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Carbonic acid, (1-methyl-2-nitro-1H-imidazol-5-yl)methyl 4-nitrophenyl ester is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

246536-87-8

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246536-87-8 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 246536-87-8 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 2,4,6,5,3 and 6 respectively; the second part has 2 digits, 8 and 7 respectively.
Calculate Digit Verification of CAS Registry Number 246536-87:
(8*2)+(7*4)+(6*6)+(5*5)+(4*3)+(3*6)+(2*8)+(1*7)=158
158 % 10 = 8
So 246536-87-8 is a valid CAS Registry Number.

246536-87-8SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 11, 2017

Revision Date: Aug 11, 2017

1.Identification

1.1 GHS Product identifier

Product name (1-methyl-2-nitro-1H-imidazol-5-yl)methyl (4-nitrophenyl)carbonate

1.2 Other means of identification

Product number -
Other names (1-methyl-2-nitro-1H-imidazol-5-yl)methyl 4-nitrophenyl carbonate

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:246536-87-8 SDS

246536-87-8Relevant academic research and scientific papers

A 2-nitroimidazole carbamate prodrug of 5-amino-1(chloromethyl)-3- [(5,6,7-trimethoxyindol-2-yl)carbonyl]-1,2-dihydro-3H-benz[e]indole (amino- seco-CBI-TMI) for use with ADEPT and GDEPT

Hay, Michael P.,Sykes, Bridget M.,Denny, William A.,Wilson, William R.

, p. 2237 - 2242 (1999)

The synthesis of a 2-nitroimidazol-5-ylmethyl carbamate prodrug 10 of the potent minor groove alkylating agent amino-seco-CBI-TMI 3 is described. Chemical, radiolytic, and enzymic reductions of a model 2-nitroimidazol-5-yl carbamate 8 show release of the amine effector upon reduction. Prodrug 10 gives a ten fold increase in cytotoxicity against human ovarian carcinoma SKOV3 cells in the presence of E. coli B nitroreductase (NTR) and a 21-fold increase in cytotoxicity against a SKOV3 cell line (SC3.2) transfected with the gene for NTR. The cytotoxicity of 10 increased 15- to 40-fold under hypoxia. Prodrug 10 has significant potential as a prodrug for use in ADEPT and GDEPT applications, and as a hypoxia-selective cytotoxin.

Hypoxia-Activated Prodrugs of PERK Inhibitors

Liew, Lydia P.,Singleton, Dean C.,Wong, Way W.,Cheng, Gary J.,Jamieson, Stephen M. F.,Hay, Michael P.

, p. 1238 - 1248 (2019/02/05)

Tumour hypoxia plays an important role in tumour progression and resistance to therapy. Under hypoxia unfolded proteins accumulate in the endoplasmic reticulum (ER) and this stress is relieved through the protein kinase R-like ER kinase (PERK) signalling

Targeting a Targeted Drug: An Approach Toward Hypoxia-Activatable Tyrosine Kinase Inhibitor Prodrugs

Karnthaler-Benbakka, Claudia,Groza, Diana,Koblmüller, Bettina,Terenzi, Alessio,Holste, Katharina,Haider, Melanie,Baier, Dina,Berger, Walter,Heffeter, Petra,Kowol, Christian R.,Keppler, Bernhard K.

, p. 2410 - 2421 (2016/11/13)

Tyrosine kinase inhibitors (TKIs), which have revolutionized cancer therapy over the past 15 years, are limited in their clinical application due to serious side effects. Therefore, we converted two approved TKIs (sunitinib and erlotinib) into 2-nitroimidazole-based hypoxia-activatable prodrugs. Kinetics studies showed very different stabilities over 24 h; however, fast reductive activation via E. coli nitroreductase could be confirmed for both panels. The anticancer activity and signaling inhibition of the compounds against various human cancer cell lines were evaluated in cell culture. These data, together with molecular docking simulations, revealed distinct differences in the impact of structural modifications on drug binding to the enzymes: whereas the catalytic pocket of the epidermal growth factor receptor (EGFR) accepted all new erlotinib derivatives, the vascular endothelial growth factor receptor (VEGFR)-inhibitory potential in the case of the sunitinib prodrugs was dramatically diminished by derivatization. In line, hypoxia dependency of ERK signaling inhibition was observed with the sunitinib prodrugs, while oxygen levels had no impact on the activity of the erlotinib derivatives. Overall, proof of principle could be shown for this concept, and the results obtained are an important basis for the future development of tyrosine kinase inhibitor prodrugs.

Synthesis and Evaluation of Nitroheterocyclic Carbamate Prodrugs for Use with Nitroreductase-Mediated Gene-Directed Enzyme Prodrug Therapy

Hay, Michael P.,Anderson, Robert F.,Ferry, Dianne M.,Wilson, William R.,Denny, William A.

, p. 5533 - 5545 (2007/10/03)

A variety of nitroheterocyclic carbamate prodrugs of phenylenediamine mustard and 5-amino-1-(chloromethyl)-3-[(5,6,7-trimethoxyindol-2-yl)carbonyl]-1, 2-dihydro-3H-benz[e]indoline (aminoseco-CBI-TMI), covering a wide range of reduction potential, were pre

Design, synthesis and evaluation of imidazolylmethyl carbamate prodrugs of alkylating agents

Hay, Michael P.,Wilson, William R.,Denny, William A.

, p. 645 - 657 (2007/10/03)

Two approaches to prodrugs of alkylating agents based on an imidazolylmethyl carbamate nucleus were explored. A 2-azido analogue (3) of the bis-carbamate carmethizole (1) displayed similar aerobic cytotoxicity to 1 in a panel of human and murine cell lines. Approaches to the 2-amino and 2- carbamoyl analogues are described. In the second approach an imidazolylmethanol was used as a 'trigger' linked via a carbamate to the alkylating agent N,N-bis(2-chlorethyl)amine (BCEA). Nitroimidazole and methylsulphinylimidazole carbamate prodrugs 6-8 were 5-20-fold less toxic than BCEA. Despite this deactivation in the prodrug form, little increase in cytotoxicity was observed under hypoxia. The data suggest that BCEA released on bioreduction is not sufficiently potent to contribute significant additional cytotoxicity. (C) 2000 Elsevier Science Ltd.

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