Furthermore, our analysis concluded to drugs (Table 2) that provide strong connection with IPF since they have been discovered by at least two out of three drug repurposing tools, with a given inhibiting score less than −0.5 against IPF. We then used our scoring formula in order to re-rank all the potential IPF inhibiting drugs, that passed the aforementioned rules, based on their inhibiting, functional, structural and side effect scores for each stage of the disease. Of all the resulting drugs and through bibliographic research regarding their connection to IPF we propose certain drugs as potential competitors against IPF. Niclosamide has been highly ranked by CoDReS for every stage of IPF, it is in the same structural cluster with other potential IPF inhibitors and has also been mentioned to reverse fibrosis on the skin and lungs of mice that had Systemic Sclerosis with pulmonary fibrosis. Due to its safety profile, niclosamide can be considered for use in clinical trials against IPF. Anisomycin and Puromycin, natural compounds that both derive from the Genus of streptomyces, seem to have potential against IPF; Anisomycin is known to inhibit the induction of ER stress and Puromycin targets inflammatory cells. Etoposide and Irinotecan are used for cancer treatment and IPF is known to have similar mechanisms with various types of cancer.
Most of the specific mechanisms (Cell communication, ecm receptor interaction, focal adhesion, cytokine-cytokine receptor interaction and colorectal cancer) that were found in all experiments, are related to fibrotic or pulmonary diseases or to other pathways that are related to IPF. This is a means to test the validity of our methods but at the same time it points out more pathways, potentially involved in IPF. As seen in Table 10, most of the aforementioned pathways are targeted by repurposed drugs from our study. This strengthens our claims for new potential repurposed drug inhibitors for IPF.
In the case of microRNAs, hsa-miR-25-3p and hsa-miR-208a-5p can inhibit genes that the FDA approved drug nintedanib targets. This finding provides an insight for a new microRNA-based treatment approach.
Finally, the action of the remaining mechanisms and drugs that were found from our analysis, may be further investigated, since they have been derived from significantly relevant genes related to IPF stages.
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