Warburg Effect,Metabolic

The Warburg Effect refers to the phenomenon that occurs in most cancer cells where instead of generating energy with a low rate of glycolysis followed by oxidizing pyruvate via the Krebs cycle in the mitochondria, the pyruvate from a high rate of glycolysis undergoes lactic acid fermentation in the cytosol. As the Krebs cycle is an aerobic process, in normal cells lactate production is reserved for anaerobic conditions. However, cancer cells preferentially utilize glucose for lactate production via this “aerobic glycolysis”, even when oxygen is plentiful. The Warburg Effect is thought to be the result of mutations to oncogenes and tumour suppressor genes. It may be an adaptation to low-oxygen environments within tumors, the result of cancer genes shutting down the mitochondria, or a mechanism to aid cell proliferation via increased glycolysis. The Warburg Effect involves numerous pathways, including growth factor stimulation, transcriptional activation, and glycolysis promotion.


Phenindione Action Pathway,Drug Action

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Phenindione (also known as Dindevan and Fenilin) 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.


Dicoumarol Action Pathway,Drug Action

Dicoumarol (also known as bishydroxycoumarin) 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.


Bopindolol Action Pathway,Drug Action

Bopindolol (also known as Sandonorm) is a selective β1 adrenergic receptor antagonist (beta blocker), which can be used for treatment of high blood pressure (hypertension) and irregular heartbeats (arrhythmias). Bopindolol 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.


Carteolol Action Pathway,Drug Action

Carteolol (also known as Cartrol or Ocupress) is a selective β1 adrenergic receptor antagonist (beta blocker), which can be used for treatment of high blood pressure (hypertension) and irregular heartbeats (arrhythmias). Carteolol 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.


Timolol Action Pathway,Drug Action

Timolol is a beta blocker medication, making it part of the antihypertensive drug class. It relieves symptoms such as tachycardia, vascular headaches, hypertension, angina and tremors. Timolol, much like propranolol or oxprenolol, begins its journey by inhibiting the beta-1 adrenergic receptors in the heart. Entering the myocyte, this activates a G-protein signalling cascade, which activates cAMP -dependent protein kinase type 1-alpha regulatory subunit. From there, cAMP-dependent protein kinase catalytic subunit alpha activates outage-dependent L-type calcium channel subunit alpha 1C and 2 other transports which bring calcium into the myocyte from outside of the cell. cAMP-dependent protein kinase catalytic subunit alpha is activated through ryanodine receptor 2, which is also transporting calcium into the myocyte from the the sarcoplasmic reticulum. The calcium and calmodulin then activate myosin light chain kinase, which is located in the smooth vascular muscle. This, paired with the calcium activating a series of troponin enzymes that activate tropomyosin enzymes in the striated muscle, results in a muscle contraction. Then in the cell membrane we have PIP2(16:0/20:3(8Z,11Z,14Z)) catalyzing into DG(14:0/14:1(9Z)/0:0) and inositol 1,4,5-triphosphate with the help of the enzyme 1-phosphatidylinositol 4,5-biphosphate phosphodiesterase beta-1. This enzyme is activated through the G-protein signalling cascade, which stems from the type-1 angiotensin II receptor. Around the cell there are many transports happening through many different transporters, leading in and out of the cell Some of the transports into the cell include sodium and calcium, while transports are also working hard to constantly export potassium from the cell. Returning to the sarcoplasmic reticulum, cardiac phospholamban inhibits the transporter sarcoplasmic/endoplasmic reticulum calcium ATPase 2, which sees water and ATP catalyzed through it to become phosphorus and ADP, while transporting calcium into the sarcoplasmic reticulum.


Sotalol Action Pathway,Drug Action

Sotalol is a beta-adrenergic receptor antagonist, which is a treatment regimen for heart failure such as abnormal heart rhythms. Sotalol inhibits response to adrenergic stimuli by competitively blocking β1-adrenergic receptors within the myocardium and β2-adrenergic receptors within bronchial and vascular smooth muscle. The electrophysiologic effects of sotalol may be due to its selective inhibition of the rapidly activating component of the potassium channel involved in the repolarization of cardiac cells.


Epinephrine Action Pathway,Drug Action

Epinephrine can be derived from phenylalanine and tyrosine and it is an active sympathomimetic hormone that can be secreted from adrenal medulla. Epinephrine can stimulate alpha-  and beta- adrenergic systems by binding on alpha-1 and beta-1 adrenergic receptors to make gastrointestinal relaxation, stimulates the heart, etc. Epinephrine can also be used to delay absorption of local anesthetics, constrict arterioles in skin and gut while dilating arterioles in leg muscles, increase glycogen hydrolysis to glucose in liver to raise up blood sugar level and breaking down lipids in adipocytes. Epinephrine can also play role as suppressive agent in immune system.


Dobutamine Action Pathway,Drug Action

Dobutamine is a type of medication that can be used for treating heart failure and cardiogenic shock. Dobutamine can bind to beta-1 adrenergic receptor on the heart cell which lead to mild chronotropic, arrhythmogenic, hypertensive and vasodilative effects. Dobutamine can also bind to beta-2 or alpha receptors. For patients with cardiac decompensation, dobutamine is required for inotropic support.


Isoprenaline Action Pathway,Drug Action

Isoprenaline (also known as isoproterenol) is a selective beta adrenergic bronchodilator that can be used for treating slow heart rate (bradycardia), heart block, and rarely for asthma. Isoprenaline can bind and inhibit beta-1 adrenergic receptor on both vascular smooth muscle, which lead to inhibition of vasoconstriction in peripheral blood vessels and adrenergic stimulation of endothelial cell function.


Arbutamine Action Pathway,Drug Action

Arbutamine is a synthetic catecholamine used to initiate a cardiac stress response to mimic exercise to detect coronary artery disease. Arbutamine has nonselective beta and weak alpha-1-adrenergic activity which causes increased chronotropic activity (increase in heart rate) and inotropic activity (increase myocardial contractility). These effects mimic the cardiovascular effects of exercise. For patients with cardiovascular artery disease, arbutamine can induce myocardial ischemia. Arbutamine is delivered via a computer controlled closed-loop system. The infusion of arbutamine is based off the heart rate feedback. The system monitors heart rate and blood pressure throughout infusion with alarms for physiological changes or problems.


Amiodarone Action Pathway,Drug Action

Amiodarone, trade name Cordarone and Nexterone, is an antianginal and a class III antiarrhythmic drug prescribed to treat irregular heart rhythms. The drug inhibits Na,K-activated myocardial adenosine triphosphatase, calcium and potassium channels and beta adrenergic receptors causing an increase in ventricular and atrial muscle action duration. This inhibition causes prevents repolarization of the cells causing heart rate to decrease and vascular resistance to decrease. Amiodarone exerts its antiarrhythmic effect by prolonging the duration of myocardial cell-action potentials. Amiodarone is unique to other class III antiarrhythmic drugs due to its effect on beta adrenergic receptors, calcium channels and sodium channels.


Levobunolol Action Pathway,Drug Action

Levobunolol (also known as Betagan) is an ophthalmic beta blocker (non-selective) that can produce cardiovascular effects and systemic pulmonary effects. Levobunolol bind to beta1-adrenergic and beta2-adrenergic receptors in heart and vascular smooth muscle to block the binding of other adrenergic neurotransmitters such as norepinephrine, which lead to decreased blood pressure, heart rate and cardiac output.


