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AMINOPLASMAL-5% E INFUSION

Product Information

Registration Status: Active

SIN05954P

AMINOPLASMAL-5% E INFUSION is approved to be sold in Singapore with effective from 1991-05-13. It is marketed by B. BRAUN SINGAPORE PTE LTD, with the registration number of SIN05954P.

This product contains Acetylcysteine 0.25g/1000ml,Alanine 6.85g/1000ml,Arginine 4.6g/1000ml,Asparagine 1.64g/1000ml,Aspartic Acid 0.65g/1000ml,Glutamic Acid 2.3g/1000ml,Glycine 3.95g/1000ml,Histidine 2.6g/1000ml,Isoleucine 2.55g/1000ml,Leucine 4.45g/1000ml,Lysine 2.8g/1000ml,Magnesium Acetate 0.56g/1000ml,Malic Acid 1.01g/1000ml,Methionine 1.9g/1000ml,N-Acetyltyrosine 0.35g/1000ml,Ornithine 1.25g/1000ml,Phenylalanine 2.55g/1000ml,Potassium Acetate 2.45g/1000ml,Proline 4.45g/1000ml,Serine 1.2g/1000ml,Sodium Acetate 3.95g/1000ml,Sodium Dihydrogen Phosphate 1.4g/1000ml,Sodium Hydroxide 0.2g/1000ml,Threonine 2.05g/1000ml,Tryptophan 0.9g/1000ml,Tyrosine 0.3g/1000ml, and Valine 2.4g/1000ml in the form of INJECTION. It is approved for INTRAVENOUS use.

This product is manufactured by B BRAUN MELSUNGEN AG in GERMANY.

It is an Over-the-counter Medicine that can be freely obtained from any retailer

Product Reference
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Description

Acetylcysteine (also known as N-acetylcysteine or N-acetyl-L-cysteine or NAC) is primarily used as a mucolytic agent and in the management of acetaminophen poisoning. It is a derivative of cysteine with an acetyl group attached to the amino group of cysteine. NAC is essentially a prodrug that is converted to cysteine (in the intestine by the enzyme aminoacylase 1) and absorbed in the intestine into the blood stream. Cysteine is a key constituent to glutathione and hence administration of acetylcysteine replenishes glutathione stores. Acetylcysteine can also be used as a general antioxidant which can help mitigate symptoms for a variety of diseases exacerbated by reactive oxygen species (ROS). For instance, acetylcysteine is commonly used in individuals with renal impairment to prevent the precipitation of acute renal failure. Acetylcysteine has been shown to have efficacy in treating mild to moderate traumatic brain injury including ischemic brain injury, particularly in reducing neuronal losses, and also reducing cognitive and neurological symptoms when administered promptly after injury. N-acetylcysteine is now widely used in the treatment of HIV, and it has reported efficacy in chronic obstructive pulmonary disease and contrast-induced nephropathy. Acetylcysteine is also being successfully used to treat a variety of neuropsychiatric and neurodegenerative disorders including cocaine, cannabis, and smoking addictions, Alzheimer's and Parkinson's diseases, autism, compulsive and grooming disorders, schizophrenia, depression, and bipolar disorder. Recent data also shows that N-acetylcysteine inhibits muscle fatigue and can be used to enhance performance in endurance events and in exercise and endurance training. Acetylcysteine is also undergoing clinical trials as RK-0202, an oral rinse for the prevention and treatment of mucositis. It is comprised of acetylcysteine in a polymer matrix.

Indication

Acetylcysteine is used mainly as a mucolytic and in the management of paracetamol (acetaminophen) overdose.

Mechanism of Action

Acetylcysteine protects against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione. It does this by producing the glutathione precursor L-cysteine. Glutathione is required to inactivate an intermediate metabolite (N-acetyl-p-benzoquinoneimine or NAPQI) of acetaminophen that is thought to be hepatotoxic. In acetaminophen overdose cases, excessive quantities of this metabolite are formed because the primary metabolic (glucuronide and sulfate conjugation) pathways become saturated. Acetylcysteine may act by reducing the metabolite to the parent compound and/or by providing sulfhydryl for conjugation of the metabolite. Experimental evidence also suggests that a sulfhydryl-containing compound such as acetylcysteine may also directly inactivate the metabolite. The mechanisms of action for acetylcysteine’s well-known mucolytic effects are different. In particular, when inhaled, acetylcysteine (and its metabolic byproduct cysteine) exerts its mucolytic action through its free sulfhydryl group, which reduces the disulfide bonds in the mucus matrix and lowers mucus viscosity. This action increases with increasing pH and is most significant at pH 7 to 9. The mucolytic action of acetylcysteine is not affected by the presence of DNA. Acetylcysteine is also an antioxidant and reduces oxidative stress. Acetylcysteine serves as a prodrug to L-cysteine which is a precursor to the biologic antioxidant, glutathione and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. This glutamate in turn acts on mGluR2/3 receptors, and at higher doses of acetylcysteine, mGluR5. Glutathione also modulates the NMDA receptor by acting at the redox site. These effects on glutamate and NMDA signaling appear to explain some of the positive neuropsychotropic effects associated with NAC. Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-κB through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis.

Pharmacokinetics

Absorption
Bioavailability is 6–10% following oral administration and less than 3% following topical administration.
Distribution
Metabolism
Hepatic. Deacetylated by the liver to cysteine and subsequently metabolized.
Elimination

Toxicity

Single intravenous doses of acetylcysteine at 1000 mg/kg in mice, 2445 mg/kg in rats, 1500 mg/kg in guinea pigs, 1200 mg/kg in rabbits and 500 mg/kg in dogs were lethal. Symptoms of acute toxicity were ataxia, hypoactivity, labored respiration, cyanosis, loss of righting reflex and convulsions.

Active Ingredient/Synonyms

(2R)-2-acetylamino-3-sulfanylpropanoic acid | (R)-2-acetylamino-3-mercaptopropanoic acid | (R)-mercapturic acid | Acetilcisteina | Acetylcysteinum | L-acetylcysteine | L-α-acetamido-β-mercaptopropionic acid | Mercapturic acid | N-acetyl-L-(+)-cysteine | N-acetyl-L-cysteine | N-acetylcysteine | NAC | Acetylcysteine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system.

Indication

Used for protein synthesis.

Mechanism of Action

L-Alanine is a non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. BCAAs are used as a source of energy for muscle cells. During prolonged exercise, BCAAs are released from skeletal muscles and their carbon backbones are used as fuel, while their nitrogen portion is used to form another amino acid, Alanine. Alanine is then converted to Glucose by the liver. This form of energy production is called the Alanine-Glucose cycle, and it plays a major role in maintaining the body's blood sugar balance.

