PF-03463275 is the novel azabicyclic glycine transporter 1 (GlyT1) inhibitor. Ketamine induced hallucinatory-like behaviors that were not reversed by PF-3463275. In contrast, all doses of PF-3463275 alleviated the deficit in spatial working memory induced by ketamine. PF-03463275 causes changes in electroretinogram (ERG) responses in albino rats. There was dose-dependent reduction in the amplitude of the rat ERG oscillatory potentials (OPs) following single subcutaneous administrations of the PF-03463275. Furthermore, the amplitude of OPs was negatively correlated to the concentration of PF-03463275 in the vitreous humor collected from rats immediately following ERG recordings. A slight increase in the amplitude and latency of the a-wave component of the ERG with PF-03463275 treatment was observed. Since the ERG changes occur in our rodent model with PF-03463275 at exposures comparable with those associated with visual disturbance in the clinic, it was proposed that the visual adverse effects reported in healthy volunteers treated with selective GlyT1 inhibitors may represent a retinal class effect. The dose-related GlyT1 occupancy of PF-03463275 is linear. While PF-03463275 did not show evidence of facilitating N-methyl-D-aspartate receptor function in the ketamine assay, it enhanced neuroplasticity in schizophrenia patients. PF-03463275 had been in phase II clinical trial for the treatment of schizophrenia. However, this development was discontinued.

Cintazone is a non-steroidal anti-inflammatory drug. It is was discovered in the 1960s, and was shown to be an anti-phlogistic agent in animal studies. Clinical development of this drug is not reported.

Filanesib is a highly selective, targeted KSP inhibitor with a mechanism of action distinct from currently available myeloma therapies such as immunomodulatory drugs (IMiDs®) and proteasome inhibitors. Across multiple studies, filanesib has demonstrated activity in heavily pretreated multiple myeloma patients, with a consistent safety profile including no drug-induced peripheral neuropathy and limited non-hematologic toxicity. Adverse events are generally limited to transient, non-cumulative and predominantly asymptomatic myelosuppression (decreases in blood counts) when supportive measures are used. Alpha 1-acid glycoprotein (AAG), a plasma protein, is a potential patient selection marker for filanesib. AAG is undergoing further investigation in clinical trials and could represent the first patient selection marker for a myeloma therapy. Filanesib is in Phase II for Multiple myeloma treatment.

Mercuderamide is a mercurial diuretic. It inhibits both Na+-K+-ATPase and cyclic 3',5'-AMP-dependent protein kinase.

Azamethiphos, an organothiophosphate insecticide, initially was used in 1991 for the treatment against sea lice. However, because of reduced sensitivity in 1999, the use of this compound was terminated. Azamethiphos was re-introduced in 2008; it’s the main component of Salmosan, a pesticide presently used for treatment against sea lice. Salmosan is applied as a bath treatment and then released into the surrounding seawater

Mesabolone is a synthetic anabolic androgen.

Rebimastat (BMS-275291) is a broad-spectrum matrix metalloproteinase (MMP) inhibitor free from toxicity-related inhibition of sheddases (cleaving membrane proteins at the cell surface). This MMP2 and MMP9 inhibitor may stop the growth of cancers by stopping blood flow to the tumor (stopping them from dividing). It might also block the enzymes necessary for growth of the tumor cell. Multiple phase II trials and a phase III clinical trial have been completed, testing the efficacy and safety of the compound in prostate cancer, HIV-related Kaposi’s Sarcoma, non-small cell lung cancer (phase II and III) and breast cancer.

Tanespimycin (17-allylamino-17-demethoxygeldanamycin, 17-AAG) is a synthetic analogue of geldanamycin, an antibiotic first purified in 1970 from Streptomyces hygroscopicus. Tanespimycin is an Hsp90 inhibitor that has demonstrated the potential to disrupt the activity of multiple oncogenes and cell signaling pathways implicated in tumor growth, including HER2, a key pathway in breast cancer. Tanespimycin was being under development by Kosan Biosciences. It was in phase 3 clinical development with bortezomib for the treatment of multiple myeloma (MM). However, in 2010 the company halted development of tanespimycin, during late-stage clinical trials as a potential treatment for multiple myeloma. While no definitive explanation was given, it has been suggested that Bristol-Myers Squibb halted development over concerns of the financial feasibility of tanespimycin development given the 2014 expiry of the patent on this compound, and the relative expense of manufacture.