CPG-52364 is a potent antagonist of toll-like receptors TLR7, TLR8, TLR9. The drug was developed by Coley Pharmaceutical Group (later acquired by Pfizer) for the treatment of immune diseases and reached phase I of clinical trials presumably for systemic lupus erythematosus. However, the development of CPG-52364 was terminated by unknown reason.

MX-100 (also known as PL-100) is a benzenesulfonamide derivative patented by Pharmacor Inc as HIV aspartyl protease inhibitor. MX-100 retained excellent antiviral activity against almost all of these protease inhibitor-resistant viruses and that its performance in this regard was superior to those of atazanavir, amprenavir, indinavir, lopinavir, nelfinavir, and saquinavir. In almost every case, the increase in the EC50 for MX-100 observed with viruses containing multiple mutations in protease was far less than that obtained with the other drugs. Preclinical studies showed that MX-100 possessed suboptimal solubility and pharmacokinetic, (PK) properties, possibly hindering further development. MX-100 successfully completed preclinical and clinical development (phase I in healthy volunteers) and have been licensed to Merck in 2006

PF-04634817 is a small molecule chemokine CCR2 and CCR5 receptor dual antagonist. Treatment with PF-04634817 was associated with a modest improvement in best-corrected visual acuity, which was inferior to intravitreal ranibizumab. Analysis of the primary endpoint, Urine Albumin-to-Creatinine Ratio, indicated a modest effect of PF-04634817 in reducing albuminuria in subjects with type 2 diabetes who received angiotensin receptor blocker therapy after 12 weeks of treatment. Despite the tolerable safety profile shown by PF-04634817, clinical development was discontinued in light of the modest efficacy observed.

PBT-1033, also known as PBT-2, is a neural protective agent potentially for the treatment of Alzheimer's disease and Huntington's Disease. PBT-1033 is a moderate-affinity 8-hydroxyquinoline transition metal-ligand that acts as a synthetic chaperone, re distributing copper, zinc, and iron from locations where they are abundant to subcellular locations where they might be deficient. Delivery of copper and zinc by PBT-1033 into the cytoplasm deactivates the kinase glycogen synthase kinase 3β and the phosphatase calcineurin, both potential targets for Huntington’s disease. In aged wild-type mice, PBT-1033 improves cognitive ability and markers of neuronal plasticity and function. In Alzheimer’s disease mouse models, PBT-1033 inhibits the accumulation of amyloid β, attenuates neuropathological effects of amyloid β, including amyloid-β-induced hyperphosphorylation of tau, and improves cognition. In a 12-week, phase 2a, randomized, double-blind, placebo-controlled trial in 78 individuals with mild Alzheimer’s dementia, PBT-1033 was safe and well tolerated and significantly reduced concentrations of amyloid β42 in CSF.