The end-organ resistance to androgens has been designated as Androgen Insensitivity Syndrome (AIS), an X-linked disorder caused by mutations in the Androgen Receptor (AR) gene. It is generally accepted that defects in the AR gene prevent the normal development of both internal and external genital structures in 46,XY individuals, causing a variety of phenotypes ranging from male infertility to completely normal female external genitalia. Precise diagnosis requires clinical, hormonal and molecular investigation and is of great importance for appropriate gender assignment and management in general. The complexity of phenotypic presentation of AIS with genotype-phenotype variability of identical mutations complicates both the diagnostic procedure and genetic counseling of the affected families. More than 400 different AR gene mutations have thus far been reported but the receptor structure-function relationship and its phenotypic outcome is not yet fully understood. This review focuses on the clinical features and molecular pathophysiology of AIS and explores the relationship of the molecular defects in the AR gene to their clinical expression.

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The novel triphenyl adduct of 2‐[(2,6‐dimethylphenyl)amino]benzoic acid (HDMPA; 1), i.e., [SnPh3(DMPA)] (2), the dimeric tetraorganostannoxane [Ph2(DMPA)SnOSn(DMPA)Ph2]2 (3), and the monomeric adduct [SnPh2(DMPA)2] (4), where DMPA is monodeprotonated HDMPA, have been prepared and structurally characterized by means of IR, 1H‐NMR, and 13C‐NMR spectroscopy. The structures of 1 and 2 have been determined by X‐ray crystallography. Single‐crystal X‐ray‐diffraction analysis of 1 revealed that there are two molecules in the asymmetric unit, HD1 and HD2, differing in conformation, both forming centrosymmetric dimers linked by H‐bonds between the carboxylic O‐atoms. X‐Ray analysis of 2 revealed a pentacoordinate structure containing Ph3Sn coordinated to the carboxylato group. Significant CH/π interactions and intramolecular H‐bonds stabilize the structures of 1 and 2, which self‐assembled via CH/π and π/π‐stacking interactions. The Ph3Sn adduct 2 was found to be a promising antimycobacterial lead compound, displaying activity against Mycobacterium tuberculosis H37Rv. The cytotoxiciy in the Vero cell line is also reported.

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The synthesis and spectral characterisation of novel organotin complexes [SnMe2(lorn)] (1) and [SnBu2(lorn)] (2) of the potent and widely used anti‐inflammatory drug lornoxicam, H2lorn, are reported. Crystal structure determinations of complexes1 and 2 showed that the ligand is doubly deprotonated at the oxygen and amide nitrogen atoms and is coordinated to the SnR2 fragment via four‐ and six‐membered chelate rings. The monomers of 1 are linked through intermolecular hydrogen bonds of C−H‐‐O type and through C−H−π intermolecular interactions. There are two similar molecules in the asymmetric unit of 2. The dimers of 2 are arranged in polymers with a stacking of alternate parallel chains and are linked through intermolecular hydrogen bonds of C−H‐‐O type, and through C−H−π intermolecular interactions. An extended network of Sn−O−Sn, C−H‐‐O and C−H‐‐π contacts lead to aggregation and a supramolecular assembly. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)

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