XG-102 (also known as brimapitide), a D-stereoisomer of a c-Jun-N-terminal kinase-1111 was developed in a biocompatible gel formulation for the treatment of sudden sensorineural hearing loss with a single-dose administration into the middle ear. It’s a cell-penetrating peptide which inhibits the JNK stress kinase. JNK is activated following various types of cochlear insults (stress) that cause acute inner ear hearing loss and plays a key role in apoptosis of sensory cells as well as in inflammatory responses. By blocking JNK, AM-111 protects stress-injured cochlear cells and helps to prevent or reduce chronic hearing loss. Auris Medical's otoprotective drug AM-111 has been granted orphan drug status by the U.S. Food and Drug Administration (FDA) for the treatment of acute sensorineural hearing loss (ASNHL), a condition which may occur following various inner ear injuries. In addition, XG-102 was studied in phase III clinical trials in the treatment of acute inner ear hearing loss and in the reduction of post-cataract surgery intraocular inflammation. Besides, XG-102 is advancing through pre-clinical development with programs in ocular inflammation, urology, nephrology and Alzheimer’s disease.

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.

Vorasidenib (also known as AG 881) was developed as an isocitrate dehydrogenase (IDH) type 1 in the cytoplasm and type 2 in the mitochondria, with potential antineoplastic activity. It is known that IDH is an essential enzyme for cellular respiration in the tricarboxylic acid (TCA) cycle. Isocitrate dehydrogenases 1 and 2 (IDH1/2) are homodimeric enzymes that catalyze the conversion of isocitrate to α-ketoglutarate (α-KG) in the tricarboxylic acid cycle. Vorasidenib participated in phase I clinical trials in patients with advanced hematologic malignancies and in gliomas.

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.

LX-7101 (Lexicon Pharmaceuticals) was advanced to Phase-I clinical trials for treatment open-angle glaucoma or ocular hypertension. This drug is a potent inhibitor of LIM-kinase 2 (LIMK2) kinase and inhibits to less extent LIMK1 and Rho-associated protein kinase 2 (ROCK2).

Squaric acid is a dibasic organic acid and useful intermediate in a variety of synthetic reactions involving the synthesis of photosensitive squarylium dyes and inhibitors of protein tyrosine phosphatases. Medically, squaric acid dibutyl ester or dibutyl squarate derives from a squaric acid is used for the treatment of warts.