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Showing 21 - 30 of 48704 pathways
SMPDB ID Pathway Chemical Compounds Proteins


Pw000070 View Pathway

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency

4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency (SSADH; Gamma-hydroxybutyric acidemia) inhibits the formation of succinate from GABA. This deficiency results in urinary excretion of 4-hydroxybutyric acid. In vivo proton MR also indicates elevated GABA levels as compared with an age-matched control. Symptoms include ataxia, chorea or athetosis, motor retardation, seizures, macrocephaly and delayed or abnormal speech development.


Pw000476 View Pathway

5-Oxoprolinase Deficiency

5-oxoprolinase deficiency can be caused by heterozygous or homozygous mutation in the OPLAH gene (5-Oxoprolinase). Patients are relatively asymptomatic but they do exhibit high levels of urinary excretion of 5-oxoproline. Patients also exhibit plasma 5-oxoproline levels of about 0.18 mM or higher. Patients tend to exhibit transient hypoglycemia.


Pw000074 View Pathway


5-Oxoprolinuria (5-Oxoprolinase deficiency) is a result of a defect in the gamma-glutamyl cycle due to either 5-oxoprolinase or glutathione synthetase deficiency. In the case of glutathione synthetase deficiency, the glycine is not incorporated into gamma-glutamylcysteine. In the case of 5-oxoprolinase, however, pyroglutamic acid accumulates. Symptoms include anemia, mental retardation, metabolic acidosis, respiratory distress and urolithiasis.


Pw000714 View Pathway
Drug Action

Abacavir Action Pathway

Abacavir (also known as Ziagen or Epzicom) is an antiviral agent that is used for treating HIV/AID. Cellular enzyme converts abacavir to its activate metabolite, carbovir triphosphate, for inhibiting HIV-1 reverse transcriptase (RT) by competing with dGTP, which is the natural substrate of RT. Without HIV-1 reverse transcriptase, complementary DNA (cDNA) could not be generated; therefore, viral DNA couldn't be completed.


Pw000291 View Pathway
Drug Action

Abciximab Action Pathway

Abciximab (also known as c7E3 Fab) is integrin (integrin alpha-IIb and integrin beta-3) receptor antagonist. Binding of abciximab to integrin receptor will block any large molecule to attach on the receptor, which will lead to block any associated signal transduction pathways.


Pw000364 View Pathway
Drug Action

Acebutolol Action Pathway

Acebutolol (also known as Sectral or Prent) is a selective β1 adrenergic receptor antagonist (beta blocker), which can be used for treatment of high blood pressure (hypertension) and irregular heartbeats (arrhythmias). Acebutolol also has the ability to mild intrinsic sympathomimetic activity (ISA) with effective range of dosage. Adrenaline (also known as epinephrine) can activate β1 adrenergic receptor so that the heart rate and output will be increased. Renin is a hormone that generated from kidney, which could lead to constriction of blood vessels. Beta blockers could efficiently prohibit renin release.


Pw000312 View Pathway
Drug Action

Acenocoumarol Action Pathway

Acenocoumarol (also known as Nitrowarfarin or Sinthrome) is an anticoagulant that inhibit the liver enzyme vitamin K reductase, which cause Vitamin K1 2,3-epoxide could not be catalyzed by vitamin K reductase to form vitamin KH2, the reduced form of vitamin K. Vitamin K-dependent coagulation factors (II, VII, IX, and X) requires its cofactor, vitamin K to facilitate the activation and gamma-carboxylation. Inhibition of vitamin K reductase results in reduced concentration of vitamin KH2, which will ultimately lead to decreased coagulability of the blood and reduced cleavage of fibrinogen into fibrin.


Pw000687 View Pathway
Drug Action

Acetaminophen Action Pathway

Acetaminophen (also named paracetamol or APAP) is not a Nonsteroidal anti-inflammatory drugs (NSAIDs). However, it still can be used to treat pain and fever. Acetaminophen can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of acetaminophen.


Pw000616 View Pathway
Drug Metabolism

Acetaminophen Metabolism Pathway

Acetaminophen (APAP) is metabolized primarily in the liver. Glucuronidation is the main route, accounting for 45-55% of APAP metabolism, and is mediatied by UGT1A1, UGT1A6, UGT1A9, UGT2B15 in the liver and UGT1A10 in the gut. APAP can also by metabolized via sulfation, accounting for 30-35% of the metabolism. In the liver, this step is catalyzed by the sulfotransferases SULT1A1, SULT1A3, SULT1A4, SULT1E1 and SULT2A1. Moreover, APAP can also be activated to form the toxic N-acetyl-p-benzoquinone imine (NAPQI) under the mediation of CYP3A4, CYP2E1, CYP2D6 CYP1A2, CYP2E1 and CYP2A6.


Pw000128 View Pathway
Drug Action

Acetylsalicylic Acid Action Pathway

Acetylsalicylic acid, also known as ASA or aspirin, belongs to a class of drugs known as non-steroidal anti-inflammatory drugs (NSAIDs). In addition to its anti-inflammatory properties, aspirin also acts as an analgesic, antipyretic and antithrombotic agent. Like most other NSAIDs, aspirin exerts its therapeutic effects by inhibiting prostaglandin G/H synthase 1 and 2, better known as cyclooxygenase-1 and -2 or simply COX-1 and -2. COX-1 and -2 catalyze the conversion of arachidonic acid to prostaglandin G2 and prostaglandin G2 to prostaglandin H2. Prostaglandin H2 is the precursor to a number of other prostaglandins, such as prostaglandin E2, involved in pain, fever and inflammation. The antipyretic properties of aspirin arise from inhibition of prostaglandin E2 synthesis in the preoptic region of the hypothalamus. Interference with adhesion and migration of granulocytes, polymorphonuclear leukocytes and macrophages at sites of inflammation account for its anti-inflammatory effects. The analgesic effects of aspirin likely occur due to peripheral action at the site of injury and possibly within the CNS. Aspirin is unique from other NSAIDs in that it is an irreversible COX inhibitor. Aspirin irreversibly acetylates a serine side chain of COX rendering the enzyme inactive. Enzyme activity can only be regained by production of more cyclooxygenase. This unique property of aspirin and its higher selectivity for COX-1 over COX-2 makes it an effective antiplatelet agent. Platelets contain COX-1, a key enzyme in the production thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation. Since platelets lack the ability to make more enzyme, TXA2 production is inhibited for the lifetime of the platelet (approximately 8 – 12 days). Aspirin is commonly used at low doses to prevent cardiovascular events such as strokes and heart attacks. At higher doses, aspirin may be used as an analgesic, anti-inflammatory and antipyretic. Aspirin may cause gastric irritation and bleeding by inhibiting the synthesis of prostaglandins that enhance and maintain the protective gastric mucous layer.
Showing 21 - 30 of 48704 pathways