Metipranolol Action Pathway,Drug Action

Metipranolol (also known as Betanol or Disorat) is an  beta blocker (non-selective) that can used as an antihypertensive, antiarrhythmic and antiglaucoma agent. Metipranolol binds to beta1-adrenergic and beta2-adrenergic receptors in heart and vascular smooth muscle. Metipranolol demonstrates low intrinsic sympathomimetic activity, and weak local anesthetic (membrane-stabilizing) and myocardial depressant activity. Metipranolol can also reduce the producion of aqueous humor.


Bevantolol Action Pathway,Drug Action

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.


Practolol Action Pathway,Drug Action

Practolol (also known as Eraldin or Dalzic) is a beta blocker (non-selective) that are used for treat high blood pressure or chest pain. Practolol bind to beta1-adrenergic receptors in heart and vascular smooth muscle to block the binding of other adrenergic neurotransmitters such as norepinephrine, which lead to decreased blood pressure, heart rate and cardiac output. Practolol can also bind beta-2 adrenergic receptors in juxtaglomerular apparatus and bronchiole smooth muscle. In juxtaglomerular apparatus, practolol can prevent the production of aldosterone and angiotensin II by inhibiting renin production, which lead to prevention of water retention and vasoconstriction. In bronchiole smooth muscle, binding of practolol to beta-2 adrenergic receptors can also prevent vasoconstriction.


Bupranolol Action Pathway,Drug Action

Bupranolol is a nonselective beta-blocker with structural similarity to propanolol. Both drugs do not have intrinsic sympathomimetic activity. It competes with catecholamines for binding beta-1 adrenergic receptors in the heart to inhibit sympathetic activation. This inhibition causes decreased heart rate, cardiac output, blood pressure


Tramadol Action Action Pathway,Drug Action

Tramadol is an analgesic drug consisting of two enantiomer forms (+)-Tramadol and (-)-Tramadol. Both contribute to pain relief by inhibiting pain transmission in the spinal cord via different mechanisms. (+)-Tramadol is a selective agonist of the mu receptor (OP3) inhibiting serotonin reuptake, while (-)-Tramadol inhibits norepinephrine reuptake in the central nervous system. Although tramadol is structurally related to codeine and morphine, it’s affinity for the mu receptor compared to other opioids is significantly less. Therefore tramadol is used when treatment with strong opioids is not necessary since it’s pharmacodynamic and pharmacokinetic properties suggest the low likelihood of patients becoming dependent.


Propoxyphene Action Pathway,Drug Action

Propoxyphene is an analgesic in the opioid category. It primarily acts on the G protein coupled receptors, OP3. Propoxyphene binding to OP3 causes GTP exchange for GDP and inhibit adenylate cyclase causing decreased intracellular cAMP. This leads to the inhibition of nociceptive neurotransmitters such as: substance P, GABA, dopamine, acetylcholine and noradrenaline. Opioids inhibit vasopressin, somatostatin, insulin and glucagon release. Propoxyphene also causes the closure of voltage-gated calcium channels and opens potassium channels causing the hyperpolarization of the membrane and decreasing neuronal excitability. This further reduces the feeling of pain.


Levorphanol Action Pathway,Drug Action

Levorphanol (also known as  Levo-Dromoran) is an opioid medication that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of levorphanol will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Therefore, levorphanol can reduce nerve conduction and decrease neurotransmitter release; so that perception of pain signals can be blocked.


Anileridine Action Pathway,Drug Action

Anileridine (also known as Leritine) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of anileridine will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.


Diphenoxylate Action Pathway,Drug Action

Diphenoxylate (also known as Difenossilato or Lomotil) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of diphenoxylate will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.


Dezocine Action Pathway,Drug Action

Dezocine (also known as Dalgan) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of dezocine will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.


Levomethadyl Acetate Action Action Pathway,Drug Action

Levomethadyl acetate (also known as LAAM) is a synthetic synthetic opioid analgesic with multiple actions quantitatively similar to those as morphine, the most prominent of which involve the central nervous system and organs composed of smooth muscle. However, levomethadyl acetate is more active and more toxic than morphine. Levomethadyl acetate can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of levomethadyl acetate will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Therefore, methadyl acetate can reduce nerve conduction and decrease neurotransmitter release; so that perception of pain signals can be blocked. Levomethadyl acetate can also open calcium-dependent inwardly rectifying potassium channels (OP1 receptor agonist) to reduce neuronal excitability as well as lead to hyperpolarization.


Methadyl Acetate Action Pathway,Drug Action

Methadyl Acetate (also known as Acetylmethadol) is a synthetic opioid analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of methadyl acetate will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Therefore, methadyl acetate can reduce nerve conduction and decrease neurotransmitter release; so that perception of pain signals can be blocked.


3-Methylthiofentanyl Action Pathway,Drug Action

Methadyl Acetate  (also known as Acetylmethadol) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of methadyl acetate  will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.


Dimethylthiambutene Action Pathway,Drug Action

Dimethylthiambutene (also known as Ohton or Aminobutene) is an opioid analgesic and substrate for mu-type opioid receptor which can be used for relieving  pain. Dimethylthiambutene can act on mu-opiod receptor on neurons located at central nervous system. Binding of dimethylthiambutene on mu-type opioid receptor can activate associated G(i) proteins, which inhibits adenylate cyclase and reduce intracellular cAMP level. G(i) protein can also open potassium channels and close calcium channels to result in hyperpolarize on neuron. Binding of dimethylthiambutene on mu-type opioid receptor will eventually relieving the pain by reducing nerve conduction and neurotransmitter release.


Ethylmorphine Action Pathway,Drug Action

Ethylmorphine (also known as codethyline and dionine) is an opioid analgesic. Ethylmorphine can be metabolized to form morphine by cytochrome P450 2D6 (CYP2D6). Morphine can bind the mu-type opioid receptor on central nervous system (CNS) to reduce the pain. Morphine can also bind and inhibit gamma-Aminobutyric acid (GABA) inhibitory interneurons. These interneurons can inhibit the descending pain inhibition pathway; therefore, without the interneurons, pain modulation will go downstream.


Leucine Stimulation on Insulin Signaling,Signaling

The branched chain amino acid (BCAA) leucine is able to signal transduction pathways that modulate translation initiation for protein synthesis in skeleton muscles. In the presence of leucine, hyperphosphorylation of 4E-BP1 causes its affinity for eIF4E to be lowered. This allows eIF4F protein complexes to recognize, unfold and guide the mRNA to the 43S preinitiation complex thereby increasing translation initiation. In addition, leucine has a transient affect on the release of insulin and/or enhances sensitivity of muscle cells to insulin. A culmination of both signals at the mammalian target of rapamycin (mTOR) and perhaps other signaling, such as PKCδ, are needed for maximum translation initiation to occur.


Levallorphan Action Pathway,Drug Action

Levallorphan (also known as Lorfan and Naloxifan) is a type of medication that can be used for treating drug overdoses and respirotry depression. Levallorphan can bind to mu-type opioid receptor and kappa-type opioid receptor on neuron of central nerves system (CNS). Effects of opioids such as respiratory depression, hypotension and sedation can be prevented or reversed by levallorphan. Levallorphan can also be used for treating pentazocine which is a type of psychotomimetic and dysphoric effects of agonist-antagonists.


