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Pathways

PathWhiz ID Pathway Meta Data

PW146171

Pw146171 View Pathway
drug action

Cetyl alcohol Drug Metabolism Action Pathway

Homo sapiens

PW146215

Pw146215 View Pathway
drug action

Cetylpyridinium Drug Metabolism Action Pathway

Homo sapiens

PW144316

Pw144316 View Pathway
drug action

Cevimeline Drug Metabolism Action Pathway

Homo sapiens

PW128284

Pw128284 View Pathway
drug action

Cevimeline M1 Saliva Excretion Action Pathway

Homo sapiens
Cevimeline is a muscarinic agonist with parasympathomimetic activities that is used for the symptomatic treatment of dry mouth in patients with Sjögren's Syndrome. It is administered as an oral tablet and can be found under the brand name Evoxac. Cevimeline is a parasympathomimetic agent that act as an agonist at the muscarinic acetylcholine receptors M1 and M3. Muscarinic agonists in sufficient dosage can increase secretion of exocrine glands, such as salivary and sweat glands and increase tone of the smooth muscle in the gastrointestinal and urinary tracts. The M1 receptors are common in secretory glands (exocrine glands such as salivary and sweat glands), and their activation results in an increase in secretion from the secretory glands. Therefore, as saliva excretion is increased, the symptoms of dry mouth are relieved.

PW128285

Pw128285 View Pathway
drug action

Cevimeline M3 Salivary Gland Smooth Muscle Contraction Action Pathway

Homo sapiens
Cevimeline is a muscarinic agonist with parasympathomimetic activities that is used for the symptomatic treatment of dry mouth in patients with Sjögren's Syndrome. It can be found under the brand name Evoxac. Cevimeline is a parasympathomimetic agent that act as an agonist at the muscarinic acetylcholine receptors M1 and M3. Muscarinic agonists such as cevimeline bind and activate the muscarinic M1 and M3 receptors. The M1 receptors are common in secretory glands (exocrine glands such as salivary and sweat glands), and their activation results in an increase in secretion from the secretory glands. The M3 receptors are found on smooth muscles and in many glands which help to stimulate secretion in salivary glands, and their activation generally results in smooth muscle contraction and increased glandular secretions. Therefore, as saliva excretion is increased, the symptoms of dry mouth are relieved. Salivary secretion is largely dependent upon the activation of acinar cell fluid transport, achieved through intracellular formation of inositol triphosphate and elevated calcium concentration and activation of ion transporting proteins. Sustained salivary secretion requires influx of extracellular calcium across the plasma membrane of acinar cells, which is referred to as store-operated calcium entry. Possible side effects of using Civimeline may include bladder pain, body aches, and difficulty breathing.

PW122269

Pw122269 View Pathway
physiological

charlie

Homo sapiens

PW145785

Pw145785 View Pathway
drug action

Chenodeoxycholic acid Drug Metabolism Action Pathway

Homo sapiens

PW121715

Pw121715 View Pathway
disease

CHILD Syndrome

Mus musculus
CHILD Syndrome, (Congenital Hemidysplasia with Icthyosiform Erythroderma and Limb Defects; Ichthyosiform Eruthroderma, Unilateral, with Epsilateral Malformations, Especially Absence Deformity of Limbs) is caused by a mutation in the gene encoding NADH steroid dehydrogenase-like protein (NSDHL). A defect in sterol-4 alpha-carboxylate 3-dehydrogenase, which normally catalyzes the reaction 3-beta-hydroxy-4-beta-methyl-5-alpha-cholest-7-ene-4-alpha-carboxylate + NAD+ = 4-alpha-methyl-5-alpha-cholest-7-en-3-one + CO2 + NADH, causes accumulation of 8(9)cholestenol and 8-dehydrocholesterol in plasma. Symptoms of CHILD syndrome include hearing defects, hemidysplasia, unilateral hypomelia, ichthyosiform nevi, limb abnormalities, lung hypoplasia, and punctate calcifications.

PW127201

Pw127201 View Pathway
disease

CHILD Syndrome

Homo sapiens
CHILD Syndrome, (Congenital Hemidysplasia with Icthyosiform Erythroderma and Limb Defects; Ichthyosiform Eruthroderma, Unilateral, with Epsilateral Malformations, Especially Absence Deformity of Limbs) is caused by a mutation in the gene encoding NADH steroid dehydrogenase-like protein (NSDHL). A defect in sterol-4 alpha-carboxylate 3-dehydrogenase, which normally catalyzes the reaction 3-beta-hydroxy-4-beta-methyl-5-alpha-cholest-7-ene-4-alpha-carboxylate + NAD+ = 4-alpha-methyl-5-alpha-cholest-7-en-3-one + CO2 + NADH, causes accumulation of 8(9)cholestenol and 8-dehydrocholesterol in plasma. Symptoms of CHILD syndrome include hearing defects, hemidysplasia, unilateral hypomelia, ichthyosiform nevi, limb abnormalities, lung hypoplasia, and punctate calcifications.

PW121940

Pw121940 View Pathway
disease

CHILD Syndrome

Rattus norvegicus
CHILD Syndrome, (Congenital Hemidysplasia with Icthyosiform Erythroderma and Limb Defects; Ichthyosiform Eruthroderma, Unilateral, with Epsilateral Malformations, Especially Absence Deformity of Limbs) is caused by a mutation in the gene encoding NADH steroid dehydrogenase-like protein (NSDHL). A defect in sterol-4 alpha-carboxylate 3-dehydrogenase, which normally catalyzes the reaction 3-beta-hydroxy-4-beta-methyl-5-alpha-cholest-7-ene-4-alpha-carboxylate + NAD+ = 4-alpha-methyl-5-alpha-cholest-7-en-3-one + CO2 + NADH, causes accumulation of 8(9)cholestenol and 8-dehydrocholesterol in plasma. Symptoms of CHILD syndrome include hearing defects, hemidysplasia, unilateral hypomelia, ichthyosiform nevi, limb abnormalities, lung hypoplasia, and punctate calcifications.