Geclosporin (Cyclosporine) is an immunosuppressive agent, that is used to prevent rejection of a transplanted organ by the body. Geclosporin is isolated from a fungus, Beauveria nivea, and was first discovered in 1970. By suppressing the immune system, this drug prevents white blood cells from rejecting the transplanted organ. Geclosporin primarily does this by suppressing T cells and T cell cytokine production, but also acts in other ways, for example by inhibiting growth and activation of B cells and antigen presenting cells, and by reducing antibody production. Geclosporin is usually combined with other compounds, and has been studied as potential treatment for a large range of disorders. It is used for the treatment of several other conditions, such as severe recalcitrant plaque psoriasis, severe active rheumatoid artritis, and to prevent rejection of donor cells as a result of bone marrow transplantation. Relapse after discontinuation of this compound is to be expected, and therefore, patients should receive maintenance therapy at the lowest effective dosage. The most common adverse events are hypertrichosis, gingival hyperplasia, and neurological and gastrointestinal effects. Renal dysfunction is also possible, but irreversible damage is rare.

G749 is a Fms-like tyrosine receptor kinase 3 (FLT3) inhibitor and a promising next-generation drug candidate for the treatment of relapsed and refractory acute myeloid leukemia (AML) patients with various FLT3-ITD/FLT3-TKD mutants that shows the ability to overcome drug resistance. It demonstrated potent and sustained inhibition of the FLT3 wild type and mutants including FLT3-ITD, FLT3-D835Y, FLT3-ITD/N676D, and FLT3-ITD/F691L in cellular assays. G749 retained its inhibitory potency in various drug-resistance milieus such as patient plasma, FLT3 ligand surge, and stromal protection. It also displayed potent antileukemic activity in bone marrow blasts from AML patients regardless of FLT3 mutation status, including those with little or only minor responses to AC220 or PKC412. Oral administration of G749 yielded complete tumor regression and increased life span in animal models.

BMS-690514 is a potent, reversible oral inhibitor of epidermal growth factor receptor (EGFR/HER-1), HER-2 and -4, and vascular endothelial growth factor receptors (VEGFRs)-1 to -3 offering targeted inhibition of tumour growth and vascularisation in a single agent. Bristol-Myers Squibb was developing BMS 690514, as an oral treatment for cancer. BMS-690514 had being in phase II for the treatment of breast cancer; non-small cell lung cancer, but later these studies were discontinued.

Nacubactam (FPI-1459) was developed as an antibacterial drug. Nacubactam successfully has completed phase I clinical trials for the treatment of serious gram-negative bacterial infections. The drug is currently being developed for the treatment of complicated urinary tract infection, hospital-acquired bacterial pneumonia, ventilator-associated bacterial pneumonia, and complicated intra-abdominal infections. FPI-1459 works through several mechanisms of action, inhibiting a number of beta-lactamase enzymes as well as certain bacterial cell wall enzymes. In January 2019, FPI-1459 received Fast Track and Qualified Infectious Disease Product designations from the U.S. Food and Drug Administration (FDA).

11C-JHU75528 (also known as 11C-OMAR) is a radiotracer with suitable imaging properties for quantification of cannabinoid receptor, CB1R in the human brain. 11C-JHU75528 is participating in an ongoing phase I clinical trial to examine whether the use of cannabis alters CB1R availability in females and if the severity of cannabis withdrawal is correlated with CB1 receptor availability.