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SummaryThe synthesis of [MX 3 (CO) 3 ] 2 -(M = ,88 Re, Re, "Tc) directly from the corresponding permetallates is described. Intermediates and byproducts have been isolated and characterized. Preliminary direct labeling studies at r.t. revealed a slow but irreversible incorporation of "[ 188 Re(CO) 3 ] + " into intact antibodies. The best yield was 40% after 20 h with 0.8 mg/ml of intact antibody. To elucidate possible coordination sites in proteins, the synthesis and formation of model complexes has been investigated by means of Ή NMR spectroscopy and X-ray structure analysis. A high tendency for imidazole (im) coordination has been found and is examplified in the model complexes [ReBr(histamine)-(CO) 3 ] and [Re 2^-OH) 2 (im) 2 (CO) 6 ], which structures will be presented. Additionally, complexation with the macrocyclic thioether ligand [20-aneS6] was studied in order to establish a postlabeling protocol with this type of chelator. The structure of {Tc(CO) 3 } 2 ]2+ will be presented.

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Methods have been developed for the preparation of terminal p-idophenyl-substituted alpha- and beta-methyl-branched long-chain fatty acids. The syntheses and physical properties of 14-(p-iodophenyl)-2(RS)-methyltetradecanoic acid and 15-p-iodophenyl)-3(RS)-methylpentadecanoic acid are described. The radioiodinated agents are of interest as a result of the expected pronounced uptake and prolonged myocardial retention that may result from the inhibition of fatty acid metabolism. Tissue distribution studies in rats with 14-(p-[125I]iodophenyl)-2(RS)-methyltetradecanoic acid and 15-(p-[125I]iodophenyl)-3(RS)-methylpentadecanoic acid show significant heart uptake and prolonged retention accompanied by low in vivo deiodination and high blood levels. A comparison of the heart uptake of the radioiodinated methyl-branched fatty acids and their unbranched analogues has demonstrated a greater myocardial retention of the methyl-branched fatty acids than the unbranched analogues. These results suggest that the mechanism of myocardial retention results from steric or chemical inhibition of the metabolism of these fatty acids by the presence of the methyl group.

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