The novel seven coordinate complex [(n Bu)2Sn(C10H8N2O3)(C2H5OH)]2 (C10H8N2O32- is the dinegative ion of 2 oxo propionic acid benzoyl hydrazone) was synthesized by the reaction of (n Bu)2SnO with 2 oxo propionic acid ...The novel seven coordinate complex [(n Bu)2Sn(C10H8N2O3)(C2H5OH)]2 (C10H8N2O32- is the dinegative ion of 2 oxo propionic acid benzoyl hydrazone) was synthesized by the reaction of (n Bu)2SnO with 2 oxo propionic acid benzoyl hydrazone in 1∶ 1 molar ratio in benzene ethanol (V/V, 3/1), and its structure was characterized by X ray single crystal diffraction. The crystal belongs to a tetragonal system with space group I41/a, a=2.4890(2)nm, b=2.4890(2)nm, c=1.5170(3)nm, V=9.398(2)nm3, Z=8, F(000)=3968, Dc=1.366g· cm- 3, and the structure was refined to final R1=0.0530, wR2=0.0971. The structure of the title complex is described as a dimer through weak interactions of Sn… O bonding and hydrogen bond. The tin atoms rendered seven coordination in a distorted pentagonal bipyramid geometry structure, four oxygen atoms [O1, O2, O2# 1 and O4] and one nitrogen atom N2 formed the equatorial plane and C11 Sn1 C15 is the axis. CCDC: 212696.展开更多
Gemcitabine is a pyrimidine nucleoside analog that becomes triphosphorylated intracellularly where it competitively inhibits cytidine incorporation into DNA strands. Another mechanism-of-action of gemcitabine (diphosp...Gemcitabine is a pyrimidine nucleoside analog that becomes triphosphorylated intracellularly where it competitively inhibits cytidine incorporation into DNA strands. Another mechanism-of-action of gemcitabine (diphosphorylated form) involves irreversible inhibition of the enzyme ribonucleotide reductase thereby preventing deoxyribonucleotide synthesis. Functioning as a potent chemotherapeutic gemcitabine promote decreases in neoplastic cell proliferation and apoptosis which is frequently found to be effective for the treatment of several leukemias and a wide spectrum of carcinomas. A brief plasma half-life in part due to rapid deamination and chemotherapeutic-resistance restricts the utility of gemcitabine in clinical oncology. Selective “targeted” delivery of gemcitabine represents a potential molecular strategy for simultaneously prolonging its plasma half-life and minimizing innocient tissues and organ systems exposure to chemotherapy. The molecular design and an organic chemistry based synthesis reaction is described that initially generates a UV-photoactivated gemcitabine intermediate. In a subsequent phase of the synthesis method the UV-photoactivated gemcitabine intermediate is covalently bonded to a monoclonal immunoglobulin yielding an end-product in the form of gemcitabine-(C4-amide)-[anti-HER2/neu]. Analysis by SDS-PAGE/chemiluminescent auto-radiography did not detect evidence of gemcitabine-(C4-amide)-[anti-HER2/neu] polymerization or degradative fragmentation while cell-ELISA demonstrated retained binding-avidity for HER2/neu trophic membrane receptor complexes highly over-expressed by chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3). Compared to chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3), the covalent immunochemotherapeutic, gemcitabine-(C4-amide)-[anti-HER2/neu] is anticipated to exert greater levels of cytotoxic anti-neoplastic potency against other neoplastic cell types like pancreatic carcinoma, small-cell lung carcinoma, neuroblastoma, glioblastoma, oral squamous cell carcinoma, cervical epitheliod carcinoma, or leukemia/lymphoid neoplastic cell types based on their reported sensitivity to gemcitabine and gemcitabine covalent conjugates.展开更多
To synthesize and study the relation between structure and characteristics of Co-Cbond of coenzym B<sub>12</sub> model compounds, it is an effective way to understand the fac-tors which can influence the s...To synthesize and study the relation between structure and characteristics of Co-Cbond of coenzym B<sub>12</sub> model compounds, it is an effective way to understand the fac-tors which can influence the stabilities of Co-C bond and the mechanism of mutasecatalyzed substrate rearrangement. Unfortunately knowledge about micro reaction mecha-nism of the model compounds is limited. W. N. Lipscomb calculated the展开更多