Buprenorphine Action Pathway,Drug Action

Buprenorphine, trade name subutex, suboxone, zubsolv and bunavail, is a partial agonist of mu-opioid receptors and a kappa-opioid receptor antagonist and is prescribed for opioid addiction to prevent cravings and symptoms of withdrawal. The binding of these receptors causes hyperpolarization and decreased neuronal excitability. Buprenorphine has a longer duration of action due to its slow dissociation from the receptor. This long rate of action causes a long clinical effect and decreases physical dependence. Buprenorphine can also prevent opioid use by inhibiting exogenous opioid effects. This elimination of the rush from the opioid can block the reinforcing behaviour of the drug and may treat opioid addiction. Buprenorphine is available on its own or in combination with naloxone.


Alvimopan Action Pathway,Drug Action

Alvimopan is prescribed to treat patient opioid-induced constipation, a common side effect of opioid therapy. This side effect results in delayed discharge for hospitalized patients following surgery. Alvimopan helps to increase gastrointestinal recovery following surgery for a shorter hospital stay. Opioids bind opioid receptors in the gut causing inhibition of gut motility which results in constipation. Alvimopan is a peripherally acting mu-opioid antagonist. The drug acts in the gastrointestinal tract by competing to bind the mu-opioid receptor. Alvimopan differs from other peripherally acting mu-receptor antagonists such as, methylnaltrexone, by the presence of a quaternary amine.


Pentazocine Action Pathway,Drug Action

Pentazocine (also known as Talwin) is a type of medication that can relieve moderate to severe pain. Pentazocine can bind to mu-type opioid receptor and kappa-type opioid receptor on neuron of central nerves system (CNS). Binding of pentazocine on mu-type opioid receptor and kappa-type opioid receptor can lead to decreased level of neuronal excitability and hyperpolarization. After binding to the receptor, pentazocine will slowly dissociate.


Naltrexone Action Pathway,Drug Action

Naltrexone (also known as ReVia and Vivitrol) is a competitive antagonist of mu-type opioid receptor in the central nervous system (CNS). Naltrexone is also a type of medication that are used for manage opioid or alcohol dependence. Binding of naltrexone can prevent the effects that caused by endogenous opioids, which results in antagonization of effects of opiates such as respiratory depression or drug craving.


Naloxone Action Pathway,Drug Action

Naloxone (also known as Narcan) is a competitive antagonist of mu-type opioid receptor in the central nervous system (CNS). Naloxone is also a type of medication that are used for manage opioid or alcohol dependence. Binding of naloxone can prevent the effects that caused by endogenous opioids, which results in antagonization of effects of opiates such as respiratory depression or drug craving. In recent study, naloxone shows that it can also bind to kappa and gamma-opioid receptors.


Dihydromorphine Action Pathway,Drug Action

Dihydromorphine (also known as Paramorfan or Paramorphan) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of dihydromorphine acetate  will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.


Ketobemidone  Action Pathway,Drug Action

Ketobemidone (also known as Ketogan) is analgesic that can bind to mu-type opioid receptor to activate associated G-protein in the sensory neurons of central nervous system (CNS), which will reduce the level of intracellular cAMP by inhibiting adenylate cyclase. The binding of ketobemidone acetate  will eventually lead to reduced pain because of decreased nerve conduction and release of neurotransmitter. Hyperpolarization of neuron is caused by inactivation of calcium channels and activation of potassium channels via facilitated by G-protein.


Nalbuphine Action Pathway,Drug Action

Nalbuphine (also known as Rubuphine and Nubain) is a competitive antagonist of mu-type and kappa-type opioid receptor in the central nervous system (CNS). Nalbuphine is also a type of medication that are mainly used for treat pain. Binding of nalbuphine can prevent the effects that caused by endogenous opioids, which results in antagonization of effects of opiates such as respiratory depression or drug craving.


Antipyrine Action Pathway,Drug Action

Antipyrine (also named Fenazone or Phenazone) is often used for testing the effect of other drugs on drug-metabolizing enzymes in the liver. Antipyrine 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 antipyrine.


Antrafenine Action Pathway,Drug Action

Antrafenine (also named Stakane) acts as an anti-inflammatory and analgesic drug. It is not widely used as it has largely been replaced by newer drugs. Antrafenine 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 antrafenine.


Carprofen Action Pathway,Drug Action

Carprofen (also named Rimadyl or Imadyl) is a nonsteroidal anti-inflammatory drug that can treat various joint pain or post-operative pain. Carprofen 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 Carprofen.


Etoricoxib Action Pathway,Drug Action

Etoricoxib (also named as Arcoxia) is a COX-2 selective inhibitor. It can be used to treat fever, pain, swelling, inflammation, and platelet aggregation. Etoricoxib 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.


Fenoprofen Action Pathway,Drug Action

Fenoprofen (also named Nalfon) is a nonsteroidal anti-inflammatory drug. Fenoprofen 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 Fenoprofen.


Flurbiprofen Action Pathway,Drug Action

Flurbiprofen (also named Ansaid or Froben) is a nonsteroidal anti-inflammatory drugs. It is used for treatment of moderate pain. Flurbiprofen 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 flurbiprofen.


Magnesium Salicylate Action Pathway,Drug Action

Magnesium Salicylate is a nonsteroidal anti-inflammatory drug. It can be used to treat mild to moderate muscular pain such as headaches, general back pain and other joint pain. Magnesium Salicylate 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 Magnesium Salicylate.


Lumiracoxib Action Pathway,Drug Action

Lumiracoxib (also named Prexige) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used as the mediators of certain kinds of intraocular inflammation. Lumiracoxib 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.


Lornoxicam Action Pathway,Drug Action

Lornoxicam (also named Chlortenoxicam or Xefocam) is a nonsteroidal anti-inflammatory drug. It can be used to treat moderate pain such as pain relieving. It can also treat swelling and fever reducing. Lornoxicam 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 Lornoxicam.


Phenylbutazone Action Pathway,Drug Action

Phenylbutazone (also named fenilbutazona or butazolidin or bute) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat the pain and fever in animal. However, Phenylbutazone is not approved in United State and United Kingdom for human use anymore because of severe adverse effects. Phenylbutazone 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 phenylbutazone.


Nepafenac Action Pathway,Drug Action

Nepafenac (also named nevanac or ilevro or amfenac amide)  is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain and inflammation that is associated with cataract surgery. Nepafenac 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 nepafenac.


Trisalicylate-Choline Action Pathway,Drug Action

Trisalicylate-Choline (also named Choline Magnesium Trisalicylate) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain and fever. Trisalicylate-Choline 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 trisalicylate-choline.


Tolmetin Action Pathway,Drug Action

Tolmetin (also named Tolectin) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to reduce pain, swelling, tenderness, and stiffness. Tolmetin 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 tolmetin.


Tiaprofenic Acid Action Pathway,Drug Action

Tiaprofenic Acid (also named tiaprofensaeure and surgam) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain (especially arthritic pain). Tiaprofenic 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 tiaprofenic.


Tenoxicam Action Pathway,Drug Action

Tenoxicam (also named mobiflex and tilcotil) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to reduce inflammation, swelling, stiffness, and pain that are associated with various diseases such as tendinitis, bursitis and etc. Tenoxicam 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 tenoxicam.


Salsalate Action Pathway,Drug Action

Salsalate (also named Salflex, Disalcid or Salsitab) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to treat pain, fever and inflammation. Salsalate 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 salsalate.


