Recilisib (also known as EX-RAD or ON-01210) is a radioprotectant, which means that this compound can protect cells from harmful effects of ionizing radiation. Unlike other radioprotectors, recilisib is not a free-radical scavenger or responsible for cell cycle arrest. Recilisib was suggested to have a different radiation protection mechanism involving DNA repair pathways. This compound has been studied as prophylactic (use prior to radiation exposure) and therapeutic (after exposure to radiation) drug. In studies with healthy volunteers, recilisib was rapidly absorbed and well-tolerated, with only mild adverse events. Phase I clinical trials have been completed.

Phencynonate (PHH) is a novel anticholinergic compound. It is structurally similar to scopolamine, possesses both muscarinic and nicotinic antagonistic properties as well as anti-NMDA properties. It has been developed as a safe and effective drug for the prevention of motion sickness in tablet form, it also demonstrates clear anticonvulsant effectiveness after soman poisoning in a rat model. S-isomer was more effective against motion sickness and had not anxiogenic action at therapeutic doses. S-isomer has the higher affinity and activity for mAChR in cerebral cortex and acted as a competitive mAChR antagonist. PHH was able to suppress chronic unpredictable mild stress (CUMS)-induced oxidative stress and enhance the antioxidant capacity and antioxidant proteins activity, such as superoxide dismutase 2 (SOD2) and peroxiredoxin 6 (Prdx6). PHH ameliorated CUMS-induced depressive phenotypes by up-regulating SIRT6 deacetylation activity. PHH-mediating SIRT6 pathway is required for antidepressant response and PHH can be used as a novel therapeutic to effectively treat depression. Phencynonate is in phase III clinical trials for the treatment of vertigo.

PG-116800 is a member of the hydroxyproline-based hydroxamic acid class of matrix metalloproteinase (MMP) inhibitors. PG-116800 did not modify matrix structure in osteoarthritic patients. Also, it had unexpected side effects on muscle and skeleton; it limited joint mobility, and caused arthralgia, hand oedema, palmar fibrosis, Dupuytren’s contracture and persistent tendon thickness or nodules. PG-116800 failed to reduce left ventricular remodeling or improve clinical outcomes after myocardial infarction.

OSI-027 is an orally bioavailable mammalian inhibitor of mTOR kinase and has antineoplastic activity. OSI-027 binds to and inhibits of the catalytic site of mTOR, which is a central part of two protein complexes, mTORC1 and mTORC2, which may result in tumor cell apoptosis and a decrease in tumor cell proliferation. OSI-027 is in phase I clinical trial for the investigation on patients with advanced solid tumors or lymphoma.

Resolvin E1 (RvE1 or RX-10001) is a trihydroxy eicosapentaenoic acid metabolite that has a role as an anti-inflammatory agent and a human xenobiotic metabolite. This compound binds to leukotriene B4 (BLT-1) on neutrophils and to ERV-1/ChemR23 on monocyte/macrophages. Resolvin E1 has been shown to reverse experimental periodontitis and dysbiosis in rats. Furthermore, in a murine model of Alzheimer’s disease, Resolvin E1 (in combination with lipoxin A4) decreased neuroinflammation. Resolvin E1 was also suggested as a potential therapeutic target for psoriasis. A phase I clinical trial to test drug safety in healthy volunteers has been completed in 2009.

Acorafloxacin (JNJ-Q2) is a fluoroquinolone that was developed by Furiex Pharmaceuticals (a subsidiary of Forest Laboratories) for the treatment of complicated skin and and soft tissue infections. Acorafloxacin was originally developed by Janssen, then licensed to Furiex Pharmaceuticals (now a part of Actavis). JNJ-Q2 has excellent in vitro and in vivo activity against a variety of Gram-positive and Gram-negative organisms. In vitro studies indicate that JNJ-Q2 has potent activity against pathogens responsible for acute bacterial skin and skin structure infections (ABSSSI) and community-acquired bacterial pneumonia (CABP), such as Staphylococcus aureus and Streptococcus pneumoniae. JNJ-Q2 also has been shown to have a higher barrier to resistance compared to other agents in the class and it remains highly active against drug-resistant organisms, including methicillin-resistant S. aureus, ciprofloxacin-resistant methicillin-resistant S. aureus, and drug-resistant S. pneumoniae. In two Phase II studies, the efficacy of JNJ-Q2 was comparable to linezolid for ABSSSI and moxifloxacin for CABP. Furthermore, JNJ-Q2 was well tolerated, with adverse event rates similar to or less than other fluoroquinolones. Acorafloxacin inhibits MuRF enzyme, required for cell wall synthesis. Acorafloxacin directly inhibits bacterial DNA synthesis by halting the activity of DNA gyrase (responsible for negative helical supercoiling) and DNA topoisomerase IV (responsible for separating the nucleotide strands). Fast track designation and qualified infectious disease product designation (QIDP) was granted by FDA for the treatment of bacterial infections in 2013.

Vidofludimus (SC12267; 4SC-101) is a novel oral immunomodulator inhibiting dihydroorotate dehydrogenase (DHODH) and the expression of proinflammatory cytokines including interleukin-17 (IL17A and IL17F) and interferon-gamma. This drug is in the clinical trial for the treatment of inflammatory bowel diseases and Rheumatoid arthritis.