文摘The novel seven coordinate complex [(n Bu)2Sn(C10H8N2O3)(C2H5OH)]2 (C10H8N2O32- is the dinegative ion of 2 oxo propionic acid benzoyl hydrazone) was synthesized by the reaction of (n Bu)2SnO with 2 oxo propionic acid benzoyl hydrazone in 1∶ 1 molar ratio in benzene ethanol (V/V, 3/1), and its structure was characterized by X ray single crystal diffraction. The crystal belongs to a tetragonal system with space group I41/a, a=2.4890(2)nm, b=2.4890(2)nm, c=1.5170(3)nm, V=9.398(2)nm3, Z=8, F(000)=3968, Dc=1.366g· cm- 3, and the structure was refined to final R1=0.0530, wR2=0.0971. The structure of the title complex is described as a dimer through weak interactions of Sn… O bonding and hydrogen bond. The tin atoms rendered seven coordination in a distorted pentagonal bipyramid geometry structure, four oxygen atoms [O1, O2, O2# 1 and O4] and one nitrogen atom N2 formed the equatorial plane and C11 Sn1 C15 is the axis. CCDC: 212696.
文摘Gemcitabine is a pyrimidine nucleoside analog that becomes triphosphorylated intracellularly where it competitively inhibits cytidine incorporation into DNA strands. Another mechanism-of-action of gemcitabine (diphosphorylated form) involves irreversible inhibition of the enzyme ribonucleotide reductase thereby preventing deoxyribonucleotide synthesis. Functioning as a potent chemotherapeutic gemcitabine promote decreases in neoplastic cell proliferation and apoptosis which is frequently found to be effective for the treatment of several leukemias and a wide spectrum of carcinomas. A brief plasma half-life in part due to rapid deamination and chemotherapeutic-resistance restricts the utility of gemcitabine in clinical oncology. Selective “targeted” delivery of gemcitabine represents a potential molecular strategy for simultaneously prolonging its plasma half-life and minimizing innocient tissues and organ systems exposure to chemotherapy. The molecular design and an organic chemistry based synthesis reaction is described that initially generates a UV-photoactivated gemcitabine intermediate. In a subsequent phase of the synthesis method the UV-photoactivated gemcitabine intermediate is covalently bonded to a monoclonal immunoglobulin yielding an end-product in the form of gemcitabine-(C4-amide)-[anti-HER2/neu]. Analysis by SDS-PAGE/chemiluminescent auto-radiography did not detect evidence of gemcitabine-(C4-amide)-[anti-HER2/neu] polymerization or degradative fragmentation while cell-ELISA demonstrated retained binding-avidity for HER2/neu trophic membrane receptor complexes highly over-expressed by chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3). Compared to chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3), the covalent immunochemotherapeutic, gemcitabine-(C4-amide)-[anti-HER2/neu] is anticipated to exert greater levels of cytotoxic anti-neoplastic potency against other neoplastic cell types like pancreatic carcinoma, small-cell lung carcinoma, neuroblastoma, glioblastoma, oral squamous cell carcinoma, cervical epitheliod carcinoma, or leukemia/lymphoid neoplastic cell types based on their reported sensitivity to gemcitabine and gemcitabine covalent conjugates.
基金Project supported by the National Natural Science Foundation of China.
文摘To synthesize and study the relation between structure and characteristics of Co-Cbond of coenzym B<sub>12</sub> model compounds, it is an effective way to understand the fac-tors which can influence the stabilities of Co-C bond and the mechanism of mutasecatalyzed substrate rearrangement. Unfortunately knowledge about micro reaction mecha-nism of the model compounds is limited. W. N. Lipscomb calculated the