Salicylate-Sodium Action Pathway,Drug Action

Salicylate-sodium (also named salsonin or clin) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used for relieving pain and reducing fever. Salicylate-sodium 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 salicylate-sodium.


Salicylic Acid Action Pathway,Drug Action

Salicylic acid (also named rutranex or salonil) is a nonsteroidal anti-inflammatory drug. Salicylic acid is also an important active metabolite of aspirin (acetylsalicylic acid). It can be used to reduce pain and fever. Salicylic acid 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 Salicylic acid.


Acetaminophen  Action Pathway,Drug Action

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.


Tobramycin Action Pathway,Drug Action

Tobramycin (also named aktob or tobi) is an aminoglycoside antibiotic that can be used to treat various gram-negative bacterial infections such as the species of Pseudomonas. Bacterial 30S ribosomal subunit protein and four nucleotides of 16S rRNA will be bound with tobramycin irreversibly to cause misreading of mRNA; so that formation of mRNA could be prevented because of incorrect insertion of amino acids to polypeptide will result nonfunctional or toxic peptides. Therefore, there is no protein synthesis for bacteria.


Tigecycline Action Pathway,Drug Action

Tigecycline is a glycylcycline, a class of antibiotics derived from tetracycline. Tigecycline has broad spectrum antibacterial abilities and is not susceptible to traditional tetracycline resistance mechanisms such as ribosomal protection and efflux by tetracycline-specific pumps. Tigecycline inhibits bacterial protein synthesis by binding to the A site of the 16s rRNA on the 30S ribosomal subunit. By binding to the A site, tigecycline prevents tRNA from docking onto the 16S rRNA with it’s codon ultimately halting the addition of amino acids to elongate peptide chains used in protein structures.


Arbekacin Action Pathway,Drug Action

Arbekacin, trade name Habekacin, is an aminoglycoside antibiotic derived from dibekacin that inhibits bacterial protein synthesis. Arbekacin is prescribed to patients with sepsis and pneumonia resulting from MRSA. Arbekacin binds the bacterial 50S and 30S ribosomal subunit proteins and prevents the formation of the initiation complex with messenger RNA. More specifically, Arbekacin 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 causes interference of 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. Arbekacin is effective at treating Gram-positive bacteria like Staphylococcus aureus and Staphylococcus epidermidis and Gram-negative bacteria such as Pseudomonas aeruginosa.


Paromomycin Action Pathway,Drug Action

Paromomycin (also known as Aminosidin) is an antimicrobial that can be used for treatment of various parasitic infections. By binding to the A site of ribosomal RNA complexes, paramomycin can lead to production of incorrect polypeptide chain in bacteria, which cause incorrect protein production and eventually, the death of bacteria. Therefore, paramomycin can kill bacteria by inhibiting their protein synthesis that lead to bacterial death.


Methylhistidine Metabolism,Metabolic

Methylhistidine is a modified amino acid that is produced in myocytes during the methylation of actin and myosin. It is also formed from the methylation of L-histidine, which takes the methyl group from S-adenosylmethionine and forms S-adenosylhomocysteine as a byproduct.After its formation in the myocytes, methylhistidine enters the blood stream and travels to the kidneys, where it is excreted in the urine.Methylhistidine is present in the blood and urine in higher concentrations after skeletal muscle protein breakdown, which can occur due to disease or injury. Because of this, it can be used to judge how much muscle breakdown is occurring. Methylhistidine levels are also affected by diet, and may differ between vegetarian diets and those containing meats.


Thyroid Hormone Synthesis,Metabolic

Thyroid hormone synthesis is a process that occurs in the thyroid gland in humans that results in the production of thyroid hormones which regulate many different processes in the body, such as metabolism, temperature regulation and growth/development. Thyroid hormone synthesis begins in the nucleus of a thyroid follicular cell, as thyroglobulin synthesis occurs here and is transported to the endoplasmic reticulum. From there, thyroglobulin transported through endocytosis into the intracellular space, and then transported through exocytosis to the follicle colloid. There, thyroglobulin is joined by iodide that has been transported from the blood, through the thyroid follicular cell and arrived in the the follicle colloid using pendrin, and hydrogen peroxide to be catalyzed by thyroid peroxidase, creating thyroglobulin + iodotyrosine. Then, iodide, hydrogen peroxide and thyroidperoxidase create thyroglobulin + 3,5-diiodo-L-tyrosine. Thyroglobulin+3,5-diiodo-L-tyrosine then joins with hydrogen peroxide and thyroid peroxidase to create thyroglobulin + 2-aminoacrylic acid and thyroglobulin+liothyronine. Thyroglobulin + liothyronine then goes through two processes, the first being its transportation into the cell and undergoing of proteolysis, which is followed by liothyronine being transported into the bloodstream. The second process is thyroglobulin + liothyronine being catalyzed by thyroid peroxidase and resulting in the production of thyroglobulin + thyroxine. Thyroglobulin + thyroxine is then transported back into the cell, undergoes proteolysis, and thyroxine alone is transported back out of the cell and into the bloodstream.


Apparent Mineralocorticoid Excess Syndrome,Disease

Apparent mineralocorticoid excess (AME) is an autosomal recessive form of low-renin hypertension associated with low aldosterone, metabolic alkalosis, hypernatremia, and hypokalemia. The disorder is due to a congenital defect in 11-beta-hydroxysteroid dehydrogenase type II (HSD11B2) activity, resulting in decreased conversion of biologically active cortisol to inactive cortisone; this defect allows cortisol to act as a ligand for the mineralocorticoid receptor, resulting in sodium retention and volume expansion. There is a favorable therapeutic response to spironolactone (review by Ferrari, 2010).


3-beta (β)-hydroxysteroid dehydrogenase (HSD) deficiency is an inherited disorder that affects hormone-producing glands including the gonads (ovaries in females and testes in males) and the adrenal glands.Mutations in the HSD3B2 gene cause 3β-HSD deficiency. The HSD3B2 gene provides instructions for making the 3β-HSD enzyme. This enzyme is found in the gonads and adrenal glands. The 3β-HSD enzyme is involved in the production of many hormones, including cortisol, aldosterone, androgens, and estrogen. Cortisol has numerous functions such as maintaining energy and blood sugar levels, protecting the body from stress, and suppressing inflammation.


It is a metabolic disorder characterized by increased levels of 2-oxoadipate and 2-hydroxyadipate in the urine.  Patients can have mild to severe intellectual disability, muscular hypotonia, developmental delay, ataxia, and epilepsy.  Most cases are asymptomatic.


27-Hydroxylase Deficiency,Disease

Sterol 27-hydroxylase is a mitochondrial cytochrome P-450 species (CYP27) that catalyzes the first step in the degradation of steroid side chain in cholesterol to produce bile acids in the liver. When there are low concentrations of 27-Hydroxylase, patients will exhibit cerebrotendinous xanthomatosis, an autosomal recessive disorder characterized by the accumulation of cholestanol and cholesterol due to the inability to break down the lipids. The formation of xanthomas (deposits of lipids) in the nervous system and tendons will cause symptoms such as dementia, ataxia, and cataracts. Other symptoms may include damaged liver cells and body tissues.


