Amcasertib is an orally administered investigational agent designed to inhibit cancer stemness pathways, including Nanog, by targeting stemness kinases. Amcasertib is undergoing multiple Phase I and Phase II studies as monotherapy and combination therapy for treating a range of tumor types.

Adolor Corporation and Pfizer were developing an orally available and selective opioid delta (δ) receptor agonist, ADL 5747 (also known as PF 04856881), for the treatment of pain. ADL-5747 showed efficient pain-reducing properties in the two preclinical models of chronic pain. Their effects were mediated by δ-opioid receptors, with a main contribution of receptors expressed on peripheral Nav1.8-positive neurons. ADL-5747 had been in phase II clinical trials for the treatment of pain. However, this studies on this drug candidate were discontinued in 2010.

There is no information about biological o medical application of ferrous orotate. But is known, that this substance may be used for nutritional purposes to food supplements.

p53 is a critical tumor suppressor and is the most frequently inactivated gene in human cancer. Inhibition of the interaction of p53 with its negative regulator MDM2 represents a promising clinical strategy to treat p53 wild-type tumors. AMG 232 is a potential best-in-class inhibitor of the MDM2-p53 interaction and is currently in clinical trials. Based on X-ray cocrystal structures a model of AMG 232 bound to MDM2 was developed. The model shows that the m-chlorophenyl, the p-chlorophenyl, and C-linked isopropyl fragments of AMG 232 bind to the Leu 26(p53), Trp 23(p53), and Phe 19(p53) pockets of MDM2, respectively. The carboxylic acid forms a salt bridge with His 96 and the isopropyl sulfone forms a novel interaction with the glycine shelf region of MDM2. AMG 232 in phase II in combination with trametinib and dabrafenib in subjects with metastatic melanoma; in phase I for the treatment of solid tumors, multiple myeloma and Acute Myeloid Leukemia.

4‐Chlorokynurenine (AV-101) is a neuropharmaceutical drug candidate in development for the treatment of major depressive disorder. Pharmacology studies conducted in rodent models have demonstrated AV-101’s antihyperalgesic activity in models of facilitated pain processing was seen at serum concentrations ranging from 150–300 M. In addition, AV-101 has been shown to be neuroprotective activity against an intrahippocampal injection of quinolinic acid, reductions in seizures, and antidepressive activity. An oral prodrug, AV-101, which, in the brain, is converted into one of the most potent and selective GlyB site antagonists of the NMDAR, has been demonstrated to be active in animal models of neuropathic pain. The two Phase 1 studies were designed to assess the safety and pharmacokinetics of AV-101, over a wide dose range, after daily dosing for 14-days. AV-101 has excellent safety and PK characteristics providing support for advancing AV-101 into Phase 2 studies in neuropathic pain.