Active Ingredient/Synonyms

(2S)-2-aminopropanoic acid | (S)-2-aminopropanoic acid | (S)-alanine | Alanine | L-2-Aminopropionic acid | L-Alanin | L-alpha-Alanine | L-α-alanine | L-Alanine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An essential amino acid that is physiologically active in the L-form.

Indication

Used for nutritional supplementation, also for treating dietary shortage or imbalance.

Mechanism of Action

Many of supplemental L-arginine's activities, including its possible anti-atherogenic actions, may be accounted for by its role as the precursor to nitric oxide or NO. NO is produced by all tissues of the body and plays very important roles in the cardiovascular system, immune system and nervous system. NO is formed from L-arginine via the enzyme nitric oxide synthase or synthetase (NOS), and the effects of NO are mainly mediated by 3,'5' -cyclic guanylate or cyclic GMP. NO activates the enzyme guanylate cyclase, which catalyzes the synthesis of cyclic GMP from guanosine triphosphate or GTP. Cyclic GMP is converted to guanylic acid via the enzyme cyclic GMP phosphodiesterase. NOS is a heme-containing enzyme with some sequences similar to cytochrome P-450 reductase. Several isoforms of NOS exist, two of which are constitutive and one of which is inducible by immunological stimuli. The constitutive NOS found in the vascular endothelium is designated eNOS and that present in the brain, spinal cord and peripheral nervous system is designated nNOS. The form of NOS induced by immunological or inflammatory stimuli is known as iNOS. iNOS may be expressed constitutively in select tissues such as lung epithelium. All the nitric oxide synthases use NADPH (reduced nicotinamide adenine dinucleotide phosphate) and oxygen (O2) as cosubstrates, as well as the cofactors FAD (flavin adenine dinucleotide), FMN (flavin mononucleotide), tetrahydrobiopterin and heme. Interestingly, ascorbic acid appears to enhance NOS activity by increasing intracellular tetrahydrobiopterin. eNOS and nNOS synthesize NO in response to an increased concentration of calcium ions or in some cases in response to calcium-independent stimuli, such as shear stress. In vitro studies of NOS indicate that the Km of the enzyme for L-arginine is in the micromolar range. The concentration of L-arginine in endothelial cells, as well as in other cells, and in plasma is in the millimolar range. What this means is that, under physiological conditions, NOS is saturated with its L-arginine substrate. In other words, L-arginine would not be expected to be rate-limiting for the enzyme, and it would not appear that supraphysiological levels of L-arginine which could occur with oral supplementation of the amino acid^would make any difference with regard to NO production. The reaction would appear to have reached its maximum level. However, in vivo studies have demonstrated that, under certain conditions, e.g. hypercholesterolemia, supplemental L-arginine could enhance endothelial-dependent vasodilation and NO production.

Pharmacokinetics

Absorption
Absorbed from the lumen of the small intestine into the enterocytes. Absorption is efficient and occurs by an active transport mechanism.
Distribution
Metabolism
Some metabolism of L-arginine takes place in the enterocytes. L-arginine not metabolized in the enterocytes enters the portal circulation from whence it is transported to the liver, where again some portion of the amino acid is metabolized.
Elimination

Toxicity

Oral supplementation with L-arginine at doses up to 15 grams daily are generally well tolerated. The most common adverse reactions of higher doses from 15 to 30 grams daily are nausea, abdominal cramps and diarrhea. Some may experience these symptoms at lower doses.

Active Ingredient/Synonyms

(2S)-2-amino-5-(carbamimidamido)pentanoic acid | (2S)-2-amino-5-guanidinopentanoic acid | (S)-2-amino-5-guanidinopentanoic acid | (S)-2-Amino-5-guanidinovaleric acid | Arg | Arginine | L-(+)-Arginine | L-Arg | L-Arginin | R | L-Arginine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A non-essential amino acid that is involved in the metabolic control of cell functions in nerve and brain tissue. It is biosynthesized from aspartic acid and ammonia by asparagine synthetase. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed)

Indication

Used for nutritional supplementation, also for treating dietary shortage or imbalance.

Mechanism of Action

Asparagine, a non-essential amino acid is important in the metabolism of toxic ammonia in the body through the action of asparagine synthase which attaches ammonia to aspartic acid in an amidation reaction. Asparagine is also used as a structural component in many proteins.

Active Ingredient/Synonyms

(2S)-2-amino-3-carbamoylpropanoic acid | (2S)-2,4-diamino-4-oxobutanoic acid | (S)-2-amino-3-carbamoylpropanoic acid | (S)-Asparagine | 2-Aminosuccinamic acid | alpha-aminosuccinamic acid | Asn | Asparagine | Aspartamic acid | L-2-aminosuccinamic acid | L-Asparagin | L-Asparagine | L-aspartic acid beta-amide | L-aspartic acid β-amide | N | α-aminosuccinamic acid | L-Asparagine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter.

Indication

There is no support for the claim that aspartates are exercise performance enhancers, i.e. ergogenic aids.

Mechanism of Action

There are also claims that L-aspartate has ergogenic effects, that it enhances performance in both prolonged exercise and short intensive exercise. It is hypothesized that L-aspartate, especially the potassium magnesium aspartate salt, spares stores of muscle glycogen and/or promotes a faster rate of glycogen resynthesis during exercise. It has also been hypothesized that L-aspartate can enhance short intensive exercise by serving as a substrate for energy production in the Krebs cycle and for stimulating the purine nucleotide cycle.

Pharmacokinetics

Absorption
Absorbed from the small intestine by an active transport process
Distribution
Metabolism
Elimination

Toxicity

Mild gastrointestinal side effects including diarrhea. LD50 (rat) > 5,000 mg/kg.

Active Ingredient/Synonyms

(S)-2-aminobutanedioic acid | (S)-2-aminosuccinic acid | 2-Aminosuccinic acid | Asp | Aspartic acid | D | L-Asp | L-Asparaginsaeure | L-Asparaginsäure | L-Aspartate | L-Aspartic acid | L-Aspartic Acid |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. An oral formulation of L-glutamine was approved by the FDA in July 2017 for use in sickle cell disease [L892]. This oral formulation is marketed under the tradename Endari by Emmaus Medical.

Indication

Used for nutritional supplementation, also for treating dietary shortage or imbalance. Used to reduce the acute complications of sickle cell disease in adult and pediatric patients 5 years of age and older [FDA Label].