3-Phosphoglycerate dehydrogenase deficiency is a disorder of L-serine biosynthesis that is characterized by congenital microcephaly, psychomotor retardation, and seizures.The disorder is caused by homozygous or compound heterozygous or homozygous mutation in the gene encoding phosphoglycerate dehydrogenase on chromosome 1p12. Defects in the gene lead to a decrease of Glycine and Serine.


Cystinuria,Disease

Cystinuria is an autosomal disorder characterized by impaired epithelial cell transport of cystine and dibasic amino acids (lysine, ornithine, and arginine) in the proximal renal tubule and gastrointestinal tract. The impaired renal reabsorption of cystine and its low solubility causes the formation of calculi in the urinary tract, resulting in obstructive uropathy, pyelonephritis, and, rarely, renal failure (summary by Barbosa et al., 2012). Cystinuria can be caused by mutation in the SLC3A1 amino acid transporter gene, which encodes the heavy subunit of the renal amino acid transporter and is located on chromosome 2p, and/or by mutation in the SLC7A9 gene, which encodes the light subunit and is located on chromosome 19.


Rolitetracycline Action Pathway,Drug Action

Rolitetracycline is a broad spectrum second antibiotic formed by the N-aminomethylation of the carboxamide function of tetracycline. Classified as a second generation tetracycline due to it’s semi-synthesis, rolitetracycline like tetracycline inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit. This prevents tRNA from interacting with the ribosome ultimately halting the addition of amino acids to peptide chains used in protein synthesis.


Methacycline Action Pathway,Drug Action

Methacycline is a type of tettracycline antibiotic, which can inhibiting the aminoacyl-tRNA bind to mRNA-ribosome complex (16S part of 30S ribosomal subunit). Binding og mRNA-ribosome complex can prevent translation of RNA to protein which result in inhibtion of cell growth.


Lincomycin Action Pathway,Drug Action

Lincomycin is a lincosamid antibiotic that can effectively aganist aerobic gram-positive cocci, aerobic gram-positive bacilli as well as anaerobic gram-positive sporeforming bacilli in vitro. Lincomycin is derived from yeast Streptomyces lincolnensis. Lincomycin can bind and inhibit 50S subunits of bacterial ribosomes to prevent protein synthesis, which result in cell death.


Chloramphenicol Action Pathway,Drug Action

Chloramphenicol, trade names Pentamycetin and Chloromycetin, is a broad spectrum antibiotic originally derived from Streptomyces venezuelae. It inhibits protein synthesis by binding the 50S ribosomal subunit to prevent bacterial growth. Bacterial resistance has occurred through decreased uptake or permeability, ribosomal mutation and inactivation by acetylation. Adverse side effects such as aplastic anemia, bone-marrow suppression or Gray syndrome in neonates and infants have resulted in limited use.  However, due to ampicillin-resistance bacterial meningitis there has been a renewed interest in the drug.


Troleandomycin Action Pathway,Drug Action

Troleandomycin is a macrolide antibiotic that is similar to erythromycin. It is active in vitro against the following gram-positive organisms: Streptococcus pyogenes and Diplococcus pneumoniae. Troleandomycin acts by penetrating the bacterial cell membrane and reversibly binding to the 50 S subunit of bacterial ribosomes or near the "P" or donor site so that binding of tRNA (transfer RNA) to the donor site is blocked. Translocation of peptides from the "A" or acceptor site to the "P" or donor site is prevented, and subsequent protein synthesis is inhibited.


Josamycin Action Pathway,Drug Action

Josamycin is a macrolide antibiotic that is synthesized from Streptomyces narbonensis which can against various pathogens. Josamycin inhibits protein biosynthesis of bacteria by binding to ribosomal 50S subunit reversibly, which lead to inhibition of translocation of peptidyl tRNA. This action is mainly bacteriostatic, but can also be bactericidal in high concentrations. Macrolides can be accumulated within leukocytes, and transport into infection site later on.


Temocapril Metabolism Pathway,Drug Metabolism

Benazepril, brand name Lotensin, belongs to the class of drugs known as angiotensin-converting enzyme (ACE) inhibitors and is used primarily to lower high blood pressure (hypertension). This drug can also be used in the treatment of congestive heart failure and type II diabetes. Benazepril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form benazeprilat via cleavage of its ester group by the liver. Angiotensin-converting enzyme (ACE) is a component of the body's renin–angiotensin–aldosterone system (RAAS) and cleaves inactive angiotensin I into the active vasoconstrictor angiotensin II. ACE (or kininase II) also degrades the potent vasodilator bradykinin. Consequently, ACE inhibitors decrease angiotensin II concentrations and increase bradykinin concentrations resulting in blood vessel dilation and thereby lowering blood pressure.


Roxatidine Acetate Action Pathway,Drug Action

Roxatidine acetate is an anti-ulcer agent, that works through antagonizing the histamine H2 receptor. It is used to reduce abdominal pain, heartburn, acid indigestion and acid reflux. The pathway begins in the stomach, where roxatidine acetate inhibits the histamine H2 receptor on the surface of the parietal cell. Now in the gastric endothelial cell, potassium-transporting ATPase units are inhibited by G-Protein signalling cascade through somatostatin receptor type 4, which is activated by somatostatin. At the same time, potassium-transporting ATPase is activated by the G-protein signalling cascade, through histamine H2 receptor which is inhibited by ranitidine, gastrin/cholecystokinin type B receptor, and muscarinic acetylcholine receptor M3 which are activated by histamine, gastrin and acetylcholine, respectively. The potassium transporting ATPase also converts water and ATP to a phosphate molecule and ADP. Alongside the transporters, potassium is brought into the cell. Carbonic anhydrase 1 uses water and carbon dioxide to create hydrogen carbonate and a hydrogen ion, which are both transported out of the endothelial cell, into the gastric lumen. A chloride ion is transported into the gastric endothelial cell through a chloride anion exchanger and is transported out of the cell through a chloride intracellular channel protein 2, back into the gastric lumen.


Metiamide Action Pathway,Drug Action,Metiamide is a histamine H2-receptor antagonist that can bind and inhibit histamine H2-receptor to prevent the histamine effects on basolateral memrbane in gastric parietal cell. Binding and inhibition of histamine H2-receptor can lead to decreased gastric acid secretion so that lowering gastric volume as well as acidity.


Betazole Action Pathway,Drug Action

Betazole, also known as ametazole and Histalog, is a histamine H2 agonist that causes an increase in gastric acid secretion. Betazole is commonly used to evaluate acid production. Betazole binds to the H2 receptor to enhance the G protein signaling cascade to increase gastric secretion into the lumen. Gastric acid digests protein and absorbs calcium, iron and vitamin B12. Gastric acidity may also interfere with medication bioavailability. Measuring gastric acid secretion is useful to manage diseases involving acid production such as gastroesophageal reflux disease.


Abacavir Action Pathway,Drug Action

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.


Delavirdine Action Pathway,Drug Action

Delavirdine (also known as Rescriptor) is a non-nucleoside reverse transcriptase inhibitor (NNRTI) that can be used for treating HIV-1. Delavirdine can bind and inhibit the reverse transcriptase so that the DNA polymerase activities can be prevented, which lead to disruption of the enzyme's catalytic site and eventually lead to prevention of cell growth.


