% water

Abdampfrückstand

<0.0005%

Brechungsindex

n20/D 1.379 (lit.)

bp

80 °C (lit.)
80 °C

mp (Schmelzpunkt)

−87 °C (lit.)

Dichte

0.805 g/mL at 25 °C (lit.)

λ

H₂O reference

UV-Absorption

λ: 330 nm A_max: 1.00
λ: 340 nm A_max: 0.10
λ: 350-400 nm A_max: 0.01

SMILES String

CC(CC)=O

InChI

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

InChIKey

ZWEHNKRNPOVVGH-UHFFFAOYSA-N

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Piktogramme

GHS02,GHS07

Signalwort

Danger

H-Sätze

H225,H319,H336

P-Sätze

P210 - P233 - P240 - P241 - P242 - P305 + P351 + P338

Gefahreneinstufungen

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

Zielorgane

Central nervous system

Zusätzliche Gefahrenhinweise

EUH066

Lagerklassenschlüssel

3 - Flammable liquids

WGK

WGK 1

Flammpunkt (°F)

30.2 °F - closed cup

Flammpunkt (°C)

-1 °C - closed cup

Persönliche Schutzausrüstung

Eyeshields, Faceshields, Gloves, type ABEK (EN14387) respirator filter

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Metabolites of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in smokers' urine.

S G Carmella et al.

Cancer research, 53(4), 721-724 (1993-02-15)

Metabolites of the tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, a potent pulmonary carcinogen, have been quantified in the urine of 11 smokers. They were not detected in nonsmokers' urine. The metabolites, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronide, were detected in quantities of 0.23-1.0 and 0.57-6.5

The effect of solvent extraction on the lipids of the stratum corneum in relation to observed immediate whitening of the skin.

L B Goldsmith et al.

Contact dermatitis, 19(5), 348-350 (1988-11-01)

Irritant contact dermatitis along with an increased transepidermal water loss can result from exposing the skin to solvents. A study of the interaction of various solvents with human stratum corneum was made using thin-layer chromatography. Comparison of 10 solvents (trichloroethylene

BRAFV600E Co-opts a Conserved MHC Class I Internalization Pathway to Diminish Antigen Presentation and CD8+ T-cell Recognition of Melanoma.

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

Phosphorylation status determines the opposing functions of Smad2/Smad3 as STAT3 cofactors in TH17 differentiation.

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

Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia.

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

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