Pathways

PathWhiz ID Pathway Meta Data

PW127798

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drug action

Deflazacort Action Action Pathway

Homo sapiens
Deflazacort, also known as Emflaza, is a corticosteroid used to treat Duchenne muscular dystrophy (DMD). This dystrophy is an inherited disorder resulting from mutations of the dystrophin gene, which is important for muscle function. This causes serious muscle weakness and progressive breathing and cardiovascular disabilitiy. Deflazacort exerts anti-inflammatory activity in DMD, likely improving various symptoms, including muscle weakness and cardiorespiratory symptoms in addition to delaying their onset. Deflazacort is a corticosteroid prodrug with an active metabolite, 21-deflazacort that results from its activation by plasma esterases. 21-deflazacort binds to the glucocorticoid receptor to exert anti-inflammatory and immunosuppressive effects on the body.The exact mechanism by which deflazacort exerts its therapeutic effects in patients with DMD is unknown but likely occurs via its anti-inflammatory activities. By binding to the glucocorticoid receptor, it probably influences transcription factors AP-1 and NF-kB to block the transcription of COX-2/prostaglandin G/H synthase 2 which reduces the amount of prostanoids being produced from arachidonic acid. Prostanoids such as PGI2 and thromboxane A2 influence effects of inflammation through vasoconstriction/dilation, pain sensitivity and platelet aggregation. 21-deflazacort could also affects the promoter of annexin-1, an important inflammatory protein as it affects leukocytes and blocks phospholipase A2 which reduces the amount of arachidonic acid being cleaved from the phospholipid bilayer. Reducing the amount of arachidonic acid formed further decreases concentrations of prostanoids mentioned calming inflammation.

PW127797

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drug action

Felbamate Action Pathway (new)

Homo sapiens
Felbamate is an anticonvulsant used to treat severe epilepsy, particularly in adults. The mechanism by which Felbamate exerts its anticonvulsant activity is unknown, but in animal tests felbamate has properties in common with other marketed anticonvulsants. In vitro studies have found that it may be an antagonist at the strychnine-insensitive glycine-recognition site of the N-methyl-D-aspartate(NMDA) receptor-ionophore complex. This antagonism of the NMDA receptor blocks the glutamate from activating the receptor and prevents calcium from entering the neuron. This causes hyperpolarization of the neuron which increases the threshold for neuron activation, increasing the seizure threshold and decreasing seizure spread. It has also been indicated that Felbamate has inhibitory actions on GABA receptors and benzodiazepine receptors.

PW127796

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drug action

Edoxaban Action Pathway

Homo sapiens
Edoxaban is a novel oral anticoagulant, used to prevent or reduce the risk of stroke and systemic embolism specifically used for patients who have nonvalvular atrial fibrillation. Edoxaban is administered orally, it can be taken with or without food. It selectively inhibits factor Xa so the cleavage of prothrombin to thrombin is inhibited. Without thrombin, the conversion of fibrinogen to fibrin cannot occur and stops the clotting cascade from proceeding. Metabolized minimally by hydrolysis in the liver and primarily eliminated through the urine. Edoxaban increases the risk of major bleeding such as intracranial hemorrhage and gastrointestinal bleeding. Edoxaban should not be co-administered with other anti-coagulants, anti-platelets, or thrombolytics as it increases the risk of bleeding. Due to the anticoagulant properties herbs and supplements with anticoagulant and antiplatelet activity should be avoided this includes garlic, ginger, bilberry, danshen, piracetam and ginkgo biloba.

PW127795

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drug action

Desirudin Action Pathway

Homo sapiens
Desirudin is an inhibitor of thrombin, similar in structure to hirudin a naturally occurring anticoagulant peptide produced by salivary glands in leeches. This drug is administered to prevent deep vein thrombosis, some possible side effects include bleeding gums, blood collecting under the skin, coughing up blood, bruising and difficulty breathing and or swallowing. Desirudin binds to the active site of thrombin inhibiting the conversion of fibrinogen to fibrin, due to this stopping the formation of a blood clot. This is usually administered subcutaneously, it is then metabolized and eliminated via the kidney. Due to the anticoagulant properties herbs and supplements with anticoagulant and antiplatelet activity should be avoided, this includes ginger, garlic, bilberry, danshen, piracetam and ginkgo biloba.

