7Z-Calcipotriol is an isomeric impurity in vitamin D analog calcipotriol. Synthesis of 7Z-Calcipotriol was disclosed by Japanese company Kuraray Co in a patent application JP 06316558.

Tegafur (INN, BAN, USAN) is a chemotherapeutic fluorouracil prodrug used in the treatment of cancers. It is a component of the combination drugs tegafur/uracil and tegafur/gimeracil/oteracil. UFT is an anticancer medication composed of a fixed molar ration (1:4) of tegafur and uracil. This drug is commonly used in the treatment of head and neck cancer, gastric cancer, colorectal cancer, hepatic cancer, gallbladder cancer, bile-duct cancer, pancreatic cancer, lung cancer, breast cancer, bladder cancer, prostatic cancer, or uterine cervical cancer. In the body, tegafur is converted into 5-fluorouracil (5-FU), the active antineoplastic metabolite. The mechanism of cytotoxicity of 5-FU is thought to be derived from the fact that 5-fluoro-deoxyuridine-monophosphate (FdUMP), the active metabolite of 5-FU, competes with deoxyuridine-monophosphate (dUMP), thereby inhibiting thymidylate synthase and subsequently DNA synthesis. Another active metabolite of 5-FU, 5-fluorouridine-triphosphate (FUTP) is integrated into cellular RNA, inhibiting RNA function. Uracil, when combined with tegafur, enhances the antitumor activity of 5-FU due to higher 5-FU concentrations in the tumor tissue versus normal surrounding tissue compared with tegafur alone. Uracil inhibits degradation of the released 5-FU. The combination of these two drugs enhances the antitumor activity of Tegafur.

Methotrexate is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the "S" phase (of the cell cycle), stopping normal development and division. Methotrexate inhibits folic acid reductase which is responsible for the conversion of folic acid to tetrahydrofolic acid. At two stages in the biosynthesis of purines and at one stage in the synthesis of pyrimidines, one-carbon transfer reactions occur which require specific coenzymes synthesized in the cell from tetrahydrofolic acid. Tetrahydrofolic acid itself is synthesized in the cell from folic acid with the help of an enzyme, folic acid reductase. Methotrexate looks a lot like folic acid to the enzyme, so it binds to it quite strongly and inhibits the enzyme. Thus, DNA synthesis cannot proceed because the coenzymes needed for one-carbon transfer reactions are not produced from tetrahydrofolic acid because there is no tetrahydrofolic acid. Methotrexate selectively affects the most rapidly dividing cells (neoplastic and psoriatic cells). Methotrexate is indicated in the treatment of gestational choriocarcinoma, chorioadenoma destruens and hydatidiform mole. In acute lymphocytic leukemia, methotrexate is indicated in the prophylaxis of meningeal leukemia and is used in maintenance therapy in combination with other chemotherapeutic agents. Methotrexate is also indicated in the treatment of meningeal leukemia. Methotrexate is used alone or in combination with other anticancer agents in the treatment of breast cancer, epidermoid cancers of the head and neck, advanced mycosis fungoides (cutaneous T cell lymphoma), and lung cancer, particularly squamous cell and small cell types. Methotrexate is also used in combination with other chemotherapeutic agents in the treatment of advanced stage non-Hodgkin’s lymphomas. Methotrexate is indicated in the symptomatic control of severe, recalcitrant, disabling psoriasis. Methotrexate is indicated in the management of selected adults with severe, active rheumatoid arthritis (ACR criteria), or children with active polyarticular-course juvenile rheumatoid arthritis.

Solasodine is an aglycone of solamargine and solasonine, which are the major solasodine glycosides present in numerous species of the solanaceae family including potato, tomato or garden egg plant etc. In Phase II clinical trial was shown that solasodine glycosides exhibit anticancer activity against skin cancer. The effects of aglycone solasodine on cancer cells have also been investigated. Solasodine inhibits the growth of human colon and liver cancer cell. In addition, solasodine effectively inhibits proliferation of HER2-overexpressing breast cancer cells and inhibits invasion of human lung cancer cells. Solasodine possesses CNS activities such as antipyretic, anticonvulsant and memory enhancing effects. Also, solasodine has been found to possess diuretic, antifungal, hepatoprotective, immunomodulatory, anti-spermatogenetic and antiandrogenic effects.

