Publications by authors named "Ksenya M Tabakmakher"

Monanchocidin A (MonA) is a novel marine alkaloid with promising anti-cancer properties. We recently demonstrated its high efficacy in human urogenital cancers including germ cell tumors. Here, we applied a global proteome screening approach to investigate molecular targets and biological processes affected by MonA in the human cisplatin-resistant germ cell cancer cell line NCCIT-R.

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New pentacyclic guanidine alkaloids, normonanchocidins A, B and D (1-3) along with the earlier known monanchocidin A were isolated from the Far-Eastern marine sponge Monanchora pulchra. Structures of 1-3 were elucidated using ID- and 2D-NMR spectroscopic and mass spectrometric data. Compound 1 and a mixture of 2 and 3 (1:1) exhibited cytotoxic activities against human leukemia THP-1 cells with IC50 values of 2.

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Urupocidins A and B (1 and 2), bisguanidine alkaloids with an unprecedented skeleton system, derived from polyketide precursors and containing an unusual N-alkyl-N-hydroxyguanidine moiety, have been isolated from the sponge Monanhora pulchra. The structures of 1 and 2, including absolute configuration, were established using the detailed analysis of 1D and 2D NMR, CD, and mass spectra as well as chemical transformations. Compound 1 increases nitric oxide production in murine macrophages via inducing iNOS expression.

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A new pentacyclic guanidine alkaloid, monanchomycalin C (1), along with the earlier known ptilomycalin A (2), were isolated from the Far-Eastern marine sponge Monanchora pulchra. The structure of 1 was elucidated using 1D and 2D NMR spectroscopic and ma ss spectrometric da ta. Compounds 1 and 2 exhibited cytotoxic activities against human breast cancer MDA-MB-231 cells with IC50 values of 8.

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New marine natural products, pulchranins B and C (2 and 3), were isolated from the marine sponge Monanchora pulchra and their structures were established using NMR and MS analysis. Compounds 2 and 3 were moderately active as inhibitors of TRPV1 (EC50 value of 95 and 183 microM, respectively) and less potent against TRPV3 and TRPA1 receptors.

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