Methyl 3-carbazolecarboxylate - CAS 97931-41-4
Catalog number: 97931-41-4
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C14H11NO2
Molecular Weight:
225.2
COA:
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Description:
Methyl 3-carbazolecarboxylate isolated from the herbs of Micromelum sp.
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Purity:
> 95%
Appearance:
Yellow powder
Synonyms:
Methyl 9H-carbazole-3-carboxylate
MSDS:
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Quality Standard:
Enterprise Standard
Quantity:
Milligrams-Grams
Chemical Family:
Alkaloids
1.Structural Modifications to Quaternary Ammonium Polymer Coagulants to Inhibit N-Nitrosamine Formation.
Zeng T1,2,3, Li RJ4, Mitch WA2,3. Environ Sci Technol. 2016 Apr 20. [Epub ahead of print]
Quaternary ammonium cationic polymers, such as poly(diallyldimethylammonium chloride) (polyDADMAC) and epichlorohydrin-dimethylamine (Epi-DMA), are commonly used by water utilities to enhance removal of particles and dissolved organic matter (DOM) from raw waters. Unfortunately, chloramination of waters treated with quaternary ammonium polymers leads to the formation of carcinogenic N-nitrosodimethylamine (NDMA). In this study, two approaches were developed to modify polyDADMAC and Epi-DMA to inhibit N-nitrosamine formation. The first approach involved treatment of polymers with methyl iodide (MeI), an alkylating agent, to convert polymer-bound tertiary amine groups to less chloramine-reactive quaternary ammonium groups. The second approach involved synthesis of polymers bearing less chloramine-reactive quaternary ammonium groups with dipropylamino (DPA) substituents. Treatment with MeI reduced NDMA formation from polymers by ∼75%, while synthesis of DPA-based polymers eliminated NDMA formation and formed N-nitrosodipropylamine, which is 10-fold less carcinogenic than NDMA, at 20-fold lower yields.
2.Synthesis, antiproliferative and multidrug resistance reversal activities of heterocyclic α,β-unsaturated carbonyl compounds.
Sun JF1, Hou GG1, Zhao F1, Cong W1, Li HJ1, Liu WS1, Wang C1. Chem Biol Drug Des. 2016 Apr 20. doi: 10.1111/cbdd.12777. [Epub ahead of print]
A series of heterocyclic α,β-unsaturated carbonyl compounds (1a-1d, 2a-2d, 3a-3d, 4a-3d and 5a-5d) with 1,5-diaryl-3-oxo-1,4-pentadienyl pharmacophore were synthesized for the development of anticancer and multidrug resistance reverting agents. The antiproliferative activities were tested against nine human cancer cell lines. Approximately 73% of the IC50 values were below 5 μM, while 35% of these figures were submicromolar, and compounds 3a-3d with 4-trifluoro methyl in the arylidene benzene rings were the most potent, since their IC50 values are between 0.06-3.09 μM against all cancer cell lines employed. Meanwhile, their MDR reversal properties and cellular uptake were further examined. The data displayed that all of these compounds could reverse MDR, particularly, compounds 3a and 4a demonstrated both potent MDR reverting properties and strong antiproliferative activities, which can be taken as leading molecules for further research of dual effect agents in tumor chemotherapy.
3.The dose makes the poison: from glutamate-mediated neurogenesis to neuronal atrophy and depression.
Rubio-Casillas A, Fernández-Guasti A. Rev Neurosci. 2016 Apr 20. pii: /j/revneuro.ahead-of-print/revneuro-2015-0066/revneuro-2015-0066.xml. doi: 10.1515/revneuro-2015-0066. [Epub ahead of print]
Experimental evidence has demonstrated that glutamate is an essential factor for neurogenesis, whereas another line of research postulates that excessive glutamatergic neurotransmission is associated with the pathogenesis of depression. The present review shows that such paradox can be explained within the framework of hormesis, defined as biphasic dose responses. Low glutamate levels activate adaptive stress responses that include proteins that protect neurons against more severe stress. Conversely, abnormally high levels of glutamate, resulting from increased release and/or decreased removal, cause neuronal atrophy and depression. The dysregulation of the glutamatergic transmission in depression could be underlined by several factors including a decreased inhibition (γ-aminobutyric acid or serotonin) or an increased excitation (primarily within the glutamatergic system). Experimental evidence shows that the activation of N-methyl-D-aspartate receptor (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (AMPAR) can exert two opposite effects on neurogenesis and neuron survival depending on the synaptic or extrasynaptic concentration.
4.Discovery and Optimization of Potent, Selective, and in Vivo Efficacious 2-Aryl Benzimidazole BCATm Inhibitors.
Deng H1, Zhou J1, Sundersingh F1, Messer JA1, Somers DO2, Ajakane M3, Arico-Muendel CC1, Beljean A2, Belyanskaya SL1, Bingham R2, Blazensky E4, Boullay AB3, Boursier E3, Chai J1, Carter P2, Chung CW2, Daugan A3, Ding Y1, Herry K3, Hobbs C2, Humphries E4, ACS Med Chem Lett. 2016 Feb 8;7(4):379-84. doi: 10.1021/acsmedchemlett.5b00389. eCollection 2016.
To identify BCATm inhibitors suitable for in vivo study, Encoded Library Technology (ELT) was used to affinity screen a 117 million member benzimidazole based DNA encoded library, which identified an inhibitor series with both biochemical and cellular activities. Subsequent SAR studies led to the discovery of a highly potent and selective compound, 1-(3-(5-bromothiophene-2-carboxamido)cyclohexyl)-N-methyl-2-(pyridin-2-yl)-1H-benzo[d]imidazole-5-carboxamide (8b) with much improved PK properties. X-ray structure revealed that 8b binds to the active site of BACTm in a unique mode via multiple H-bond and van der Waals interactions. After oral administration, 8b raised mouse blood levels of all three branched chain amino acids as a consequence of BCATm inhibition.
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CAS 97931-41-4 Methyl 3-carbazolecarboxylate

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