Luminespib (NVP-AUY922) is a highly potent isoxazole-based, nongeldanamycin HSP90 inhibitor that inhibits the adenosine triphosphatase activity of HSP90. Luminespib is a highly potent HSP90 inhibitor for HSP90α/β with IC50 of 13 nM /21 nM in cell-free assays, weaker potency against the HSP90 family members GRP94 and TRAP-1, exhibits the tightest binding of any small-molecule HSP90 ligand. Luminespib potently inhibited in vitro growth in all 41 NSCLC cell lines evaluated with IC50 less than 100 nM. IC100 value less than 40 nM was seen in 36 of 41 lines. Luminespib (NVP-AUY922) has greater potency, reduced hepatotoxicity, and lower dependence on DT-diaphorase than the first-generation HSP90 inhibitors. Luminespib was discovered in a multiparameter lead optimization program based on a high-throughput screening hit methodology developed jointly by The Institute of Cancer Research, UK and the pharmaceutical company Vernalis. It has been licensed to Novartis. Luminespib activity is independent of NQO1/DT-diaphorase, maintained in drug-resistant cells and under hypoxic conditions. The molecular signature of HSP90 inhibition, comprising induced HSP72 and depleted client proteins, was readily demonstrable. Pre-clinical studies proved that Luminespib acts via several processes (cytostasis, apoptosis, invasion, and angiogenesis) to inhibit tumor growth and metastasis. These results helped Luminespib to enter clinical trials for various cancers including breast cancers. From 2011 to 2014 it was in Phase II clinical trials.

Licochalcone A (LicA) is a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch and has a wide spectrum of pharmacological activities such as anti-oxidant, anti-bacterial, anti-viral, and anti-cancer. However, its pharmacological mechanism is not well defined. The anti-Inflammatory effects of LicA on IL-1β-Stimulated human osteoarthritis chondrocytes was reached by activating Nrf2 signaling pathway. LicA showed anti-proliferative and apoptotic effects in breast cancer cells through regulating Sp1 and apoptosis-related proteins in a dose- and a time-dependent manner. In addition, the chemotherapeutic potential of LicA for treatment of human cervical cancer was achieved by inhibition of PI3K/Akt/mTOR signaling.

Lucitanib (E-3810) is a novel multi-kinase inhibitor currently in clinical trials for its anti-angiogenic and anti-tumor activity. A Phase I/IIa clinical trial of lucitanib was initiated in 2010 and has demonstrated multiple objective responses in FGFR1 gene-amplified breast cancer patients, and objective responses were also observed in patients with tumors often sensitive to VEGFR inhibitors, such as renal cell and thyroid cancer. Lucitanib is an oral, potent inhibitor of the tyrosine kinase activity of fibroblast growth factor receptors 1 through 3 (FGFR1-3), vascular endothelial growth factor receptors 1 through 3 (VEGFR1-3) and platelet-derived growth factor receptors alpha and beta (PDGFR alpha-beta). The most common adverse events were hypertension, asthenia, and proteinuria.

Dihydromyricetin is a flavonoid component from the Ampelopsis species japonica, megalophylla, and grossedentata; Cercidiphyllum japonicum; Hovenia dulcis; Rhododendron cinnabarinum; some Pinus species; and some Cedrus species, as well as Salix sachalinensis. Dihydromyricetin exerts a more rapid antidepressant-like effect than does a typical antidepressant, in association with enhancement of BDNF expression and inhibition of neuroinflammation. Dihydromyricetin inhibited the proliferative potential of fibroblasts in the lung cancer cells through targeting the activation of Erk1/2 and Akt. Therefore, there is scope for dihydromyricetin to be evaluated further for the treatment of lung cancer. Dihydromyricetin supplementation improves glucose and lipid metabolism as well as various biochemical parameters in patients with nonalcoholic fatty liver disease, and the therapeutic effects of dihydromyricetin are likely attributable to improved insulin resistance and decreases in the serum levels of tumor necrosis factor-alpha, cytokeratin-18, and fibroblast growth factor 21.

PF-3758309 was developed as an ATP-competitive inhibitor of PAK4. In cells, PF-3758309 inhibits phosphorylation of the PAK4 substrate GEF-H1 (IC50 = 1.3 nM) and anchorage-independent growth of a panel of tumor cell lines (IC50 = 4.7 nM). PF-3758309 blocks the growth of multiple human tumor xenografts, with a plasma EC50 value of 0.4 nM in the most sensitive model. PF-3758309 is antiproliferative and induces apoptosis in an HCT116 tumor model.

Darbufelone mesylate is a dual inhibitor of cellular prostaglandin and leukotriene production. Darbufelone potently inhibits PGHS-2 (IC50 = 0.19 uM) but is much less potent with PGHS-1 (IC50= 20 uM). Darbufelone is a dual inhibitor of cellular PGF2R and LTB4 production. Darbufelone is orally active and nonulcerogenic in animal models of inflammation and arthritis. Darbufelone mesylate was in phase III clinical trials by Pfizer and Zhuhai United Laboratories for the treatment of rheumatoid arthritis.