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.

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.

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.

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.

Dabigatran (Pradaxa, Prazaxa) is an anticoagulant medication that can be taken by mouth. FDA approved on October 19, 2010. Dabigatran directly inhibits thrombin in a concentration-dependent, reversible, specific, and competitive manner which results in a prolongation of aPTT (partial thromboplastin time), ECT (Ecarin clotting time), and TT (thrombin time). It may increase INR but this laboratory parameter is relatively insensitive to the activity of dabigatran. Dabigatran is indicated for the prevention of venous thromboembolic events in patients who have undergone elective hip or knee replacement surgery (based on RE-NOVATE, RE-MODEL, and RE-MOBILIZE trials). In 2010, it was approved in the US and Canada for prevention of stroke and systemic embolism in patients with atrial fibrillation (approval based on the RE-LY trial). Contraindications: severe renal impairment (CrCL < 30 ml/min); haemorrhagic manifestations, bleeding diathesis or spontaneous or pharmacologic impairment of haemostasis; lesions at risk of clinically significant bleeding (e.g. extensive cerebral infarction (haemorrhagic or ischemic) in the last 6 months, active peptic ulcer disease); concomitant treatment with P-glycoprotein inhibitors (e.g. oral ketoconazole, verapamil); and those with known hypersensitivity to dabigatran, dabigatran etexilate or any ingredient used in the formulation or component of the container. As of December 2012, dabigatran is contraindicated in patients with mechanical prosthetic heart valves.

Dabigatran (Pradaxa, Prazaxa) is an anticoagulant medication that can be taken by mouth. FDA approved on October 19, 2010. Dabigatran directly inhibits thrombin in a concentration-dependent, reversible, specific, and competitive manner which results in a prolongation of aPTT (partial thromboplastin time), ECT (Ecarin clotting time), and TT (thrombin time). It may increase INR but this laboratory parameter is relatively insensitive to the activity of dabigatran. Dabigatran is indicated for the prevention of venous thromboembolic events in patients who have undergone elective hip or knee replacement surgery (based on RE-NOVATE, RE-MODEL, and RE-MOBILIZE trials). In 2010, it was approved in the US and Canada for prevention of stroke and systemic embolism in patients with atrial fibrillation (approval based on the RE-LY trial). Contraindications: severe renal impairment (CrCL < 30 ml/min); haemorrhagic manifestations, bleeding diathesis or spontaneous or pharmacologic impairment of haemostasis; lesions at risk of clinically significant bleeding (e.g. extensive cerebral infarction (haemorrhagic or ischemic) in the last 6 months, active peptic ulcer disease); concomitant treatment with P-glycoprotein inhibitors (e.g. oral ketoconazole, verapamil); and those with known hypersensitivity to dabigatran, dabigatran etexilate or any ingredient used in the formulation or component of the container. As of December 2012, dabigatran is contraindicated in patients with mechanical prosthetic heart valves.

Fingolimod (FTY720) is a sphingosine 1-phosphate receptor modulator indicated and approved for the treatment of relapsing-remitting multiple sclerosis. Fingolimod (trade name Gilenya, Novartis) is metabolized by sphingosine kinase to the active metabolite, fingolimod-phosphate. Fingolimod-phosphate is a sphingosine 1-phosphate receptor modulator, and binds with high affinity to sphingosine 1-phosphate receptors 1, 3, 4, and 5. Fingolimod-phosphate blocks the capacity of lymphocytes to egress from lymph nodes, reducing the number of lymphocytes in peripheral blood. The mechanism by which fingolimod exerts therapeutic effects in multiple sclerosis is unknown, but may involve reduction of lymphocyte migration into the central nervous system. Fingolimod was approved as a first-in-class, orally active drug for relapsing multiple sclerosis in 2010, and its applications in other disease conditions are currently under clinical trials.

Cabazitaxel (JEVTANA®) is an antineoplastic agent belonging to the taxane class and is used to treat people with prostate cancer that has progressed despite treatment with docetaxel. It is prepared by semi-synthesis with a precursor extracted from yew needles (10-deacetylbaccatin III). Cabazitaxel (JEVTANA®) is a microtubule inhibitor. It binds to tubulin and promotes its assembly into microtubules while simultaneously inhibiting disassembly. This leads to the stabilization of microtubules, which results in the inhibition of mitotic and interphase cellular functions. The cell is then unable to progress further into the cell cycle, being stalled at metaphase, thus triggering apoptosis of the cancer cell.

Cabazitaxel (JEVTANA®) is an antineoplastic agent belonging to the taxane class and is used to treat people with prostate cancer that has progressed despite treatment with docetaxel. It is prepared by semi-synthesis with a precursor extracted from yew needles (10-deacetylbaccatin III). Cabazitaxel (JEVTANA®) is a microtubule inhibitor. It binds to tubulin and promotes its assembly into microtubules while simultaneously inhibiting disassembly. This leads to the stabilization of microtubules, which results in the inhibition of mitotic and interphase cellular functions. The cell is then unable to progress further into the cell cycle, being stalled at metaphase, thus triggering apoptosis of the cancer cell.

Dabigatran (Pradaxa, Prazaxa) is an anticoagulant medication that can be taken by mouth. FDA approved on October 19, 2010. Dabigatran directly inhibits thrombin in a concentration-dependent, reversible, specific, and competitive manner which results in a prolongation of aPTT (partial thromboplastin time), ECT (Ecarin clotting time), and TT (thrombin time). It may increase INR but this laboratory parameter is relatively insensitive to the activity of dabigatran. Dabigatran is indicated for the prevention of venous thromboembolic events in patients who have undergone elective hip or knee replacement surgery (based on RE-NOVATE, RE-MODEL, and RE-MOBILIZE trials). In 2010, it was approved in the US and Canada for prevention of stroke and systemic embolism in patients with atrial fibrillation (approval based on the RE-LY trial). Contraindications: severe renal impairment (CrCL < 30 ml/min); haemorrhagic manifestations, bleeding diathesis or spontaneous or pharmacologic impairment of haemostasis; lesions at risk of clinically significant bleeding (e.g. extensive cerebral infarction (haemorrhagic or ischemic) in the last 6 months, active peptic ulcer disease); concomitant treatment with P-glycoprotein inhibitors (e.g. oral ketoconazole, verapamil); and those with known hypersensitivity to dabigatran, dabigatran etexilate or any ingredient used in the formulation or component of the container. As of December 2012, dabigatran is contraindicated in patients with mechanical prosthetic heart valves.