Mechanism of Action

Supplemental L-glutamine's possible immunomodulatory role may be accounted for in a number of ways. L-glutamine appears to play a major role in protecting the integrity of the gastrointestinal tract and, in particular, the large intestine. During catabolic states, the integrity of the intestinal mucosa may be compromised with consequent increased intestinal permeability and translocation of Gram-negative bacteria from the large intestine into the body. The demand for L-glutamine by the intestine, as well as by cells such as lymphocytes, appears to be much greater than that supplied by skeletal muscle, the major storage tissue for L-glutamine. L-glutamine is the preferred respiratory fuel for enterocytes, colonocytes and lymphocytes. Therefore, supplying supplemental L-glutamine under these conditions may do a number of things. For one, it may reverse the catabolic state by sparing skeletal muscle L-glutamine. It also may inhibit translocation of Gram-negative bacteria from the large intestine. L-glutamine helps maintain secretory IgA, which functions primarily by preventing the attachment of bacteria to mucosal cells. L-glutamine appears to be required to support the proliferation of mitogen-stimulated lymphocytes, as well as the production of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma). It is also required for the maintenance of lymphokine-activated killer cells (LAK). L-glutamine can enhance phagocytosis by neutrophils and monocytes. It can lead to an increased synthesis of glutathione in the intestine, which may also play a role in maintaining the integrity of the intestinal mucosa by ameliorating oxidative stress. The exact mechanism of the possible immunomodulatory action of supplemental L-glutamine, however, remains unclear. It is conceivable that the major effect of L-glutamine occurs at the level of the intestine. Perhaps enteral L-glutamine acts directly on intestine-associated lymphoid tissue and stimulates overall immune function by that mechanism, without passing beyond the splanchnic bed. The exact mechanism of L-glutamine's effect on NAD redox potential is unknown but is thought to involve increased amounts of reduced glutathione made available by glutamine supplementation [FDA Label]. This improvement in redox potential reduces the amount of oxidative damage which sickle red blood cells are more susceptible to. The reduction in cellular damage is thought to reduce chronic hemolysis and vaso-occlusive events.

Pharmacokinetics

Absorption
Absorption is efficient and occurs by an active transport mechanism. Tmax is 30 minutes after a single dose [FDA Label]. Absorption kinetics following multiple doses has not yet been determined.
Distribution
Volume of distribution is 200 mL/kg after intravenous bolus dose [FDA Label].
Metabolism
Exogenous L-glutamine likely follows the same metabolic pathways as endogenous L-glutamine which is involved in the formation of glutamate, proteins, nucleotides, and amino acid sugars [FDA Label].
Elimination

Toxicity

Doses of L-glutamine up to 21 grams daily appear to be well tolerated. Reported adverse reactions are mainly gastrointestinal and not common. They include constipation and bloating. There is one older report of two hypomanic patients whose manic symptoms were exacerbated following the use of 2 to 4 grams daily of L-glutamine. The symptoms resolved when the L-glutamine was stopped. These patients were not rechallenged, nor are there any other reports of this nature. The most common adverse effects observed in clinical trials of Endari were constipation (21%), nausea (19%), headache (18%), abdominal pain (17%), cough (16%), extremity pain (13%), back pain (12%), and chest pain (12%) [FDA Label].

Active Ingredient/Synonyms

(2S)-2-amino-4-carbamoylbutanoic acid | (2S)-2,5-diamino-5-oxopentanoic acid | (S)-2,5-diamino-5-oxopentanoic acid | Glutamic acid 5-amide | Glutamic acid amide | Glutamine | L-(+)-glutamine | L-2-aminoglutaramic acid | L-glutamic acid γ-amide | L-Glutamin | L-Glutaminsäure-5-amid | Levoglutamide | Q | L-Glutamine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter.

Indication

Supplemental glycine may have antispastic activity. Very early findings suggest it may also have antipsychotic activity as well as antioxidant and anti-inflammatory activities.

Mechanism of Action

In the CNS, there exist strychnine-sensitive glycine binding sites as well as strychnine-insensitive glycine binding sites. The strychnine-insensitive glycine-binding site is located on the NMDA receptor complex. The strychnine-sensitive glycine receptor complex is comprised of a chloride channel and is a member of the ligand-gated ion channel superfamily. The putative antispastic activity of supplemental glycine could be mediated by glycine's binding to strychnine-sensitive binding sites in the spinal cord. This would result in increased chloride conductance and consequent enhancement of inhibitory neurotransmission. The ability of glycine to potentiate NMDA receptor-mediated neurotransmission raised the possibility of its use in the management of neuroleptic-resistant negative symptoms in schizophrenia.
Animal studies indicate that supplemental glycine protects against endotoxin-induced lethality, hypoxia-reperfusion injury after liver transplantation, and D-galactosamine-mediated liver injury. Neutrophils are thought to participate in these pathologic processes via invasion of tissue and releasing such reactive oxygen species as superoxide. In vitro studies have shown that neutrophils contain a glycine-gated chloride channel that can attenuate increases in intracellular calcium and diminsh neutrophil oxidant production. This research is ealy-stage, but suggests that supplementary glycine may turn out to be useful in processes where neutrophil infiltration contributes to toxicity, such as ARDS.

Pharmacokinetics

Absorption
Absorbed from the small intestine via an active transport mechanism.
Distribution
Metabolism
Hepatic
Elimination

Toxicity

ORL-RAT LD50 7930 mg/kg, SCU-RAT LD50 5200 mg/kg, IVN-RAT LD50 2600 mg/kg, ORL-MUS LD50 4920 mg/kg; Doses of 1 gram daily are very well tolerated. Mild gastrointestinal symptoms are infrequently noted. In one study doses of 90 grams daily were also well tole.

Active Ingredient/Synonyms

Aminoacetic acid | Aminoessigsäure | Aminoethanoic acid | Gly | Glycin | Glycocoll | Glykokoll | Glyzin | Leimzucker | Glycine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An essential amino acid that is required for the production of histamine.

Indication

The actions of supplemental L-histidine are entirely unclear. It may have some immunomodulatory as well as antioxidant activity. L-histidine may be indicated for use in some with rheumatoid arthritis. It is not indicated for treatment of anemia or uremia or for lowering serum cholesterol.

