Sodium aceneuramate is a sodium salt of aceneuramic acid (sialic acid). It is an effective inhalant expectorant. Inhalation of sodium aceneuramate repaired inflammation in the airway, and caused bronchitic rabbits to produce sputa with a low viscosity, similar to normal air-way secretions. Sodium aceneuramate protected the mucociliary transport impaired bycigarette smoke in a dose-dependent manner. The results suggest that sodium aceneuramate may participate in the defense mechanism in the airway against irritant gases. Sodium aceneuramate inhibited bronchial anaphylaxis and the release of histamine into bronchoalveolar lavages. Sodium aceneuramate has an action which elevates the viscoelasticity of secretions in the respiratory tract.

Gestaclone was developed as a progesterone receptor agonist; however, this compound has never been marketed. Information about the current use of this compound is not available.

Exherin is a small, cyclic pentapeptide vascular-targeting agent with potential antineoplastic and antiangiogenic activities. ADH-1 selectively and competitively binds to and blocks N-cadherin, which may result in disruption of tumor vasculature, inhibition of tumor cell growth, and the induction of tumor cell and endothelial cell apoptosis. In murine melanoma xenografts, ADH-1 in combination with melphalan significantly reduced tumor growth up to 30-fold over melphalan alone. ADH-1 enhancement of response to melphalan was associated with increased formation of DNA adducts, increased apoptosis, and intracellular signaling changes. In a pilot study (phase I trial), ADH-1 intravenous pretreatment before chemotherapy in metastatic melanoma completely destroyed tumors in half of patients

Nolpitantium (SR-140333) is a highly selective nonpeptide antagonist of neurokinin-1 (NK1) receptor. Nolpitantium potently, selectively and competitively inhibited substance P binding to NK1 receptors from various animal species, including humans. In vitro, it was a potent antagonist in functional assays for NK1 receptors such as [Sar9, Met(O2)11]substance P-induced endothelium-dependent relaxation of rabbit pulmonary artery and contraction of guinea-pig ileum. Up to 1 mkM, Nolpitantium had no effect in bioassays for NK2 and NK3 receptors. The antagonism exerted by Nolpitantium toward NK1 receptors was apparently non-competitive, with pD2' values between 9.65 and 10.16 in the different assays. Nolpitantium also blocked in vitro [Sar9, Met(O2)11]substance P-induced release of acetylcholine from rat striatum. In vivo, Nolpitantium exerted highly potent antagonism toward [Sar9, Met(O2)11]substance P-induced hypotension in dogs, bronchoconstriction in guinea-pig) and plasma extravasation in rats. Nolpitantium was found to be effective in the modulation of the inflammatory response and airway remodeling in mice. Nolpitantium is reported to cause antagonism of the SP-induced relaxations of human isolated intralobar pulmonary arterial rings. Nolpitantium also blocked the activation of rat thalamic neurons after nociceptive stimulation. Nolpitantium has been shown to reduce the severity of inflammation in trinitrobenzene sulfonic acid-induced colitis in the rat colon. Nolpitantium inhibited mustard oil-induced plasma protein extravasations in the dorsal skin of the rat hind paw. Nolpitantium had been in some phase II clinical trials but further studies were discontinued.

PCI-27483 is a reversible small-molecule inhibitor of activated factor VII (factor VIIa) with potential antineoplastic and antithrombotic activities. FVII, a serine protease, becomes activated (FVIIa) upon binding with TF forming the FVIIa/TF complex, which induces intracellular signaling pathways by activating protease activated receptor 2 (PAR-2). Upon subcutaneous administration, factor VIIa inhibitor PCI-27483 selectively inhibits factor FVIIa in the VIIa/TF complex, which may prevent PAR-2 activation and PAR2-mediated signal transduction pathways, thereby inhibiting tumor cell proliferation, angiogenesis, and metastasis of TF-overexpressing tumor cells. A phase I study in healthy volunteers was conducted to assess the PD and PK profiles of PCI- 27483 following a single, SC injection. The halflife of PCI-27483 was 10-12 h. The International Normalized Ratio (INR) was strongly correlated with drug plasma concentration. PCI-27483 was well tolerated. This compound has being evaluated in a phase Ib/II trial in patients with pancreatic cancer receiving treatment with gemcitabine. However, no recent development has been reported. The compound was originally developed by Celera, then licensed to Pharmacyclics (acquired by Abbvie in 2015) later. In 2012, the product was licensed to Novo Nordisk by Pharmacyclics for disease outside of oncology.

DBPR-108 is a potent, selective, and orally bioavailable dipeptide-derived inhibitor of DPP4 with IC50 of 15 nM; no inhibition on DDP8 and DPP9, which is in phase I clinical trial as a potential treatment of type 2 diabetes.