Ticagrelor (known trade names Brilinta, Brilique and Possia) is a P2Y12 platelet inhibitor. Brilinta has been approved by the US Food and Drug administration (FDA) in 2011 and is indicated to reduce the rate of cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ACS) or a history of myocardial infarction. Brilinta also reduces the rate of stent thrombosis in patients who have been stented for treatment of ACS. Ticagrelor and its major metabolite reversibly interact with the platelet P2Y12 ADP-receptor to prevent signal transduction and platelet activation. Ticagrelor and its active metabolite are approximately equipotent. In vitro metabolism studies demonstrate that ticagrelor and its major active metabolite are weak inhibitors of CYP3A4, potential activators of CYP3A5 and inhibitors of the P-gp transporter. Most common adverse reactions are bleeding 12% and dyspnea 14%.

Vandetanib, 4-anilinoquinazoline, is an anti-cancer drug that with the potential for use in a broad range of tumour types. In 2011 vandetanib (trade name Caprelsa) was approved by the FDA to treat nonresectable, locally advanced, or metastatic medullary thyroid cancer in adult patients. In vitro studies have shown that vandetanib inhibits the tyrosine kinase activity of the EGFR and VEGFR families, RET, BRK, TIE2, and members of the EPH receptor and Src kinase families. These receptor tyrosine kinases are involved in both normal cellular function and pathologic processes such as oncogenesis, metastasis, tumor angiogenesis, and maintenance of the tumor microenvironment. Vandetanib was shown to inhibit epidermal growth factor (EGF)-stimulated receptor tyrosine kinase phosphorylation in tumor cells and endothelial cells and VEGF-stimulated tyrosine kinase phosphorylation in endothelial cells. Vandetanib administration reduced tumor cell-induced angiogenesis, tumor vessel permeability, and inhibited tumor growth and metastasis in mouse models of cancer.

TAK-536 (generic name: azilsartan) is an angiotensin II type 1 receptor blocker, discovered by Takeda and its mechanism of action is to lower blood pressure by inhibiting action of a vasopressor hormone Angiotensin II. Angiotensin II type 1 receptor antagonists have become an important drug class in the treatment of hypertension and heart failure. TAK-536 is in phase III clinical trial for treatment hypertension. This drug also known as active metabolite of the prodrug azilsartan medoxomil (also known as azilsartan kamedoxomil), but in some countries azilsartan rather than its prodrug is used for oral treatment.

Rivaroxaban (trade name Xarelto) is an oral anticoagulant. It is the first available orally active direct factor Xa inhibitor. Upon oral administration, rivaroxaban selectively binds to both free factor Xa and factor Xa bound in the prothrombinase complex. This interferes with the conversion of prothrombin (factor II) to thrombin and eventually prevents the formation of cross-linked fibrin clots. Rivaroxaban does not affect existing thrombin levels. Activation of factor X to factor Xa (FXa) via the intrinsic and extrinsic pathways plays a central role in the cascade of blood coagulation. Xarelto is indicated to reduce the risk of stroke and systemic embolism in patients with nonvalvular atrial fibrillation, treatment and prophylaxis of deep vein thrombosis (DVT) which may lead to PE in patients undergoing knee or hip replacement surgery, pulmonary embolism (PE) and for the reduction in the risk of recurrence of deep vein thrombosis and of pulmonary embolism following initial 6 months treatment for DVT and/or PE.

Deferiprone (trade name Ferriprox) is an iron chelator indicated for the treatment of patients with transfusional iron overload due to thalassemia syndromes when current chelation therapy is inadequate. Deferiprone is an orally bioavailable bidentate ligand with iron chelating activity. Deferiprone binds to iron in a 3:1 (ligand:iron) molar ratio. By binding to iron, deferiprone is able to remove excess iron from the body. All the adverse effects of deferiprone are considered reversible, controllable and manageable. These include agranulocytosis with frequency of about 0.6%, neutropenia 6%, musculoskeletal and joint pains 15%, gastrointestinal complains 6% and zinc deficiency 1%.

Vilazodone is a serotonergic antidepressant. The mechanism of the antidepressant effect of vilazodone is not fully understood but is thought to be related to its inhancement of serotonergic activity in the CNS through selective inhibition of serotonin reuptake. Vilazodone is also a partial agonist at serotonergic 5-HT1A receptors; however, the net result of this action on serotonergic transmission and its role in vilazodone’s antidepressant effect are unknown. The side effects include activation of mania/hypomania in patients with bipolar disorder, seizures can occur with treatment in patients with a seizure disorder.

Ioflupane I-123 (trade name DaTscan) is a radioiodinated cocaine analogue synthesized from a key starting material Sn FP-CT via oxidative iododestannylation with sodium (123I)-iodide. Ioflupane I-123 binds reversibly with high affinity to the dopamine transporter (DaT) protein, a marker for presynaptic terminals in dopaminergic nigrostriatal neurons. It has been developed as a dopamine transporter imaging agent for single photon emission computed tomography (SPECT) which is claimed to be sensitive enough to differentiate changes in the nigrostriatal dopaminergic system in patients with Parkinsonism and healthy controls. DaTSCAN is unable to discriminate between Parkinson's Disease, Multiple System Atrophy and Progressive Supranuclear Palsy. DaTscan is an adjunct to other diagnostic evaluations. Headache, nausea, vertigo, dry mouth, or dizziness of mild to moderate severity as well as hypersensitivity reactions and injection-site pain have been reported. The DaTscan injection may contain up to 6% of free iodide (iodine 123 or I-123). To decrease thyroid accumulation of I-123, the thyroid gland has to be blocked at least one hour before administration of DaTscan because of the long-term risk for thyroid neoplasia. DaTscan was first approved in the European Union (EU) on July 27, 2000. It is also approved in Israel, Switzerland and in the United States (a total of 33 countries).

Clobazam belongs to the 1,5-benzodiazepine class of drugs with antiepileptic properties. It has been used to treat anxiety and epilepsy since 1970s. In the US clobazam was approved for marketing in October of 2011 for the adjunctive treatment of seizures associated with Lennox-Gastaut syndrome. It is also approved for adjunctive therapy for epilepsy in patients who have not responded to first-line drugs and in children who are refractory to first-line drugs. The mechanism of action for clobazam is not fully understood but is thought to involve what is known as potentiation of GABAergic neurotransmission resulting from binding at a benzodiazepine site at the GABA(A) receptor. Possible side effects: constipation, fever, drowsiness, sedation, ataxia, aggressive behavior, lethargy, drooling, and irritability. Other side effects include: urinary tract infection, pneumonia, cough, dysphagia, dysarthria, bronchitis, insomnia, fatigue, decreased appetite, and increased appetite.

Ezogabine (U.S. adopted name) or retigabine (international nonproprietary name) is one of a family of aminopyrroles with anticonvulsant activity. It is used as an adjunctive treatment for partial epilepsies in treatment-experienced adult patients. The drug was approved by the European Medicines Agency under the trade name Trobalt and by the United States Food and Drug Administration (FDA), under the trade name Potiga. The mechanism by which ezogabine exerts its therapeutic effects has not been fully elucidated. In vitro studies indicate that ezogabine enhances transmembrane potassium currents mediated by the KCNQ (Kv7.2 to 7.5) family of ion channels. By activating KCNQ channels, ezogabine is thought to stabilize the resting membrane potential and reduce brain excitability. This mechanism of action is unique among antiepileptic drugs, and may hold promise for the treatment of other neurologic conditions, including migraine, tinnitus and neuropathic pain. In vitro studies suggest that ezogabine may also exert therapeutic effects through augmentation of GABA-mediated currents.