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Pathways

PathWhiz ID Pathway Meta Data

PW176362

Pw176362 View Pathway
metabolic

Ambroxol Predicted Metabolism Pathway

Homo sapiens
Metabolites of Ambroxol are predicted with biotransformer.

PW127753

Pw127753 View Pathway
drug action

Amcinonide Action Pathway

Homo sapiens
Amcinonide is a topical corticosteroid used for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Amcinonide is a selective glucocorticoid receptor (GC) agonist. 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 the effects of inflammation through vasoconstriction/dilation, pain sensitivity, and platelet aggregation. Amcinonide 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 the concentrations of prostanoids mentioned calming inflammation. Also, amcinonide has a weak affinity for the progesterone receptor, and virtually no affinity for the mineralocorticoid, estrogen, or androgen receptors. This molecule is administered as a topical cream or ointment.

PW144416

Pw144416 View Pathway
drug action

Amcinonide Drug Metabolism Action Pathway

Homo sapiens

PW146416

Pw146416 View Pathway
drug action

Amifampridine Drug Metabolism Action Pathway

Homo sapiens

PW132337

Pw132337 View Pathway
metabolic

Amifostine Drug Metabolism

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

PW145231

Pw145231 View Pathway
drug action

Amifostine Drug Metabolism Action Pathway

Homo sapiens

PW000351

Pw000351 View Pathway
drug action

Amikacin Action Pathway

Homo sapiens
Amikacin is an aminoglycoside antibiotic that inhibits bacterial protein synthesis. Amikacin binds irreversibly to the bacterial 30S ribosomal subunit protein and 16S rRNA and prevents the formation of the initiation complex with messenger RNA. More specifically, amikacin binds four nucleotides of the 16S rRNA and a single amino acid of protein S12. This interferes with the decoding site in the vicinity of nucleotide 1400 in 16S rRNA of the 30S subunit. This region interacts with the wobble base of the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so that incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides, and the breakup of polysomes into nonfunctional monosomes. Aminoglycosides are useful in treating infections from mycobacteria such as, tuberculosis, and aerobic Gram-negative bacteria including, Pseudomonas, Acinetobacter and Enterobacter. Aminoglycosides can also treat Gram-positive bacterial infections but are inferior to other available antibiotics. Aminoglycosides may be used in combination with penicillin type antibiotics. Aminoglycosides are not an effective treatment for anaerobic bacteria, fungi and viruses.

PW125985

Pw125985 View Pathway
drug action

Amikacin Action Pathway (new)

Homo sapiens
Amikacin is a semi-synthetic aminoglycoside antibiotic that is used to treat infections caused by both positive and negative strains of Gram bacteria, as it is considered bacteriocidal. It is commonly administered intravenously or intramuscular injection, and is used to successfully treat bacterial infections caused by Pseudomonas species, Escherichia coli, species of indole-positive Proteus, indole-negative Proteus, Providencia species, Klebsiella-Enterobacter-Serratia species, and Acinetobacter species. Amikacin enters the bacterial cell and interacts in the cytosol with the bacterial ribosome 30S subunit, this interferes with mRNA binding and tRNA acceptor sites which halts protein synthesis. With protein synthesis inhibited this leads to the formation of non-functional and defective peptides. The structure of Amikacin allows it to enter the body and minimize enzymatic deactivation, this is helpful as it reduces bacterial resistance to the drug. 94%-98% of Amikacin is eliminated by the kidneys, relatively unchanged within a 24 hour period. Patients with renal impairment have more difficulty clearing Amikacin and doses have to be adjusted accordingly so no harm comes to the patient. If Amikacin accumulates or too much is administered it can lead to nephrotoxicity, ototoxicity, and neuromuscular blockade. Caution should be taken by patients who are pregnant or breastfeeding as the possible effects of Amikacin on fetal development are unknown and could potentially be harmful.

PW144601

Pw144601 View Pathway
drug action

Amikacin Drug Metabolism Action Pathway

Homo sapiens

PW124026

Pw124026 View Pathway
drug action

Amiloride Action Action Pathway

Homo sapiens
Amiloride is a K+ (potassium-sparing diuretics) that works by directly blocking the epithelial sodium channel mainly in the distal convoluted tubule in the nephrons of the kidney in Homo Sapiens. This pathway focuses on the action of the diuretic Amiloride on the ENaC of the distal convoluted tubule which works by inhibiting sodium reabsorption. This promotes the loss of sodium in the sodium-potassium pump as well as water from the body, but without depleting potassium. Amiloride exerts its potassium-sparing effect through the inhibition of sodium reabsorption at the distal convoluted tubule, cortical collecting tubule, and collecting duct; this decreases the net negative potential of the tubular lumen and reduces both potassium and hydrogen secretion and their subsequent excretion. Amiloride is not an aldosterone antagonist and its effects are seen even in the absence of aldosterone. Usage of this drug alleviates symptoms of edema (swelling), oliguria (decreased urine output), high blood pressure, hypokalemia in patients taking diuretics.