PW127794

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drug action

Metipranolol Action Pathway (New)

Homo sapiens
Metipranolol is a cardioselective beta blocker. It can be administered orally, where it passes through hepatic portal circulation, and enters the bloodstream and travels to act on cardiomyocytes. In bronchial and vascular smooth muscle, metipranolol can compete with epinephrine for beta-2 adrenergic receptors. By competing with catecholamines for adrenergic receptors, it inhibits sympathetic stimulation of the heart. The reduction of neurotransmitters binding to beta receptor proteins in the heart inhibits adenylate cyclase type 1. Because adenylate cyclase type 1 typically activates cAMP synthesis, which in turn activates PKA production, which then activates SRC and nitric oxide synthase, its inhibition causes the inhibition of cAMP, PKA, SRC and nitric oxide synthase signaling. Following this chain of reactions, we see that the inhibition of nitric oxide synthase reduces nitric oxide production outside the cell which results in vasoconstriction. On a different end of this reaction chain, the inhibition of SRC in essence causes the activation of Caspase 3 and Caspase 9. This Caspase cascade leads to cell apoptosis. The net result of all these reactions is a decreased sympathetic effect on cardiac cells, causing the heart rate to slow and arterial blood pressure to lower; thus, metipranolol administration and binding reduces resting heart rate, cardiac output, afterload, blood pressure and orthostatic hypotension. By prolonging diastolic time, it can prevent re-infarction. One potentially less than desirable effect of non-selective beta blockers like metipranolol is the bronchoconstrictive effect exerted by antagonizing beta-2 adrenergic receptors in the lungs. Clinically, it is used to increase atrioventricular block to treat supraventricular dysrhythmias. Metipranolol also reduce sympathetic activity and is used to treat ocular hypertension or open-angle glaucoma. Blockage of beta-2 receptors causes smooth muscle constriction allowing for the inflow of aqueous humour in the eye to be reduce, effectively reducing the intraocular pressure and aiding in glaucoma. Some side effects of using metipranolol may include changes in vision, difficulty breathing, irregular heartbeat, and bloody nose.

PW127793

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drug action

Cortisone Acetate Action Action Pathway

Homo sapiens
Cortisone acetate is a steroid hormone used for the relief of a wide variety of endocrine, rheumatic, collagen, dermatologic, allergic, ophtalmic, respiratory, hematologic, neoplastic, edamatous, and gastrointestinal diseases and disorders. This molecule is a prodrug and needs to be activated by a dehydrogenase in the liver. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. The duration of action is moderate as it is generally given once daily. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. By binding to the glucocorticoid receptor, it influences transcription factors AP-1 and NF-kB to block the transcription of COX-2/prostaglandin G/H synthase 2 which reduces the amount of prostanoids being produced from arachidonic acid. Prostanoids such as PGI2 and thromboxane A2 influence effects of inflammation through vasoconstriction/dilation, pain sensitivity and platelet aggregation. Cortisone ac├ętate also affects the promoter of annexin-1, an important inflammatory protein as it affects leukocytes and blocks phospholipase A2 which reduces the amount of arachidonic acid being cleaved from the phospholipid bilayer. Reducing the amount of arachidonic acid formed further decreases concentrations of prostanoids mentioned calming inflammation. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections.

PW127791

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drug action

Betrixaban Action Pathway

Homo sapiens
Betrixaban is an anticoagulant that targets and inhibits factor Xa in order to prevent venous thromboembolism. Due to its interaction with factor Xa, the coagulant factor is no longer free and unable to form the prothrombinase complex. Betrixaban is administered orally and rapidly absorbed, if taken with the consumption of food its bioavailability will be reduced greatly. It has minimal hepatic metabolism due to this does not run the risk of accumulation if the liver is impaired. It is mainly eliminated via the gastrointestinal system, feces and urine. Some possible adverse effects are bleeding, hypersensitivity and minimal hepatotoxicity. The anticoagulant does interact with food, this means herbs and supplements with anticoagulant and antiplatelet activity should be avoided such as garlic, ginger, bilberry, dansen, piracetam and ginkgo biloba. Betrixaban should be taken with food despite the bioavailability being decreased and this should also be taken at the same time every day.

