Two series of 22 and 15 atom cyclic enkephalins incorporating a diversely substituted guanidine bridge have been prepared to assess the potential effect of the bridge substitutions on their opioid activity profile. The most notable results were obtained with the shortest cyclic analogues, which showed a significant variation of their binding affinity toward μ and δ opioid receptors in relation to bridge substitution. NMR studies were performed to rationalize these data. Some small analogues were found to exist as at least one major and one minor stable forms, which could be separated by chromatography. In particular, the compounds 13 and 14 with a cyclic substituent were separated in three isomers and the basis of this multiplicity was explored by 2D NMR spectroscopy. All compounds were agonists with slight selectivity for the μ opioid receptor. Compounds 7a (thiourea bridge) and 10a (N-Me-guanidine bridge) showed nanomolar affinity toward μ receptor, the latter being the more selective for this receptor (40-fold).

The systems formed by palladium acetate [Pd(OAc)2] and hybrid silica materials prepared by sol‐gel from monosilylated imidazolium and disilylated dihydroimidazolium salts show catalytic activity in Suzuki–Miyaura cross‐couplings with challenging aryl bromides and chlorides. They are very efficient as recoverable catalysts with aryl bromides. Recycling is also possible with aryl chlorides, although with lower conversions. In situ formation of palladium nanoparticles has been observed in recycling experiments.

More than 160 arginine analogues modified on the C‐terminus via either an amide bond or a heterocyclic moiety (1,2,4‐oxadiazole, 1,3,4‐oxadiazole and 1,2,4‐triazole) were prepared as potential inhibitors of NO synthases (NOS). A methodology involving formation of a thiocitrulline intermediate linked through its side‐chain on a solid support followed by modification of its carboxylate group was developed. Finally, the side‐chain thiourea group was either let unchanged, S‐alkylated (Me, Et) or guanidinylated (Me, Et) to yield respectively after TFA treatment the corresponding thiocitrulline, S‐Me/Et‐isothiocitrulline and N‐Me/Et‐arginine substrate analogues. They all were tested against three recombinant NOS isoforms. Several compounds containing a S‐Et‐ or a S‐Me‐Itc moiety and mainly belonging to both the dipeptide‐like and 1,2,4‐oxadiazole series were shown to inhibit nNOS and iNOS with IC50 in the 1–50 μM range. Spectral studies confirmed that these new compounds interacted at the heme active site. The more active compounds were found to inhibit intra‐cellular iNOS expressed in RAW264.7 and INS‐1 cells with similar efficiency than the reference compounds L‐NIL and SEIT.