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279246-01-4

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279246-01-4 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 279246-01-4 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 2,7,9,2,4 and 6 respectively; the second part has 2 digits, 0 and 1 respectively.
Calculate Digit Verification of CAS Registry Number 279246-01:
(8*2)+(7*7)+(6*9)+(5*2)+(4*4)+(3*6)+(2*0)+(1*1)=164
164 % 10 = 4
So 279246-01-4 is a valid CAS Registry Number.

279246-01-4Relevant academic research and scientific papers

Titanium(IV) chloride-mediated carbocyclization of 1,6-Enynes: Selective synthesis of 3-Azabicyclo[3.1.0]hexanes and functionalized allenes by controlling the reaction temperature

Zhang, Zhen,Shi, Min

, p. 2610 - 2614 (2011)

1,6-Enynes can be transformed into 3-azabicyclo[3.1.0]hexanes and functionalized allenes in moderate to good yields along with moderate to high diastereoselectivities by controlling the reaction temperature in the presence of titanium(IV) chloride. A plausible mechanism is proposed. 1,6-Enynes can be transformed into 3-azabicyclo[3.1.0]hexanes and functionalized allenes respectively in moderate to goodyields along with moderate to high diastereoselectivities by controlling the reaction temperature in the presence of titanium(IV) chloride. A plausible mechanism is proposed.

Discovery of Sulfonamide-Derived Agonists of SOS1-Mediated Nucleotide Exchange on RAS Using Fragment-Based Methods

Sarkar, Dhruba,Olejniczak, Edward T.,Phan, Jason,Coker, Jesse A.,Sai, Jiqing,Arnold, Allison,Beesetty, Yugandhar,Waterson, Alex G.,Fesik, Stephen W.

, p. 8325 - 8337 (2020/09/21)

The nucleotide exchange factor Son of Sevenless (SOS) catalyzes the activation of RAS by converting it from its inactive GDP-bound state to its active GTP-bound state. Recently, we have reported the discovery of small-molecule allosteric activators of SOS1 that can increase the amount of RAS-GTP in cells. The compounds can inhibit ERK phosphorylation at higher concentrations by engaging a feedback mechanism. To further study this process, we sought different chemical matter from an NMR-based fragment screen using selective methyl labeling. To aid this process, several Ile methyl groups located in different binding sites of the protein were assigned and used to categorize the NMR hits into different classes. Hit to lead optimization using an iterative structure-based design paradigm resulted in compounds with improvements in binding affinity. These improved molecules of a different chemical class increase SOS1cat-mediated nucleotide exchange on RAS and display cellular action consistent with our prior results.

Potent arylsulfonamide inhibitors of tumor necrosis factor-α converting enzyme able to reduce activated leukocyte cell adhesion molecule shedding in cancer cell models

Nuti, Elisa,Casalini, Francesca,Avramova, Stanislava I.,Santamaria, Salvatore,Fabbi, Marina,Ferrini, Silvano,Marinelli, Luciana,La Pietra, Valeria,Limongelli, Vittorio,Novellino, Ettore,Cercignani, Giovanni,Orlandini, Elisabetta,Nencetti, Susanna,Rossello, Armando

experimental part, p. 2622 - 2635 (2010/08/20)

Activated leukocyte cell adhesion molecule (ALCAM) plays a relevant role in tumor biology and progression. Our previous studies showed that ALCAM is expressed at the surface of epithelial ovarian cancer (EOC) cells and is released in a soluble form by ADAM-17-mediated shedding. This process is relevant to EOC cell motility and invasiveness, which is reduced by nonspecific inhibitors of ADAM-17. For this reason, ADAM-17 may represent a new useful target in anticancer therapy. Herein, we report the synthesis and biological evaluation of new ADAM-17 inhibitors containing an arylsulfonamidic scaffold. Among the new potential inhibitors, two very promising compounds 17 and 18 were discovered, with a nanomolar activity for ADAM-17 isolated enzyme. These compounds proved to be also the most potent in inhibiting soluble ALCAM release in cancer cells, showing a nanomolar activity on A2774 and SKOV3 cell lines

Discovery of a potent CDK2 inhibitor with a novel binding mode, using virtual screening and initial, structure-guided lead scoping

Richardson, Christine M.,Nunns, Claire L.,Williamson, Douglas S.,Parratt, Martin J.,Dokurno, Pawel,Howes, Rob,Borgognoni, Jenifer,Drysdale, Martin J.,Finch, Harry,Hubbard, Roderick E.,Jackson, Philip S.,Kierstan, Peter,Lentzen, Georg,Moore, Jonathan D.,Murray, James B.,Simmonite, Heather,Surgenor, Allan E.,Torrance, Christopher J.

, p. 3880 - 3885 (2008/02/08)

Virtual screening against a pCDK2/cyclin A crystal structure led to the identification of a potent and novel CDK2 inhibitor, which exhibited an unusual mode of interaction with the kinase binding motif. With the aid of X-ray crystallography and modelling,

NMR-based modification of matrix metalloproteinase inhibitors with improved bioavailability

Hajduk, Philip J.,Shuker, Suzanne B.,Nettesheim, David G.,Craig, Richard,Augeri, David J.,Betebenner, David,Albert, Daniel H.,Guo, Yan,Meadows, Robert P.,Xu, Lianhong,Michaelides, Michael,Davidsen, Steven K.,Fesik, Stephen W.

, p. 5628 - 5639 (2007/10/03)

The NMR-based discovery of biaryl hydroxamate inhibitors of the matrix metalloproteinase stromelysin (MMP-3) has been previously described (Hajduk et al. J. Am. Chem. Soc. 1997, 119, 5818-5827). While potent in vitro, these inhibitors exhibited no in vivo activity due, at least in part, to the poor pharmacokinetic properties of the alkylhydroxamate moiety. To circumvent this liability, NMR-based screening was implemented to identify alternative zinc-chelating groups. Using this technique, 1-naphthyl hydroxamate was found to bind tightly to the protein (KD = 50 μM) and was identified as a candidate for incorporation into the lead series. On the basis of NMR-derived structural information, the naphthyl hydroxamate and biaryl fragments were linked together to yield inhibitors of this enzyme that exhibited improved bioavailability. These studies demonstrate that the NMR-based screening of fragments can be effectively applied to improve the physicochemical or pharmacokinetic profile of lead compounds.

Inhibitors of matrix metalloproteinases

-

, (2008/06/13)

Compounds having the formula and pharmaceutically acceptable salts and prodrugs thereof are matrix metalloproteinase inhibitors. Also disclosed are matrix metalloproteinase-inhibiting compositions and methods of inhibiting matrix metalloproteinase in a ma

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