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This dissertation describes development of inhibitors targeting two enzymes regarding bacterial RNA polymerase (RNAP) and steroid 11β-hydroxylase (CYP11B1) for wound healing. During our quest for novel bacterial RNAP inhibitors as infective agents, two studies have been launched and involved in artifacts. In one study, compound I-1was identified as a hit compound. Later, an impurity with a structure of polymeric carboxylic acids originating from I-1 was discovered and proven to be responsible for the biological activity. The polymer acted as a negatively charged ligand interacting very efficiently with the protein surface of E. coli RNAP via electrostatic interaction and blocking the DNA channel. In the other study, we focused on CBR703, which was reported to inhibit bacterial RNAP and biofilm formation, considering it to be a good candidate for further optimization. While synthesized derivatives of CBR703 did not result in more active RNAP inhibitors, we observed promising antibacterial activities. These again correlated with a significant cytotoxicity towards mammalian cells. Furthermore, the promising effects on biofilm formation were uncovered to be artifacts. Topical application of CYP11B1 inhibitors to reduce cutaneous cortisol is a novel strategy to promote chronic wound healing. To satisfy this application, inhibitors were developed to possess specific metabolic profile: stable in wound fluid and unstable in liver. The potent inhibitor III-34 (IC50 = 5 nM) was very stable in plasma (t1/2 >> 150 min), which is similar to wound fluid in composition, whereas it was fast metabolized in human liver S9 fraction (t1/2 = 16 min) to avoid impairing adrenal steroidogenesis. It also showed no mutagenic effects and was selective CYP17 and CYP19. Therefore it is a promising candidate for further in vivo evaluation.