PW127790

Pw127790 View Pathway
drug action

Memantine Action Pathway

Homo sapiens
Memantine is an N-methyl-D-aspartate (NMDA) receptor antagonist, also know by the brand names Axura, Ebixa, Marixino, Namenda, Namenda 49 Titration Pack, and Namzaric, which is used to treat and manage moderate to severe dementia. Glutamate is a neurotransmitter in the brain that leads to neuronal excitabiity and excessive stimulation in Alzheimer's Disease, so the inhibition of it helps with Alzheimer's Disease. Memantine has also shown minimal activity for GABA, benzodiazepine, dopamine, adrenergic, histamine, and glycine receptors. It has also shwon minimal activity on voltage-dependent Ca2+, Na+, or K+ channels. Memantine inhibits the influx of calcium caused by chronic NMDA receptor activation by glutamate. The Memantine binds to NMDA receptors, which prevents glutamate from activating the receptor which further prevents the influx of calcium. This leads to an improvement of Alzheimer's dementia symptoms, such as increased cognition. At lower concentrations, often used in clinical settings, it can also enhance neuronal synaptic plasticity in the brain, improve memory, and act as a neuroprotectant against the destruction of neurons. Despite the antagonistic effects against NMDA receptors, Memantine has not been proven to prevent or retard the neurodegeneration seen in patients diagnosed with Alzheimer's disease. It only treats symptoms of Alzheimer's disease.

PW127789

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drug action

Labetalol Action Pathway (New)

Homo sapiens
Labetalol is a non-selective beta blocker and is a racemic mixture of 2 diastereoisomers . It can be administered orally, where it passes through hepatic portal circulation, and enters the bloodstream and travels to act on cardiomyocytes. In bronchial and vascular smooth muscle, labetalol can compete with epinephrine for beta-2 adrenergic receptors. By competing with catecholamines for adrenergic receptors, it inhibits sympathetic stimulation of the heart. The reduction of neurotransmitters binding to beta receptor proteins in the heart inhibits adenylate cyclase type 1. Because adenylate cyclase type 1 typically activates cAMP synthesis, which in turn activates PKA production, which then activates SRC and nitric oxide synthase, its inhibition causes the inhibition of cAMP, PKA, SRC and nitric oxide synthase signaling. Following this chain of reactions, we see that the inhibition of nitric oxide synthase reduces nitric oxide production outside the cell which results in vasoconstriction. On a different end of this reaction chain, the inhibition of SRC in essence causes the activation of Caspase 3 and Caspase 9. This Caspase cascade leads to cell apoptosis. The net result of all these reactions is a decreased sympathetic effect on cardiac cells, causing the heart rate to slow and arterial blood pressure to lower; thus, labetalol administration and binding reduces resting heart rate, cardiac output, afterload, blood pressure and orthostatic hypotension. By prolonging diastolic time, it can prevent re-infarction. One potentially less than desirable effect of non-selective beta blockers like labetalol is the bronchoconstrictive effect exerted by antagonizing beta-2 adrenergic receptors in the lungs. Clinically, it is used to increase atrioventricular block to treat supraventricular dysrhythmias. Labetalol also reduce sympathetic activity and is used to treat hypertension, angina, migraine headaches, and hypertrophic subaortic stenosis. Labetalol can be found under the brand name Trandate, and some side effects of using this drug may include dizziness, headaches, and stomach pain.

PW127788

Pw127788 View Pathway
drug action

Esmolol Action Pathway (New)

Homo sapiens
Esmolol is a cardioselective beta 1 blocker. It can be administered orally, where it passes through hepatic portal circulation, and enters the bloodstream and travels to act on cardiomyocytes. In bronchial and vascular smooth muscle, esmolol can compete with epinephrine for beta-2 adrenergic receptors. By competing with catecholamines for adrenergic receptors, it inhibits sympathetic stimulation of the heart. The reduction of neurotransmitters binding to beta receptor proteins in the heart inhibits adenylate cyclase type 1. Because adenylate cyclase type 1 typically activates cAMP synthesis, which in turn activates PKA production, which then activates SRC and nitric oxide synthase, its inhibition causes the inhibition of cAMP, PKA, SRC and nitric oxide synthase signaling. Following this chain of reactions, we see that the inhibition of nitric oxide synthase reduces nitric oxide production outside the cell which results in vasoconstriction. On a different end of this reaction chain, the inhibition of SRC in essence causes the activation of Caspase 3 and Caspase 9. This Caspase cascade leads to cell apoptosis. The net result of all these reactions is a decreased sympathetic effect on cardiac cells, causing the heart rate to slow and arterial blood pressure to lower; thus, esmolol administration and binding reduces resting heart rate, cardiac output, afterload, blood pressure and orthostatic hypotension. By prolonging diastolic time, it can prevent re-infarction. Esmolol also reduce sympathetic activity and is used to treat hypertension, angina, migraine headaches, and hypertrophic subaortic stenosis. Some side effects of using esmolol may include light headedness, wheezing, and swelling of the hands and feet. It can be found under the brand name Brevibloc.