Mechanism of Action

Since the actions of supplemental L-histidine are unclear, any postulated mechanism is entirely speculative. However, some facts are known about L-histidine and some of its metabolites, such as histamine and trans-urocanic acid, which suggest that supplemental L-histidine may one day be shown to have immunomodulatory and/or antioxidant activities. Low free histidine has been found in the serum of some rheumatoid arthritis patients. Serum concentrations of other amino acids have been found to be normal in these patients. L-histidine is an excellent chelating agent for such metals as copper, iron and zinc. Copper and iron participate in a reaction (Fenton reaction) that generates potent reactive oxygen species that could be destructive to tissues, including joints.
L-histidine is the obligate precursor of histamine, which is produced via the decarboxylation of the amino acid. In experimental animals, tissue histamine levels increase as the amount of dietary L-histidine increases. It is likely that this would be the case in humans as well. Histamine is known to possess immunomodulatory and antioxidant activity. Suppressor T cells have H2 receptors, and histamine activates them. Promotion of suppressor T cell activity could be beneficial in rheumatoid arthritis. Further, histamine has been shown to down-regulate the production of reactive oxygen species in phagocytic cells, such as monocytes, by binding to the H2 receptors on these cells. Decreased reactive oxygen species production by phagocytes could play antioxidant, anti-inflammatory and immunomodulatory roles in such diseases as rheumatoid arthritis.
This latter mechanism is the rationale for the use of histamine itself in several clinical trials studying histamine for the treatment of certain types of cancer and viral diseases. In these trials, down-regulation by histamine of reactive oxygen species formation appears to inhibit the suppression of natural killer (NK) cells and cytotoxic T lymphocytes, allowing these cells to be more effective in attacking cancer cells and virally infected cells.

Pharmacokinetics

Absorption
Absorbed from the small intestine via an active transport mechanism requiring the presence of sodium.
Distribution
Metabolism
Elimination

Toxicity

ORL-RAT LD50 > 15000 mg/kg, IPR-RAT LD50 > 8000 mg/kg, ORL-MUS LD50 > 15000 mg/kg, IVN-MUS LD50 > 2000 mg/kg; Mild gastrointestinal side effects.

Active Ingredient/Synonyms

(S)-4-(2-Amino-2-carboxyethyl)imidazole | (S)-a-Amino-1H-imidazole-4-propanoic acid | (S)-alpha-amino-1H-Imidazole-4-propanoic acid | (S)-alpha-Amino-1H-imidazole-4-propionic acid | (S)-α-amino-1H-Imidazole-4-propanoic acid | HIS | Histidina | L-(−)-histidine | L-Histidin | L-Histidine | Histidine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An essential branched-chain aliphatic amino acid found in many proteins. It is an isomer of leucine. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels. [PubChem]

Indication

The branched-chain amino acids may have antihepatic encephalopathy activity in some. They may also have anticatabolic and antitardive dyskinesia activity.

Mechanism of Action

(Applies to Valine, Leucine and Isoleucine)
This group of essential amino acids are identified as the branched-chain amino acids, BCAAs. Because this arrangement of carbon atoms cannot be made by humans, these amino acids are an essential element in the diet. The catabolism of all three compounds initiates in muscle and yields NADH and FADH2 which can be utilized for ATP generation. The catabolism of all three of these amino acids uses the same enzymes in the first two steps. The first step in each case is a transamination using a single BCAA aminotransferase, with a-ketoglutarate as amine acceptor. As a result, three different a-keto acids are produced and are oxidized using a common branched-chain a-keto acid dehydrogenase, yielding the three different CoA derivatives. Subsequently the metabolic pathways diverge, producing many intermediates.
The principal product from valine is propionylCoA, the glucogenic precursor of succinyl-CoA. Isoleucine catabolism terminates with production of acetylCoA and propionylCoA; thus isoleucine is both glucogenic and ketogenic. Leucine gives rise to acetylCoA and acetoacetylCoA, and is thus classified as strictly ketogenic.
There are a number of genetic diseases associated with faulty catabolism of the BCAAs. The most common defect is in the branched-chain a-keto acid dehydrogenase. Since there is only one dehydrogenase enzyme for all three amino acids, all three a-keto acids accumulate and are excreted in the urine. The disease is known as Maple syrup urine disease because of the characteristic odor of the urine in afflicted individuals. Mental retardation in these cases is extensive. Unfortunately, since these are essential amino acids, they cannot be heavily restricted in the diet; ultimately, the life of afflicted individuals is short and development is abnormal The main neurological problems are due to poor formation of myelin in the CNS.

Pharmacokinetics

Absorption
Absorbed from the small intestine by a sodium-dependent active-transport process
Distribution
Metabolism
Hepatic
Elimination

Toxicity

Symptoms of hypoglycemia, increased mortality in ALS patients taking large doses of BCAAs

Active Ingredient/Synonyms

(2S,3S)-2-Amino-3-methylpentanoic acid | 2-Amino-3-methylvaleric acid | alpha-amino-beta-methylvaleric acid | I | Ile | Isoleucine | L-Isoleucine | α-amino-β-methylvaleric acid | L-Isoleucine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An essential branched-chain amino acid important for hemoglobin formation. [PubChem]

Indication

Indicated to assist in the prevention of the breakdown of muscle proteins that sometimes occur after trauma or severe stress.

Mechanism of Action

This group of essential amino acids are identified as the branched-chain amino acids, BCAAs. Because this arrangement of carbon atoms cannot be made by humans, these amino acids are an essential element in the diet. The catabolism of all three compounds initiates in muscle and yields NADH and FADH2 which can be utilized for ATP generation. The catabolism of all three of these amino acids uses the same enzymes in the first two steps. The first step in each case is a transamination using a single BCAA aminotransferase, with a-ketoglutarate as amine acceptor. As a result, three different a-keto acids are produced and are oxidized using a common branched-chain a-keto acid dehydrogenase, yielding the three different CoA derivatives. Subsequently the metabolic pathways diverge, producing many intermediates. The principal product from valine is propionylCoA, the glucogenic precursor of succinyl-CoA. Isoleucine catabolism terminates with production of acetylCoA and propionylCoA; thus isoleucine is both glucogenic and ketogenic. Leucine gives rise to acetylCoA and acetoacetylCoA, and is thus classified as strictly ketogenic. There are a number of genetic diseases associated with faulty catabolism of the BCAAs. The most common defect is in the branched-chain a-keto acid dehydrogenase. Since there is only one dehydrogenase enzyme for all three amino acids, all three a-keto acids accumulate and are excreted in the urine. The disease is known as Maple syrup urine disease because of the characteristic odor of the urine in afflicted individuals. Mental retardation in these cases is extensive. Unfortunately, since these are essential amino acids, they cannot be heavily restricted in the diet; ultimately, the life of afflicted individuals is short and development is abnormal The main neurological problems are due to poor formation of myelin in the CNS.

