Drogenation of 15 proceeded cleanly only with selenium dioxide in neutral, strictly anhydrous tert-butyl alcohol to give 12. Compound 13 was prepared by reaction of 17-acetyl-19-nortestosterone with iodine-potassium iodate followed by selenium dioxide dehydrogenation, alternatively from epoxidation of 16 to 17, chromium trioxide-pyridine oxidation and selenium dioxide dehydrogenation. Dehydrogenation of 17β-hydroxy-19-nor-5α-androstan-3-one gave 1-en-3-one, which with alkaline hydrogen peroxide gave 18 stereospecifically. Reduction of 1-en-3-one gave 19, which were epoxidized and oxidized to 18 stereoisomers. 14 was prepared from dehydrogenation of 18's more abundant isomer. These epoxyenones are stable, undergo aromatization under acidic conditions, suggesting they may be intermediates in catechol estrogen biosynthesis. Biological evaluation: compounds 12-14 were inactive on bacteriophage PM2 DNA; compound 13 (2 μM) was as active as 3-methylcholanthrene in transforming Balb/c 3T3 cells, more effective than estradiol by two orders of magnitude, 12 and 14 inactive. Considerable progress has been made in complement system research, its role in diseases like rheumatoid arthritis. Synthetic modulators are a treatment approach. Chlorazol Fast Pink B (I) was a promising inhibitor. Modified I to get IIb (polyanionic, no azo). Synthesis of IIb: 5-nitrobenzenedisulfonic acid → acid chloride → bis(p-tert-butylphenyl) ester → amine → condensed with 1,3,6-naphthalenetrisulfonyl chloride → IIa → deprotected to IIb. Biological: IIb was more active than I and suramin in complement inhibition, no tissue-staining. Synthesis of new 8-(arythio)-, 8-(alkylthio)-, NG-alkyl- and NG-dialkyl-8-substituted cAMP derivatives. Based on protein kinase activation, β-butyl-8-(benzylthio)-cAMP (26) was selected, which increased blood flow by 85% in vivo without increasing heart rate. Large-scale synthesis: N1-alkylation → Dimroth rearrangement → reduction → bromination → nucleophilic displacement with benzyl mercaptan. These derivatives are potent inotropic agents, may treat myocardial infarction.