Didanosine Action Pathway,Drug Action

Didanosine (ddl) can be metabolized into dideoxyadenosine triphosphate (ddATP) by series of reaction. Dideoxyadenosine triphosphate can bind and inhibit HIV reverse transcriptase enzyme competitively against natural dATP. Dideoxyadenosine triphosphate will terminate the viral DNA chain to make it missing 3'-OH group so that formation of 5' to 3' phosphodiester could be prevented, which 5' to 3' phosphodiester is required for DNA chain elongation and result in terminated DNA growth.


Efavirenz Action Pathway,Drug Action

Efavirenz (also known as Sustiva) is a nucleoside reverse transcriptase inhibitor (NRTI) for treating HIV infection by inhibiting the transcriptase reversibly. Efavirenz is phosphorylated to its active triphosphorylated form so that it can compete with deoxycytidine 5'-triphosphate to inhibit HIV-1 reverse transcriptase, which lead to early chain termination.


Emtricitabine Action Pathway,Drug Action

Emtricitabine (also known as FTC) is a nucleoside reverse transcriptase inhibitor (NRTI) for treating HIV infection by inhibiting the transcriptase reversibly. Emtricitabine is phosphorylated to form emtricitabine 5'-triphosphate so that emtricitabine 5'-triphosphate can compete with deoxycytidine 5'-triphosphate to inhibit HIV-1 reverse transcriptase, which lead to early chain termination. Emtricitabine 5'-triphosphate can also incorporate into viral DNA to inhibit the activity of HIV-1 reverse transcriptase (RT).


Lamivudine  Action Pathway,Drug Action

Lamivudine (also known as 3TC) is an antiretroviral drug that can be used to treat HIV/AIDS. Lamivudine is phosphorylated to lamivudine triphosphate (L-TP), which is its active metabolite. Lamivudine triphosphate (L-TP) can bind and inhibit the HIV reverse transcriptase as well as HBV polymerase, which lead to DNA chain termination.


Nevirapine  Action Pathway,Drug Action

Nevirapine (also named as Viramune or BIRG587) is a medication that are used for the treatment of HIV/AIDS (especially HIV-1). Nevirapine binds and inhibits reverse transcriptase to create interruption on catalytic site of enzyme so that it can prevent the activities of RNA-dependent and DNA-dependent DNA polymerase, which lead to no complementary DNA (cDNA) produced.


Rilpivirine Action Pathway,Drug Action,Rilpivirine is non-nucleoside reverse transcriptase inhibitor (NNRTI) which is used for the treatment of HIV-1 infections in treatment-naive patients. It binds to reverse transcriptase which results in a block in RNA and DNA- dependent DNA polymerase activities. One such activity is HIV-1 replication. Intracellular phosphorylation is not necessary for its antiviral activity.

Rilpivirine, sold as Edurant, is an antiretroviral drug that works as a non-nucleoside reverse transcriptase inhibitor (NNRTI) to treat HIV infections.NNRTI drugs work by entering the cell that HIV is present in, and binding to HIV's reverse transcriptase protein. This inactivates it, preventing HIV from being able to produce cDNA from its RNA genome, effectively stopping it from replicating its genome and spreading. While NNRTIs are able to prevent HIV from replicating, it does not destroy the virus, and it is only useful to help slow down the progression of the disease, not curing it.


Stavudine Action Pathway,Drug Action,Stavudine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Stavudine is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis.

Acquired immunodeficiancy syndrome (AIDS) is generally accepted to be a consequence of infection with the retrovirus designated as human immunodeficiency virus (HIV-l). Stavudine is a potent and selective inhibitor of HIV-replication and of cytopathic effects in a variety of mammalian cells, and is relatively non-toxic to the uninfected human T-cell line H9. Stavudine, phosphorylates cellular enzymes to the mono-, di-, and triphosphates and is ultimately incorporated into the DNA of growing cells. A significant amount of radioactivity appears in the alkaline labile fraction of cells which are treated with Stavudine, due to terminal addition of Stavudine to DNA and the resultant chain termination.


Zalcitabine Action Pathway,Drug Action

Zalcitabine (ddc) is a dideoxynucleoside antiretroviral drug that when used in combination with zidovudine improves the viral load and CD4+ cell count of patients infected with Human Immunodeficiency Virus Type 1 (HIV-1). Zalcitabine is phosphorylated to it’s active form metabolite 2′,3′-dideoxycytidine 5′-triphosphate (ddCTP) in both healthy and infected cells. ddCTP competes with deoxycytidine triphosphate inhibiting the enzyme reverse transcriptase from using the substrates to elongate the viral DNA strand ultimately halting HIV replication.


Zidovudine Action Pathway,Drug Action

The discovery of AIDS prompted the search for agents that block the HIV replication process. Zidovudine (AZT) is a nucleoside analogue of thymidine, and was shown to reduce considerably the mortality of patients with AIDS. Zidovudine is toxic to the hemtopoietic system, causing anemia and neutropenia. It is clear, however, that disease progression can occur during continued administration of zidovudine. Moreover, zidovudine is not effective in treating Kaposi sarcoma, a common complication of HIV infection. Zidovudine therapy is also associated with a high incidence of toxicity, primarily bone marrow suppression, that requires dosage reduction or discontinuation of the therapy.


Activation of PKC Through G Protein-Coupled Receptor,Signaling

G protein-coupled receptors sense stimuli outside the cell and transmit signals across the plasma membrane. Activation of protein kinase C (PKC) is one of the common signaling pathways. When a class of GPCRs are activated by a ligand, they activate Gq protein to bind GTP instead of GDP. After the Gq becomes active, it activates phospholipase C (PLC) to cleave the membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacyl glycerol (DAG). IP3 can bind Ins3P receptor to open calcium channel by diffusion from cytoplasm to ER. Activated calcium channel will release the calcium from ER into cytoplasm. Calcium can activate the kinase activity of PKC.


The Oncogenic Action of 2-Hydroxyglutarate,Disease

The compound 2-hydroxyglutarate is the product of gain-of-function mutations producing mutIDH1 and mutIDH2 in the cytosolic and mitochondrial isoforms of isocitrate dehydrogenase (IDH). This compound is derived from the TCA cycle. The compound 2-hydroxyglutarate is sufficiently similar in structure to 2-oxogluratate (2OG) to inhibit a range of 2OG-dependent dioxygenases,including histone lysine demethylases (KDMs) and the ten-eleven translocation (TET) family of 5-methylcytosine (5mC) hydroxylases. In turn, this leads to modulations of HIF-mediated hypoxia responses and alterations in gene expression through global epigenetic remodelling that may contribute to malignant transformation.


The Oncogenic Action of Succinate,Disease

Hypoxia-inducible factor In many tumours, oxygen availability becomes limited (hypoxia) very quickly during cancer development. The major regulator of the response to hypoxia is the HIF transcription factor. Under normal oxygen levels, the protein levels of HIF alpa is very low due to constant degradation, mediated by a sequence of post-translational modification events catalyzed by the enzymes PHD1,2 and 3, (also known as EglN2,1 and 3). Under hypoxic conditions, HIF alpha escapes hydroxylation and degration. Succinate dehydrogenase (SDH)  is a collection of housekeeping genes (SDHA,B,C,D), but mutations in those genes allows for succinate to accumulate and cross the mitochondrial barrier through a dicarboxylate carrier.  Once in the cytosol, it inhibits the activity of the PHD1,2 and 3 since succinate is a product of the enzyme, it acts as feedback inhibition.


