Aluminum complexes with new non-symmetric ferrocenyl amidine ligands and their application in CO2 transformation into cyclic carbonates.

A set of alkyl aluminum complexes supported by non-symmetric ferrocenyl amidine ligands were used as catalysts for the preparation of cyclic carbonates from epoxides and carbon dioxide using Bu4NI as a co-catalyst. A modified method for the synthesis of aminoferrocene allowed us to obtain this precursor in quantitative yield. Treatment of aminoferrocene with the corresponding acetimidoyl chloride afforded the desired ferrocenyl amidine ligands L1H, (E)-N-(2,6-diisopropylphenyl)-N'-(ferrocenyl)acetimidamide, and L2H, (E)-N-(2,6-dimethylphenyl)-N'-(ferrocenyl)acetimidamide. The reaction of these ligands with 1.0 or 0.5 equiv. of AlMe3 led to the synthesis of aminoferrocene based aluminum complexes ((L1)AlMe2 (1), (L2)AlMe2 (2), (L1)2AlMe (3), and (L2)2AlMe (4)) in excellent yields, which were characterized by spectroscopic and X-ray diffraction methods. In addition, we have studied their electrochemical properties and complex 1 was found to be the most active catalyst for the formation of cyclic carbonates 6a-j from their corresponding epoxides 5a-j and CO2.

Synthesis of 4(3H)quinazolinimines with selective cytotoxic effect on human acute promyelocytic leukemia cells.

We synthesized a new family of six 4(3H)quinazolinimines based on the reaction between (E)-N-(2-cyanophenyl)benzimidoyl chloride and substituted anilines reaching the formation of their corresponding C2, N3-substituted quinazoliniminium chlorides. This method provides novel, direct and flexible access to diverse substituted 4(3H)quinazolinimines. New compounds obtained following the proposed synthesis were fully characterized and, including the thirteen 4(3H)quinazolinimines synthesized by this method and previously reported by us, were used to study its cytotoxic effect on neoplastic cell lines. The mechanism involved in cell toxicity was also studied. Results showed that these compounds were highly cytotoxic, in particular on Human Promyelocytic Leukemia cells (HL60) and Chronic Myelogenous Leukemia cells (K562) when compared with conventional antineoplastic drugs such as etoposide and cisplatin. The mechanism associated to cytotoxic effect was mainly apoptosis, which not was decreased by antioxidant addition, thereby suggesting that the compounds exert apoptotic death through a mechanism unrelated with oxidative stress.

Synthesis of 4(3H)quinazolinimines by reaction of (E)-N-(aryl)-acetimidoyl or -benzimidoyl chloride with amines.

An efficient one-step method to access 4(3H)quinazolinimines by reaction of phenylchloroimines with 2-aminobenzonitrile is described. The reaction of (E)-N-(2-cyanophenyl)benzimidoyl chloride with substituted anilines that yields a number of their corresponding C2, N3-substituted quinazoliniminium chlorides or neutral products is also reported. These methods provide direct and flexible access to diverse substituted iminoquinazolines substituted at the C2, N3-positions. All the new compounds were fully characterized and six examples are given with their single-crystal X-ray structure.