Sodium sulfate S-35 is a radiotracer used in research and diagnostics.

Cefilavancin is a covalently-linked glycopeptide-cephalosporin (beta-lactam) heterodimer antibiotic that exhibits substantially greater activity than its component parts against Gram-positive bacteria.

AMG-925, a dual FLT3/CDK4 inhibitor, has been developed to overcome resistance to FLT3 inhibitors, which is a serious clinical issue in treating acute myelogenous leukemia (AML). AMG-925 inhibits FLT3, including many FLT3 mutants reported to date. AMG-925 inhibits the proliferation of a panel of human tumor cell lines including Colo205 (Rb(+)) and U937 (FLT3(WT)) and induced cell death in MOLM13 (FLT3(ITD)) and even in MOLM13 (FLT3(ITD, D835Y)), which exhibits resistance to a number of FLT3 inhibitors currently under clinical development. At well-tolerated doses, AMG-925 leads to significant growth inhibition of MOLM13 xenografts in nude mice, and the activity correlates with inhibition of STAT5 and Rb phosphorylation. AMG-925 is in Phase I clinical trials for the treatment of Acute myeloid leukaemia.

Adomeglivant, also known as LY2409021, is a potent and selective glucagon receptor antagonist. Adomeglivant lowers blood glucose in healthy people and in those with type 2 diabetes. Blockade of glucagon signalling in patients with type 2 diabetes is well tolerated and results in substantial reduction of fasting and postprandial glucose with minimal hypoglycaemia, but with reversible increases in aminotransferases. Adomeglivant had been in phase II clinical trials by Eli Lilly for the treatment of type 2 diabetes mellitus. However, this research has been discontinued.

Mapreg is developing pregnenolone methyl ether (MAP4343), an injectable neurosteroid stimulator of the tubulin polymerisation and neurite growth stimulator. The synthetic pregnenolone-derivative MAP4343 (3β-methoxy-preg-nenolone) binds in vitro to microtubule-associated-protein 2 (MAP2), stimulates the polymerization of tubulin, enhances the extension of neurites and protects neurons against neurotoxic agents. MAP4343 has been selected after screening of a large library ofnatural and synthetic steroids. MAP4343 has similar in vitro activity as pregnenolone; it cannot be converted into metabolites with hormonal activities, and has been shown to have in vivo beneficial effects in rat models of spinal cord injury. MAP4343 has an interesting pharmacological profile because no in vitro affinity for any CNS neurotransmitter receptor was found. MAP4343 has been shown to have antidepressant efficacy in rats. In the rat isolation-rearing model of depression, administration of MAP4343 showed persistent efficacy in recovering recognition memory deficit, stronger and more rapid anxiolytic activity, and more rapid rescue of passive coping behavior compared with FLX. The behavioral effects of MAP4343 correlated with changes in α-tubulin isoforms in the hippocampus, amygdala, and pre-frontal cortex (PFC). Its efficacy was also assessed in vivo with the most commonly used thoracic spinal cord compression/contusion models in rats. In the three models used, the post-traumatic subcutaneous injection of MAP4343 significantly improved the recovery of locomotor function after spinal cord injury, as shown by an earlier and more complete recovery compared to vehicle-treated rats. The results obtained in three different rat models of spinal cord injury demonstrate the beneficial effects of this therapeutic strategy and identify MAP4343 as a potential treatment for acute spinal cord injury. MAP4343 received EU Orphan Drug designation for spinal cord injury. MAP4343 is in phase II clinical trials by Mapreg for the treatment of depression and in phase I clinical trials for the treatment of spinal cord injury and traumatic brain injury.

Sergliflozin, a novel oral selective low-affinity sodium glucose cotransporter (SGLT2) inhibitor, improves hyperglycemia by suppressing renal glucose reabsorption, in which SGLT2 participates as a dominant transporter. Its prodrug form, sergliflozin etabonate, is orally available and is converted to sergiflozin upon absorption. Development of sergliflozin has been discontinued in favor of remogliflozin.