The Oncogenic Action of Fumarate,Disease

Hypoxia-inducible factor In many tumours, oxygen availability becomes limited (hypoxia) very quickly during cancer development. The major regulator of the response to hypoxia is the HIF transcription factor. Under normal oxygen levels, the protein levels of HIF alpa is very low due to constant degradation, mediated by a sequence of post-translational modification events catalyzed by the enzymes PHD1,2 and 3, (also known as EglN2,1 and 3). Under hypoxic conditions, HIF alpha escapes hydroxylation and degration. Fumarate hydratase (FH) is a housekeeping gene, but mutations in this gene allows for fumarate to accumulate and cross the mitochondrial barrier through a dicarboxylate carrier. Once in the cytosol, it inhibits the activity of the PHD1,2 and 3 since it is chemically similar to succinate. Having a double bond in the centre of the dicarboxylic acid, fumarate is a rigid molecule compared to succinate making it a probable possibility for fumarate to interacts better with PHDs.


Glutaminolysis and Cancer,Disease

The glutaminolysis pathway catabolizes glutamine to generate ATP and lactate. Glutamine not only provides a major substrate for respiration but also for the synthesis of other macromolecules, such as nucleotides, proteins and hexosamines. It also  macromolecule biosynthesis, glutaminolysis also has an important role in regulating redox balance, mTOR signaling, apoptosis and autophagy.High extracellular glutamine concentrations stimulate tumor growth and are essential for cell transformation. The transportation of glutamine in and out regulates mTOR activation to coordinate cell growth and proliferation.Glutaminolysis is a series of biochemical reactions by which glutamine is degraded into glutamate, aspartate, CO2, pyruvate, lactate, alanine and citrate.Glutamine is imported through ASCT2 and SN2, once inside the cell, it can be deaminated into glutamate. Glutamate is converted into Oxoglutaric acid which then is incorporated into the TCA cycle. Once it reaches malic acid, it is transported outside the mitochondria and transformed into pyruvic acid and lactate.The oxoglutaric acid can also be transformed into citric acid which then gets turned into acetyl coa and get incorporated into the lipid synthesis


Sarcosine Oncometabolite Pathway ,Disease

Sarcosine levels have been found to be higher in prostate cancer cells. The expression of sarcosine biosynthetic enzyme, glycine N-methyltransferase (GNMT), is elevated in cancer tissues, while sarcosine dehydrogenase (SARDH) and pipecolic acid oxidase (PIPOX), which metabolize sarcosine, were reduced. Consistent with this, GNMT promoted the oncogenic potential of prostate cells by facilitating sarcosine production, while SARDH and PIPOX reduced the oncogenic potential of prostate cells by metabolizing sarcosine.


The Oncogenic Action of L-2-Hydroxyglutarate in Hydroxyglutaric aciduria ,Disease

Hydroxyglutaric aciduria is a rare genetic disorder. Both isoforms are believed to have autosomal recessive inheritance. The compound 2-hydroxyglutarate is the product of gain-of-function mutations producing mutIDH1 and mutIDH2 in the cytosolic and mitochondrial isoforms of isocitrate dehydrogenase (IDH). This compound is derived from the TCA cycle. The compound 2-hydroxyglutarate shares enough structural similarity to 2-oxogluratate (2OG) to inhibit a range of 2OG-dependent dioxygenases, including histone lysine demethylases (KDMs) and the ten-eleven translocation (TET) family of 5-methylcytosine (5mC) hydroxylases. This results in modulations of HIF-mediated hypoxia responses and alterations in gene expression through global epigenetic remodelling that may contribute to malignant transformation. L-2-hydroxyglutarate dehydrogenase (L2HGDH) converts L-2-hydroxyglutarate to α-ketoglutaric acid. L-2-Hydroxyglutarate is an oncometabolite and is produced by gain-of-function IDH mutations. When IDH is mutated, L-2-Hydroxyglutaric acid production is increased. L-2-hydroxyglutarate is a competitive inhibitor of 2OG-dependent dioxygenases resulting in genetic changes and malignancies.


The Oncogenic Action of D-2-Hydroxyglutarate in Hydroxyglutaric aciduria ,Disease

Hydroxyglutaric aciduria  is a rare genetic disorder. Both isoforms are believed to have autosomal recessive inheritance. The compound 2-hydroxyglutarate is the product of gain-of-function mutations producing mutIDH1 and mutIDH2 in the cytosolic and mitochondrial isoforms of isocitrate dehydrogenase (IDH). This compound is derived from the TCA cycle. The compound 2-hydroxyglutarate shares structural similarity with 2-oxogluratate (2OG) to inhibit a range of 2OG-dependent dioxygenases, including histone lysine demethylases (KDMs) and the ten-eleven translocation (TET) family of 5-methylcytosine (5mC) hydroxylases. This results in modulations of HIF-mediated hypoxia responses and alterations in gene expression through global epigenetic remodelling that may contribute to malignant transformation. 2-Hydroxyglutarate dehydrogenase (D2HGDH) converts D-2-hydroxyglutarate (D-2HG) to α-ketoglutaric acid. The enzyme D-3-phosphoglycerate dehydrogenase (PHGDH) catalyzes the NADH-dependent reduction of α-ketoglutarate (AKG) to D-2HG.  D-2-Hydroxyglutarate is an oncometabolite produced from IDH mutations.  A mutation in IDH causes high concentrations of D-2-Hydroxyglutaric acid. D-2-hydroxyglutarate is a competitive inhibitor of 2OG-dependent dioxygenases resulting in genetic changes and malignancies.


Phosphatidylcholines (PC) are a class of phospholipids that incorporate a phosphocholine headgroup into a diacylglycerol backbone. They are the most abundant phospholipid in eukaryotic cell membranes and has both structural and signalling roles. In eukaryotes, there exist two phosphatidylcholine biosynthesis pathways: the Kennedy pathway and the methylation pathway. The Kennedy pathway begins with the direct phosphorylation of free choline into phosphocholine followed by conversion into CDP-choline and subsequently phosphatidylcholine. It is the major synthesis route in animals. The methylation pathway involves the 3 successive methylations of phosphatidylethanolamine to form phosphatidylcholine.  The first reaction of the Kennedy pathway involves the cytosol-localized enzyme choline/ethanolamine kinase catalyzing the conversion of choline into phosphocholine. Second, choline-phosphate cytidylyltransferase, localized to the endoplasmic reticulum membrane, catalyzes the conversion of phosphocholine to CDP-choline. Last, choline/ethanolaminephosphotransferase catalyzes phosphatidylcholine biosynthesis from CDP-choline. It requires either magnesium or manganese ions as cofactors.  A parallel Kennedy pathway forms phosphatidylethanolamine from ethanolamine - the only difference being a different enzyme, ethanolamine-phosphate cytidylyltransferase, catalyzing the second step.   Phosphatidylethanolamine is also synthesized from phosphatidylserine in the mitochondrial membrane by phosphatidylserine decarboxylase.  Phosphatidylethanolamine funnels into the methylation pathway in which phosphatidylethanolamine N-methyltransferase (PEMT) then catalyzes three sequential N-methylation steps to convert phosphatidylethanolamine to phosphatidylcholine. PEMT uses S-adenosyl-L-methionine as a methyl donor.


