Apeptico is developing solnatide (AP301), a dry powder inhalation and an inhaled aerosol formulation of a synthetic peptide for the treatment of acute lung injury, acute respiratory distress syndrome and pulmonary oedema caused by lung infection or high altitude. The AP301 peptide mimics the lectin-like domain of TNF-α. The synthetic peptide AP301 is composed of 17 amino acids and contains an intramolecular disulfide bond between the N-terminal and the C-terminal cysteine. AP301 interacts with the endothelial sodium channel (ENaC) and activates pulmonary liquid clearance both in vitro and in animal studies. The specific interaction of AP301 with both endogenously and heterologously expressed ENaC requires precedent binding to glycosylated extracellular loop(s). Solnatide has been granted Orphan Drug Designation for “Treatment of Primary Graft Dysfunction following Lung Transplantation” and for “Treatment of Pseudohypoaldosteronism Type 1B” by the Food and Drug Administration.

Tiprelestat (Elafin) is a potent Human neutrophil elastase inhibitor. Elafin is identical to the human protein elafin with high specificity for tissue destroying and inflammation promoting proteases. The development program of Elafin is focused on the late stage development of Elafin in major surgery and early stage development in pulmonary arterial hypertension (PAH). Elafin has received orphan drug designations in the USA and the EU for esophageal cancer surgery (ECS) and PAH. Tiprelestat is in phase II clinical trials for the treatment of myocardial reperfusion injury, postoperative inflammation and in phase I clinical trial for the treatment of pulmonary arterial hypertension.

Disitertide (P144) is a TGF-β1 antagonist peptide. Disitertide prevents TGF-β1-dependent inhibition of MV1Lu proliferation in vitro and markedly reduces binding of TGF-β1 to its receptors. P144 blocked TGF-beta1-dependent stimulation of a reporter gene under the control of human alpha2(I) collagen promoter. Intraperitoneal administration of P144 also showed potent antifibrogenic activity in vivo in the liver of rats receiving CCl4. These rats also showed a significant decrease in the number of activated hepatic stellate cells as compared with those treated with saline only. P144 decreased proliferation, migration, invasiveness, and tumorigenicity in vitro, whereas apoptosis and anoikis were significantly increased for glioblastoma cell lines. SMAD2 phosphorylation was reduced, together with a downregulation of SKI and an upregulation of SMAD7 at both transcriptional and translational levels. Additionally, P144 was able to impair tumor growth and increase survival in an in vivo flank model. This findings suggest a potential effect of P144 in vitro and in vivo that is mediated by regulation of transcriptional target genes of the TGF-β pathway, suggesting a therapeutic potential of P144 for glioblastoma treatment. Topical application of disitertide may promote scar maturation and clinical improvement of hypertrophic scar morphology features in an "in vivo" model in nude mice after two weeks of treatment.