Active Ingredient/Synonyms

(2S)-2-Amino-4-methylpentanoic acid | (2S)-alpha-2-Amino-4-methylvaleric acid | (2S)-alpha-Leucine | (S)-(+)-Leucine | (S)-Leucine | 2-Amino-4-methylvaleric acid | L | L-Leucin | L-Leuzin | Leu | Leucine | L-Leucine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

L-Lysine (abbreviated as Lys or K) is an α-amino acid with the chemical formula HO2CCH(NH2)(CH2)4NH2. This amino acid is an essential amino acid, which means that humans cannot synthesize it. Its codons are AAA and AAG. L-Lysine is a base, as are arginine and histidine. The ε-amino group often participates in hydrogen bonding and as a general base in catalysis. Common posttranslational modifications include methylation of the ε-amino group, giving methyl-, dimethyl-, and trimethyllysine. The latter occurs in calmodulin. Other posttranslational modifications include acetylation. Collagen contains hydroxylysine which is derived from lysine by lysyl hydroxylase. O-Glycosylation of lysine residues in the endoplasmic reticulum or Golgi apparatus is used to mark certain proteins for secretion from the cell.

Indication

Supplemental L-lysine has putative anti-herpes simplex virus activity. There is preliminary research suggesting that it may have some anti-osteoporotic activity.

Mechanism of Action

Proteins of the herpes simplex virus are rich in L-arginine, and tissue culture studies indicate an enhancing effect on viral replication when the amino acid ratio of L-arginine to L-lysine is high in the tissue culture media. When the ratio of L-lysine to L-arginine is high, viral replication and the cytopathogenicity of herpes simplex virus have been found to be inhibited. L-lysine may facilitate the absorption of calcium from the small intestine.

Pharmacokinetics

Absorption
Absorbed from the lumen of the small intestine into the enterocytes by an active transport process
Distribution
Metabolism
Hepatic
Elimination

Active Ingredient/Synonyms

(S)-2,6-diaminohexanoic acid | (S)-lysine | (S)-α,ε-diaminocaproic acid | 6-ammonio-L-norleucine | L-2,6-Diaminocaproic acid | L-lys | L-Lysin | LYS | Lysina | Lysine | Lysine acid | Lysinum | L-Lysine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

Magnesium acetate tetrahydrate is a hydrated form of anhydrous magnesium acetate salt with the chemical formula of Mg(CH3COO)2 • 4H2O. As a salt form of magnesium, magnesium acetate is one of the bioavailable forms of magnesium and forms a very water soluble compound. Magnesium is an essential element and second most abundant cation in the body that plays a key role in maintaining normal cellular function such as production of ATP and efficient enzyme activity. Magnesium acetate tetrahydrate can be used as an electrolyte supplementation or a reagent in molecular biology experiments.

Indication

Used as magnesium salf-containing laxatives to prevent constipation. It can bring synergistic effect to restore normal bowel function when using in combination with aluminum salts that induce bowel retention [T28]. Magnesium acetate tetrahydrate is used as a source of water and electrolytes when combined with dextrose and other salts to form intravenous infusions. This injection can be used for patients with carbohydrate or magnesium deficiency, insulin hypoglycemia, constipation or hypertension during pregnancy.

Mechanism of Action

Magnesium ions electrostatically stabilize the adenylyl cyclase complex and enhance its catalytic actions and production of cAMP. They also regulate the level of phosphorylation in various pathways by formation of transition state of phosphoryl transfer reaction by protein kinases and stabilize ATP binding to protein kinases via electrostatic interactions [A19416]. Many metabolic enzymes involved in glycolysis and Krebs cycle are magnesium-dependent. Magnesium-containing laxatives cause diarrhea through water retention and increased fecal mass that stimulates peristalsis. When used as an electrolyte supplementation, magnesium acetate tetrahydrate induces diuresis and metabolic alkalinizing effect. Magnesium ions enhance reactivity of arteries to vasoconstrictors, promotes vasoconstriction, and increases peripheral resistance, leading to increased blood pressure [A19412] through potential competition with calcium ions in the vascular system. Magnesium ions also regulate other ions entering and exiting the cell membrane by acting as a ligand in N-methyl-D-aspartate receptor.

Pharmacokinetics

Absorption
Intestinal absorption is achieved mainly through passive diffusion.
Distribution
Magnesium ions display approximate volume of distribution of 0.2 to 0.4 L/kg
Metabolism
Elimination

Toxicity

Predicted oral LD50 value is >2000mg/kg. In case of mild to moderate toxicity, it may cause irritation in case of skin or eye contact,and nausea or vomiting from ingestion and inhalation. In overdose, magnesium impairs neuromuscular transmission, manifested as weakness and hyporeflexia. Early manifestations of severe toxicity are lethargy, hyporeflexia, followed by weakness, paralysis, hypotension, ECG changes (prolonged PR and QRS intervals), CNS depression, seizures, and respiratory depression.

Active Ingredient/Synonyms

Acetic acid, magnesium salt, tetrahydrate | Magnesium diacetate tetrahydrate | Magnesium acetate tetrahydrate |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

Malic Acid has been used in trials studying the treatment of Xerostomia, Depression, and Hypertension.

Active Ingredient/Synonyms

Malic Acid | Malic Acid |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals.

Indication

Used for protein synthesis including the formation of SAMe, L-homocysteine, L-cysteine, taurine, and sulfate.

Mechanism of Action

The mechanism of the possible anti-hepatotoxic activity of L-methionine is not entirely clear. It is thought that metabolism of high doses of acetaminophen in the liver lead to decreased levels of hepatic glutathione and increased oxidative stress. L-methionine is a precursor to L-cysteine. L-cysteine itself may have antioxidant activity. L-cysteine is also a precursor to the antioxidant glutathione. Antioxidant activity of L-methionine and metabolites of L-methionine appear to account for its possible anti-hepatotoxic activity. Recent research suggests that methionine itself has free-radical scavenging activity by virtue of its sulfur, as well as its chelating ability.

Pharmacokinetics

Absorption
Absorbed from the lumen of the small intestine into the enterocytes by an active transport process.
Distribution
Metabolism
Hepatic
Elimination

Toxicity

Doses of L-methionine of up to 250 mg daily are generally well tolerated. Higher doses may cause nausea, vomiting and headache. Healthy adults taking 8 grams of L-methionine daily for four days were found to have reduced serum folate levels and leucocytosis. Healthy adults taking 13.9 grams of L-methionine daily for five days were found to have changes in serum pH and potassium and increased urinary calcium excretion. Schizophrenic patients given 10 to 20 grams of L-methionine daily for two weeks developed functional psychoses. Single doses of 8 grams precipitated encephalopathy in patients with cirrhosis.

