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1018331-52-6

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1018331-52-6 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 1018331-52-6 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,0,1,8,3,3 and 1 respectively; the second part has 2 digits, 5 and 2 respectively.
Calculate Digit Verification of CAS Registry Number 1018331-52:
(9*1)+(8*0)+(7*1)+(6*8)+(5*3)+(4*3)+(3*1)+(2*5)+(1*2)=106
106 % 10 = 6
So 1018331-52-6 is a valid CAS Registry Number.

1018331-52-6Relevant articles and documents

Synthesis and unexpected oxidization of the tricyclic core of ugibohlin, isophakellin, and styloguanidine

Chang, Chia-Wei,Wu, Chi-Cheng,Chang, Yung-Yu,Lin, Chia-Chi,Chien, Tun-Cheng

, p. 10459 - 10468 (2013)

A series of 4-substituted 5,6,7,9-tetrahydropyrrolo[2,3-f]indolizin-9-ones, representing the tricyclic core skeleton of ugibohlin, isophakellin, and styloguanidine, were synthesized via an intramolecular Vilsmeier-Haack reaction. This reaction allows the chemoselective C-C bond formation between the pyrrole C3 and proline C5 of N-[(pyrrol-2-yl)carbonyl]prolinamides to construct the B-ring without the protection of the pyrrole nitrogen. Unexpected oxidizative property of the tricyclic core skeleton was observed, which could illuminate understanding of the biological formation of these marine secondary metabolites.

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Yamada et al.

, p. 381 (1973)

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Targeting the Src Homology 2 (SH2) Domain of Signal Transducer and Activator of Transcription 6 (STAT6) with Cell-Permeable, Phosphatase-Stable Phosphopeptide Mimics Potently Inhibits Tyr641 Phosphorylation and Transcriptional Activity

Mandal, Pijus K.,Morlacchi, Pietro,Knight, J. Morgan,Link, Todd M.,Lee, Gilbert R.,Nurieva, Roza,Singh, Divyendu,Dhanik, Ankur,Kavraki, Lydia,Corry, David B.,Ladbury, John E.,McMurray, John S.

, p. 8970 - 8984 (2015/12/09)

Signal transducer and activator of transcription 6 (STAT6) transmits signals from cytokines IL-4 and IL-13 and is activated in allergic airway disease. We are developing phosphopeptide mimetics targeting the SH2 domain of STAT6 to block recruitment to phosphotyrosine residues on IL-4 or IL-13 receptors and subsequent Tyr641 phosphorylation to inhibit the expression of genes contributing to asthma. Structure-affinity relationship studies showed that phosphopeptides based on Tyr631 from IL-4Rα bind with weak affinity to STAT6, whereas replacing the pY+3 residue with simple aryl and alkyl amides resulted in affinities in the mid to low nM range. A set of phosphatase-stable, cell-permeable prodrug analogues inhibited cytokine-stimulated STAT6 phosphorylation in both Beas-2B human airway cells and primary mouse T-lymphocytes at concentrations as low as 100 nM. IL-13-stimulated expression of CCL26 (eotaxin-3) was inhibited in a dose-dependent manner, demonstrating that targeting the SH2 domain blocks both phosphorylation and transcriptional activity of STAT6.

Aminocarbonyloxymethyl ester prodrugs of flufenamic acid and diclofenac: Suppressing the rearrangement pathway in aqueous media

Ribeiro, Lina,Silva, Nuno,Iley, Jim,Rautio, Jarkko,Jaervinen, Tomi,Mota-Filipe, Helder,Moreira, Rui,Mendes, Eduarda

, p. 32 - 40 (2007/10/03)

Aminocarbonyloxymethyl ester prodrugs are known to undergo rearrangement in aqueous solutions to form the corresponding N-acylamine side product via an O → N intramolecular acyl transfer from the carbamate conjugate base. Novel aminocarbonyloxymethyl esters of diclofenac and flufenamic acid containing amino acid amide carriers were synthesized and evaluated as potential prodrugs displaying less ability to undergo rearrangement. These compounds were prepared in reasonable yield by a four-step synthetic method that uses the appropriate N-Boc-protected amino acid N-hydroxysuccinimide ester and secondary amine and chloromethyl chloroformate as key reactants. Their reactivity in pH 7.4 buffer and 80% human plasma at 37°C was assessed by RP-HPLC. The aminocarbonyloxymethyl esters containing a secondary carbamate group derived from amino acids such as glycine or phenylalanine were hydrolyzed quantitatively to the parent drug both in non-enzymatic and enzymatic conditions, with no rearrangement product being detected. The oral bioavailability in rats was determined for selected diclofenac derivatives. These derivatives displayed a bioavailability of 25 to 68% relative to that of diclofenac, probably due to their poor aqueous solubility and lipophilicity. These results suggest that further optimization of aminocarbonyloxymethyl esters as potential prodrugs for non-steroidal anti-inflammatory drugs require the use of amino acid carriers with ionizable groups to improve aqueous solubility.

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