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PathWhiz ID Pathway Meta Data

PW128615

Pw128615 View Pathway
drug action

Vanoxerine Dopamine Reuptake Inhibitor Action Pathway

Homo sapiens
Vanoxerine is an investigational drug that is a selective dopamine transporter antagonist that has not been approved for therapeutic use but is indicated to help treat cocaine addiction. It was developed as a treatment for depression but was found to have a higher affinity for the dopamine reuptake transporter with a slower dissociation rate than cocaine, indicating its use in cocaine addiction. Vanoxerine does have a moderate potential to be abused by humans as it stimulates the nervous system through the reuptake of norepinephrine and dopamine, which prolongs their duration in the synapse so that they can bind more readily to the receptors. This drug can inhibit cocaine binding sites at the dopamine transporters. The mechanism is not fully understood, but may be similar to other dopamine reuptake inhibitors where Vanoxerine would cross the blood-brain barrier through diffusion. Dopamine is synthesized in the ventral tegmental area of the brain from tyrosine being synthesized into L-dopa by the enzyme Tyrosine 3-monooxygenase . L-Dopa is then synthesized into dopamine with the enzyme aromatic-L-amino-acid decarboxylase. Dopamine then travels to the prefrontal cortex, which is released into the synapse when the neuron is stimulated and fires. Vanoxerine binds to the sodium-dependent dopamine transporter, preventing dopamine from re-entering the presynaptic neuron. The dopamine then binds to Dopamine D4 receptors on the postsynaptic membrane. The dopamine D4 receptor activates the Gi protein cascade which inhibits adenylate cyclase. This prevents adenylate cyclase from catalyzing ATP into cAMP.

PW144966

Pw144966 View Pathway
drug action

Vardenafil Drug Metabolism Action Pathway

Homo sapiens

PW176415

Pw176415 View Pathway
metabolic

Vardenafil Predicted Metabolism Pathway

Homo sapiens
Metabolites of Vardenafil are predicted with biotransformer.

PW145352

Pw145352 View Pathway
drug action

Varenicline Drug Metabolism Action Pathway

Homo sapiens

PW144258

Pw144258 View Pathway
drug action

Vasopressin Drug Metabolism Action Pathway

Homo sapiens

PW000447

Pw000447 View Pathway
protein

Vasopressin Regulation of Water Homeostasis

Homo sapiens
The vasopressin V2 receptor is found in the kidneys. It serves a role in maintaining corporal water homeostasis. Malfunction of this receptor can lead to Nephrogenic Diabetes Insipidus. Vasopressin (aka Antidiuretic hormone) activates both follicle-stimulating hormone receptor as well as the V2 receptor G protein complex. From this complex, Guanine nucleotide binding protein G(s) protein reacts with Adenylate Cyclase Type 2, Adeonsine Triphosphate, as well as GTP and magnesium to produce cAMP and Pyrophosphate. cAMP then activates PKA (protein kinase A) which leads to changes in the concentration of water in urine.

PW109223

Pw109223 View Pathway
protein

Vasopressin Regulation of Water Homeostasis

Bos taurus
The vasopressin V2 receptor is found in the kidneys. It serves a role in maintaining corporal water homeostasis. Malfunction of this receptor can lead to Nephrogenic Diabetes Insipidus. Vasopressin (aka Antidiuretic hormone) activates both follicle-stimulating hormone receptor as well as the V2 receptor G protein complex. From this complex, Guanine nucleotide binding protein G(s) protein reacts with Adenylate Cyclase Type 2, Adeonsine Triphosphate, as well as GTP and magnesium to produce cAMP and Pyrophosphate. cAMP then activates PKA (protein kinase A) which leads to changes in the concentration of water in urine.

PW109263

Pw109263 View Pathway
protein

Vasopressin Regulation of Water Homeostasis

Rattus norvegicus
The vasopressin V2 receptor is found in the kidneys. It serves a role in maintaining corporal water homeostasis. Malfunction of this receptor can lead to Nephrogenic Diabetes Insipidus. Vasopressin (aka Antidiuretic hormone) activates both follicle-stimulating hormone receptor as well as the V2 receptor G protein complex. From this complex, Guanine nucleotide binding protein G(s) protein reacts with Adenylate Cyclase Type 2, Adeonsine Triphosphate, as well as GTP and magnesium to produce cAMP and Pyrophosphate. cAMP then activates PKA (protein kinase A) which leads to changes in the concentration of water in urine.

PW109175

Pw109175 View Pathway
protein

Vasopressin Regulation of Water Homeostasis

Mus musculus
The vasopressin V2 receptor is found in the kidneys. It serves a role in maintaining corporal water homeostasis. Malfunction of this receptor can lead to Nephrogenic Diabetes Insipidus. Vasopressin (aka Antidiuretic hormone) activates both follicle-stimulating hormone receptor as well as the V2 receptor G protein complex. From this complex, Guanine nucleotide binding protein G(s) protein reacts with Adenylate Cyclase Type 2, Adeonsine Triphosphate, as well as GTP and magnesium to produce cAMP and Pyrophosphate. cAMP then activates PKA (protein kinase A) which leads to changes in the concentration of water in urine.

PW000237

Pw000237 View Pathway
drug action

Vatalanib Action Pathway

Homo sapiens
Vatalanib is an anti-VEGFR molecule 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. Vatalanib exerts its effect by binding to intracellular tyrosine kinase domain of VEGFR-2 and preventing receptor autophosphorylation and activation of downstream pathways, resulting in suppression of angiogenesis.