Loader

Pathways

PathWhiz ID Pathway Meta Data

PW132369

Pw132369 View Pathway
metabolic

Bethanidine Drug Metabolism

Homo sapiens
Bethanidine is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Bethanidine passes through the liver and is then excreted from the body mainly through the kidney.

PW144347

Pw144347 View Pathway
drug action

Bethanidine Drug Metabolism Action Pathway

Homo sapiens

PW146746

Pw146746 View Pathway
drug action

Betiatide Drug Metabolism Action Pathway

Homo sapiens

PW128030

Pw128030 View Pathway
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.

PW146520

Pw146520 View Pathway
drug action

Betrixaban Drug Metabolism Action Pathway

Homo sapiens

PW146533

Pw146533 View Pathway
drug action

Betulinic Acid Drug Metabolism Action Pathway

Homo sapiens

PW000236

Pw000236 View Pathway
drug action

Bevacizumab Action Pathway

Homo sapiens
Bevacizumab is a humanized anti-VEGF monoclonal antibody used in the treatment of cancer. Cancer cells tend to overexpress VEGF, which stimulates angiogenesis, facilitating cancer growth and metastasis. The majority of VEGF’s effects are mediated through its binding to the VEGFR-2 receptor on endothelial cell surfaces. Upon binding, the receptor autophosphorylates and initiates a signalling cascade, starting with the activation of CSK. CSK phosphorylates Raf-1, which subsequently phosphorylates MAP kinase kinase, which phosphorylates MAP kinase. The activated MAP kinase enters the nucleus and stimulates the expression of angiogenic factors resulting in increased cell proliferation, migration, permeability, invasion, and survival. Binding of VEGF to VEGFR-2 also activates phospholipase C PIP2 into DAG and IP3. DAG may be involved in the activation of Raf-1 leading to angiogenesis, while IP3 activates PI3K and triggers calcium release from the endoplasmic reticulum. This ultimately leads to the activation of nitric oxide synthase and the production of nitric oxide, which stimulates vasodilation and increases vascular permeability. In cancer, VEGF has also been shown to bind to the VEGFR-1 receptor. However, its effects on angiogenesis are unclear at the moment. There are some evidence to show that VEGFR-1 may cross-talk with VEGFR-2 and initiate the signalling cascades described above. Bevacizumab exerts its effect by binding to extracellular VEGF and preventing its binding to receptors on the endothelial cell surfaces. This in turns inhibits the MAP and IP3 and supresses angiogenesis.

PW124122

Pw124122 View Pathway
drug action

Bevacizumab VEGF Inhibitor Action Pathway

Homo sapiens
Bevacizumab is a humanized monoclonal antibody administered intravenously to treat cancers such as colorectal cancer; non-small cell lung cancer; glioblastoma; hepatocellular cancer; renal cell carcinoma; cervical cancer; and epithelial ovarian, fallopian tube, or primary peritoneal cancer. It targets vascular endothelial growth factor (VEGF) in the blood. When cancer grows and spreads, the blood and oxygen supplies become insufficient. In response, the tumor cells secrete VEGF which enters the blood and binds the VEGF receptor-1 and VEGF receptor-2 on endothelial cells in the blood vessels. This activates the VEGF signaling pathway in the endothelial cells which promotes the growth of new blood vessels to supply the cancer cells with a greater blood and oxygen supply. Bevacizumab binds to VEGF in the blood and inactivates it, preventing its interaction with the VEGF receptors. The VEGF signaling pathway is not activated and angiogenesis does not occur. The cancer cells are starved of blood and oxygen, preventing the growth and spread of cancer. Bevacizumab may have side effects like epistaxis, headache, dizziness, fatigue, hypertension, rhinitis, dry skin, back pain, excessive bleeding, skin rash, poor wound healing, hemorrhage, thrombosis, renal dysfunction and bowel, stomach or nasal septum perforation.

PW000645

Pw000645 View Pathway
drug action

Bevantolol Action Pathway

Homo sapiens
Bevantolol hydrocholride, also known as bevantolol, is a cardioselective beta blocker prescribed to treat angina pectoris and hypertension. Bevantolol is an antagonist of beta-1 adrenoreceptors to block the G protein signalling cascade and inhibit epinephrine induced sympathetic activation such as, increased heart rate. It does not have intrinsic sympathomimetic activity therefore does not stimulate beta-adrenergic receptors. This results in a decrease in preload and blood pressure.

PW124257

Pw124257 View Pathway
drug action

Bevantolol Beta Blocker Cardiac Action Pathway

Homo sapiens
Bevantolol is a beta blocker and calcium channel blocker. It is an oral drug used for the treatment of angina pectoris and hypertension. It targets the myocytes in heart where it acts mainly as a beta-1 adrenergic receptor antagonist, but also an L-type calcium channel blocker. It exerts it’s effects by inhibiting beta-1 adrenergic receptors, which is coupled to the G-protein signaling cascade. Inhibition of this receptor prevents activation of the signaling cascade which activates protein kinase. Protein kinase is required to activate calcium channels in the cell membrane, causing them to open and allow Ca2+ to enter the cell. Ca2+ activates the ryanodine receptor on the sarcoplasmic reticulum, which transports Ca2+ from the sarcoplasmic reticulum into the cytosol. Ca2+ in the cytosol binds to troponin to cause muscle contraction. Since protein kinase activation does not occur, there is a low concentration of Ca2+ in the cell. The low concentration of Ca2+ means that less Ca2+ binds to troponin, reducing inotropy/muscle contraction. In cardiac pacemaker cells a decrease in intracellular Ca2+ decreases the slope of phase 4 of the action potential. The time taken to reach threshold is longer, therefore, the heart rate is decreased. Due to the decreased force of contraction and heart rate, the blood pumped of the heart exerts less force on the blood vessels, thus the blood pressure decreases. This is also effective for treating angina because lowering the heart rate and force of contraction reduces the oxygen demand and how hard the heart has to work. Possible side effects from taking bevantolol include fatigue, headache, dizziness, edema and gastrointestinal upset.