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Merck
CN

224235

Sigma-Aldrich

N,N′-六亚甲基双乙酰胺

98%

别名:

N,N′-二乙酰基-1,6-己二胺, HMBA

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About This Item

线性分子式:
CH3CONH(CH2)6NHCOCH3
CAS号:
分子量:
200.28
MDL编号:
UNSPSC代码:
12352100
PubChem化学物质编号:
NACRES:
NA.22

方案

98%

mp

128-129 °C (lit.)

溶解性

water: soluble 5%, clear, colorless

官能团

amide

SMILES字符串

CC(=O)NCCCCCCNC(C)=O

InChI

1S/C10H20N2O2/c1-9(13)11-7-5-3-4-6-8-12-10(2)14/h3-8H2,1-2H3,(H,11,13)(H,12,14)

InChI key

BNQSTAOJRULKNX-UHFFFAOYSA-N

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应用

N,N′-Hexamethylene bis(acetamide) was used as an inducing agent in obtaining mononuclear cells from the peripheral blood (PB) sample by Ficoll-Hypaque gradient separation.

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Maria Chatzopoulou et al.
European journal of medicinal chemistry, 50, 75-80 (2012-02-22)
Based on previous studies on bis-acetamides that act as hybrid polar compounds to induce leukemia cell differentiation, an attempt was made to bioisosterically replace the amide moiety with the lipophilic non-classical bioisostere tetrazole. A pyrrole group was also included in
Xuguang Zhu et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 23(2), 430-440 (2016-07-22)
New therapeutic approaches are needed for patients with thyroid cancer refractory to radioiodine treatment. An inhibitor of bromodomain and extraterminal domain (BET) proteins, JQ1, shows potent antitumor effects in hematological cancers and solid tumors. To evaluate whether JQ1 is effective
J P Brody et al.
Cancer, 75(10), 2474-2483 (1995-05-15)
A 63-year-old male presented with fever, a subcutaneous nodule, gingival hypertrophy, lacrimal gland enlargement, and no lymphadenopathy or hepatosplenomegaly, but had anemia, thrombocytopenia, and peripheral blood (PB) plus bone marrow (BM) involvement by leukemic cells. There was minimal response to
Richard L Thompson et al.
PLoS pathogens, 5(3), e1000352-e1000352 (2009-03-28)
The mechanism controlling the exit from herpes simplex virus latency (HSV) is of central importance to recurrent disease and transmission of infection, yet interactions between host and viral functions that govern this process remain unclear. The cascade of HSV gene
Wali Hafezi et al.
PLoS pathogens, 8(5), e1002679-e1002679 (2012-05-17)
Following productive, lytic infection in epithelia, herpes simplex virus type 1 (HSV-1) establishes a lifelong latent infection in sensory neurons that is interrupted by episodes of reactivation. In order to better understand what triggers this lytic/latent decision in neurons, we

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