Active Ingredient/Synonyms

(2S)-2-amino-4-(methylsulfanyl)butanoic acid | (S)-2-amino-4-(methylthio)butanoic acid | (S)-2-amino-4-(methylthio)butyric acid | (S)-methionine | L-(−)-methionine | L-a-Amino-g-methylthiobutyric acid | L-Methionin | L-Methionine | L-α-amino-γ-methylmercaptobutyric acid | M | Met | Methionine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

N-acetyltyrosine, also referred to as N-acetyl-L-tyrosine, is used in place of as a tyrosine precursor. [DB00135] is a non-essential amino acid with a polar side group. N-acetyltyrosine is administered as parenteral nutrition or intravenous infusion due to its enhanced solubility compared to tyrosine [A32652]. It is typically administered as a source of nutritional support where oral nutrition is inadequate or cannot be tolerated.

Indication

N-acetyltyrosine is indicated, in combination with several other amino acids and dextrose, as a peripherally administered source of nitrogen for nutritional support in patients with adequate stores of body fat in whom, for short periods, oral administration cannot be tolerated, is undesirable, or inadequate [FDA Label]. It is also indicated, with other amino acids, 5-10% dextrose, and fat emulsion, for parenteral nutrition to preserve protein and reduce catabolism in stress conditions where oral administration is inadequate [FDA Label]. When administered with other amino acids and concentrated dextrose, it is indicated for central vein infusion to prevent or reverse negative nitrogen balance in patients where the alimentary tract by the oral, gastrostomy, or jejestomy routes cannot or should not be used or in patients in which gastrointestinal absorption of protein is impaired, metabolic requirements for protein are substantially increased, or morbidity and mortality may be reduced by replacing amino acids lost from tissue breakdown [FDA Label]

Mechanism of Action

Used as a source of [DB00135]. See [DB00135] for more information on its role and pharmacology.

Active Ingredient/Synonyms

(+)-(2s)-2-(acetylamino)-3-(4-hydroxyphenyl)propanoic acid | (2s)-2-acetylamino-3-(4-hydroxyphenyl)propanoic acid | Acetyl tyrosine | L-N-acetyltyrosine | Melanowhite-A | N-acetyl-L-tyrosine | N-acetyl-tyrosine | N-acetyltyrosin | N-acetyltyrosine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

Ornithine is an amino acid produced in the urea cycle by the splitting off of urea from arginine. It is a central part of the urea cycle, which allows for the disposal of excess nitrogen. L-Ornithine is a precursor of citrulline and arginine.

Indication

Used for nutritional supplementation, also for treating dietary shortage or imbalance. It has been claimed that ornithine improves athletic performance, has anabolic effects, has wound-healing effects, and is immuno-enhancing.

Mechanism of Action

L-Ornithine is metabolised to L-arginine. L-arginine stimulates the pituitary release of growth hormone. Burns or other injuries affect the state of L-arginine in tissues throughout the body. As De novo synthesis of L-arginine during these conditions is usually not sufficient for normal immune function, nor for normal protein synthesis, L-ornithine may have immunomodulatory and wound-healing activities under these conditions (by virtue of its metabolism to L-arginine).

Pharmacokinetics

Absorption
Absorbed from the small intestine via a sodium-dependent active transport process
Distribution
Metabolism
Ornithine undergoes extensive metabolism in the liver to L-arginine, polyamines, and proline, and several other metabolites.
Elimination

Toxicity

Oral, rat LD50 = 10000 mg/kg

Active Ingredient/Synonyms

(S)-2,5-Diaminopentanoate | (S)-2,5-Diaminopentanoic acid | (S)-2,5-diaminovaleric acid | (S)-alpha,delta-Diaminovaleric acid | (S)-ornithine | (S)-α,δ-diaminovaleric acid | L-Ornithine | levo-ornithine | Ornithine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An essential aromatic amino acid that is a precursor of melanin; dopamine; noradrenalin (norepinephrine), and thyroxine.

Indication

L-phenylalanine may be helpful in some with depression. It may also be useful in the treatment of vitiligo. There is some evidence that L-phenylalanine may exacerbate tardive dyskinesia in some schizophrenic patients and in some who have used neuroleptic drugs.

Mechanism of Action

The mechanism of L-phenylalanine's putative antidepressant activity may be accounted for by its precursor role in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain norepinephrine and dopamine levels are thought to be associated with antidepressant effects.
The mechanism of L-phenylalanine's possible antivitiligo activity is not well understood. It is thought that L-phenylalanine may stimulate the production of melanin in the affected skin

Pharmacokinetics

Absorption
Absorbed from the small intestine by a sodium dependent active transport process.
Distribution
Metabolism
Hepatic. L-phenylalanine that is not metabolized in the liver is distributed via the systemic circulation to the various tissues of the body, where it undergoes metabolic reactions similar to those that take place in the liver.
Elimination

Toxicity

L-phenylalanine will exacerbate symptoms of phenylketonuria if used by phenylketonurics. L-phenylalanine was reported to exacerbate tardive dyskinesia when used by some with schizophrenia.

Active Ingredient/Synonyms

(S)-2-Amino-3-phenylpropionic acid | (S)-alpha-Amino-beta-phenylpropionic acid | 3-phenyl-L-alanine | beta-Phenyl-L-alanine | F | Phe | Phenylalanine | β-phenyl-L-alanine | L-Phenylalanine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.



Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

L-Proline is one of the twenty amino acids used in living organisms as the building blocks of proteins. Proline is sometimes called an imino acid, although the IUPAC definition of an imine requires a carbon-nitrogen double bond. Proline is a non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons.

Indication

L-Proline is extremely important for the proper functioning of joints and tendons and also helps maintain and strengthen heart muscles.

Mechanism of Action

Glycogenic, by L-Proline oxidase in the kidney, it is ring-opened and is oxidized to form L-Glutamic acid. L-Ornithine and L-Glutamic acid are converted to L-Proline via L-Glutamic acid-gamma-semialdehyde. It is contained abundantly in collagen, and is intimately involved in the function of arthrosis and chordae.

Active Ingredient/Synonyms

(-)-2-Pyrrolidinecarboxylic acid | (−)-(S)-proline | (−)-2-pyrrolidinecarboxylic acid | (−)-proline | (2S)-pyrrolidine-2-carboxylic acid | (S)-2-Carboxypyrrolidine | (S)-2-Pyrrolidinecarboxylic acid | (S)-pyrrolidine-2-carboxylic acid | 2-Pyrrolidinecarboxylic acid | L-(−)-proline | L-alpha-pyrrolidinecarboxylic acid | L-Prolin | L-pyrrolidine-2-carboxylic acid | L-α-pyrrolidinecarboxylic acid | P | Prolina | Proline | Prolinum | L-Proline |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines; pyrimidines; and other amino acids.

Indication

Used as a natural moisturizing agent in some cosmetics and skin care products.