Phosphatidylcholines (PC) are a class of phospholipids that incorporate a phosphocholine headgroup into a diacylglycerol backbone. They are the most abundant phospholipid in eukaryotic cell membranes and has both structural and signalling roles. In eukaryotes, there exist two phosphatidylcholine biosynthesis pathways: the Kennedy pathway and the methylation pathway. The Kennedy pathway begins with the direct phosphorylation of free choline into phosphocholine followed by conversion into CDP-choline and subsequently phosphatidylcholine. It is the major synthesis route in animals. The methylation pathway involves the 3 successive methylations of phosphatidylethanolamine to form phosphatidylcholine. The first reaction of the Kennedy pathway involves the cytosol-localized enzyme choline/ethanolamine kinase catalyzing the conversion of choline into phosphocholine. Second, choline-phosphate cytidylyltransferase, localized to the endoplasmic reticulum membrane, catalyzes the conversion of phosphocholine to CDP-choline. Last, choline/ethanolaminephosphotransferase catalyzes phosphatidylcholine biosynthesis from CDP-choline. It requires either magnesium or manganese ions as cofactors. A parallel Kennedy pathway forms phosphatidylethanolamine from ethanolamine - the only difference being a different enzyme, ethanolamine-phosphate cytidylyltransferase, catalyzing the second step. Phosphatidylethanolamine is also synthesized from phosphatidylserine in the mitochondrial membrane by phosphatidylserine decarboxylase. Phosphatidylethanolamine funnels into the methylation pathway in which phosphatidylethanolamine N-methyltransferase (PEMT) then catalyzes three sequential N-methylation steps to convert phosphatidylethanolamine to phosphatidylcholine. PEMT uses S-adenosyl-L-methionine as a methyl donor.


Phosphatidylethanolamines (PE) are a class of phospholipids that incorporate a phosphoric acid headgroup into a diacylglycerol backbone. They are the second most abundant phospholipid in eukaryotic cell membranes, and contrary to phosphatidylcholine, it is concentrated with phosphatidylserine in the cell membrane's inner leaflet. In Homo sapiens, there exist two phosphatidylethanolamine biosynthesis pathways. In the visualization, all enzymes that are dark green in colour are membrane-localized. The first pathway synthesizes phosphatidylethanolamine from ethanolamine via the Kennedy pathway. First, the cytosol-localized enzyme choline/ethanolamine kinase catalyzes the conversion of choline into phosphocholine. Second, choline-phosphate cytidylyltransferase, localized to the endoplasmic reticulum membrane, catalyzes the conversion of phosphocholine to CDP-choline. Last, choline/ethanolaminephosphotransferase catalyzes phosphatidylcholine biosynthesis from CDP-choline. It requires either magnesium or manganese ions as cofactors. Phosphatidylethanolamine is also synthesized from phosphatidylserine at the mitochondrial inner membrane by phosphatidylserine decarboxylase. Phosphatidylserine, itself, is synthesized using a base-exchange reaction with phosphatidylcholine. This reaction is catalyzed by phosphatidylserine synthase which is located in the endoplasmic reticulum membrane.


De Novo Triacylglycerol Biosynthesis,Metabolic

A triglyceride (TG, triacylglycerol, TAG, or triacylglyceride) is an ester derived from glycerol and three fatty acids.  De novo biosynthesis of triglycerides is also known as the phosphatidic acid pathway, and it is mainly associated with the liver and adipose tissue.  All membrane-localized enzymes are coloured dark green in the image.  First, dihydroxyacetone phosphate (or glycerone phosphate) from glycolysis is used by the cytosolic enzyme glycerol-3-phosphate dehydrogenase [NAD(+)] to synthesize sn-glycerol 3-phosphate.  Second, the mitochondrial outer membrane enzyme glycerol-3-phosphate acyltransferase esterifies an acyl-group to the sn-1 position of sn-glycerol 3-phosphate to form 1-acyl-sn-glycerol 3-phosphate (lysophosphatidic acid or LPA).  The next three steps are localized to the endoplasmic reticulum membrane.  The enzyme 1-acyl-sn-glycerol-3-phosphate acyltransferase converts LPA into phosphatidic acid (1,2-diacyl-sn-glycerol 3-phosphate) by esterifying an acyl-group to the sn-2 position of the glycerol backbone.  Next, magnesium-dependent phosphatidate phosphatase catalyzes the conversion of phosphatidic acid into diacylglycerol.  Last, the enzyme diacylglycerol O-acyltransferase synthesizes triacylglycerol from diacylglycerol and a fatty acyl-CoA.


De Novo Triacylglycerol Biosynthesis TG(10:0/10:0/10:0),Metabolic

A triglyceride (TG, triacylglycerol, TAG, or triacylglyceride) is an ester derived from glycerol and three fatty acids. Triglycerides are the main constituents of body fat in humans and other animals, as well as vegetable fat. They are also present in the blood to enable the bidirectional transference of adipose fat and blood glucose from the liver, and are a major component of human skin oils. (Wikipedia) De novo biosynthesis of triglycerides is also known as the phosphatidic acid pathway, and it is mainly associated with the liver and adipose tissue. All membrane-localized enzymes are coloured dark green in the image. First, dihydroxyacetone phosphate (or glycerone phosphate) from glycolysis is used by the cytosolic enzyme glycerol-3-phosphate dehydrogenase [NAD(+)] to synthesize sn-glycerol 3-phosphate. Second, the mitochondrial outer membrane enzyme glycerol-3-phosphate acyltransferase esterifies an acyl-group to the sn-1 position of sn-glycerol 3-phosphate to form 1-acyl-sn-glycerol 3-phosphate (lysophosphatidic acid or LPA). The next three steps are localized to the endoplasmic reticulum membrane. The enzyme 1-acyl-sn-glycerol-3-phosphate acyltransferase converts LPA into phosphatidic acid (1,2-diacyl-sn-glycerol 3-phosphate) by esterifying an acyl-group to the sn-2 position of the glycerol backbone. Next, magnesium-dependent phosphatidate phosphatase catalyzes the conversion of phosphatidic acid into diacylglycerol. Last, the enzyme diacylglycerol O-acyltransferase synthesizes triacylglycerol from diacylglycerol and a fatty acyl-CoA.


De Novo Triacylglycerol Biosynthesis TG(16:0/16:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/18:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/18:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/18:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/18:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/20:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:1(9Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:1(9Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/18:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/18:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/18:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/20:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/20:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/20:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(20:0/20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(20:0/20:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(20:0/20:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/20:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/16:1(9Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/16:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/16:1(9Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/16:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/16:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/20:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/20:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/18:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/18:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/18:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/20:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(20:1(11Z)/20:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/14:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/14:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/14:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/14:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:0/16:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/14:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/14:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/14:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/16:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(16:1(9Z)/18:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/14:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/14:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/14:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/14:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/16:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:0/18:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/14:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/14:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/16:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/16:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/16:1(9Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/16:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/18:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(11Z)/18:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/14:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/18:1(11Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(18:1(9Z)/18:1(9Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(8:0/8:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(12:0/12:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:1(9Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:1(9Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:1(11Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/15:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/14:1(9Z)/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/16:1(9Z)/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(11Z)/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/18:1(9Z)/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/20:1(11Z)/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/22:1(13Z)/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(14:0/24:1(15Z)/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/14:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/15:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/16:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/14:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/22:1(13Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/18:0/24:1(15Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/24:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/16:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/18:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/18:1(9Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/20:1(11Z)),Metabolic


De Novo Triacylglycerol Biosynthesis TG(15:0/20:0/22:1(13Z)),Metabolic