GSK-2636771 is a potent, orally bioavailable, PI3Kβ-selective inhibitor, sensitive to PTEN null cell lines. GSK-2636771 shows selectively inhibitory activity in PTEN null cell lines (human prostate adenocarcinoma PC-3 and breast cancer HCC70) with EC50 of 36 nM and 72 nM, respectively. GSK-2636771 significantly decreases cell viability in p110β-reliant PTEN-deficient PC3 prostate and BT549 and HCC70 breast cancer cell lines, and leads to a marked decrease of AKT phosphorylation only in the control prostate and breast cancer cell lines. On April 1 2016 GlaxoSmithKine completes a phase-I/II trial for Solid tumours (Late-stage disease) in USA, United Kingdom and South Korea (NCT01458067).

Diaziquone is an aziridinylbenzoquinone with properties suggestive of an alkylating agent. The drug has shown broad antitumor activity against numerous transplantable murine tumors including curative activity against several intracerebrally implanted tumors. Diaziquone is rapidly and extensively metabolized by the liver. Diaziquone is a potent marrow suppressive agent inducing significant degrees of leukopenia, granulocytopenia, and thrombocytopenia in humans. Thrombocytopenia is often severe. Diaziquone alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. This agent can also form free radicals, thereby initiating DNA damage via DNA strand breaks. Due to its lipophilicity, diaziquone readily crosses the blood brain barrier. In phase I and preliminary phase II trials, diaziquone has demonstrated activity against primary brain tumors. Little activity has been seen in other tumor categories.

BMS 599626 is a selective and efficacious inhibitor of HER1 and HER2 with IC50 of 20 nM and 30 nM. BMS-599626 is identified as an ATP-competitive inhibitor for HER1 and as an ATP-noncompetitive inhibitor for HER2. BMS-599626 inhibits the proliferation of tumor cells expressing high levels of HER1 and/or HER2, including Sal2, BT474, N87, KPL-4, HCC202, HCC1954, HCC1419, AU565, ZR-75-30, MDA-MB-175, GEO, and PC9 cells. In a phase I trial of solid tumour patients receiving BMS 599626 no doselimiting toxicities were observed during the first cycle. Grade 1 or 2 drugrelated effects were reported and included diarrhoea, nausea, vomiting, rash, fatigue, musculoskeletal pain/cramp and cough. BristolMyers Squibb discontinued development of BMS 599626 for cancer in July 2015

Lodoxamide ethyl, diethyl N,N'-(2-chloro-5-cyano-m-phenylene) dioxamate, is an orally active candidate for the treatment of asthma and other allergic diseases. Lodoxamide ethyl prevents mast cell mediator release during allergic reactions in rats, guinea pigs, and monkeys at doses well below toxic levels. Lodoxamide ethyl does not interfere with antigen-antibody interaction, does not antagonize the effects of histamine or slow-reacting substance of anaphylaxis, and does not have direct antiinflammatory effects. Lodoxamide ethyl has been proven capable of preventing bronchospasm in humans when the subject was given 1, 3, or 10 mg of the drug orally prior to challenge with an antigen.

Bucrylate (isobutyl cyanoacrylate) is a liquid tissue adhesive for transcatheter embolization. It is used in radiological and endoscopic interventions to occlude vessels and to stop bleedings. In comparison with sponges, coils and plugs, bucrylate is inexpensive and achieves immediate, irreversible and complete occlusion of the vessel irrespective of coagulation deficiencies.

Tixanox is an antiallergic drug. It blocks histamine release from human lung induced by anti-IgE. Tixanox has been shown to be orally active against exercise-induced asthma in man.

FLUFENISAL is a compound related to aspirin structurally, chemically, and pharmacologically. It was in clinical development as an analgesic and anti-inflammatory agent. However, its development was discontinued due to lack of sufficient superiority over aspirin.

Zearalenone (ZEN) is a toxic non-steroidal mycoestrogen produced by fungi that widely contaminate agricultural products, eliciting estrogenic responses by mimicking sex steroid hormones. Zearalenone is biosynthesised through a polyketide pathway by a variety of Fusarium fungi including Fusarium graminearum (Gibberella zeae), Fusarium culmorum, Fusarium equiseti, Fusarium crookwellense, Fusarium cerealis and Fusarium semitectum. Zearalenone and its derivatives share similar molecular mechanisms and activity with estrogens. They interact with the estrogen receptors (ERa and ERb) leading to functional and morphological changes in the reproductive system in both animals and humans. Zearalenone exposure is associated with the estrogenic syndrome and infertility in animals and premature thelarche and precocious puberty in girls. In animal models, it was found that prepubertal exposure to a low dose of Zearalenone, decreased breast cancer risk. When prepubertal rats were treated with 20 lg (1 mg ⁄ kg body weight) of Zearalenone, a significant reduction of both the incidence and multiplicity of DMBA-induced mammary tumours was noted. Zearalenone has been used to treat postmenopausal symptoms in women.

PGD2 (Prostaglandin D2) is a major cellular regulator, has been shown to bind different receptors: D prostanoid receptor (DP) and chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2). PGD2 reportedly inhibits platelet aggregation, the proliferation of cells, and activation of neutrophils. This compound is also a potent vasodilator that also relaxes smooth muscle but causes contraction of the bronchial airways. PGD2 promotes T cell migration via CRTH2 and aggravates asthma. In contrast, there have been some studies suggesting that PGD2 exerts anti-inflammatory effects via DP, such as inhibiting the migration and activation of neutrophils, basophils, dendritic cells and T cells. Elevated levels of prostaglandin D2 (PGD2) have been shown to be present in the bald scalp of androgenic alopecia (AGA) patients and was suggested the PGD(2)-GPR44 pathway as a potential target for treatment. Also was revealed, that PGD2 might be a new target for asthma therapy, PGD2 in serum and BALF were lower in the treated group than in the untreated group.