Mechanism of Action

L-Serine plays a role in cell growth and development (cellular proliferation). The conversion of L-serine to glycine by serine hydroxymethyltransferase results in the formation of the one-carbon units necessary for the synthesis of the purine bases, adenine and guanine. These bases when linked to the phosphate ester of pentose sugars are essential components of DNA and RNA and the end products of energy producing metabolic pathways, ATP and GTP. In addition, L-serine conversion to glycine via this same enzyme provides the one-carbon units necessary for production of the pyrimidine nucleotide, deoxythymidine monophosphate, also an essential component of DNA.

Active Ingredient/Synonyms

(S)-2-Amino-3-hydroxypropanoic acid | (S)-Serine | alpha-Amino-beta-hydroxypropionic acid | beta-Hydroxyalanine | L-Serine | Ser | Serina | Serinum | Serine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

Sodium Acetate is chemically designated CH3COONa, a hygroscopic powder very soluble in water. Sodium acetate could be used as additives in food, industry, concrete manufacture, heating pads and in buffer solutions. Medically, sodium acetate is important component as an electrolyte replenisher when given intravenously. It is mainly indicated to correct sodium levels in hyponatremic patients. It can be used also in metabolic acidosis and for urine alkalinization.

Indication

Injection, USP 40 mEq is indicated as a source of sodium, for addition to large volume intravenous fluids to prevent or correct hyponatremia in patients with restricted or no oral intake. It is also useful as an additive for preparing specific intravenous fluid formulas when the needs of the patient cannot be met by standard electrolyte or nutrient solutions. Sodium acetate and other bicarbonate precursors are alkalinising agents, and can be used to correct metabolic acidosis, or for alkalinisation of the urine.

Mechanism of Action

It works as a source of sodium ions especially in cases of hyponatremic patients. Sodium has a primary role in regulating extracellular fluid volume. It controls water distribution, fluid and electrolyte balance and the osmotic pressure of body fluids. Sodium is also involved in nerve conduction, muscle contraction, acid-base balance and cell nutrient uptake.

Pharmacokinetics

Absorption
It is readily available in the circulation after IV administration.
Distribution
Metabolism
In liver, sodium acetate is being metabolized into bicarbonate. To form bicarbonate, acetate is slowly hydrolyzed to carbon dioxide and water, which are then converted to bicarbonate by the addition of a hydrogen ion.
Elimination

Toxicity

LD50: 25956 mg/kg (Rat.)

Active Ingredient/Synonyms

acetic acid, sodium salt | Acetic acid, sodium salt (1:1) | anhydrous sodium acetate | Natriumazetat | Sodium acetate anhydrous | Sodium acetate, anhydrous | Sodium acetate,anhydrous | Sodium acetate |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.



Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

Sodium hydroxide is also known as _lye_ or _soda_ , or _caustic soda_ [L1971]. At room temperature, sodium hydroxide is a white crystalline odorless solid that absorbs moisture from the air. It is a synthetically manufactured substance. When dissolved in water or neutralized with acid it releases substantial amounts of heat, which may prove sufficient to ignite combustible materials. Sodium hydroxide is highly corrosive [L1965]. Sodium hydroxide is generally used as a solid or a diluted in a 50% solution. This chemical is used to manufacture soaps, rayon, paper, explosives, dyestuffs, and petroleum products [L1965]. It is also used in processing cotton fabric, laundering and bleaching, metal cleaning and processing, oxide coating, electroplating, and electrolytic extracting. It is commonly found in commercial drain/ oven cleaners [L1965]. According to the the FDA, sodium hydroxide is considered a direct food recognized as safe, where it serves as a pH control agent and follows good manufacturing guidelines [L1967]. Interestingly, sodium hydroxide has been studied for its use in the treatment of prion disease (as occurs in mad cow disease and kuru). The use of this compound has been shown to effectively reduce prion levels in an in vitro inactivation assay [A32334].

Indication

Used to destroy or kill the nail matrix (matrixectomies) [L1968].

Mechanism of Action

Because of its high-level alkalinity, sodium hydroxide in aqueous solution directly causes bond breakage in proteins (especially disulfide bridges). Hair and fingernails are found to be dissolved after 20 hours of direct contact with sodium hydroxide at pH values higher than 9.2 [L1975]. Sodium hydroxide has depilatory effects which have been described after accidental contact with solutions in the workplace. The breakage of bonds in proteins may lead to severe necrosis to the application site. The level of corrosion depends on the period of contact with the tissue, and on the concentration of sodium hydroxide [L1975].

Pharmacokinetics

Absorption
There are no quantitative data for the absorption of sodium hydroxide through the skin. Solutions which contain 50 % sodium hydroxide have been shown to be corrosive and lethal when applied dermally to mice [L1977].
Distribution
Metabolism
Elimination

Toxicity

Human poisoning cases indicate that a dose of 10 grams orally is fatal [L1970]. Sodium hydroxide is toxic by oral ingestion [L1965]. Sodium hydroxide is corrosive to all tissues. Concentrated vapors lead to serious damage to the eyes and respiratory system. Oral ingestion of sodium hydroxide, which occurs frequently in children, causes severe tissue necrosis, with stricture formation of the esophagus, often resulting in death. Contact with the skin may result in contact dermatitis, hair loss, as well as necrosis due to severe irritation [L1972]. Increased incidence of esophageal carcinoma after severe intoxication with sodium hydroxide has been reported in man. In animal studies, long-term dermal contact with substances leading to pH changes in the skin causes the development of tumors, as a result of severe tissue irritation and reparative cell growth [L1977]. Mutagenic for mammalian somatic cells. May cause damage to the following organs: mucous membranes, upper respiratory tract, skin, eyes [MSDS]. Tumors are not to be expected if the effects of irritation are prevented [L1977]. To date, there are no relevant studies of the prenatal toxic effects of sodium hydroxide [L1977].

Active Ingredient/Synonyms

caustic soda | lye | soda lye | sodium hydrate | white caustic | Sodium hydroxide |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [PubChem]

Indication

L-Threonine makes up collagen, elastin, and enamel protein. It aids proper fat metabolism in the liver, helps the digestive and intestinal tracts function more smoothly, and assists in metabolism and assimilation.

Mechanism of Action

L-Threonine is a precursor to the amino acids glycine and serine. It acts as a lipotropic in controlling fat build-up in the liver. May help combat mental illness and may be very useful in indigestion and intestinal malfunctions. Also, threonine prevents excessive liver fat. Nutrients are more readily absorbed when threonine is present.

Active Ingredient/Synonyms

(2S,3R)-(-)-Threonine | (2S)-threonine | 2-Amino-3-hydroxybutyric acid | L-(-)-Threonine | L-2-Amino-3-hydroxybutyric acid | L-alpha-amino-beta-hydroxybutyric acid | L-Threonin | L-α-amino-β-hydroxybutyric acid | Thr | Threonine | L-Threonine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor of indole alkaloids in plants. It is a precursor of serotonin (hence its use as an antidepressant and sleep aid). It can be a precursor to niacin, albeit inefficiently, in mammals.

