Chryseriol (Chrysoeriol) is a methoxylated flavone of great scientific interest because of its promising antioxidant, antiinflammatory, antitumor, antimicrobial, antiviral, and free radical scavenging activities. Chryseriol is a promising inhibitor of protein kinase CK2α and CK2α', the catalytic subunits of CK2, with IC50 values of 250 and 34 nM for CK2α and CK2α', respectively. Chrysoeriol produced a noncompetitive and mixed inhibition of pancreatic lipase with IC50=158uM. Chryseriol is a dual c‑Met and VEGFR2 kinase inhibitor. The results of docking experiments revealed that chrysoeriol was able to efficiently bind in the active site cavity of c‑Met and VEGFR2. The results of enzymatic assays showed relatively high binding affinities of chrysoeriol to c‑Met (Kd=12 uM) and VEGFR2 (Kd=11 uM). Chrysoeriol selectively inhibited human recombinant CYP1B1-mediated 7-ethoxyresorufin-O-deethylation (EROD) activity 5-fold more than that of CYP1A1-mediated activity in a competitive manner. Additionally, chrysoeriol inhibited E(2) hydroxylation catalyzed by CYP1B1, but not by CYP1A1. So chrysoeriol is a chemopreventive natural ingredient that can selectively inhibit CYP1B1 activity and prevent the formation of carcinogenic 4-OHE(2) from E(2.). Chrysoeriol was a selective PI3K-AKT-mTOR pathway inhibitor. It restrained the proliferation of human multiple myeloma cells, but didn't affect proliferation of PBMNCs from normal donors. It might exhibit the cell cycle regulatory effect via the inhibition of PI3K-AKT-mTOR signal pathway. The US Food and Drug Administration (FDA) recently granted orphan drug approval for Chrysoeriol, a cannabis-based drug used to treat acute myeloid leukaemia, which was developed by Jamaican scientist Dr Henry Lowe.

Menatetrenone (INN), also known as MK4, is a vitamin K compound used as a hemostatic agent, and also as adjunctive therapy for the pain of osteoporosis. MK4 is marketed for the osteoporosis indication in Japan by Eisai Co., under the trade name Glakay. Has several mechanism of actions: (1) Acceleration of osteogenesis. In human osteoblast cultures, calcification was accelerated by administration of menatetrenone at a concentration of 2.25 × 10-6 mol/L alone or when it was coadministered with 1,25(OH)2D3. The osteocalcin content in the cell layers was increased by coadministration with 1,25(OH)2D3. 2. Inhibition of bone resorption. In organ cultures of mouse calvaria, at concentrations of 3 × 10-6 to 3 × 10-5 mol/L, menatetrenone inhibited bone resorption induced by IL-1α, PGE2, PTH and 1,25(OH)2D3. In mouse bone marrow cell cultures, at concentrations of 3 × 10-6 to 1 × 10-5 mol/L, menatetrenone inhibited the induction of osteoclast release by 1,25(OH)2D3. 3. Effect on serum level of osteocalcin. Menatetrenone was administered to patients with osteoporosis at a dose of 45 mg/day for 2 years. Menatetrenone increased the serum level of osteocalcin and decreased the serum level of Glu-osteocalcin.

Ubenimex is a dipeptide, which specificallyinhibits the activity of leukotriene A4 hydrolase, aminopeptidase B and leucine aminopeptidase of the cell membrane. The drug was isolated from Streptomyces oliooreticuli in 1976 in Nippon Kayaku, Japan and approved for the treatment of acute non-lymphocytic leukemia under the name Bestatin. In the USA the drug is currentlu in Phase II for the treatment of pulmonary arterial hypertension and lymphedema.

Tamibarotene (brand name: Amnolake), also called retinobenzoic acid, is orally active, the synthetic retinoid, developed to overcome all-trans retinoic acid (ATRA) resistance, with potential antineoplastic activity against acute promyelocytic leukemia (APL). Tamibarotene is a specific agonist for retinoic acid receptor alpha/beta. It is currently marketed only in Japan and early trials have demonstrated that it tends to be better tolerated than ATRA. It has also been investigated as a possible treatment for Alzheimer's disease, multiple myeloma, and Crohn's disease.

Vosaroxin is a small molecule and a naphthyridine analogue with antineoplastic activity. This quinolone-based topoisomerase II inhibitor is a new therapeutic for acute myeloid leukemia (AML). Being a DNA intercalating topoisomerase II inhibitor that causes the induction of apoptosis via double-strand DNA breaks vosoroxin is chemically distinct from other topoisomerase inhibitors with its stable quinolone-based core. Due to the stability of this core, vosaroxin is not associated with significant formation of toxic metabolites, free radicals, or reactive oxygen species, which are associated with off-target organ damage and cardiotoxicity. Furthermore, vosaroxin evades two common mechanisms of drug resistance, as it is not a substrate for the P-glycoprotein efflux pump and its activity is maintained in cells with p53 deletion. Vosaroxin has beeт tested in several investigator-sponsored studies, both as a single-agent and in combination with other therapies, for the treatment of AML and myelodysplastic syndromes. Both the U.S. Food and Drug Administration (FDA) and European Commission have granted orphan drug designation to vosaroxin for the treatment of AML. Additionally, vosaroxin has been granted fast track designation by the FDA for the potential treatment of relapsed or refractory AML in combination with cytarabine. Vosaroxin is an investigational drug that has not been approved for use in any jurisdiction. The trademark name QINPREZO is conditionally accepted by the FDA and the EMA as the proprietary name for the vosaroxin drug product candidate.