O-Desmethyl tramadol (O-Desmethyltramadol, O-DSMT) is a metabolite of tramadol. O-Desmethyltramadol is an opioid analgesic and the main active metabolite of tramadol. (+)-O-Desmethyltramadol is the most important metabolite of tramadol produced in the liver after tramadol is consumed. This metabolite is considerably more potent as a μ-opioid agonist than the parent compound. O-desmethyl tramadol, inhibits 5-hydroxytryptamine type 2C receptors expressed in xenopus oocytes. O-desmethyl tramadol inhibits functions of M(1) receptors but has little effect on those of M(3) receptors. O-desmethyl tramadol has been widely used clinically and has analgesic activity.

CNDAC (TAK-109) is an analog of the nucleoside deoxycytidine with potential antineoplastic activity. CNDAC is incorporated into DNA and induces single-strand breaks, which are converted into double-strand breaks (DSBs) when cells go through a second S phase. This results in the cell cycle arrest in the S and G2/M phases, DNA fragmentation, and tumor cell apoptosis. Sapacitabine, a prodrug of CNDAC, is being developed by the US biotechnology company Cyclacel for the treatment of hemalogical cancers and solid tumors.

2,2-DIMETHYLBUTYRIC ACID (HQK-1001) is an orally administered SCFAD (Short Chain Fatty Acid Derivative), which has shown an excellent safety profile and biologic effects on fetal hemoglobin induction and red blood cell production in the laboratory, relevant animal models, and in clinical trials carried out in healthy human subjects as well as patients with sickle cell disease and beta thalassemia. The compound has received Orphan Drug Designation in the United States and Europe for both sickle cell disease and beta thalassemia. HemaQuest Pharmaceuticals was developing HQK-1001 for the oral treatment of sickle cell anaemia and beta thalassaemia. HQK-1001 has been evaluated in phase II trials for beta thalassaemia and sickle cell anaemia.

Decoglurant is a negative allosteric modulator of the mGlu2 and mGlu receptors developed by Roche. Decoglurant was investigated in a phase 2 clinical trials in patients with major depressive disorder. Negative results were reported and the development was discontinued in 2015.

Rigosertib sodium (ON 01910.Na) is a small molecule inhibitor of critical pathways important in the growth and survival of cancer cells, being developed by Onconova Therapeutics ("Onconova") for the treatment of hematologic malignancies and solid tumors. Rigosertib (ON-01910) is a non-ATP-competitive inhibitor of PLK1 with IC50 of 9 nM in a cell-free assay. It shows 30-fold greater selectivity against Plk2 and no activity to Plk3. Extensive Phase I and Phase II studies with rigosertib have been conducted at leading institutions in the U.S. and abroad in more than 450 patients with solid tumors and hematological cancers, including MDS and AML. MDS and AML are blood disorders widely recognized as difficult to manage, with limited therapeutic options available for patients, especially those with drug-resistant disease. The multi-site Phase III ONTIME trial in MDS patients is under a Special Protocol Assessment (SPA) from the U.S. FDA and is being supported by an award from the Therapeutics Acceleration Program (TAP) of the Leukemia and Lymphoma Society (LLS). FDA has granted Orphan Drug Designation for the use of rigosertib in MDS. The clinical program in solid tumors is also advancing with initiation of the Phase II/III combination ONTRAC trial (ON 01910.Na TRial in Patients with Advanced Pancreatic Cancer) and Phase II single agent trial in ovarian cancer. In Japan, SymBio is developing rigosertib for the treatment of refractory/relapsed HR-MDS (IV form) and first-line LR-MDS (oral form).

AT7519M or AT7519, a small molecule inhibitor of cyclin-dependent kinases 1, 2, 4, 5, and 9, participated in phase II clinical trials in patients with relapsed or refractory chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL). As a result, in CLL, some patients had tumor reductions, but the objective response rate (ORR) was low. In MCL, activity was noted with ORR of 27%. In addition, AT7519M was studied in patients with previously treated multiple myeloma, to understand whether the drug alone or in combination with bortezomib were effective treatments. Recent experiments also have shown that AT7519 is a promising drug for the treatment of high-risk neuroblastoma patients with MYCN amplification. It is known, that MYCN-dependent neuroblastomas have low cure rates with current multimodal treatment.

Deoxyspergualin is a derivative of the antitumor antibiotic spergualin, that used as an immunosuppressive drug. Deoxyspergualin shows immunosuppressive activity both in vitro and in vivo, affecting B-lymphocyte, T-lymphocyte and macrophage/monocyte function. In rodents and human cell systems, Deoxyspergualin shows a dose-dependent inhibition of primary and secondary responses to T-, B- and antigen-presenting cell-dependent reactions. Deoxyspergualin also blocks nuclear translocation of NF-kB in a pre-B-cell line, thereby affecting NF-kB driven transcription of the kappa light chain. Deoxyspergualin inhibits desoxyhypusine synthase, the first enzyme in the formation of active eukaryotic translation initiation factor 5A. This factor is important for the stabilization of certain mRNA transcripts (TNF-a and others). The immunosuppressive properties of Deoxyspergualin have been demonstrated in preclinical animal studies including Systemic lupus erythematosus models. In humans with glucocorticoidresistant kidney transplant rejection, Deoxyspergualin shows the same efficacy rate as the strongly T-cell depleting anti-CD3 monoclonal antibody. Deoxyspergualin has been licensed in Japan for acute renal allograft rejection since 1994. In 2003, an open clinical trial successfully tested Deoxyspergualin in patients with persistent ANCA-associated vasculitis. Adverse events (AE) were common but rarely led to treatment discontinuation. Against this background, Deoxyspergualin was granted an orphan drug status for the treatment of Wegener’s granulomatosis by the European Medicines Agency (EMA).

Bioresmethrin is a synthetic pyrethroid insecticide. It is the (+)-trans isomer of resmethrin which itself contains a minimum of 30% bioresmethrin. Bioresmethrin is the [1R, trans] isomer of resmethrin and has greater insecticidal activity than the racemic mixture. Bioresmethrin is a potent contact insecticide effective against a wide range of household insects, plant pests, grain pests and insects found in animal housing. It exhibits a high order of insecticidal activity, which when coupled with its excellent toxicological properties, makes it potentially one of the safest and most useful insecticides now being produced.