Veliparib (ABT-888) is a potent inhibitor of PARP, has good oral bioavailability, can cross the blood-brain barrier, and potentiates temozolomide, platinums, cyclophosphamide, and radiation in syngeneic and xenograft tumor models. AbbVie is developing veliparib for the treatment of cancers. Clinical trials are underway worldwide, investigating veliparib primarily as part of a combination therapy in oncology indications such as brain, colorectal, melanoma, ovarian, prostate and pancreatic cancers.

Levonadifloxacin is the S-(-) isomer of the benzoquinolizine fluoroquinolone nadifloxacin and is two- to four-fold more active than the racemic mixture. Levonadifloxacin is a potent antibacterial agent against Gram-positive bacteria especially against methicillin resistance Staphylococcus aureus. It also possesses potent bactericidal activity against other resistant variants like quinolone-resistant Staphylococcus aureus, vancomycin and glycopeptide intermediate Staphylococcus aureus and vancomycin resistant Staphylococcus aureus. Intravenous dosage form developed to treat complicated skin and skin structure infections and has recently completed Phase III studies in India and Phase I studies in USA.

Tolafentrine is phosphodiesterase 3/4 (PDE3/4) inhibitor. Treatment of endothelial cells with tolafentrine significantly decreased asymmetrical dimethylarginine-induced apoptosis via a cAMP/PKA-dependent pathway by induction of dimethylarginine dimethylaminohydrolase 2 (DDAH2). Chronic nebulization of PDE3/4 inhibitor significantly attenuated monocrotaline-induced hemodynamic, gas exchange abnormalities, vascular remodeling, and right heart hypertrophy. When chronically nebulized from day 28 to 42 (12 daily aerosol maneuvers), after full establishment of severe pulmonary hypertension, tolafentrine reversed about 60% of all hemodynamic abnormalities in rats, right heart hypertrophy and monocrotaline-induced structural lung vascular changes, including the proportion of pulmonary artery muscularization. Tolafentrine was developed as therapeutic agent for the treatment of asthma. However, this development was discontinued.

Barasertib (AZD1152) is a dihydrogen phosphate prodrug of a pyrazoloquinazoline Aurora kinase inhibitor [AZD1152–hydroxyquinazoline pyrazol anilide (HQPA)] and is converted rapidly to the active AZD1152-HQPA in plasma. AstraZeneca was developing the aurora kinase inhibitor, barasertib (AZD 1152) as a therapeutic for cancer. AZD1152-HQPA is a highly potent and selective inhibitor of Aurora B (Ki, 0.36nmol/L) compared with Aurora A (Ki, 1,369nmol/L) and has a high specificity versus a panel of 50 other kinases. Consistent with inhibition of Aurora B kinase, addition of AZD1152-HQPA to tumour cells in vitro induces chromosome misalignment, prevents cell division, and consequently reduces cell viability and induces apoptosis. Barasertib (AZD1152) potently inhibited the growth of human colon, lung, and haematologic tumour xenografts (mean tumour growth inhibition range, 55% to ≥100%; P < 0.05) in immunodeficient mice. Detailed pharmacodynamic analysis in colorectal SW620 tumour-bearing athymic rats treated i.v. with Barasertib (AZD1152) revealed a temporal sequence of phenotypic events in tumours: transient suppression of histone H3 phosphorylation followed by accumulation of 4N DNA in cells (2.4-fold higher compared with controls) and then an increased proportion of polyploid cells (>4N DNA, 2.3-fold higher compared with controls). Histologic analysis showed aberrant cell division that was concurrent with an increase in apoptosis in AZD1152-treated tumours. Bone marrow analyses revealed transient myelosuppression with the drug that was fully reversible following cessation of Barasertib (AZD1152) treatment. Barasertib (AZD1152) was in phase III for the treatment of Acute myeloid leukaemia, but later these studies were discontinued.

LEIOPYRROLE is an antispasmodic agent.

LANIQUIDAR is a P-glycoprotein inhibitor. It was used in trials studying the treatment of breast cancer.