Indication

Tryptophan may be useful in increasing serotonin production, promoting healthy sleep, managing depression by enhancing mental and emotional well-being, managing pain tolerance, and managing weight.

Mechanism of Action

A number of important side reactions occur during the catabolism of tryptophan on the pathway to acetoacetate. The first enzyme of the catabolic pathway is an iron porphyrin oxygenase that opens the indole ring. The latter enzyme is highly inducible, its concentration rising almost 10-fold on a diet high in tryptophan. Kynurenine is the first key branch point intermediate in the pathway. Kynurenine undergoes deamniation in a standard transamination reaction yielding kynurenic acid. Kynurenic acid and metabolites have been shown to act as antiexcitotoxics and anticonvulsives. A second side branch reaction produces anthranilic acid plus alanine. Another equivalent of alanine is produced further along the main catabolic pathway, and it is the production of these alanine residues that allows tryptophan to be classified among the glucogenic and ketogenic amino acids. The second important branch point converts kynurenine into 2-amino-3-carboxymuconic semialdehyde, which has two fates. The main flow of carbon elements from this intermediate is to glutarate. An important side reaction in liver is a transamination and several rearrangements to produce limited amounts of nicotinic acid, which leads to production of a small amount of NAD+ and NADP+.

Toxicity

Oral rat LD50: > 16 gm/kg. Investigated as a tumorigen, mutagen, reproductive effector. Symptoms of overdose include agitation, confusion, diarrhea, fever, overactive reflexes, poor coordination, restlessness, shivering, sweating, talking or acting with excitement you cannot control, trembling or shaking, twitching, and vomiting.

Active Ingredient/Synonyms

(2S)-2-amino-3-(1H-indol-3-yl)propanoic acid | (S)-alpha-Amino-beta-(3-indolyl)-propionic acid | (S)-Tryptophan | (S)-α-amino-1H-indole-3-propanoic acid | L-(-)-Tryptophan | L-(−)-tryptophan | L-β-3-indolylalanine | Trp | Tryptophan | W | L-Tryptophan |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine; thyroid hormones; and melanin.

Indication

Tyrosine is claimed to act as an effective antidepressant, however results are mixed. Tyrosine has also been claimed to reduce stress and combat narcolepsy and chronic fatigue, however these claims have been refuted by some studies.

Mechanism of Action

Tyrosine is produced in cells by hydroxylating the essential amino acid phenylalanine. This relationship is much like that between cysteine and methionine. Half of the phenylalanine required goes into the production of tyrosine; if the diet is rich in tyrosine itself, the requirements for phenylalanine are reduced by about 50%. The mechanism of L-tyrosine's antidepressant activity can be accounted for by the precursor role of L-tyrosine in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain norepinephrine and dopamine levels are thought to be associated with antidepressant effects.

Pharmacokinetics

Absorption
L-tyrosine is absorbed from the small intestine by a sodium-dependent active transport process.
Distribution
Metabolism
In the liver, L-tyrosine is involved in a number of biochemical reactions, including protein synthesis and oxidative catabolic reactions. L-tyrosine that is not metabolized in the liver is distributed via the systemic circulation to the various tissues of the body.
Elimination

Toxicity

L-Tyrosine has very low toxicity. There have been very few reports of toxicity. LD50 (oral, rat) > 5110 mg/kg.

Active Ingredient/Synonyms

(−)-α-amino-p-hydroxyhydrocinnamic acid | (2S)-2-amino-3-(4-hydroxyphenyl)propanoic acid | (S)-(-)-Tyrosine | (S)-2-Amino-3-(p-hydroxyphenyl)propionic acid | (S)-3-(p-Hydroxyphenyl)alanine | (S)-alpha-amino-4-Hydroxybenzenepropanoic acid | (S)-Tyrosine | (S)-α-amino-4-hydroxybenzenepropanoic acid | 4-hydroxy-L-phenylalanine | L-Tyrosin | Tyr | Tyrosine | Y | L-Tyrosine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. [PubChem]

Indication

Promotes mental vigor, muscle coordination, and calm emotions. May also be of use in a minority of patients with hepatic encephalopathy and in some with phenylketonuria.

Mechanism of Action

(Applies to Valine, Leucine and Isoleucine)
This group of essential amino acids are identified as the branched-chain amino acids, BCAAs. Because this arrangement of carbon atoms cannot be made by humans, these amino acids are an essential element in the diet. The catabolism of all three compounds initiates in muscle and yields NADH and FADH2 which can be utilized for ATP generation. The catabolism of all three of these amino acids uses the same enzymes in the first two steps. The first step in each case is a transamination using a single BCAA aminotransferase, with a-ketoglutarate as amine acceptor. As a result, three different a-keto acids are produced and are oxidized using a common branched-chain a-keto acid dehydrogenase, yielding the three different CoA derivatives. Subsequently the metabolic pathways diverge, producing many intermediates.
The principal product from valine is propionylCoA, the glucogenic precursor of succinyl-CoA. Isoleucine catabolism terminates with production of acetylCoA and propionylCoA; thus isoleucine is both glucogenic and ketogenic. Leucine gives rise to acetylCoA and acetoacetylCoA, and is thus classified as strictly ketogenic.
There are a number of genetic diseases associated with faulty catabolism of the BCAAs. The most common defect is in the branched-chain a-keto acid dehydrogenase. Since there is only one dehydrogenase enzyme for all three amino acids, all three a-keto acids accumulate and are excreted in the urine. The disease is known as Maple syrup urine disease because of the characteristic odor of the urine in afflicted individuals. Mental retardation in these cases is extensive. Unfortunately, since these are essential amino acids, they cannot be heavily restricted in the diet; ultimately, the life of afflicted individuals is short and development is abnormal The main neurological problems are due to poor formation of myelin in the CNS.

Pharmacokinetics

Absorption
Absorbed from the small intestine by a sodium-dependent active-transport process.
Distribution
Metabolism
Hepatic
Elimination

Toxicity

Symptoms of hypoglycemia, increased mortality in ALS patients taking large doses of BCAAs.

Active Ingredient/Synonyms

(2S)-2-Amino-3-methylbutanoic acid | (S)-Valine | 2-Amino-3-methylbutyric acid | L-(+)-alpha-Aminoisovaleric acid | L-alpha-Amino-beta-methylbutyric acid | Val | Valine | L-Valine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.

References

  1. Health Science Authority of Singapore - Reclassified POM
  2. Drugbank

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